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In New Zealand, age standardised hospitalisation rates for ischaemic heart disease (IHD) and its most important clinical manifestation, myocardial infarction (MI), have steadily decreased over the last 10 years.1,2 However, despite this good news, Māori, Pacific and South Asian peoples continue to have higher IHD hospitalisation rates, and Māori and Pacific peoples have higher IHD mortality rates compared to European.3,4 The reasons for these differences are complex and incompletely understood. The All New Zealand Acute Coronary Syndrome Quality Improvement (ANZACS-QI) registry collects a comprehensive dataset for all patients presenting to New Zealand public hospitals with an ACS (acute coronary syndrome) who undergo investigation with a coronary angiogram. The ANZACS-QI registry is linked via an encrypted identifier to national administrative datasets to augment data and to track patient outcomes.5 Our aim was to use this contemporary real-world national cohort, in patients presenting with their first MI, to better understand the extent to which differences in the clinical presentation, cardiovascular disease (CVD) risk factors, comorbidity and in-hospital treatment explain the divergence in outcomes between ethnic groups.

Methods

Cohort

New Zealand residents aged ≥20 years hospitalised with their first MI between 1 January 2014 and 31 December 2017 and who underwent coronary angiography were identified from the ANZACS-QI registry.

The ANZACS-QI registry is a web-based electronic database that captures a mandatory dataset which includes patient demographics, admission ACS risk stratification, cardiovascular risk factors, investigations and management, inpatient outcomes and medications prescribed at discharge. The patients captured in the registry are linked via an encrypted unique National Health Identifier (NHI) to national hospitalisation, mortality and pharmaceutical dispensing national datasets. Details regarding the ANZACS-QI programme, registry data collection and linkage to national datasets have been previously reported.5 Data collected in ANZACS-QI has been previously described in detail.5,6 The registry is subject to monthly auditing to ensure capture of >95% of all patients admitted with suspected ACS who are investigated with coronary angiography, and annual audit to check the accuracy of data entry.

Data and definitions

MI was defined according to the contemporary universal definition.7Sociodemographic variables and residency status were derived from the linked national dataset. For patients in whom more than one ethnic group was recorded, ethnicity was prioritised, in accordance with health sector protocols, in the following order: indigenous Māori, Pacific, Indian, Other Asian and European/other.8 European /other included all those identifying as European as well as a small number of people from the Middle East, Africa and Latin America. Fijian Indian people are categorised as ‘Indian’, as opposed to ‘Pacific’. Socioeconomic deprivation was assessed by the NZDep13 score, a census-based small area 10-point index of deprivation based on the person’s domicile.9 Clinical presentation variables from the ANZACS-QI registry included type of MI (ST-elevation MI (STEMI) or non ST-elevation MI (NSTEMI)), known prior congestive heart failure (CHF), components of the Global Registry of Acute Coronary Events (GRACE) in-hospital mortality risk score (including Killip class, admission heart rate and blood pressure, cardiac arrest on admission, electrocardiogram findings, troponin level, admission creatinine),10 left ventricular ejection fraction (LVEF) assessed by transthoracic echo or left ventriculogram, coronary artery disease extent on angiography. Killip class was divided into those without (Class I) and with acute heart failure (Classes II–IV).11 Left ventricular ejection fraction (LVEF) assessment was classified into normal (≥50%), mild impairment (40–49%), moderate to severe impairment (<40%), and not quantified further. Coronary artery disease (CAD) extent was defined by the findings at angiography and were grouped into one of the following: (i) no significant CAD, defined as the absence of any stenosis with ≥50% diameter loss in the epicardial vessels, (ii) significant (≥50% stenosis) single vessel coronary disease, (iii) significant (≥50% stenosis) double vessel coronary artery disease, (iv) significant three-vessel disease and/or left main stem (LMS) disease ≥50%. Due to the use of multiple different Troponin assays across New Zealand, the peak troponin values for each patient were stratified into quintiles for each separate assay. eGFR at admission was calculated using the CKD-EPI equation in ml/min and reported in CKD stages one (>90ml/min), two (60–90ml/min), three (30–60ml/min), four (15–30ml/min) and five (<15ml/min).12 Cardiovascular disease risk factors, history and comorbidity variables included: smoking status defined as current, ex-smoker or never smoker, diabetes mellitus, hypertension (HT), low-density lipoprotein (LDL) and total cholesterol (TC) to high-density lipoprotein (HDL) ratio, body mass index (BMI), history of chronic obstructive pulmonary disease (COPD), history of congestive heart failure (CHF) and prior atherosclerotic CVD—defined as a prior diagnosis or history of transient ischaemic attack or ischaemic stroke, peripheral vascular disease or radiological evidence of vascular disease.

Investigation and management variables were coronary revascularisation by percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). Discharge medications were: aspirin, P2Y12 inhibitor (clopidogrel or ticagrelor), statins, angiotensin converting enzyme inhibitors (ACEIs) and beta-blockers. Dual anti-platelet therapy (DAPT) was aspirin plus a P2Y12 inhibitor.

Outcomes

All-cause mortality up to one year after the index admission date was obtained by linkage to the national mortality database.

Statistical analysis

Categorical variables were summarised as frequency and percentage and continuous variables as mean and standard deviation (SD). Comparisons across ethnic groups were made using Pearson’s chi-square test, one-way ANOVA or a Kruskall Wallis test, as appropriate. Multivariable Cox regression models were used to estimate the hazard ratio of each ethnicity compared to European/other for all-cause mortality and 30-day post admission all-cause mortality outcomes in four models: Model One—unadjusted ; Model Two—adjusted by age and sex ; Model Three—adjusted by age, sex, worst Killip class, EF categories, CAD extent, troponin quintile, cardiac arrest, MI sub-type, prior CHF, prior CVD, smoking, diabetes, TC:HDL, hypertension, eGFR, COPD; Model Four—Model Three variables plus coronary revascularisation (PCI or CABG), medications (statin, ACEI/ARB, beta blocker, DAPT) at discharge. Cumulative mortality plots stratify time to death by ethnic group.

The proportional hazards assumptions were tested by plotting the standardised score residuals over time. The assumptions were met. All tests of statistical significance were two tailed and a p-value <0.05 was considered statistically significant. Data were analysed using SAS version 9.4 (SAS Institute, Cary, NC), and cumulative mortality plots were created using RStudio version 1.2.1335.

Ethical approval

This research was performed as part of the VIEW-ANZACS-QI research programme. Ethics approval was obtained from the Northern Region Ethics Committee (AKY/03/12/314) and Multi-Region Ethics Committee (MEC/01/19/EXP and MEC/11/EXP/078).

Results

There were 17,404 patients with a first ever MI. European/other comprised 76% of the population, Māori 11.5%, Pacific 5.1%, Indian 4.3% and other Asian 2.9%. Patient demographics are shown in Table 1. Two thirds of patients were men and the mean age was 64 years. Māori, Pacific and Indian patients presented at a younger age (mean age 58–59 years) compared with other Asian and European/other patients (mean age 61 and 66 years respectively). Over half (55%) of Māori, Pacific and Indian patients were admitted with their first MI before age 60 years, compared with 35% of other Asian and 29% of European/other patients.

Table 1: Baseline demographics.

All values are number of patients and frequency (%) unless otherwise specified.

Clinical presentation (Table 2)

Māori patients were the most likely to present with cardiac arrest. Māori and Pacific patients were 1.5 to 2 times more likely to have acute heart failure than European/others (17%, 19.5%, 11.5%, respectively), while 26% of Pacific patients and 21% of Māori patients had moderate-severe LV impairment, but only 15% of European/others. This was despite a similar proportion of each ethnic group having myocardial necrosis in the highest quintile (based on troponin levels). At coronary angiography nearly half of all patients had obstructive disease in more than one coronary artery. Pacific and Indian patients had more severe three-vessel disease and/or left main coronary artery disease (38% and 33%) than Māori, Other Asian or European/other patients (25%, 26.5% and 26%). The proportion of STEMIs was similar for Māori, Indian and European/other groups but lower for Pacific patients and slightly higher for Other Asian patients. While only 3.1% of the overall cohort had advanced (Stage 4 or 5) CKD, Pacific (11.4%) and Māori (5.8%) were markedly over-represented, with 4.2% of Indian people also affected. In contrast, only 2% of European/other patients had advanced CKD.

Table 2: Clinical presentation.

Values are number of patients and frequency (%) unless otherwise specified. CAD, coronary artery disease; NSTEMI, non-ST segment elevation myocardial infarction; STEMI, ST segment elevation myocardial infarction; eGFR, estimated glomerular filtration rate.

Atherosclerotic CVD risk factors and medical history (Table 3)

Nearly half of Pacific and Indian patients had diabetes, 30% of Māori, 29% of Other Asian and 16% of European/others. Of those with BMI recorded, 33.8% of Maori and 44.2% of Pacific compared to 23.7% of European/others had a BMI in the obese range (Indian 18.4% and Other Asian 9.5%). Mean TC:HDL was highest in Māori and lowest in Other Asian patients with intermediate levels in other groups. Nearly half of Māori and a third of Pacific patients were current smokers compared with less than a quarter of other ethnic groups. Māori patients, correspondingly, were more likely to have COPD. Māori and Pacific patients were twice as likely to have a diagnosis of prior CHF compared with non-Māori/non-Pacific.

Table 3: Cardiovascular risk factors.

Values are number of patients and frequency (%) unless otherwise specified. BMI, body mass index; TC:HDL, total cholesterol to high-density lipoprotein ratio; COPD, chronic obstructive pulmonary disease; CVD, cardiovascular disease; CHF, congestive heart failure.

Treatment (Table 4)

Overall, 74.5 % of patients underwent coronary revascularisation: 61.6% with PCI and 12.9% by CABG. Revascularisation was highest for Other Asian patients (77%) followed by European/others (75%), Indian (72%), Pacific (70.5%) and Māori (67%). Compared to European/other patients, Māori, Pacific and Indian patients had higher rates of CABG and lower rates of PCI consistent with their higher prevalence of diabetes and among Pacific and Indian patients, diffuse coronary artery disease. Indian people were equally likely to receive PCI as European/other patients. However, Māori and Pacific patients were less likely to receive PCI and less likely overall to receive coronary intervention. There was a high level of prescription of aspirin and statin medication at discharge with only minor ethnic differences. Use of a P2Y12 anti-platelet agent was higher in European/other than other groups and use of ACEI/ARB was highest in Māori, Pacific and Indian patients.

Table 4: Post MI management.

Values are number of patients and frequency (%) unless otherwise specified. PCI: percutaneous intervention. CABG: coronary artery bypass graft.

Outcomes (Table 5, Figure 1)

The unadjusted one-year cumulative mortality was highest for Pacific (8.8%) followed by Māori (7.6%), European/others (4.9%), Other Asians (4.8%) and lowest in Indian (3.5%). The age and sex adjusted cumulative mortality is shown in Figure 1. There is a steep early hazard for all ethnic groups which is greatest in Māori, Pacific and Indian patients. Beyond this early phase, there is only minimal incremental increase in mortality in European/other, Indian and Other Asian patients but a steady incremental increase in Māori and Pacific mortality, leading to progressive divergence of the mortality curves. After adjusting for age-group and sex, Māori and Pacific, but not Indian or Other Asian patients, had significantly higher all-cause mortality at one year compared with the European/other reference group. (HR 2.55, (95% CI 2.12–3.07), HR 2.98 (95% CI 2.34–3.81), for Māori and Pacific respectively). When further adjusted for differences in clinical presentation, clinical history and cardiovascular risk factors the excess mortality risk for Māori and Pacific patients compared with European/others was reduced but a substantial differential persisted (HR 1.77, (95% CI 1.44–2.19), HR 1.42, (95% CI 1.07–1.83). Further adjustment for differences in mode of revascularisation and discharge medications made little difference (HR 1.72, (95% CI 1.39–2.12), HR 1.35 (95% CI 1.01–1.80).

Table 5: All-cause mortality in the year after a first MI: multivariable models.

CAD, Coronary artery disease; VD, vessel disease; ACS, Acute coronary syndrome; CVD, Cardiovascular Disease; CHF, Congestive heart failure; TC:HDL, total cholesterol to high density lipoprotein ratio; eGFR, Estimated glomerular filtration rate; COPD, Chronic obstructive pulmonary disease; DAPT, Dual antiplatelet therapy. For detailed description of the multi-variable regression models please refer to the statistical analysis section above.

Figure 1: Age and sex adjusted cumulative mortality.

Discussion

In this real-world nationwide study, Māori and Pacific people presenting with their first myocardial infarction were younger, but had more advanced cardiac disease, were more acutely unwell, and had higher case fatality rates at one year compared with New Zealand European/other patients. In particular, Māori and Pacific patients were more likely to have acute heart failure and LV dysfunction, and Māori were more likely to present with a cardiac arrest, despite a similar ratio of STEMI to NSTEMIs. Indian and Other Asian patients presenting with their first MI were also younger than New Zealand European/other patients. Pacific peoples, followed by Indian, were more likely to have severe obstructive coronary artery disease at their first admission than other ethnic groups. There were differences in the burden of modifiable cardiovascular risk factors with smoking and associated COPD most frequent in Māori and Pacific patients. Pacific and Indian peoples had the highest prevalence of diabetes, with higher prevalence also observed among Māori and Other Asian people compared to the European/other group. Despite having similarly high prevalence of diabetes and hypertension, fewer Indian patients had advanced CKD than Pacific patients. Indian patients also had less advanced CKD than Māori patients despite diabetes being less frequent in Māori.

The age and sex adjusted one-year mortality was 2.5 times and 3 times higher for Māori and Pacific patients, respectively, compared to European/others, while Indian and Other Asian patients had outcomes similar to European/others. After adjustment for differences in the clinical presentation, risk factors and comorbidity, the excess mortality associated with Māori or Pacific ethnicity was significantly attenuated, although remained at about 1.8 times and 1.4 times higher risk, respectively. Adjustment for differences in in-hospital treatment did not modify this further. These findings suggest that at least half of the inequity in outcomes for Māori, and three quarters for Pacific people, is associated with differences in preventable or modifiable clinical factors, and could therefore be reduced by improvements in healthcare delivery in primary care and in the acute, community-to-secondary care interface. The remaining—unaccounted for—differences in mortality require further study, but may include differences in other modifiable factors including medical comorbidities and inequities in healthcare access and delivery both before hospitalisation and post-discharge.

What is already known

In New Zealand, despite ongoing reductions in IHD mortality, there are persisting major ethnic inequalities in IHD mortality, with Māori and Pacific patients having approximately double the European age standardised mortality rate.4 Ischaemic heart disease accounts for 40.2% of Māori deaths in those aged less than 65 years, compared to 10.5% of non-Māori deaths.13 Furthermore, we have previously reported similarly disproportionate rates of IHD mortality both in Māori and Pacific patients who die before they can be hospitalised, as well as those who die after a hospitalisation.3,14 The causes of inequity in IHD outcomes will be multifactorial, including differential exposure to CVD risk factors, socioeconomic deprivation, and unequal access to healthcare, utilisation of primary prevention and treatment. The majority of premature IHD incidence is attributable to uncontrolled but potentially modifiable risk factors.15,16

In this study we have shown, at a national level, that there are ethnic differences in potentially modifiable risk factors which can be identified across the care continuum, from primordial prevention in primary care through to post-hospital discharge. These potentially modifiable factors explain at least half of the inequity in outcomes observed.

Ethnic differences in clinical presentation

Māori patients were more likely to present with a cardiac arrest. Cardiac arrest is associated with worse outcome post-MI but its impact can be ameliorated by effective CPR and early cardioversion.17,18 The most effective way to improve access to defibrillation is to reduce the time between symptom onset and the call for medical help with subsequent ambulance attendance or utilisation of community automated external defibrillators. Despite community programmes in New Zealand aimed at increasing recognition of MI symptoms and encouraging people to call for help there remain long delays in making the call. In the ANZACS-QI national cohort of patients with STEMI the median delay to call for help was 45 minutes for ambulance-transported patients and 97 minutes for those self-transported to hospital. That delay was more common in older people, Māori and Indian peoples and those self-transported to hospital.19

Both Māori and Pacific peoples were more likely to present with acute heart failure and worse LV systolic function. Both of these are associated with more adverse outcomes after MI.20,21 They may be presenting with larger heart attacks, although the similar proportions of all ethnic groups in the highest quintile of peak Troponin T, a measure of MI size,22 argues against this. An alternative explanation is that Māori and Pacific patients have more pre-existing cardiac disease, making them more susceptible to developing acute heart failure despite similar amounts of acute myocardial necrosis. Both of these explanations point to possible interventions. Delayed presentation reduces the opportunity for early medical treatment and revascularisation of both culprit and non-culprit coronary lesions. Remarkably, over a quarter of patients in all ethnic groups and over a third of Pacific and Indian patients had severe three vessel or left main stem coronary artery disease when they presented with their first MI. Because an acute MI is usually due to sudden occlusion of one coronary artery these patients must have had pre-existing but unrecognised obstructive CAD prior to their first MI. Earlier identification of both asymptomatic coronary artery disease and heart failure/LV dysfunction, and their determinants, are an opportunity to modify the disease course using well established lifestyle and pharmacological interventions.

The comparatively higher rate of MI without obstructive coronary artery disease in Maori, and to a lesser extent in Pacific patients also requires further investigation—in particular whether these patients have atherosclerotic plaque rupture or, alternatively, have other cardiac disease (cardiomyopathy and arrhythmia) for which other management is required.

Ethnic differences in modifiable longer-term determinants of risk

The most clinically important ethnic differences in CVD risk factors included excess smoking and associated COPD in Māori, excess diabetes in Pacific, Indian and Māori patients, and excess CKD in Pacific and to a lesser extent in Māori and Indian patients. Our group has described and discussed the differences in traditional risk factors in an earlier, smaller ANZACS-QI cohort.23 Both smoking and diabetes mellitus and their clinical sequelae are potentially preventable risk factors.24,25 Although CKD is not a traditional risk factor it is predominantly caused by poorly controlled diabetes and high blood pressure, and is in that sense, a surrogate for those more traditional, treatable risk factors. In our multivariable analysis and a prior ANZACS-QI report, advanced CKD conferred a 5–10-fold excess mortality risk compared with patients with normal renal function.26 Of importance, despite having similar high rates of diabetes, Indian patients had less advanced CKD than Pacific patients. Indian patients were also less likely to have advanced CKD than Maori patients, despite having more frequent diabetes.

The triad of diabetes, high blood pressure and CKD are important determinants of the LV dysfunction and pre-clinical CAD discussed above. The causative pathway is complex—diabetes and high blood pressure are in part determined, and potentially modifiable, by lifestyle factors including physical activity, diet and weight which are in turn related to the wider determinants of health including poverty, education, housing and institutionalised and interpersonal racism.27,28 Of note, nearly half of the Māori and Pacific patients in this cohort lived in the poorest geographical quintile in New Zealand and a higher burden of cardiovascular risk factors and multi-morbidity is associated with higher levels of deprivation.29,30

Ethnic differences in treatment

Adjustment for differences in treatment in the multivariable analysis had only a minor impact on the risk estimates of each variable. All patients in this cohort underwent coronary angiography, but there were small differences in overall revascularisation rates and type of revascularisation. In particular revascularisation occurred among 75% of European/others, 70.5% in Pacific and 67% in Māori patients. This difference has been reported and investigated in depth in prior reports. At one large metropolitan hospital where this difference was studied this was largely explained by differences in the nature of the CAD, with more non-obstructive disease in Māori and Pacific which does not require revascularisation, combined with more diffuse small vessel coronary artery disease in some patients with diabetes, which is not suitable for revascularisation and is more appropriately treated medically.6 However, in another hospital anatomic and clinical factors did not explain all the differences in revascularisation between ethnic groups.31 Each cardiology unit in the country should audit their practice and review processes to ensure that institutional racism does not contribute to the observed lower rate of invasive coronary investigation and management in Maori and Pacific.32 Māori and Pacific patients had lower rates of dual anti-platelet therapy prescription on discharge in this study, likely due to the more frequent finding of non-obstructive CAD and the higher rates of CABG. In New Zealand, contrary to guidelines, the use of DAPT for these two indications is known to be low,33,34 and an opportunity for improvement.

Ethnic differences in outcomes

This study has established that at least half of the excess in ACS mortality between European/other and Māori and three-quarters of that between Pacific and European /other patients, is related to potentially modifiable or preventable clinical factors and could therefore be reduced markedly. Modification of these factors span the continuum of care and life course from primordial prevention of risk factors to primary prevention management of risk factors in the community, to acute pre-hospital and in-hospital care, and then to post-discharge secondary prevention in primary care. This and prior studies referenced above have documented ethnic differences in risk factors and clinical management at each stage in this continuum. In many cases the differences are small but cumulatively may add up to a large impact on outcome. The implication of this finding is that improvement initiatives are required to identify and address barriers to appropriate care for Maori and Pacific people at every stage in the continuum. It is likely that disparities in cardiovascular risk are perpetuated by the wider determinants of health including poverty, education, housing and institutionalised and interpersonal racism, and that addressing these determinants will be required to achieve equitable health outcomes. Further research is needed to determine the relative importance of these various factors.

Limitations

Only patients who received a coronary angiogram in the public health system of New Zealand were included in this study. However, given other data showing excess IHD mortality in Māori and Pacific patients out of hospital it is likely that similar conclusions apply to those patients. With further variable refinement, some differences in risk between ethnic groups might have been more marked. For example we have previously reported more suboptimal glycaemic control and proteinuria in Pacific compared with European patients.6 Those variables are not available at a national level for inclusion in this study. We did not adjust for post-discharge medication adherence but have previously reported differences by ethnicity.6,35,36 We had no access to other variables which might be very important including physical activity, family support, health literacy level and health beliefs.

Conclusion

In New Zealand, at first presentation with MI, Māori, Pacific and Indian patients are younger, have more advanced cardiac disease and a greater burden of CVD risk factors compared with European/others, and there is a three-fold variation in one-year mortality based on ethnicity. Over half of this inequity in outcomes is associated with differences in potentially preventable or modifiable factors and could therefore be reduced by improvements in primordial and primary prevention in the community, and in healthcare delivery in primary and secondary care and at the community-to-secondary care interface.

Summary

Abstract

Aim

Ischaemic heart disease (IHD) mortality rates after myocardial infarction (MI) are higher in Māori and Pacific compared to European people. The reasons for these differences are complex and incompletely understood. Our aim was to use a contemporary real-world national cohort of patients presenting with their first MI to better understand the extent to which differences in the clinical presentation, cardiovascular (CVD) risk factors, comorbidity and in-hospital treatment explain the mortality outcomes for Māori and Pacific peoples.

Method

New Zealand residents (≥20 years old) hospitalised with their first MI (2014–2017), and who underwent coronary angiography, were identified from the All New Zealand Acute Coronary Syndrome Quality Improvement (ANZACS-QI) registry. All-cause mortality up to one year after the index admission date was obtained by linkage to the national mortality database.

Results

There were 17,404 patients with a first ever MI. European/other comprised 76% of the population, Māori 11.5%, Pacific 5.1%, Indian 4.3% and Other Asian 2.9%. Over half (55%) of Māori, Pacific and Indian patients were admitted with their first MI before age 60 years, compared with 29% of European/other patients. Māori and Pacific patients had a higher burden of traditional and non-traditional cardiovascular risk factors, and despite being younger, were more likely to present with heart failure and, together with Indian peoples, advanced coronary disease at presentation with first MI. After adjustment for age and sex, Māori and Pacific, but not Indian or Other Asian patients had significantly higher all-cause mortality at one year compared with the European/other reference group (HR 2.55 (95% CI 2.12–3.07), HR 2.98 (95% CI 2.34–3.81) for Māori and Pacific respectively). When further adjusted for differences in clinical presentation, clinical history and cardiovascular risk factors, the excess mortality risk for Māori and Pacific patients was reduced substantially, but a differential persisted (HR 1.77 (95% CI 1.44–2.19), HR 1.42 (95% CI 1.07–1.83)) which was not further reduced by adjustment for differences in in-hospital management and discharge medications.

Conclusion

In New Zealand patients after their first MI there is a three-fold variation in one-year mortality based on ethnicity. At least half of the inequity in outcomes for Māori, and three-quarters for Pacific people, is associated with differences in preventable or modifiable clinical factors present at, or prior to, presentation.

Author Information

Janine Mazengarb, Cardiology Trainee, Counties Manukau District Health Board; Corina Grey, Public Health Physician, Auckland District Health Board; Mildred Lee, Biostatistician, Counties Manukau District Health Board; Katrina Poppe, Heart Foundation Hynds Senior Fellow, School of Population Health, University of Auckland, Auckland; Suneela Mehta, Public Health Physician and Senior Research Fellow, School of Population Health, University of Auckland, Auckland; Matire Harwood, Associate Professor, Department of General Practice and Primary Care, University of Auckland, Auckland; Wil Harrison, Cardiologist, Counties Manukau District Health Board; Nicki Earle, Heart Foundation Research Fellow, Department of Medicine, University of Auckland, Auckland; Rod Jackson, Professor, School of Population Health, University of Auckland, Auckland; Andrew Kerr, Cardiologist, Counties Manukau District Health Board; Adjunct Associate Professor of Medicine, University of Auckland, Auckland.

Acknowledgements

ANZACS-QI programme implementation, coordination and analysis: The ANZACS-QI software was developed and supported by Enigma Solutions. Programme implementation is coordinated by the National Institute for Health Innovation (NIHI) at the University of Auckland. The ANZACS-QI programme is funded by the NZ Ministry of Health. We thank the the National Health Board Analytic Services and Pharmac for enabling use of the national data sets. We also thank the VIEW team at the School of Population Health, University of Auckland for the curation and linkage of the national data. ANZACS-QI Governance group: Andrew Kerr (chair), Dean Boddington, Gary Sutcliffe, Gerry Devlin, Harvey White, John Edmond, Jonathon Tisch, Kim Marshall, Mayanna Lund, Michael Williams (deputy chair), Nick Fisher, Seif El Jack, Sue Riddle. ANZACS-QI Project management: Kristin Sutherland (Project Manager), Charmaine Flynn (Northern coordinator), Maxine Rhodes (Southern coordinator). Data analysis: Mildred Lee. Editorial assistant: Julia Kerr. Data management: Billy Wu (SOPH), Michelle Jenkins (NIHI), John Faatui (NIHI). We acknowledge all the New Zealand cardiologists, physicians, nursing staff and radiographers and all the patients who have supported and contributed to ANZACS-QI. ANZACS-QI hospital coordinators: Ascot Angiography: Summerscales, I. Money, J. Ashburton: Wilson, S. Auckland Hospital Belz, L. Stewart, R. Marshall, K. Bay of Islands: Cochran, G. Christchurch Hospital: Jackson, M, Sutherland J, McLaren S. Clutha Hospital: Reed, G. Campbell, B, McElrea J. Dargaville: Cripps, J. Katipa, K. Dunedin Hospital: Foote, C. Dunstan: Nixon, G. Shaw, M, Klahn R. Gisborne: Low, T. Gore: Lindley, G, Whitten C. Grey Base Hospital: Smith, L, Jennings M. Hawke’s Bay Hospital Soldiers Memorial: Brown, G. Grant, P. Hutt Hospital: Pinfold, S. Ferrier, K. Kitchen, R. Kaikoura Hospital: McCullough C. Kaitaia Hospital: Thompson, R. Smith, N. Lakes District Hospital: Burt, J. Mercy Angiography: Shah, A. Ubod, B. Mercy Heart Centre: Hall, S. Middlemore: Mcintosh, R. McLachlan, A. Midland Cardiovascular Services: Phillips, K. Nelson Hospital: Besley, J. Abernethy, H. North Shore Hospital: Gray, L. Oamaru: Gonzales, R, Clare L. Palmerston North Hospital: Kinloch, D. Rawene Hospital: Dorsay, C. Rotorua Hospital: Colby, C. Southland Hospital: Byers, R, Ghosh P. St Georges Hospital: Lissette, J, Lewis K. Taranaki Base Hospital: Ternouth, I. Spurway, M. Taumaranui: Pointon, L. Taupo Hospital: McAnanay, J. Tauranga Hospital: Goodson, J. Te Kuiti: Te Wano, T. Thames: Stutchbury, D. Timaru Hospital: Addidle, D. Tokoroa: Huitema, V. Waikato Hospital: Emerson, C. Pilay, R. Wairarapa Hospital: Matthews, T. Wairau Hospital: Langford, S, Ballagh D. Waitakere Hospital: Long, L. Waitemata Hospital: Newcombe, R. Wakefield Private Hospital: Murphy, S. Wellington Hospital: Scott, B, Wylie D. Whakatane Hospital: Bentley-Smith, M. Whanganui Hospital: Thompson, T. Whangarei Hospital: Vallancey, S.

Correspondence

Adjunct Associate Professor Andrew Kerr, Department of Cardiology, Middlemore Hospital, Otahuhu, Auckland 93311.

Correspondence Email

a.kerr@auckland.ac.nz

Competing Interests

Dr Mehta, Dr Kerr and Dr Poppe report grants from Health Research Council of New Zealand during the conduct of the study. Dr Grey and Dr Poppe report grants from Heart Foundation of New Zealand during the conduct of the study.

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19. Kerr A, Lee M, Grey C, et al. Acute reperfusion for ST-elevation myocardial infarction in New Zealand (2015–2017): patient and system delay (ANZACS-QI 29). New Zealand Medical Journal. 2019; 132:41–59.

20. Fox KAA, Dabbous OH, Goldberg RJ, et al. Prediction of risk of death and myocardial infarction in the six months after presentation with acute coronary syndrome: prospective multinational observational study (GRACE).[see comment]. BMJ. 2006; 333:1091.

21. Sutton NR, Li S, Thomas L, et al. The association of left ventricular ejection fraction with clinical outcomes after myocardial infarction: Findings from the Acute Coronary Treatment and Intervention Outcomes Network (ACTION) Registry-Get With the Guidelines (GWTG) Medicare-linked database. American Heart Journal. 2016; 178:65–73.

22. Panteghini M, Cuccia C, Bonetti G, Giubbini R, Pagani F, Bonini E. Single-point cardiac troponin T at coronary care unit discharge after myocardial infarction correlates with infarct size and ejection fraction. Clin Chem. 2002; 48:1432–6.

23. Earle NJ, Poppe KK, Doughty RN, Rolleston A, Kerr AJ, Legget ME. Clinical Characteristics and Burden of Risk Factors Among Patients With Early Onset Acute Coronary Syndromes: The ANZACS-QI New Zealand National Cohort (ANZACS-QI 17). Heart, Lung & Circulation. 2018; 27:568–75.

24. Hu FB, Manson JE, Stampfer MJ, et al. Diet, lifestyle, and the risk of type 2 diabetes mellitus in women. NEJM. 2001; 1:790–7.

25. Rana JS, Li TY, Manson JE, Hu FB. Adiposity compared with physical inactivity and risk of type 2 diabetes in women. Diabetes Care. 2007; 30:53–8.

26. Pilmore HL, Xiong F, Choi Y, et al. Impact of chronic kidney disease on mortality and cardiovascular outcomes after acute coronary syndrome: A nationwide data linkage study (ANZACS-QI 44). Nephrology. 2020; 27:27.

27. Curtis E, Harwood M, Riddell T, et al. Access and society as determinants of ischaemic heart disease in indigenous populations. Heart, Lung & Circulation. 2010; 19:316–24.

28. Harris R, Tobias M, Jeffreys M, Waldegrave K, Karlsen S, Nazroo J. Racism and health: the relationship between experience of racial discrimination and health in New Zealand. Social Science & Medicine. 2006; 63:1428–41.

29. Kerr AJ, McLachlan A, Furness S, et al. The burden of modifiable cardiovascular risk factors in the coronary care unit by age, ethnicity, and socioeconomic status—PREDICT CVD-9. New Zealand Medical Journal. 2008; 121:20–33.

30. Barnett K, Mercer SW, Norbury M, Watt G, Wyke S, Guthrie B. Epidemiology of multimorbidity and implications for health care, research, and medical education: a cross-sectional study. Lancet. 2012; 380:37–43.

31. Sandiford P, El-Jack SS, Scott AG, Crengle SM, Bramley DM. Different needs or treated differently? Understanding ethnic inequalities in coronary revascularisation rates. Heart, Lung & Circulation. 2015; 24:960–8.

32. Grey C, Jackson R, Wells S, et al. Ethnic Differences in Coronary Revascularisation following an Acute Coronary Syndrome in New Zealand: A National Data-linkage Study (ANZACS-QI 12). Heart, Lung & Circulation. 2016; 25:820–8.

33. Williams MJA, Barr PR, Lee M, Poppe KK, Kerr AJ. Outcome after myocardial infarction without obstructive coronary artery disease. Heart. 2018; 29:29.

34. Wei D, Wang T. Contemporary audit of prescribing patterns following coronary arrtery bypass grafting. Heart, Lung and Circulation. 2019; 28.

35. Grey C, Jackson R, Wells S, et al. Maintenance of statin use over 3 years following acute coronary syndromes: a national data linkage study (ANZACS-QI-2). Heart. 2014; 100:770–4.

36. Kerr A, Turaga M, Grey C, Lee M, McLachlan A, Devlin G. Initiation and maintenance of statins and aspirin after acute coronary syndromes (ANZACS-QI 11). Journal of Primary Health Care. 2016; Published on line:doi:10.1071/HC16013.

Contact diana@nzma.org.nz
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In New Zealand, age standardised hospitalisation rates for ischaemic heart disease (IHD) and its most important clinical manifestation, myocardial infarction (MI), have steadily decreased over the last 10 years.1,2 However, despite this good news, Māori, Pacific and South Asian peoples continue to have higher IHD hospitalisation rates, and Māori and Pacific peoples have higher IHD mortality rates compared to European.3,4 The reasons for these differences are complex and incompletely understood. The All New Zealand Acute Coronary Syndrome Quality Improvement (ANZACS-QI) registry collects a comprehensive dataset for all patients presenting to New Zealand public hospitals with an ACS (acute coronary syndrome) who undergo investigation with a coronary angiogram. The ANZACS-QI registry is linked via an encrypted identifier to national administrative datasets to augment data and to track patient outcomes.5 Our aim was to use this contemporary real-world national cohort, in patients presenting with their first MI, to better understand the extent to which differences in the clinical presentation, cardiovascular disease (CVD) risk factors, comorbidity and in-hospital treatment explain the divergence in outcomes between ethnic groups.

Methods

Cohort

New Zealand residents aged ≥20 years hospitalised with their first MI between 1 January 2014 and 31 December 2017 and who underwent coronary angiography were identified from the ANZACS-QI registry.

The ANZACS-QI registry is a web-based electronic database that captures a mandatory dataset which includes patient demographics, admission ACS risk stratification, cardiovascular risk factors, investigations and management, inpatient outcomes and medications prescribed at discharge. The patients captured in the registry are linked via an encrypted unique National Health Identifier (NHI) to national hospitalisation, mortality and pharmaceutical dispensing national datasets. Details regarding the ANZACS-QI programme, registry data collection and linkage to national datasets have been previously reported.5 Data collected in ANZACS-QI has been previously described in detail.5,6 The registry is subject to monthly auditing to ensure capture of >95% of all patients admitted with suspected ACS who are investigated with coronary angiography, and annual audit to check the accuracy of data entry.

Data and definitions

MI was defined according to the contemporary universal definition.7Sociodemographic variables and residency status were derived from the linked national dataset. For patients in whom more than one ethnic group was recorded, ethnicity was prioritised, in accordance with health sector protocols, in the following order: indigenous Māori, Pacific, Indian, Other Asian and European/other.8 European /other included all those identifying as European as well as a small number of people from the Middle East, Africa and Latin America. Fijian Indian people are categorised as ‘Indian’, as opposed to ‘Pacific’. Socioeconomic deprivation was assessed by the NZDep13 score, a census-based small area 10-point index of deprivation based on the person’s domicile.9 Clinical presentation variables from the ANZACS-QI registry included type of MI (ST-elevation MI (STEMI) or non ST-elevation MI (NSTEMI)), known prior congestive heart failure (CHF), components of the Global Registry of Acute Coronary Events (GRACE) in-hospital mortality risk score (including Killip class, admission heart rate and blood pressure, cardiac arrest on admission, electrocardiogram findings, troponin level, admission creatinine),10 left ventricular ejection fraction (LVEF) assessed by transthoracic echo or left ventriculogram, coronary artery disease extent on angiography. Killip class was divided into those without (Class I) and with acute heart failure (Classes II–IV).11 Left ventricular ejection fraction (LVEF) assessment was classified into normal (≥50%), mild impairment (40–49%), moderate to severe impairment (<40%), and not quantified further. Coronary artery disease (CAD) extent was defined by the findings at angiography and were grouped into one of the following: (i) no significant CAD, defined as the absence of any stenosis with ≥50% diameter loss in the epicardial vessels, (ii) significant (≥50% stenosis) single vessel coronary disease, (iii) significant (≥50% stenosis) double vessel coronary artery disease, (iv) significant three-vessel disease and/or left main stem (LMS) disease ≥50%. Due to the use of multiple different Troponin assays across New Zealand, the peak troponin values for each patient were stratified into quintiles for each separate assay. eGFR at admission was calculated using the CKD-EPI equation in ml/min and reported in CKD stages one (>90ml/min), two (60–90ml/min), three (30–60ml/min), four (15–30ml/min) and five (<15ml/min).12 Cardiovascular disease risk factors, history and comorbidity variables included: smoking status defined as current, ex-smoker or never smoker, diabetes mellitus, hypertension (HT), low-density lipoprotein (LDL) and total cholesterol (TC) to high-density lipoprotein (HDL) ratio, body mass index (BMI), history of chronic obstructive pulmonary disease (COPD), history of congestive heart failure (CHF) and prior atherosclerotic CVD—defined as a prior diagnosis or history of transient ischaemic attack or ischaemic stroke, peripheral vascular disease or radiological evidence of vascular disease.

Investigation and management variables were coronary revascularisation by percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). Discharge medications were: aspirin, P2Y12 inhibitor (clopidogrel or ticagrelor), statins, angiotensin converting enzyme inhibitors (ACEIs) and beta-blockers. Dual anti-platelet therapy (DAPT) was aspirin plus a P2Y12 inhibitor.

Outcomes

All-cause mortality up to one year after the index admission date was obtained by linkage to the national mortality database.

Statistical analysis

Categorical variables were summarised as frequency and percentage and continuous variables as mean and standard deviation (SD). Comparisons across ethnic groups were made using Pearson’s chi-square test, one-way ANOVA or a Kruskall Wallis test, as appropriate. Multivariable Cox regression models were used to estimate the hazard ratio of each ethnicity compared to European/other for all-cause mortality and 30-day post admission all-cause mortality outcomes in four models: Model One—unadjusted ; Model Two—adjusted by age and sex ; Model Three—adjusted by age, sex, worst Killip class, EF categories, CAD extent, troponin quintile, cardiac arrest, MI sub-type, prior CHF, prior CVD, smoking, diabetes, TC:HDL, hypertension, eGFR, COPD; Model Four—Model Three variables plus coronary revascularisation (PCI or CABG), medications (statin, ACEI/ARB, beta blocker, DAPT) at discharge. Cumulative mortality plots stratify time to death by ethnic group.

The proportional hazards assumptions were tested by plotting the standardised score residuals over time. The assumptions were met. All tests of statistical significance were two tailed and a p-value <0.05 was considered statistically significant. Data were analysed using SAS version 9.4 (SAS Institute, Cary, NC), and cumulative mortality plots were created using RStudio version 1.2.1335.

Ethical approval

This research was performed as part of the VIEW-ANZACS-QI research programme. Ethics approval was obtained from the Northern Region Ethics Committee (AKY/03/12/314) and Multi-Region Ethics Committee (MEC/01/19/EXP and MEC/11/EXP/078).

Results

There were 17,404 patients with a first ever MI. European/other comprised 76% of the population, Māori 11.5%, Pacific 5.1%, Indian 4.3% and other Asian 2.9%. Patient demographics are shown in Table 1. Two thirds of patients were men and the mean age was 64 years. Māori, Pacific and Indian patients presented at a younger age (mean age 58–59 years) compared with other Asian and European/other patients (mean age 61 and 66 years respectively). Over half (55%) of Māori, Pacific and Indian patients were admitted with their first MI before age 60 years, compared with 35% of other Asian and 29% of European/other patients.

Table 1: Baseline demographics.

All values are number of patients and frequency (%) unless otherwise specified.

Clinical presentation (Table 2)

Māori patients were the most likely to present with cardiac arrest. Māori and Pacific patients were 1.5 to 2 times more likely to have acute heart failure than European/others (17%, 19.5%, 11.5%, respectively), while 26% of Pacific patients and 21% of Māori patients had moderate-severe LV impairment, but only 15% of European/others. This was despite a similar proportion of each ethnic group having myocardial necrosis in the highest quintile (based on troponin levels). At coronary angiography nearly half of all patients had obstructive disease in more than one coronary artery. Pacific and Indian patients had more severe three-vessel disease and/or left main coronary artery disease (38% and 33%) than Māori, Other Asian or European/other patients (25%, 26.5% and 26%). The proportion of STEMIs was similar for Māori, Indian and European/other groups but lower for Pacific patients and slightly higher for Other Asian patients. While only 3.1% of the overall cohort had advanced (Stage 4 or 5) CKD, Pacific (11.4%) and Māori (5.8%) were markedly over-represented, with 4.2% of Indian people also affected. In contrast, only 2% of European/other patients had advanced CKD.

Table 2: Clinical presentation.

Values are number of patients and frequency (%) unless otherwise specified. CAD, coronary artery disease; NSTEMI, non-ST segment elevation myocardial infarction; STEMI, ST segment elevation myocardial infarction; eGFR, estimated glomerular filtration rate.

Atherosclerotic CVD risk factors and medical history (Table 3)

Nearly half of Pacific and Indian patients had diabetes, 30% of Māori, 29% of Other Asian and 16% of European/others. Of those with BMI recorded, 33.8% of Maori and 44.2% of Pacific compared to 23.7% of European/others had a BMI in the obese range (Indian 18.4% and Other Asian 9.5%). Mean TC:HDL was highest in Māori and lowest in Other Asian patients with intermediate levels in other groups. Nearly half of Māori and a third of Pacific patients were current smokers compared with less than a quarter of other ethnic groups. Māori patients, correspondingly, were more likely to have COPD. Māori and Pacific patients were twice as likely to have a diagnosis of prior CHF compared with non-Māori/non-Pacific.

Table 3: Cardiovascular risk factors.

Values are number of patients and frequency (%) unless otherwise specified. BMI, body mass index; TC:HDL, total cholesterol to high-density lipoprotein ratio; COPD, chronic obstructive pulmonary disease; CVD, cardiovascular disease; CHF, congestive heart failure.

Treatment (Table 4)

Overall, 74.5 % of patients underwent coronary revascularisation: 61.6% with PCI and 12.9% by CABG. Revascularisation was highest for Other Asian patients (77%) followed by European/others (75%), Indian (72%), Pacific (70.5%) and Māori (67%). Compared to European/other patients, Māori, Pacific and Indian patients had higher rates of CABG and lower rates of PCI consistent with their higher prevalence of diabetes and among Pacific and Indian patients, diffuse coronary artery disease. Indian people were equally likely to receive PCI as European/other patients. However, Māori and Pacific patients were less likely to receive PCI and less likely overall to receive coronary intervention. There was a high level of prescription of aspirin and statin medication at discharge with only minor ethnic differences. Use of a P2Y12 anti-platelet agent was higher in European/other than other groups and use of ACEI/ARB was highest in Māori, Pacific and Indian patients.

Table 4: Post MI management.

Values are number of patients and frequency (%) unless otherwise specified. PCI: percutaneous intervention. CABG: coronary artery bypass graft.

Outcomes (Table 5, Figure 1)

The unadjusted one-year cumulative mortality was highest for Pacific (8.8%) followed by Māori (7.6%), European/others (4.9%), Other Asians (4.8%) and lowest in Indian (3.5%). The age and sex adjusted cumulative mortality is shown in Figure 1. There is a steep early hazard for all ethnic groups which is greatest in Māori, Pacific and Indian patients. Beyond this early phase, there is only minimal incremental increase in mortality in European/other, Indian and Other Asian patients but a steady incremental increase in Māori and Pacific mortality, leading to progressive divergence of the mortality curves. After adjusting for age-group and sex, Māori and Pacific, but not Indian or Other Asian patients, had significantly higher all-cause mortality at one year compared with the European/other reference group. (HR 2.55, (95% CI 2.12–3.07), HR 2.98 (95% CI 2.34–3.81), for Māori and Pacific respectively). When further adjusted for differences in clinical presentation, clinical history and cardiovascular risk factors the excess mortality risk for Māori and Pacific patients compared with European/others was reduced but a substantial differential persisted (HR 1.77, (95% CI 1.44–2.19), HR 1.42, (95% CI 1.07–1.83). Further adjustment for differences in mode of revascularisation and discharge medications made little difference (HR 1.72, (95% CI 1.39–2.12), HR 1.35 (95% CI 1.01–1.80).

Table 5: All-cause mortality in the year after a first MI: multivariable models.

CAD, Coronary artery disease; VD, vessel disease; ACS, Acute coronary syndrome; CVD, Cardiovascular Disease; CHF, Congestive heart failure; TC:HDL, total cholesterol to high density lipoprotein ratio; eGFR, Estimated glomerular filtration rate; COPD, Chronic obstructive pulmonary disease; DAPT, Dual antiplatelet therapy. For detailed description of the multi-variable regression models please refer to the statistical analysis section above.

Figure 1: Age and sex adjusted cumulative mortality.

Discussion

In this real-world nationwide study, Māori and Pacific people presenting with their first myocardial infarction were younger, but had more advanced cardiac disease, were more acutely unwell, and had higher case fatality rates at one year compared with New Zealand European/other patients. In particular, Māori and Pacific patients were more likely to have acute heart failure and LV dysfunction, and Māori were more likely to present with a cardiac arrest, despite a similar ratio of STEMI to NSTEMIs. Indian and Other Asian patients presenting with their first MI were also younger than New Zealand European/other patients. Pacific peoples, followed by Indian, were more likely to have severe obstructive coronary artery disease at their first admission than other ethnic groups. There were differences in the burden of modifiable cardiovascular risk factors with smoking and associated COPD most frequent in Māori and Pacific patients. Pacific and Indian peoples had the highest prevalence of diabetes, with higher prevalence also observed among Māori and Other Asian people compared to the European/other group. Despite having similarly high prevalence of diabetes and hypertension, fewer Indian patients had advanced CKD than Pacific patients. Indian patients also had less advanced CKD than Māori patients despite diabetes being less frequent in Māori.

The age and sex adjusted one-year mortality was 2.5 times and 3 times higher for Māori and Pacific patients, respectively, compared to European/others, while Indian and Other Asian patients had outcomes similar to European/others. After adjustment for differences in the clinical presentation, risk factors and comorbidity, the excess mortality associated with Māori or Pacific ethnicity was significantly attenuated, although remained at about 1.8 times and 1.4 times higher risk, respectively. Adjustment for differences in in-hospital treatment did not modify this further. These findings suggest that at least half of the inequity in outcomes for Māori, and three quarters for Pacific people, is associated with differences in preventable or modifiable clinical factors, and could therefore be reduced by improvements in healthcare delivery in primary care and in the acute, community-to-secondary care interface. The remaining—unaccounted for—differences in mortality require further study, but may include differences in other modifiable factors including medical comorbidities and inequities in healthcare access and delivery both before hospitalisation and post-discharge.

What is already known

In New Zealand, despite ongoing reductions in IHD mortality, there are persisting major ethnic inequalities in IHD mortality, with Māori and Pacific patients having approximately double the European age standardised mortality rate.4 Ischaemic heart disease accounts for 40.2% of Māori deaths in those aged less than 65 years, compared to 10.5% of non-Māori deaths.13 Furthermore, we have previously reported similarly disproportionate rates of IHD mortality both in Māori and Pacific patients who die before they can be hospitalised, as well as those who die after a hospitalisation.3,14 The causes of inequity in IHD outcomes will be multifactorial, including differential exposure to CVD risk factors, socioeconomic deprivation, and unequal access to healthcare, utilisation of primary prevention and treatment. The majority of premature IHD incidence is attributable to uncontrolled but potentially modifiable risk factors.15,16

In this study we have shown, at a national level, that there are ethnic differences in potentially modifiable risk factors which can be identified across the care continuum, from primordial prevention in primary care through to post-hospital discharge. These potentially modifiable factors explain at least half of the inequity in outcomes observed.

Ethnic differences in clinical presentation

Māori patients were more likely to present with a cardiac arrest. Cardiac arrest is associated with worse outcome post-MI but its impact can be ameliorated by effective CPR and early cardioversion.17,18 The most effective way to improve access to defibrillation is to reduce the time between symptom onset and the call for medical help with subsequent ambulance attendance or utilisation of community automated external defibrillators. Despite community programmes in New Zealand aimed at increasing recognition of MI symptoms and encouraging people to call for help there remain long delays in making the call. In the ANZACS-QI national cohort of patients with STEMI the median delay to call for help was 45 minutes for ambulance-transported patients and 97 minutes for those self-transported to hospital. That delay was more common in older people, Māori and Indian peoples and those self-transported to hospital.19

Both Māori and Pacific peoples were more likely to present with acute heart failure and worse LV systolic function. Both of these are associated with more adverse outcomes after MI.20,21 They may be presenting with larger heart attacks, although the similar proportions of all ethnic groups in the highest quintile of peak Troponin T, a measure of MI size,22 argues against this. An alternative explanation is that Māori and Pacific patients have more pre-existing cardiac disease, making them more susceptible to developing acute heart failure despite similar amounts of acute myocardial necrosis. Both of these explanations point to possible interventions. Delayed presentation reduces the opportunity for early medical treatment and revascularisation of both culprit and non-culprit coronary lesions. Remarkably, over a quarter of patients in all ethnic groups and over a third of Pacific and Indian patients had severe three vessel or left main stem coronary artery disease when they presented with their first MI. Because an acute MI is usually due to sudden occlusion of one coronary artery these patients must have had pre-existing but unrecognised obstructive CAD prior to their first MI. Earlier identification of both asymptomatic coronary artery disease and heart failure/LV dysfunction, and their determinants, are an opportunity to modify the disease course using well established lifestyle and pharmacological interventions.

The comparatively higher rate of MI without obstructive coronary artery disease in Maori, and to a lesser extent in Pacific patients also requires further investigation—in particular whether these patients have atherosclerotic plaque rupture or, alternatively, have other cardiac disease (cardiomyopathy and arrhythmia) for which other management is required.

Ethnic differences in modifiable longer-term determinants of risk

The most clinically important ethnic differences in CVD risk factors included excess smoking and associated COPD in Māori, excess diabetes in Pacific, Indian and Māori patients, and excess CKD in Pacific and to a lesser extent in Māori and Indian patients. Our group has described and discussed the differences in traditional risk factors in an earlier, smaller ANZACS-QI cohort.23 Both smoking and diabetes mellitus and their clinical sequelae are potentially preventable risk factors.24,25 Although CKD is not a traditional risk factor it is predominantly caused by poorly controlled diabetes and high blood pressure, and is in that sense, a surrogate for those more traditional, treatable risk factors. In our multivariable analysis and a prior ANZACS-QI report, advanced CKD conferred a 5–10-fold excess mortality risk compared with patients with normal renal function.26 Of importance, despite having similar high rates of diabetes, Indian patients had less advanced CKD than Pacific patients. Indian patients were also less likely to have advanced CKD than Maori patients, despite having more frequent diabetes.

The triad of diabetes, high blood pressure and CKD are important determinants of the LV dysfunction and pre-clinical CAD discussed above. The causative pathway is complex—diabetes and high blood pressure are in part determined, and potentially modifiable, by lifestyle factors including physical activity, diet and weight which are in turn related to the wider determinants of health including poverty, education, housing and institutionalised and interpersonal racism.27,28 Of note, nearly half of the Māori and Pacific patients in this cohort lived in the poorest geographical quintile in New Zealand and a higher burden of cardiovascular risk factors and multi-morbidity is associated with higher levels of deprivation.29,30

Ethnic differences in treatment

Adjustment for differences in treatment in the multivariable analysis had only a minor impact on the risk estimates of each variable. All patients in this cohort underwent coronary angiography, but there were small differences in overall revascularisation rates and type of revascularisation. In particular revascularisation occurred among 75% of European/others, 70.5% in Pacific and 67% in Māori patients. This difference has been reported and investigated in depth in prior reports. At one large metropolitan hospital where this difference was studied this was largely explained by differences in the nature of the CAD, with more non-obstructive disease in Māori and Pacific which does not require revascularisation, combined with more diffuse small vessel coronary artery disease in some patients with diabetes, which is not suitable for revascularisation and is more appropriately treated medically.6 However, in another hospital anatomic and clinical factors did not explain all the differences in revascularisation between ethnic groups.31 Each cardiology unit in the country should audit their practice and review processes to ensure that institutional racism does not contribute to the observed lower rate of invasive coronary investigation and management in Maori and Pacific.32 Māori and Pacific patients had lower rates of dual anti-platelet therapy prescription on discharge in this study, likely due to the more frequent finding of non-obstructive CAD and the higher rates of CABG. In New Zealand, contrary to guidelines, the use of DAPT for these two indications is known to be low,33,34 and an opportunity for improvement.

Ethnic differences in outcomes

This study has established that at least half of the excess in ACS mortality between European/other and Māori and three-quarters of that between Pacific and European /other patients, is related to potentially modifiable or preventable clinical factors and could therefore be reduced markedly. Modification of these factors span the continuum of care and life course from primordial prevention of risk factors to primary prevention management of risk factors in the community, to acute pre-hospital and in-hospital care, and then to post-discharge secondary prevention in primary care. This and prior studies referenced above have documented ethnic differences in risk factors and clinical management at each stage in this continuum. In many cases the differences are small but cumulatively may add up to a large impact on outcome. The implication of this finding is that improvement initiatives are required to identify and address barriers to appropriate care for Maori and Pacific people at every stage in the continuum. It is likely that disparities in cardiovascular risk are perpetuated by the wider determinants of health including poverty, education, housing and institutionalised and interpersonal racism, and that addressing these determinants will be required to achieve equitable health outcomes. Further research is needed to determine the relative importance of these various factors.

Limitations

Only patients who received a coronary angiogram in the public health system of New Zealand were included in this study. However, given other data showing excess IHD mortality in Māori and Pacific patients out of hospital it is likely that similar conclusions apply to those patients. With further variable refinement, some differences in risk between ethnic groups might have been more marked. For example we have previously reported more suboptimal glycaemic control and proteinuria in Pacific compared with European patients.6 Those variables are not available at a national level for inclusion in this study. We did not adjust for post-discharge medication adherence but have previously reported differences by ethnicity.6,35,36 We had no access to other variables which might be very important including physical activity, family support, health literacy level and health beliefs.

Conclusion

In New Zealand, at first presentation with MI, Māori, Pacific and Indian patients are younger, have more advanced cardiac disease and a greater burden of CVD risk factors compared with European/others, and there is a three-fold variation in one-year mortality based on ethnicity. Over half of this inequity in outcomes is associated with differences in potentially preventable or modifiable factors and could therefore be reduced by improvements in primordial and primary prevention in the community, and in healthcare delivery in primary and secondary care and at the community-to-secondary care interface.

Summary

Abstract

Aim

Ischaemic heart disease (IHD) mortality rates after myocardial infarction (MI) are higher in Māori and Pacific compared to European people. The reasons for these differences are complex and incompletely understood. Our aim was to use a contemporary real-world national cohort of patients presenting with their first MI to better understand the extent to which differences in the clinical presentation, cardiovascular (CVD) risk factors, comorbidity and in-hospital treatment explain the mortality outcomes for Māori and Pacific peoples.

Method

New Zealand residents (≥20 years old) hospitalised with their first MI (2014–2017), and who underwent coronary angiography, were identified from the All New Zealand Acute Coronary Syndrome Quality Improvement (ANZACS-QI) registry. All-cause mortality up to one year after the index admission date was obtained by linkage to the national mortality database.

Results

There were 17,404 patients with a first ever MI. European/other comprised 76% of the population, Māori 11.5%, Pacific 5.1%, Indian 4.3% and Other Asian 2.9%. Over half (55%) of Māori, Pacific and Indian patients were admitted with their first MI before age 60 years, compared with 29% of European/other patients. Māori and Pacific patients had a higher burden of traditional and non-traditional cardiovascular risk factors, and despite being younger, were more likely to present with heart failure and, together with Indian peoples, advanced coronary disease at presentation with first MI. After adjustment for age and sex, Māori and Pacific, but not Indian or Other Asian patients had significantly higher all-cause mortality at one year compared with the European/other reference group (HR 2.55 (95% CI 2.12–3.07), HR 2.98 (95% CI 2.34–3.81) for Māori and Pacific respectively). When further adjusted for differences in clinical presentation, clinical history and cardiovascular risk factors, the excess mortality risk for Māori and Pacific patients was reduced substantially, but a differential persisted (HR 1.77 (95% CI 1.44–2.19), HR 1.42 (95% CI 1.07–1.83)) which was not further reduced by adjustment for differences in in-hospital management and discharge medications.

Conclusion

In New Zealand patients after their first MI there is a three-fold variation in one-year mortality based on ethnicity. At least half of the inequity in outcomes for Māori, and three-quarters for Pacific people, is associated with differences in preventable or modifiable clinical factors present at, or prior to, presentation.

Author Information

Janine Mazengarb, Cardiology Trainee, Counties Manukau District Health Board; Corina Grey, Public Health Physician, Auckland District Health Board; Mildred Lee, Biostatistician, Counties Manukau District Health Board; Katrina Poppe, Heart Foundation Hynds Senior Fellow, School of Population Health, University of Auckland, Auckland; Suneela Mehta, Public Health Physician and Senior Research Fellow, School of Population Health, University of Auckland, Auckland; Matire Harwood, Associate Professor, Department of General Practice and Primary Care, University of Auckland, Auckland; Wil Harrison, Cardiologist, Counties Manukau District Health Board; Nicki Earle, Heart Foundation Research Fellow, Department of Medicine, University of Auckland, Auckland; Rod Jackson, Professor, School of Population Health, University of Auckland, Auckland; Andrew Kerr, Cardiologist, Counties Manukau District Health Board; Adjunct Associate Professor of Medicine, University of Auckland, Auckland.

Acknowledgements

ANZACS-QI programme implementation, coordination and analysis: The ANZACS-QI software was developed and supported by Enigma Solutions. Programme implementation is coordinated by the National Institute for Health Innovation (NIHI) at the University of Auckland. The ANZACS-QI programme is funded by the NZ Ministry of Health. We thank the the National Health Board Analytic Services and Pharmac for enabling use of the national data sets. We also thank the VIEW team at the School of Population Health, University of Auckland for the curation and linkage of the national data. ANZACS-QI Governance group: Andrew Kerr (chair), Dean Boddington, Gary Sutcliffe, Gerry Devlin, Harvey White, John Edmond, Jonathon Tisch, Kim Marshall, Mayanna Lund, Michael Williams (deputy chair), Nick Fisher, Seif El Jack, Sue Riddle. ANZACS-QI Project management: Kristin Sutherland (Project Manager), Charmaine Flynn (Northern coordinator), Maxine Rhodes (Southern coordinator). Data analysis: Mildred Lee. Editorial assistant: Julia Kerr. Data management: Billy Wu (SOPH), Michelle Jenkins (NIHI), John Faatui (NIHI). We acknowledge all the New Zealand cardiologists, physicians, nursing staff and radiographers and all the patients who have supported and contributed to ANZACS-QI. ANZACS-QI hospital coordinators: Ascot Angiography: Summerscales, I. Money, J. Ashburton: Wilson, S. Auckland Hospital Belz, L. Stewart, R. Marshall, K. Bay of Islands: Cochran, G. Christchurch Hospital: Jackson, M, Sutherland J, McLaren S. Clutha Hospital: Reed, G. Campbell, B, McElrea J. Dargaville: Cripps, J. Katipa, K. Dunedin Hospital: Foote, C. Dunstan: Nixon, G. Shaw, M, Klahn R. Gisborne: Low, T. Gore: Lindley, G, Whitten C. Grey Base Hospital: Smith, L, Jennings M. Hawke’s Bay Hospital Soldiers Memorial: Brown, G. Grant, P. Hutt Hospital: Pinfold, S. Ferrier, K. Kitchen, R. Kaikoura Hospital: McCullough C. Kaitaia Hospital: Thompson, R. Smith, N. Lakes District Hospital: Burt, J. Mercy Angiography: Shah, A. Ubod, B. Mercy Heart Centre: Hall, S. Middlemore: Mcintosh, R. McLachlan, A. Midland Cardiovascular Services: Phillips, K. Nelson Hospital: Besley, J. Abernethy, H. North Shore Hospital: Gray, L. Oamaru: Gonzales, R, Clare L. Palmerston North Hospital: Kinloch, D. Rawene Hospital: Dorsay, C. Rotorua Hospital: Colby, C. Southland Hospital: Byers, R, Ghosh P. St Georges Hospital: Lissette, J, Lewis K. Taranaki Base Hospital: Ternouth, I. Spurway, M. Taumaranui: Pointon, L. Taupo Hospital: McAnanay, J. Tauranga Hospital: Goodson, J. Te Kuiti: Te Wano, T. Thames: Stutchbury, D. Timaru Hospital: Addidle, D. Tokoroa: Huitema, V. Waikato Hospital: Emerson, C. Pilay, R. Wairarapa Hospital: Matthews, T. Wairau Hospital: Langford, S, Ballagh D. Waitakere Hospital: Long, L. Waitemata Hospital: Newcombe, R. Wakefield Private Hospital: Murphy, S. Wellington Hospital: Scott, B, Wylie D. Whakatane Hospital: Bentley-Smith, M. Whanganui Hospital: Thompson, T. Whangarei Hospital: Vallancey, S.

Correspondence

Adjunct Associate Professor Andrew Kerr, Department of Cardiology, Middlemore Hospital, Otahuhu, Auckland 93311.

Correspondence Email

a.kerr@auckland.ac.nz

Competing Interests

Dr Mehta, Dr Kerr and Dr Poppe report grants from Health Research Council of New Zealand during the conduct of the study. Dr Grey and Dr Poppe report grants from Heart Foundation of New Zealand during the conduct of the study.

1. Grey C, Jackson R, Wells S, et al. First and recurrent ischaemic heart disease events continue to decline in New Zealand, 2005–2015. Heart. 2018; 104:51–7.

2. Wang TKM, Grey C, Jiang Y, Jackson RT, Kerr AJ. Nationwide trends in acute coronary syndrome by subtype in New Zealand 2006–2016. Heart. 2019; 31:31.

3. Grey C, Jackson R, Wells S, Marshall R, Riddell T, Kerr AJ. Twenty-eight day and one-year case fatality after hospitalisation with an acute coronary syndrome: a nationwide data linkage study. Aust N Z J Public Health. 2014; 38:216–20.

4. Grey C, Jackson R, Wells S, et al. Trends in ischaemic heart disease: patterns of hospitalisation and mortality rates differ by ethnicity (ANZACS-QI 21). New Zealand Medical Journal. 2018; 131:21–31.

5. Kerr A, Williams MJ, White H, et al. The All New Zealand Acute Coronary Syndrome Quality Improvement Programme: Implementation, Methodology and Cohorts (ANZACS-QI 9). New Zealand Medical Journal. 2016; 129:23–36.

6. Kerr AJ, Mustafa A, Lee M, et al. Ethnicity and revascularisation following acute coronary syndromes: a 5-year cohort study (ANZACS-QI-3). New Zealand Medical Journal. 2014; 127:38–51.

7. Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR, White HD. Third universal definition of myocardial infarction. European Heart Journal. 2012; 33:2551–67.

8. Ministry of Health. HISO 10001:2017 Ethnicity Data Protocols. 2017.

9. Atkinson J, Salmond C, Crampton P. NZDep2013 Index of Deprivation. Dunedin: University of Otago, 2014.

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11. Killip T, 3rd, Kimball JT. Treatment of myocardial infarction in a coronary care unit. A two year experience with 250 patients. American Journal of Cardiology. 1967; 20:457–64.

12. Levey AS, Stevens LA, Schmid CH, et al. A new equation to estimate glomerular filtration rate. Annals of Internal Medicine. 2009; 150:604–12.

13. Ministry of Health. Mortality and Demographic Data 2012. Wellington, 2015.

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17. The United Kingdom Heart Attack Study Collaborative Group. Effect of time from onset to coming under care on fatality of patients with acute myocardial infarction: effect of resuscitation and thrombolytic treatment. The United Kingdom Heart Attack Study (UKHAS) Collaborative Group. Heart. 1998; 80:114–20.

18. Rea TD, Paredes VL. Quality of life and prognosis among survivors of out-of-hospital cardiac arrest. Curr Opin Crit Care. 2004; 10:218–23.

19. Kerr A, Lee M, Grey C, et al. Acute reperfusion for ST-elevation myocardial infarction in New Zealand (2015–2017): patient and system delay (ANZACS-QI 29). New Zealand Medical Journal. 2019; 132:41–59.

20. Fox KAA, Dabbous OH, Goldberg RJ, et al. Prediction of risk of death and myocardial infarction in the six months after presentation with acute coronary syndrome: prospective multinational observational study (GRACE).[see comment]. BMJ. 2006; 333:1091.

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22. Panteghini M, Cuccia C, Bonetti G, Giubbini R, Pagani F, Bonini E. Single-point cardiac troponin T at coronary care unit discharge after myocardial infarction correlates with infarct size and ejection fraction. Clin Chem. 2002; 48:1432–6.

23. Earle NJ, Poppe KK, Doughty RN, Rolleston A, Kerr AJ, Legget ME. Clinical Characteristics and Burden of Risk Factors Among Patients With Early Onset Acute Coronary Syndromes: The ANZACS-QI New Zealand National Cohort (ANZACS-QI 17). Heart, Lung & Circulation. 2018; 27:568–75.

24. Hu FB, Manson JE, Stampfer MJ, et al. Diet, lifestyle, and the risk of type 2 diabetes mellitus in women. NEJM. 2001; 1:790–7.

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26. Pilmore HL, Xiong F, Choi Y, et al. Impact of chronic kidney disease on mortality and cardiovascular outcomes after acute coronary syndrome: A nationwide data linkage study (ANZACS-QI 44). Nephrology. 2020; 27:27.

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Contact diana@nzma.org.nz
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In New Zealand, age standardised hospitalisation rates for ischaemic heart disease (IHD) and its most important clinical manifestation, myocardial infarction (MI), have steadily decreased over the last 10 years.1,2 However, despite this good news, Māori, Pacific and South Asian peoples continue to have higher IHD hospitalisation rates, and Māori and Pacific peoples have higher IHD mortality rates compared to European.3,4 The reasons for these differences are complex and incompletely understood. The All New Zealand Acute Coronary Syndrome Quality Improvement (ANZACS-QI) registry collects a comprehensive dataset for all patients presenting to New Zealand public hospitals with an ACS (acute coronary syndrome) who undergo investigation with a coronary angiogram. The ANZACS-QI registry is linked via an encrypted identifier to national administrative datasets to augment data and to track patient outcomes.5 Our aim was to use this contemporary real-world national cohort, in patients presenting with their first MI, to better understand the extent to which differences in the clinical presentation, cardiovascular disease (CVD) risk factors, comorbidity and in-hospital treatment explain the divergence in outcomes between ethnic groups.

Methods

Cohort

New Zealand residents aged ≥20 years hospitalised with their first MI between 1 January 2014 and 31 December 2017 and who underwent coronary angiography were identified from the ANZACS-QI registry.

The ANZACS-QI registry is a web-based electronic database that captures a mandatory dataset which includes patient demographics, admission ACS risk stratification, cardiovascular risk factors, investigations and management, inpatient outcomes and medications prescribed at discharge. The patients captured in the registry are linked via an encrypted unique National Health Identifier (NHI) to national hospitalisation, mortality and pharmaceutical dispensing national datasets. Details regarding the ANZACS-QI programme, registry data collection and linkage to national datasets have been previously reported.5 Data collected in ANZACS-QI has been previously described in detail.5,6 The registry is subject to monthly auditing to ensure capture of >95% of all patients admitted with suspected ACS who are investigated with coronary angiography, and annual audit to check the accuracy of data entry.

Data and definitions

MI was defined according to the contemporary universal definition.7Sociodemographic variables and residency status were derived from the linked national dataset. For patients in whom more than one ethnic group was recorded, ethnicity was prioritised, in accordance with health sector protocols, in the following order: indigenous Māori, Pacific, Indian, Other Asian and European/other.8 European /other included all those identifying as European as well as a small number of people from the Middle East, Africa and Latin America. Fijian Indian people are categorised as ‘Indian’, as opposed to ‘Pacific’. Socioeconomic deprivation was assessed by the NZDep13 score, a census-based small area 10-point index of deprivation based on the person’s domicile.9 Clinical presentation variables from the ANZACS-QI registry included type of MI (ST-elevation MI (STEMI) or non ST-elevation MI (NSTEMI)), known prior congestive heart failure (CHF), components of the Global Registry of Acute Coronary Events (GRACE) in-hospital mortality risk score (including Killip class, admission heart rate and blood pressure, cardiac arrest on admission, electrocardiogram findings, troponin level, admission creatinine),10 left ventricular ejection fraction (LVEF) assessed by transthoracic echo or left ventriculogram, coronary artery disease extent on angiography. Killip class was divided into those without (Class I) and with acute heart failure (Classes II–IV).11 Left ventricular ejection fraction (LVEF) assessment was classified into normal (≥50%), mild impairment (40–49%), moderate to severe impairment (<40%), and not quantified further. Coronary artery disease (CAD) extent was defined by the findings at angiography and were grouped into one of the following: (i) no significant CAD, defined as the absence of any stenosis with ≥50% diameter loss in the epicardial vessels, (ii) significant (≥50% stenosis) single vessel coronary disease, (iii) significant (≥50% stenosis) double vessel coronary artery disease, (iv) significant three-vessel disease and/or left main stem (LMS) disease ≥50%. Due to the use of multiple different Troponin assays across New Zealand, the peak troponin values for each patient were stratified into quintiles for each separate assay. eGFR at admission was calculated using the CKD-EPI equation in ml/min and reported in CKD stages one (>90ml/min), two (60–90ml/min), three (30–60ml/min), four (15–30ml/min) and five (<15ml/min).12 Cardiovascular disease risk factors, history and comorbidity variables included: smoking status defined as current, ex-smoker or never smoker, diabetes mellitus, hypertension (HT), low-density lipoprotein (LDL) and total cholesterol (TC) to high-density lipoprotein (HDL) ratio, body mass index (BMI), history of chronic obstructive pulmonary disease (COPD), history of congestive heart failure (CHF) and prior atherosclerotic CVD—defined as a prior diagnosis or history of transient ischaemic attack or ischaemic stroke, peripheral vascular disease or radiological evidence of vascular disease.

Investigation and management variables were coronary revascularisation by percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). Discharge medications were: aspirin, P2Y12 inhibitor (clopidogrel or ticagrelor), statins, angiotensin converting enzyme inhibitors (ACEIs) and beta-blockers. Dual anti-platelet therapy (DAPT) was aspirin plus a P2Y12 inhibitor.

Outcomes

All-cause mortality up to one year after the index admission date was obtained by linkage to the national mortality database.

Statistical analysis

Categorical variables were summarised as frequency and percentage and continuous variables as mean and standard deviation (SD). Comparisons across ethnic groups were made using Pearson’s chi-square test, one-way ANOVA or a Kruskall Wallis test, as appropriate. Multivariable Cox regression models were used to estimate the hazard ratio of each ethnicity compared to European/other for all-cause mortality and 30-day post admission all-cause mortality outcomes in four models: Model One—unadjusted ; Model Two—adjusted by age and sex ; Model Three—adjusted by age, sex, worst Killip class, EF categories, CAD extent, troponin quintile, cardiac arrest, MI sub-type, prior CHF, prior CVD, smoking, diabetes, TC:HDL, hypertension, eGFR, COPD; Model Four—Model Three variables plus coronary revascularisation (PCI or CABG), medications (statin, ACEI/ARB, beta blocker, DAPT) at discharge. Cumulative mortality plots stratify time to death by ethnic group.

The proportional hazards assumptions were tested by plotting the standardised score residuals over time. The assumptions were met. All tests of statistical significance were two tailed and a p-value <0.05 was considered statistically significant. Data were analysed using SAS version 9.4 (SAS Institute, Cary, NC), and cumulative mortality plots were created using RStudio version 1.2.1335.

Ethical approval

This research was performed as part of the VIEW-ANZACS-QI research programme. Ethics approval was obtained from the Northern Region Ethics Committee (AKY/03/12/314) and Multi-Region Ethics Committee (MEC/01/19/EXP and MEC/11/EXP/078).

Results

There were 17,404 patients with a first ever MI. European/other comprised 76% of the population, Māori 11.5%, Pacific 5.1%, Indian 4.3% and other Asian 2.9%. Patient demographics are shown in Table 1. Two thirds of patients were men and the mean age was 64 years. Māori, Pacific and Indian patients presented at a younger age (mean age 58–59 years) compared with other Asian and European/other patients (mean age 61 and 66 years respectively). Over half (55%) of Māori, Pacific and Indian patients were admitted with their first MI before age 60 years, compared with 35% of other Asian and 29% of European/other patients.

Table 1: Baseline demographics.

All values are number of patients and frequency (%) unless otherwise specified.

Clinical presentation (Table 2)

Māori patients were the most likely to present with cardiac arrest. Māori and Pacific patients were 1.5 to 2 times more likely to have acute heart failure than European/others (17%, 19.5%, 11.5%, respectively), while 26% of Pacific patients and 21% of Māori patients had moderate-severe LV impairment, but only 15% of European/others. This was despite a similar proportion of each ethnic group having myocardial necrosis in the highest quintile (based on troponin levels). At coronary angiography nearly half of all patients had obstructive disease in more than one coronary artery. Pacific and Indian patients had more severe three-vessel disease and/or left main coronary artery disease (38% and 33%) than Māori, Other Asian or European/other patients (25%, 26.5% and 26%). The proportion of STEMIs was similar for Māori, Indian and European/other groups but lower for Pacific patients and slightly higher for Other Asian patients. While only 3.1% of the overall cohort had advanced (Stage 4 or 5) CKD, Pacific (11.4%) and Māori (5.8%) were markedly over-represented, with 4.2% of Indian people also affected. In contrast, only 2% of European/other patients had advanced CKD.

Table 2: Clinical presentation.

Values are number of patients and frequency (%) unless otherwise specified. CAD, coronary artery disease; NSTEMI, non-ST segment elevation myocardial infarction; STEMI, ST segment elevation myocardial infarction; eGFR, estimated glomerular filtration rate.

Atherosclerotic CVD risk factors and medical history (Table 3)

Nearly half of Pacific and Indian patients had diabetes, 30% of Māori, 29% of Other Asian and 16% of European/others. Of those with BMI recorded, 33.8% of Maori and 44.2% of Pacific compared to 23.7% of European/others had a BMI in the obese range (Indian 18.4% and Other Asian 9.5%). Mean TC:HDL was highest in Māori and lowest in Other Asian patients with intermediate levels in other groups. Nearly half of Māori and a third of Pacific patients were current smokers compared with less than a quarter of other ethnic groups. Māori patients, correspondingly, were more likely to have COPD. Māori and Pacific patients were twice as likely to have a diagnosis of prior CHF compared with non-Māori/non-Pacific.

Table 3: Cardiovascular risk factors.

Values are number of patients and frequency (%) unless otherwise specified. BMI, body mass index; TC:HDL, total cholesterol to high-density lipoprotein ratio; COPD, chronic obstructive pulmonary disease; CVD, cardiovascular disease; CHF, congestive heart failure.

Treatment (Table 4)

Overall, 74.5 % of patients underwent coronary revascularisation: 61.6% with PCI and 12.9% by CABG. Revascularisation was highest for Other Asian patients (77%) followed by European/others (75%), Indian (72%), Pacific (70.5%) and Māori (67%). Compared to European/other patients, Māori, Pacific and Indian patients had higher rates of CABG and lower rates of PCI consistent with their higher prevalence of diabetes and among Pacific and Indian patients, diffuse coronary artery disease. Indian people were equally likely to receive PCI as European/other patients. However, Māori and Pacific patients were less likely to receive PCI and less likely overall to receive coronary intervention. There was a high level of prescription of aspirin and statin medication at discharge with only minor ethnic differences. Use of a P2Y12 anti-platelet agent was higher in European/other than other groups and use of ACEI/ARB was highest in Māori, Pacific and Indian patients.

Table 4: Post MI management.

Values are number of patients and frequency (%) unless otherwise specified. PCI: percutaneous intervention. CABG: coronary artery bypass graft.

Outcomes (Table 5, Figure 1)

The unadjusted one-year cumulative mortality was highest for Pacific (8.8%) followed by Māori (7.6%), European/others (4.9%), Other Asians (4.8%) and lowest in Indian (3.5%). The age and sex adjusted cumulative mortality is shown in Figure 1. There is a steep early hazard for all ethnic groups which is greatest in Māori, Pacific and Indian patients. Beyond this early phase, there is only minimal incremental increase in mortality in European/other, Indian and Other Asian patients but a steady incremental increase in Māori and Pacific mortality, leading to progressive divergence of the mortality curves. After adjusting for age-group and sex, Māori and Pacific, but not Indian or Other Asian patients, had significantly higher all-cause mortality at one year compared with the European/other reference group. (HR 2.55, (95% CI 2.12–3.07), HR 2.98 (95% CI 2.34–3.81), for Māori and Pacific respectively). When further adjusted for differences in clinical presentation, clinical history and cardiovascular risk factors the excess mortality risk for Māori and Pacific patients compared with European/others was reduced but a substantial differential persisted (HR 1.77, (95% CI 1.44–2.19), HR 1.42, (95% CI 1.07–1.83). Further adjustment for differences in mode of revascularisation and discharge medications made little difference (HR 1.72, (95% CI 1.39–2.12), HR 1.35 (95% CI 1.01–1.80).

Table 5: All-cause mortality in the year after a first MI: multivariable models.

CAD, Coronary artery disease; VD, vessel disease; ACS, Acute coronary syndrome; CVD, Cardiovascular Disease; CHF, Congestive heart failure; TC:HDL, total cholesterol to high density lipoprotein ratio; eGFR, Estimated glomerular filtration rate; COPD, Chronic obstructive pulmonary disease; DAPT, Dual antiplatelet therapy. For detailed description of the multi-variable regression models please refer to the statistical analysis section above.

Figure 1: Age and sex adjusted cumulative mortality.

Discussion

In this real-world nationwide study, Māori and Pacific people presenting with their first myocardial infarction were younger, but had more advanced cardiac disease, were more acutely unwell, and had higher case fatality rates at one year compared with New Zealand European/other patients. In particular, Māori and Pacific patients were more likely to have acute heart failure and LV dysfunction, and Māori were more likely to present with a cardiac arrest, despite a similar ratio of STEMI to NSTEMIs. Indian and Other Asian patients presenting with their first MI were also younger than New Zealand European/other patients. Pacific peoples, followed by Indian, were more likely to have severe obstructive coronary artery disease at their first admission than other ethnic groups. There were differences in the burden of modifiable cardiovascular risk factors with smoking and associated COPD most frequent in Māori and Pacific patients. Pacific and Indian peoples had the highest prevalence of diabetes, with higher prevalence also observed among Māori and Other Asian people compared to the European/other group. Despite having similarly high prevalence of diabetes and hypertension, fewer Indian patients had advanced CKD than Pacific patients. Indian patients also had less advanced CKD than Māori patients despite diabetes being less frequent in Māori.

The age and sex adjusted one-year mortality was 2.5 times and 3 times higher for Māori and Pacific patients, respectively, compared to European/others, while Indian and Other Asian patients had outcomes similar to European/others. After adjustment for differences in the clinical presentation, risk factors and comorbidity, the excess mortality associated with Māori or Pacific ethnicity was significantly attenuated, although remained at about 1.8 times and 1.4 times higher risk, respectively. Adjustment for differences in in-hospital treatment did not modify this further. These findings suggest that at least half of the inequity in outcomes for Māori, and three quarters for Pacific people, is associated with differences in preventable or modifiable clinical factors, and could therefore be reduced by improvements in healthcare delivery in primary care and in the acute, community-to-secondary care interface. The remaining—unaccounted for—differences in mortality require further study, but may include differences in other modifiable factors including medical comorbidities and inequities in healthcare access and delivery both before hospitalisation and post-discharge.

What is already known

In New Zealand, despite ongoing reductions in IHD mortality, there are persisting major ethnic inequalities in IHD mortality, with Māori and Pacific patients having approximately double the European age standardised mortality rate.4 Ischaemic heart disease accounts for 40.2% of Māori deaths in those aged less than 65 years, compared to 10.5% of non-Māori deaths.13 Furthermore, we have previously reported similarly disproportionate rates of IHD mortality both in Māori and Pacific patients who die before they can be hospitalised, as well as those who die after a hospitalisation.3,14 The causes of inequity in IHD outcomes will be multifactorial, including differential exposure to CVD risk factors, socioeconomic deprivation, and unequal access to healthcare, utilisation of primary prevention and treatment. The majority of premature IHD incidence is attributable to uncontrolled but potentially modifiable risk factors.15,16

In this study we have shown, at a national level, that there are ethnic differences in potentially modifiable risk factors which can be identified across the care continuum, from primordial prevention in primary care through to post-hospital discharge. These potentially modifiable factors explain at least half of the inequity in outcomes observed.

Ethnic differences in clinical presentation

Māori patients were more likely to present with a cardiac arrest. Cardiac arrest is associated with worse outcome post-MI but its impact can be ameliorated by effective CPR and early cardioversion.17,18 The most effective way to improve access to defibrillation is to reduce the time between symptom onset and the call for medical help with subsequent ambulance attendance or utilisation of community automated external defibrillators. Despite community programmes in New Zealand aimed at increasing recognition of MI symptoms and encouraging people to call for help there remain long delays in making the call. In the ANZACS-QI national cohort of patients with STEMI the median delay to call for help was 45 minutes for ambulance-transported patients and 97 minutes for those self-transported to hospital. That delay was more common in older people, Māori and Indian peoples and those self-transported to hospital.19

Both Māori and Pacific peoples were more likely to present with acute heart failure and worse LV systolic function. Both of these are associated with more adverse outcomes after MI.20,21 They may be presenting with larger heart attacks, although the similar proportions of all ethnic groups in the highest quintile of peak Troponin T, a measure of MI size,22 argues against this. An alternative explanation is that Māori and Pacific patients have more pre-existing cardiac disease, making them more susceptible to developing acute heart failure despite similar amounts of acute myocardial necrosis. Both of these explanations point to possible interventions. Delayed presentation reduces the opportunity for early medical treatment and revascularisation of both culprit and non-culprit coronary lesions. Remarkably, over a quarter of patients in all ethnic groups and over a third of Pacific and Indian patients had severe three vessel or left main stem coronary artery disease when they presented with their first MI. Because an acute MI is usually due to sudden occlusion of one coronary artery these patients must have had pre-existing but unrecognised obstructive CAD prior to their first MI. Earlier identification of both asymptomatic coronary artery disease and heart failure/LV dysfunction, and their determinants, are an opportunity to modify the disease course using well established lifestyle and pharmacological interventions.

The comparatively higher rate of MI without obstructive coronary artery disease in Maori, and to a lesser extent in Pacific patients also requires further investigation—in particular whether these patients have atherosclerotic plaque rupture or, alternatively, have other cardiac disease (cardiomyopathy and arrhythmia) for which other management is required.

Ethnic differences in modifiable longer-term determinants of risk

The most clinically important ethnic differences in CVD risk factors included excess smoking and associated COPD in Māori, excess diabetes in Pacific, Indian and Māori patients, and excess CKD in Pacific and to a lesser extent in Māori and Indian patients. Our group has described and discussed the differences in traditional risk factors in an earlier, smaller ANZACS-QI cohort.23 Both smoking and diabetes mellitus and their clinical sequelae are potentially preventable risk factors.24,25 Although CKD is not a traditional risk factor it is predominantly caused by poorly controlled diabetes and high blood pressure, and is in that sense, a surrogate for those more traditional, treatable risk factors. In our multivariable analysis and a prior ANZACS-QI report, advanced CKD conferred a 5–10-fold excess mortality risk compared with patients with normal renal function.26 Of importance, despite having similar high rates of diabetes, Indian patients had less advanced CKD than Pacific patients. Indian patients were also less likely to have advanced CKD than Maori patients, despite having more frequent diabetes.

The triad of diabetes, high blood pressure and CKD are important determinants of the LV dysfunction and pre-clinical CAD discussed above. The causative pathway is complex—diabetes and high blood pressure are in part determined, and potentially modifiable, by lifestyle factors including physical activity, diet and weight which are in turn related to the wider determinants of health including poverty, education, housing and institutionalised and interpersonal racism.27,28 Of note, nearly half of the Māori and Pacific patients in this cohort lived in the poorest geographical quintile in New Zealand and a higher burden of cardiovascular risk factors and multi-morbidity is associated with higher levels of deprivation.29,30

Ethnic differences in treatment

Adjustment for differences in treatment in the multivariable analysis had only a minor impact on the risk estimates of each variable. All patients in this cohort underwent coronary angiography, but there were small differences in overall revascularisation rates and type of revascularisation. In particular revascularisation occurred among 75% of European/others, 70.5% in Pacific and 67% in Māori patients. This difference has been reported and investigated in depth in prior reports. At one large metropolitan hospital where this difference was studied this was largely explained by differences in the nature of the CAD, with more non-obstructive disease in Māori and Pacific which does not require revascularisation, combined with more diffuse small vessel coronary artery disease in some patients with diabetes, which is not suitable for revascularisation and is more appropriately treated medically.6 However, in another hospital anatomic and clinical factors did not explain all the differences in revascularisation between ethnic groups.31 Each cardiology unit in the country should audit their practice and review processes to ensure that institutional racism does not contribute to the observed lower rate of invasive coronary investigation and management in Maori and Pacific.32 Māori and Pacific patients had lower rates of dual anti-platelet therapy prescription on discharge in this study, likely due to the more frequent finding of non-obstructive CAD and the higher rates of CABG. In New Zealand, contrary to guidelines, the use of DAPT for these two indications is known to be low,33,34 and an opportunity for improvement.

Ethnic differences in outcomes

This study has established that at least half of the excess in ACS mortality between European/other and Māori and three-quarters of that between Pacific and European /other patients, is related to potentially modifiable or preventable clinical factors and could therefore be reduced markedly. Modification of these factors span the continuum of care and life course from primordial prevention of risk factors to primary prevention management of risk factors in the community, to acute pre-hospital and in-hospital care, and then to post-discharge secondary prevention in primary care. This and prior studies referenced above have documented ethnic differences in risk factors and clinical management at each stage in this continuum. In many cases the differences are small but cumulatively may add up to a large impact on outcome. The implication of this finding is that improvement initiatives are required to identify and address barriers to appropriate care for Maori and Pacific people at every stage in the continuum. It is likely that disparities in cardiovascular risk are perpetuated by the wider determinants of health including poverty, education, housing and institutionalised and interpersonal racism, and that addressing these determinants will be required to achieve equitable health outcomes. Further research is needed to determine the relative importance of these various factors.

Limitations

Only patients who received a coronary angiogram in the public health system of New Zealand were included in this study. However, given other data showing excess IHD mortality in Māori and Pacific patients out of hospital it is likely that similar conclusions apply to those patients. With further variable refinement, some differences in risk between ethnic groups might have been more marked. For example we have previously reported more suboptimal glycaemic control and proteinuria in Pacific compared with European patients.6 Those variables are not available at a national level for inclusion in this study. We did not adjust for post-discharge medication adherence but have previously reported differences by ethnicity.6,35,36 We had no access to other variables which might be very important including physical activity, family support, health literacy level and health beliefs.

Conclusion

In New Zealand, at first presentation with MI, Māori, Pacific and Indian patients are younger, have more advanced cardiac disease and a greater burden of CVD risk factors compared with European/others, and there is a three-fold variation in one-year mortality based on ethnicity. Over half of this inequity in outcomes is associated with differences in potentially preventable or modifiable factors and could therefore be reduced by improvements in primordial and primary prevention in the community, and in healthcare delivery in primary and secondary care and at the community-to-secondary care interface.

Summary

Abstract

Aim

Ischaemic heart disease (IHD) mortality rates after myocardial infarction (MI) are higher in Māori and Pacific compared to European people. The reasons for these differences are complex and incompletely understood. Our aim was to use a contemporary real-world national cohort of patients presenting with their first MI to better understand the extent to which differences in the clinical presentation, cardiovascular (CVD) risk factors, comorbidity and in-hospital treatment explain the mortality outcomes for Māori and Pacific peoples.

Method

New Zealand residents (≥20 years old) hospitalised with their first MI (2014–2017), and who underwent coronary angiography, were identified from the All New Zealand Acute Coronary Syndrome Quality Improvement (ANZACS-QI) registry. All-cause mortality up to one year after the index admission date was obtained by linkage to the national mortality database.

Results

There were 17,404 patients with a first ever MI. European/other comprised 76% of the population, Māori 11.5%, Pacific 5.1%, Indian 4.3% and Other Asian 2.9%. Over half (55%) of Māori, Pacific and Indian patients were admitted with their first MI before age 60 years, compared with 29% of European/other patients. Māori and Pacific patients had a higher burden of traditional and non-traditional cardiovascular risk factors, and despite being younger, were more likely to present with heart failure and, together with Indian peoples, advanced coronary disease at presentation with first MI. After adjustment for age and sex, Māori and Pacific, but not Indian or Other Asian patients had significantly higher all-cause mortality at one year compared with the European/other reference group (HR 2.55 (95% CI 2.12–3.07), HR 2.98 (95% CI 2.34–3.81) for Māori and Pacific respectively). When further adjusted for differences in clinical presentation, clinical history and cardiovascular risk factors, the excess mortality risk for Māori and Pacific patients was reduced substantially, but a differential persisted (HR 1.77 (95% CI 1.44–2.19), HR 1.42 (95% CI 1.07–1.83)) which was not further reduced by adjustment for differences in in-hospital management and discharge medications.

Conclusion

In New Zealand patients after their first MI there is a three-fold variation in one-year mortality based on ethnicity. At least half of the inequity in outcomes for Māori, and three-quarters for Pacific people, is associated with differences in preventable or modifiable clinical factors present at, or prior to, presentation.

Author Information

Janine Mazengarb, Cardiology Trainee, Counties Manukau District Health Board; Corina Grey, Public Health Physician, Auckland District Health Board; Mildred Lee, Biostatistician, Counties Manukau District Health Board; Katrina Poppe, Heart Foundation Hynds Senior Fellow, School of Population Health, University of Auckland, Auckland; Suneela Mehta, Public Health Physician and Senior Research Fellow, School of Population Health, University of Auckland, Auckland; Matire Harwood, Associate Professor, Department of General Practice and Primary Care, University of Auckland, Auckland; Wil Harrison, Cardiologist, Counties Manukau District Health Board; Nicki Earle, Heart Foundation Research Fellow, Department of Medicine, University of Auckland, Auckland; Rod Jackson, Professor, School of Population Health, University of Auckland, Auckland; Andrew Kerr, Cardiologist, Counties Manukau District Health Board; Adjunct Associate Professor of Medicine, University of Auckland, Auckland.

Acknowledgements

ANZACS-QI programme implementation, coordination and analysis: The ANZACS-QI software was developed and supported by Enigma Solutions. Programme implementation is coordinated by the National Institute for Health Innovation (NIHI) at the University of Auckland. The ANZACS-QI programme is funded by the NZ Ministry of Health. We thank the the National Health Board Analytic Services and Pharmac for enabling use of the national data sets. We also thank the VIEW team at the School of Population Health, University of Auckland for the curation and linkage of the national data. ANZACS-QI Governance group: Andrew Kerr (chair), Dean Boddington, Gary Sutcliffe, Gerry Devlin, Harvey White, John Edmond, Jonathon Tisch, Kim Marshall, Mayanna Lund, Michael Williams (deputy chair), Nick Fisher, Seif El Jack, Sue Riddle. ANZACS-QI Project management: Kristin Sutherland (Project Manager), Charmaine Flynn (Northern coordinator), Maxine Rhodes (Southern coordinator). Data analysis: Mildred Lee. Editorial assistant: Julia Kerr. Data management: Billy Wu (SOPH), Michelle Jenkins (NIHI), John Faatui (NIHI). We acknowledge all the New Zealand cardiologists, physicians, nursing staff and radiographers and all the patients who have supported and contributed to ANZACS-QI. ANZACS-QI hospital coordinators: Ascot Angiography: Summerscales, I. Money, J. Ashburton: Wilson, S. Auckland Hospital Belz, L. Stewart, R. Marshall, K. Bay of Islands: Cochran, G. Christchurch Hospital: Jackson, M, Sutherland J, McLaren S. Clutha Hospital: Reed, G. Campbell, B, McElrea J. Dargaville: Cripps, J. Katipa, K. Dunedin Hospital: Foote, C. Dunstan: Nixon, G. Shaw, M, Klahn R. Gisborne: Low, T. Gore: Lindley, G, Whitten C. Grey Base Hospital: Smith, L, Jennings M. Hawke’s Bay Hospital Soldiers Memorial: Brown, G. Grant, P. Hutt Hospital: Pinfold, S. Ferrier, K. Kitchen, R. Kaikoura Hospital: McCullough C. Kaitaia Hospital: Thompson, R. Smith, N. Lakes District Hospital: Burt, J. Mercy Angiography: Shah, A. Ubod, B. Mercy Heart Centre: Hall, S. Middlemore: Mcintosh, R. McLachlan, A. Midland Cardiovascular Services: Phillips, K. Nelson Hospital: Besley, J. Abernethy, H. North Shore Hospital: Gray, L. Oamaru: Gonzales, R, Clare L. Palmerston North Hospital: Kinloch, D. Rawene Hospital: Dorsay, C. Rotorua Hospital: Colby, C. Southland Hospital: Byers, R, Ghosh P. St Georges Hospital: Lissette, J, Lewis K. Taranaki Base Hospital: Ternouth, I. Spurway, M. Taumaranui: Pointon, L. Taupo Hospital: McAnanay, J. Tauranga Hospital: Goodson, J. Te Kuiti: Te Wano, T. Thames: Stutchbury, D. Timaru Hospital: Addidle, D. Tokoroa: Huitema, V. Waikato Hospital: Emerson, C. Pilay, R. Wairarapa Hospital: Matthews, T. Wairau Hospital: Langford, S, Ballagh D. Waitakere Hospital: Long, L. Waitemata Hospital: Newcombe, R. Wakefield Private Hospital: Murphy, S. Wellington Hospital: Scott, B, Wylie D. Whakatane Hospital: Bentley-Smith, M. Whanganui Hospital: Thompson, T. Whangarei Hospital: Vallancey, S.

Correspondence

Adjunct Associate Professor Andrew Kerr, Department of Cardiology, Middlemore Hospital, Otahuhu, Auckland 93311.

Correspondence Email

a.kerr@auckland.ac.nz

Competing Interests

Dr Mehta, Dr Kerr and Dr Poppe report grants from Health Research Council of New Zealand during the conduct of the study. Dr Grey and Dr Poppe report grants from Heart Foundation of New Zealand during the conduct of the study.

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