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Glossary ACS Acute coronary syndromes ACE Angiotensin converting enzyme AF Atrial fibrillation AMI Acute myocardial infarction ARB Angiotensin receptor blocker BP Blood pressure CABG Coronary artery bypass grafting CCU Coronary care unit CPR Cardiopulmonary resuscitation CKMB Creatine kinase MB fraction DAPT Dual antiplatelet therapy ED Emergency department EF Ejection fraction GTN Glyceryl trinitrate IRA Infarct related artery IC Intracoronary IV Intravenous LV Left ventricular LDL Low density lipoprotein LBBB Left bundle branch block MI Myocardial infarction PCI Percutaneous coronary intervention r-PA Reteplase SC Subcutaneous SL Sublingual STEMI ST-elevation myocardial infarction TIMI Thrombolysis in myocardial infarction TNK Tenecteplase TPA Tissue plasminogen activator UFH Unfractionated heparin Purpose These guidelines apply to the management of patients with ST-elevation myocardial infarction (STEMI) and are an update from the 2005 guidelines.1 They have been developed by representatives of all major New Zealand hospitals including general cardiologists, invasive cardiologists, non-invasive cardiologists, emergency department physicians and experts in rehabilitation and nursing (Appendix 1). The purpose of these guidelines are to provide a summary of the most up-to-date New Zealand2 and overseas evidence as well as recommendations of recent European Society of Cardiology (2012) and US (2013)3,4 guidelines and to make recommendations based on the evidence that will lead to the best outcomes for patients with STEMI in New Zealand. The guidelines are recommended for all health providers who care for patients with STEMI. For a detailed description of the levels of evidence cited in these guidelines, please see Appendix 2. These guidelines are intended for best clinical practice. Treatments and approaches need to be modified according to individualised assessment of patients risk and likelihood to benefit as well as patient preferences. Where doctors or hospitals are not able to meet the guidelines because of resource constraints it is important that there is documentation of communication between doctors and managers clearly defining the clinical implications of any resource shortages. Management ST segment elevation on the electrocardiogram (ECG) persisting for \u226520 minutes in the context of an acute coronary syndrome (ACS) is indicative of an occluded epicardial artery. Included within this subset are those patients presenting with presumed new left bundle branch block pattern on the ECG. When patients first present with ischaemic symptoms (chest pain or a surrogate such as shortness of breath) lasting \u226520 minutes, or syncope, their management (Figure 1) depends on whether ST elevation or presumed new onset (left bundle branch block) LBBB is present on the ECG or not. If the symptoms are \u2264 12 hours, urgent reperfusion with fibrinolysis, or catheter-based reperfusion is mandatory (Appendix 2). Good nursing care is a very important component of the care of patients with STEMI. Figure 1. STEMI algorithm Diagnosis The diagnosis of STEMI is defined as new ST elevation at the J point in at least 2 contiguous leads using the cut points defined below or presumed new LBBB. Investigations ECGs An ECG should be performed <10 minutes of presentation and reviewed immediately on first assessment. Class I; Level of Evidence B The ECG criteria eligibility for reperfusion are new ST elevation at the J point in two contiguous leads. Sex differences require different cut-points for women, since J point elevation in healthy women in leads V2 and V3 is less than in men.5,6 The following cut-points should be used: \u22652 mm in men>40 years,>2.5 mm in men <40 years, or \u22651.5 mm in women in leads V2-V3, and/or \u22651 mm in other leads. ST elevation may be observed in other conditions, such as acute pericarditis, LBBB, Brugada syndrome, stress cardiomyopathy and early re-polarization pattern. Supplemental leads, as well as serial ECG recordings, should always be considered in patients that present with ischaemic chest pain and a non-diagnostic initial ECG.7 Circumflex occlusion with ECG evidence of ischaemia in the left circumflex territory of the infero-basal wall of the LV is often overlooked. With an infero-basal MI due to circumflex artery occlusion there may be marked ST segment depression in leads V1 to V4 associated with tall R waves and upright T waves in the right precordial leads (V1 to V3). The best leads for recording circumflex territory ischemia are the posterior leads in the fifth interspace; V7 at the left posterior axillary line, V8 at the left midscapular line, and V9 at the left paraspinal border. These leads should be recorded when there is a high clinical suspicion for circumflex occlusion e.g.: ST segment depression in leads V1-3 or ongoing ischaemic symptoms or haemodynamic instability and a normal ECG. Class IIa; Level of Evidence C Patients are eligible for reperfusion if ST elevation is>0.5 mm. Right ventricular leads (V3R & V4R) reflect the free wall of the right ventricle and should be recorded in patients with inferior infarction. If there is ST elevation>0.5mm, (>1 mm in men <30 years) this is diagnostic of RV infarction. Class IIa; Level of Evidence C Often patients with new LBBB may not have an acute thrombotic occlusion and the diagnosis of MI is more difficult in the presence of LBBB.8,9 However, concordant ST-segment elevation or a previous ECG may be helpful to determine the presence of an acute MI in this setting. The Sgarbossa criteria define 3 criteria for diagnosing acute MI during LBBB. The 2 criteria with independent diagnostic value were concordant ST elevation>1mm (i.e., ST elevation with positive QRS complex) and precordial V1-3 ST depression>1 mm, a third criterion of discordant ST elevation>5 mm was suggestive but not diagnostic of acute MI. Patients with old LBBB, with ST elevation changes as above, and a good ischaemic history should have acute angiography. Atypical ECG presentations that require consideration for urgent reperfusion include ventricular paced rhythm and ST-segment elevation in lead aVR. In the context of symptoms of an ACS, and widespread ST depression, ST elevation in aVR suggests proximal LAD or left main disease and should be regarded as a STEMI equivalent. If the initial ECG is normal, and there is a high clinical suspicion of ongoing MI, serial ECGs should be performed at 5 to 10 minute intervals and optimally continuous ST segment monitoring should be performed. ECGs should be obtained every 6 to 8 hours in all other patients until an established diagnosis has been made. Patients who present with a history consistent with acute myocardial ischaemia and have an ECG with new or presumed new LBBB should be classified and managed as a STEMI. The absence of ST elevation or a new LBBB pattern does not exclude the presence of epicardial coronary artery occlusion, but the benefit of reperfusion has not been demonstrated among these patients. Cardiac biomarkers Blood samples for measurement of troponin levels, which are the preferred cardiac markers,10 should be obtained within 10 minutes of presentation. Class I; Level of Evidence C Measurement should be repeated 3 hours later and again if prolonged recurrent ischaemia occurs. Decisions on immediate management of STEMI should not await biomarker results. Class I; Level of Evidence C High sensitivity (hs) troponins are detected in many individuals and for the diagnosis of MI a \u2265 50% change (rise and/or fall) above the 99th/% is required at low levels (e.g. hsTroponin T \u226515-50 ng/L) and a \u226520% change with higher levels e.g.>50 ng/L hsTroponin T.11,12 Troponins (which are specific cardiac markers), may be elevated in conditions other than an MI.13,14 CKMB should not be measured if troponin assays are available. Other blood tests Blood should also be obtained for full blood count, electrolytes, glucose, renal function, liver functions and lipids. A chest X-ray should be performed, but in the absence of clinical features suggesting aortic dissection or other differential diagnoses, not before initiation of treatment. Acute echocardiography Acute echocardiography may be a useful adjunct when the diagnosis of MI is uncertain but must not delay primary PCI or administration of fibrinolytic therapy in clear cases. Class I; Level of Evidence C Regional wall motion abnormalities occur within minutes following coronary occlusion and their presence supports but is not specific for the diagnosis of MI. Echocardiography may also suggest alternative diagnoses such as pulmonary embolism, pericardial effusion, myocarditis and aortic dissection. The absence of wall-motion abnormalities excludes major MI. Echocardiography should be performed early in patients with shock and is useful in the detection and assessment of complications such as ventricular septal defect, sub acute rupture and LV thrombus. . Computed tomographic angiography In the emergency setting, the role of computed tomographic (CT) scanning should be confined to the differential diagnosis of acute aortic dissection or pulmonary embolism. Management Pre-hospital Pre-hospital triage has been one of the biggest advances in the management of STEMI and is strongly recommended as a critical factor in reducing times to reperfusion.Class I; Level of Evidence C Availability of automated external defibrillators is a key factor in increasing survival. Class I; Level of Evidence C Patients presenting at locations requiring transport times to the nearest hospital of greater than 45 minutes,15 and \u2018first medical contact to device time\u2019>120 minutes, should be considered for administration of pre-hospital fibrinolysis. Class I; Level of Evidence B Fibrinolytic therapy should be administered in patients without contraindications (see Table 8), if there are trained medical or paramedical staff able to interpret ECGs on-site (or able to transmit the ECG for interpretation)16,17 and trained in how to administer fibrinolytic therapy. Bolus thrombolytic agents (TNK or r-PA) should be administered together with aspirin and enoxaparin (see doses below). Class I; Level of Evidence B Monitoring Continuous ECG monitoring should be performed from first medical contact in all patients with suspected MI Class I; Level of Evidence B 12-lead ECGs should be recorded to assess ST segment recovery. This is recommended to be performed at 60 minutes after start of fibrinolytic infusion. Failure of reperfusion is defined as <50% ST segment resolution Adjunctive therapies for all patients Oxygen should be administered to patients who are breathless, hypoxic (saturations <93%), or who have heart failure or cardiogenic shock. Oxygen may be harmful if saturations are>93%. Oxygen may increase afterload via arterial vasoconstriction. A recent Cochrane analysis showed increased mortality with oxygen therapy.18 Sublingual GTN and morphine or fentanyl should be administered for pain relief (observe BP and RR). IV antiemetics should be given with morphine (metoclopramide 10 mg or cyclizine 25 mg). Aspirin All patients should immediately receive aspirin 150-300 mg which should be chewed if enteric-coated and 75-150 mg continued indefinitely (if there are no contraindications).Class I; Level of Evidence A This recommendation is based on the collaborative meta-analysis of randomised trials of antiplatelet therapy showing no relation of dose with efficacy19 and information from other studies showing increased bleeding with increasing aspirin doses.20 Table 1. Pre-hospital therapies Table 2. Emergency Department therapies Reperfusion therapy Urgent reperfusion of the ischaemic myocardium by restoration of flow in the occluded epicardial coronary artery is the primary therapeutic goal in patients with STEMI who present \u2264 12 hours of symptom onset. If reperfusion therapies are initiated early after symptom onset, the infarctions are smaller, complications are reduced and survival is greater.21 When epicardial flow is restored within 30 minutes of occlusion infarction may be aborted. Reperfusion can be achieved using a strategy of primary PCI, fibrinolysis or a pharmacoinvasive approach. Primary angioplasty is superior to fibrinolytic therapy in reducing mortality, reinfarction, and stroke. Therefore the preferred reperfusion strategy for STEMI is primary angioplasty if performed by an experienced team. Class I; Level of Evidence A However there may be situations where fibrinolytic therapy is appropriate such as treatment within 1 hour of symptom onset when outcomes with fibrinolytic therapy may be similar to those achieved with primary angioplasty. Table 3. Primary angioplasty compared with fibrinolytic therapy Primary PCI preferred Fibrinolytic therapy preferred Primary PCI capable catheterisation laboratory available (door-to-balloon time <90 minutes) Primary PCI capable catheterisation laboratory not available Appropriate operator and team experience Transfer for PCI not possible \u2264120 min Duration of symptoms \u22651 hour Duration of symptoms <1 hour (and delay to laboratory) Cardiogenic shock Difficult vascular access Contraindications to fibrinolysis (Table 8) Primary PCI should be performed in patients with STEMI and cardiogenic shock or acute severe heart failure, irrespective of time delay from MI onset22-24 Class I; Level of Evidence: B Reperfusion therapy is reasonable for patients with STEMI and symptom onset within the prior 12 to 24 hours who have clinical and/or ECG evidence of ongoing ischaemia. Primary PCI is the preferred strategy in this population. Class I; Level of Evidence C Reperfusion therapy with primary PCI may be considered in stable patients presenting 12-24 hours after symptom onset. Class IIa; Level of Evidence B Primary angioplasty The catheterisation laboratory staff should be notified by a single call,25 preferably while the patient is enroute to hospital, laboratory staff should aim to arrive in the catheterisation laboratory within 20 min of being contacted. On arrival at hospital, the patient should be taken to the catheterisation laboratory as soon as catheterisation laboratory staff are available. Class IIa; Level of Evidence B Table 4. Primary angioplasty: exclusion criteria Frailty, comorbidities, procedural risk, ability to benefit, and patient preferences must be taken into account. Class I; Level of Evidence C There should be no age criteria. Peripheral vascular disease, inability to lie flat (patients can be intubated), renal impairment and severe respiratory disease are not exclusions. Table 5. Angiography and PCI Intra-aortic balloon pumping Routine use of Intra-aortic balloon pumping IABP (in patients without shock) is not recommended. Class III; Level of Evidence A The Counterpulsation to Reduce Infarct Size Pre-PCI-Acute MI (CRISP AMI) trial showed no benefit of routine insertion of an IABP in patients with anterior MI without shock,26 and showed increased bleeding, which is consistent with previous data regarding the role of IABPs in patients with acute MI without cardiogenic shock.27 Aspiration thrombectomy Aspiration thrombectomy may be considered in patients undergoing primary PCI.28-33 Class IIb, Level of Evidence B One single-centre randomised trial, the Thrombus Aspiration during Percutaneous coronary intervention in Acute myocardial infarction (TAPAS) trial,31,32 showed improvement in indices of myocardial reperfusion (ST-segment resolution and myocardial blush) with routine use of manual thrombus aspiration before a balloon or a stent was introduced into the coronary artery. One-year follow-up showed a reduction in mortality with thrombus aspiration as a secondary endpoint. In the TASTE (Thrombus Aspiration in ST-Elevation Myocardial Infarction in Scandinavia) trial 7244 patients were randomised to receive thrombus aspiration. Thrombus aspiration resulted in no difference in 30-day mortality; 2.8% vs 3.0% or other efficacy or safety endpoints. Long-term follow-up is awaited.33 Stenting Stenting is recommended over balloon angioplasty alone. Class I; Level of Evidence A Drug eluting stents are be preferred, according to standard PCI guidelines. Class IIa, Level of Evidence A Bare-metal stents should be considered in patients with high bleeding risk, inability to comply with 6 months of dual antiplatelet therapy (DAPT), or anticipated invasive or surgical procedures in the next 6 months. Culprit vessel or multivessel PCI PCI of non-culprit lesions may be considered in patients with cardiogenic shock Class IIa; Level of Evidence B and persistent ischaemia after PCI of the culprit lesion. PCI of the non-culprit lesions at the time of primary PCI may also be considered in stenosis of>50%. Class IIb; Level of Evidence B34-39.In the PRAMI (Preventive Angioplasty in Acute Myocardial Infarction) trial39 246 patients with PCI of the non-infarct culprit lesions> 50% resulted in a reduction in the endpoint of cardiovascular death, MI or refractory angina at 23 months; HR 0.35; 95% CI 0.21 - 0.58; p<0.001. There was a trend for cardiac death to be reduced; HR 0.34; 95% CI 0.11 - 1.08; p=0.07. P2Y12 inhibitors Ticagrelor Administration of ticagrelor is the preferred P2Y12 inhibitor and should be given at presentation in all patients with STEMI undergoing primary PCI, with a 180 mg loading dose, even in patients who have already received clopidogrel, and then 90 mg bid for a year. Class I; Level of Evidence B Ticagrelor should be stopped 5 days prior to surgery. This recommendation is based on one trial, the PLATelet inhibition and patient Outcome (PLATO) trial, where there was a 22% (1.4% absolute) reduction in total mortality with a significant 16% (1.9% absolute) reduction in CV death, MI and stroke with diverging event curves up to 12 months. There was an increase in non CABG-related PLATO defined major bleeding (4.5%vs 3.8%, p=0.03)40 Contraindications are those on dialysis, those with \u2265 moderate liver dysfunction, those with severe lung disease, and those with advanced conduction system disease (\u2265 Mobitz type 2). Prasugrel Prasugrel (60 mg loading dose, then 10 mg daily) can be considered for patients who are not receiving a P2Y12 inhibitor (safety of switching is not well defined) and in diabetes, where a larger effect was shown in the Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel (TRITON) trial41,42 unless patients have had a previous stroke, transient ischaemic attack, <60 kg, or are at high bleeding risk. Class I; Level of Evidence B Prasugrel is funded by PHARMAC for 7 days after STEMI and for patients who have undergone drug eluting stent implantation, angioplasty or had a bare metal stent implanted in the previous 4 weeks and are clopidogrel-allergic or have experienced stent thrombosis whilst on clopidogrel. Prasugrel should be stopped 7 days prior to surgery. Clopidogrel Clopidogrel should be considered for use in patient cohorts with contraindications to ticagrelor and prasugrel and in patients at very high bleeding risk. In general clopidogrel should not be used unless ticagrelor or prasugrel are not available or these drugs have to be stopped for a major side effect. Class I; Level of Evidence C Antithrombotic therapy with primary PCI Unfractionated heparin (UFH) Class I; Level of Evidence C or bivalirudin Class I; Level of Evidence B can be used for primary PCI. In the absence of a single trial showing benefit enoxaparin is not recommended. There have been no placebo-controlled trials evaluating UFH in primary PCI but there is a large body of experience with this agent. One large open-label trial demonstrated the superiority of bivalirudin over the combination of UFH+GP IIb/IIIa inhibitor,43 with the benefit being driven by a marked reduction in bleeding. There was also decreased thrombocytopaenia. There was an increase in stent thrombosis in the first 30 days in the bivalirudin arm. The reduction in all cause and cardiovascular mortality at 30 days, was maintained up to 3 years.43 In the EUROMAX (European Ambulance Acute Coronary Syndrome Angiography) trial pre-hospital administration of bivalirudin in 2218 patients with STEMI reduced major bleeding by 47%; 2.6% vs 6.0%; p<0.001.44 There was no difference in death. There was an increase in stent thrombosis within 24 hours (1% vs 0.2%; p=0.007). Unfractionated heparin dosing With GP IIb/IIIa receptor antagonist planned: 50-to 70 -U/kg IV bolus. With no GP IIb/IIIa receptor antagonist planned: 70-to 100 -U/kg bolus. Bivalirudin dosing Bivalirudin: 0.75-mg/kg IV bolus, then 1.75-mg/kg/h infusion with or without prior treatment with UFH. Reduce infusion to 1 mg/kg/h with estimated creatinine clearance <30 mL/min. A bolus only can be given if the procedure is expected to be <1 hour. Bivalirudin is preferred over UFH in patients at high risk of bleeding. Class I; Level of Evidence C Glycoprotein IIb/IIIa inhibitors with primary PCI Routine upstream administration of IIb/IIIa inhibitors is not recommended for PCI and stenting. Class III; Level of Evidence B IIb/IIIa inhibitors (eptifibatide Class IIB; Level of Evidence B or abxicimab Class IIB; Level of Evidence A are recommended to be considered to be given selectively when there is angiographic thrombus, embolism or slow flow. Class II; Level of Evidence B High bolus dose tirofiban can be given upstream and has shown benefit 45,46 but is no longer funded by PHARMAC. IC rather than i.v. administration of GP IIb/IIIa inhibitors has been tested in several small studies with variable results.47 In the Intracoronary Abciximab Infusion and Aspiration Thrombectomy in Patients Undergoing Percutaneous Coronary Intervention for Anterior ST Segment Elevation Myocardial Infarction (INFUSE-AMI) trial comparing IC abxicimab versus no abxicimab there was a reduction in infarct size as measured by magnetic resonance imaging (MRI).30 In the large Abciximab Intracoronary versus Intravenous Drug Application 4 in STEMI (AIDA-4) trial there was a significant reduction in heart failure at 90 days but not at 12 months (p=0.07) with IC versus IV abxicimab.48 There was no reduction in the primary composite of death, reinfarction and heart failure at one year. There have been no trials of IC IIb/IIIa administration versus placebo for poor coronary flow, distal embolisation or large thrombus burden. There has been no evidence of harm with IC administration. It is recommended that IC administration and continuing IV administration be given for 18-24 hours in these circumstances. Class IIa; Level of Evidence C Dosing Abciximab: 0.25-mg/kg IV bolus, then 0.125 mcg/kg/min (maximum 10mcg/min). IC abxicimab 0.25-mg/kg bolus. Eptifibatide: (double bolus): 180-mcg/kg IV bolus, then 2 mcg/kg/min; a second 180-mcg/kg bolus is administered 10 minutes after the first bolus. In patients with creatinine clearance <50 mL/min the infusion should be reduced by 50%. The boluses can be given IC. PCI of a non-infarct artery before hospital discharge PCI is indicated in a non-infarct artery at a time separate from the primary PCI if recurrent ischaemia occurs at rest or on mild to moderate exercise, Class I; Level of Evidence C, and is reasonable in patients with inducible ischaemia on non-invasive testing or decreased fractional flow reserve <0.80. Class IIa; Level of Evidence B Table 6. Time targets for primary PCI Table 7. Audit of primary PCI All aspects of delay should be audited with regular feedback to all parties involved. Fibrinolytic therapy Fibrinolytic therapy is recommended within 12 hours of onset of ischaemic symptoms in patients without contraindications or primary PCI cannot be performed by an experienced team within 120 minutes of first medical contact. Class I; Level of Evidence A Choice of fibrinolytic In the absence of contraindications (Table 8) a fibrin specific agent (tPA, TNK, r-PA) is most ef

Summary

Abstract

The New Zealand branch of the Cardiac Society of Australia and New Zealand have produced guidelines on the randomisation of acute coronary symptoms since 2005. These have been developed by clinicians throughout New Zealand with the aim to improve quality of care. They focus on the most effective strategies based on evidence from clinical trials. The evidence is graded and the recommendations are patient focused. Patients should be informed of the risks and benefits of treatment and share in decision making.

Aim

Method

Results

Conclusion

Author Information

ST-Elevation Acute Coronary Syndrome Guidelines Group (refer to Appendix 1), The New Zealand Branch of The Cardiac Society of Australia and New Zealand, Wellington

Acknowledgements

We are extremely grateful to Charlene Nell for excellent secretarial assistance.

Correspondence

Professor Harvey White, Green Lane Cardiovascular Service, Auckland City Hospital, Private Bag 92024, Victoria St West, Auckland 1142, New Zealand. Fax: +64 (0)9 6309915;

Correspondence Email

HarveyW@adhb.govt.nz

Competing Interests

Nil

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Facilitated PCI in patients with ST-elevation myocardial infarction. N Engl J Med. 2008;358(21):2205-17. Assessment of the Safety and Efficacy of a New Treatment Strategy with Percutaneous Coronary Intervention (ASSENT-4 PCI) investigators. Primary versus tenecteplase-facilitated percutaneous coronary intervention in patients with ST-segment elevation acute myocardial infarction (ASSENT-4 PCI): randomised trial. Lancet. 2006;367(9510):569-78. Borgia F, Goodman SG, Halvorsen S, et al. Early routine percutaneous coronary intervention after fibrinolysis vs. standard therapy in ST-segment elevation myocardial infarction: a meta-analysis. Eur Heart J. 2010;31(17):2156-69. Armstrong PW, Gershlick AH, Goldstein P, et al. Fibrinolysis or primary PCI in ST-segment elevation myocardial infarction. N Engl J Med. 2013;368(15):1379-87. White HD, Wong CK, Gao W, et al. New ST-depression: an under-recognized high-risk category of \u2018complete\u2019 ST-resolution after reperfusion therapy. Eur Heart J: ACC. 2012;1(3):210-21. Barbash GI, Birnbaum Y, Bogaerts K, et al. Treatment of reinfarction after thrombolytic therapy for acute myocardial infarction: an analysis of outcome and treatment choices in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO 1) and Assessment of the Safety of a New Thrombolytic (ASSENT 2) studies. Circulation. 2001;103(7):954-60. Ellis C., Gamble, G., Devlin G, et al; for the New Zealand Acute Coronary Syndromes (NZACS) \u2018SNAPSHOT\u2019 Audit Group. The management of acute coronary syndrome patients across New Zealand in 2012: results of a third comprehensive nationwide audit and observations of current care. N Z M J. 2013: in press. White HD, Assmann SF, Sanborn TA, et al. Comparison of percutaneous coronary intervention and coronary artery bypass grafting after acute myocardial infarction complicated by cardiogenic shock: results from the Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock (SHOCK) trial. Circulation. 2005;112(13):1992-2001. Chen ZM, Pan HC, Chen YP, et al. Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. Lancet. 2005;366(9497):1622-32. Dargie HJ. Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial. Lancet. 2001;357(9266):1385-90. Poole-Wilson PA, Swedberg K, Cleland JGF, et al. Comparison of carvedilol and metoprolol on clinical outcomes in patients with chronic heart failure in the Carvedilol or Metoprolol European Trial (COMET): a randomised controlled trial. Lancet. 2003;362(9377):7-13. Thompson PL. Should beta-blockers still be routine after myocardial infarction? Curr Opin Cardiol. 2013;28(4):399-404. ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group. ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050 patients with suspected acute myocardial infarction. Lancet. 1995;345:669-85. Latini R, Tognoni G, Maggioni AP, et al. Clinical effects of early angiotensin-converting enzyme inhibitor treatment for acute myocardial infarction are similar in the presence and absence of aspirin: systematic overview of individual data from 96,712 randomized patients. Angiotensin-converting Enzyme Inhibitor Myocardial Infarction Collaborative Group. J Am Coll Cardiol. 2000;35(7):1801-7. Pfeffer MA, McMurray JJV, Velazquez EJ, et al. Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both [Erratum in: N Engl J Med. 2004;350:203]. 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Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro heart survey on atrial fibrillation. Chest. 2010;137(2):263-72. Wallentin L, Yusuf S, Ezekowitz MD, et al. Efficacy and safety of dabigatran compared with warfarin at different levels of international normalised ratio control for stroke prevention in atrial fibrillation: an analysis of the RE-LY trial. Lancet. 2010;376(9745):975-83. Pisters R, Lane DA, Nieuwlaat R, et al. A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation: the Euro Heart Survey. Chest. 2010;138(5):1093-100. Granger CB, Alexander JH, McMurray JJ, et al. Apixaban versus warfarin in patients with atrial fibrillation. N Engl J Med. 2011;365(11):981-92. Patel MR, Mahaffey KW, Garg J, et al. Rivaroxaban versus warfarin in nonvalvular atrial fibrillation. N Engl J Med. 2011;365(10):883-91. 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Glossary ACS Acute coronary syndromes ACE Angiotensin converting enzyme AF Atrial fibrillation AMI Acute myocardial infarction ARB Angiotensin receptor blocker BP Blood pressure CABG Coronary artery bypass grafting CCU Coronary care unit CPR Cardiopulmonary resuscitation CKMB Creatine kinase MB fraction DAPT Dual antiplatelet therapy ED Emergency department EF Ejection fraction GTN Glyceryl trinitrate IRA Infarct related artery IC Intracoronary IV Intravenous LV Left ventricular LDL Low density lipoprotein LBBB Left bundle branch block MI Myocardial infarction PCI Percutaneous coronary intervention r-PA Reteplase SC Subcutaneous SL Sublingual STEMI ST-elevation myocardial infarction TIMI Thrombolysis in myocardial infarction TNK Tenecteplase TPA Tissue plasminogen activator UFH Unfractionated heparin Purpose These guidelines apply to the management of patients with ST-elevation myocardial infarction (STEMI) and are an update from the 2005 guidelines.1 They have been developed by representatives of all major New Zealand hospitals including general cardiologists, invasive cardiologists, non-invasive cardiologists, emergency department physicians and experts in rehabilitation and nursing (Appendix 1). The purpose of these guidelines are to provide a summary of the most up-to-date New Zealand2 and overseas evidence as well as recommendations of recent European Society of Cardiology (2012) and US (2013)3,4 guidelines and to make recommendations based on the evidence that will lead to the best outcomes for patients with STEMI in New Zealand. The guidelines are recommended for all health providers who care for patients with STEMI. For a detailed description of the levels of evidence cited in these guidelines, please see Appendix 2. These guidelines are intended for best clinical practice. Treatments and approaches need to be modified according to individualised assessment of patients risk and likelihood to benefit as well as patient preferences. Where doctors or hospitals are not able to meet the guidelines because of resource constraints it is important that there is documentation of communication between doctors and managers clearly defining the clinical implications of any resource shortages. Management ST segment elevation on the electrocardiogram (ECG) persisting for \u226520 minutes in the context of an acute coronary syndrome (ACS) is indicative of an occluded epicardial artery. Included within this subset are those patients presenting with presumed new left bundle branch block pattern on the ECG. When patients first present with ischaemic symptoms (chest pain or a surrogate such as shortness of breath) lasting \u226520 minutes, or syncope, their management (Figure 1) depends on whether ST elevation or presumed new onset (left bundle branch block) LBBB is present on the ECG or not. If the symptoms are \u2264 12 hours, urgent reperfusion with fibrinolysis, or catheter-based reperfusion is mandatory (Appendix 2). Good nursing care is a very important component of the care of patients with STEMI. Figure 1. STEMI algorithm Diagnosis The diagnosis of STEMI is defined as new ST elevation at the J point in at least 2 contiguous leads using the cut points defined below or presumed new LBBB. Investigations ECGs An ECG should be performed <10 minutes of presentation and reviewed immediately on first assessment. Class I; Level of Evidence B The ECG criteria eligibility for reperfusion are new ST elevation at the J point in two contiguous leads. Sex differences require different cut-points for women, since J point elevation in healthy women in leads V2 and V3 is less than in men.5,6 The following cut-points should be used: \u22652 mm in men>40 years,>2.5 mm in men <40 years, or \u22651.5 mm in women in leads V2-V3, and/or \u22651 mm in other leads. ST elevation may be observed in other conditions, such as acute pericarditis, LBBB, Brugada syndrome, stress cardiomyopathy and early re-polarization pattern. Supplemental leads, as well as serial ECG recordings, should always be considered in patients that present with ischaemic chest pain and a non-diagnostic initial ECG.7 Circumflex occlusion with ECG evidence of ischaemia in the left circumflex territory of the infero-basal wall of the LV is often overlooked. With an infero-basal MI due to circumflex artery occlusion there may be marked ST segment depression in leads V1 to V4 associated with tall R waves and upright T waves in the right precordial leads (V1 to V3). The best leads for recording circumflex territory ischemia are the posterior leads in the fifth interspace; V7 at the left posterior axillary line, V8 at the left midscapular line, and V9 at the left paraspinal border. These leads should be recorded when there is a high clinical suspicion for circumflex occlusion e.g.: ST segment depression in leads V1-3 or ongoing ischaemic symptoms or haemodynamic instability and a normal ECG. Class IIa; Level of Evidence C Patients are eligible for reperfusion if ST elevation is>0.5 mm. Right ventricular leads (V3R & V4R) reflect the free wall of the right ventricle and should be recorded in patients with inferior infarction. If there is ST elevation>0.5mm, (>1 mm in men <30 years) this is diagnostic of RV infarction. Class IIa; Level of Evidence C Often patients with new LBBB may not have an acute thrombotic occlusion and the diagnosis of MI is more difficult in the presence of LBBB.8,9 However, concordant ST-segment elevation or a previous ECG may be helpful to determine the presence of an acute MI in this setting. The Sgarbossa criteria define 3 criteria for diagnosing acute MI during LBBB. The 2 criteria with independent diagnostic value were concordant ST elevation>1mm (i.e., ST elevation with positive QRS complex) and precordial V1-3 ST depression>1 mm, a third criterion of discordant ST elevation>5 mm was suggestive but not diagnostic of acute MI. Patients with old LBBB, with ST elevation changes as above, and a good ischaemic history should have acute angiography. Atypical ECG presentations that require consideration for urgent reperfusion include ventricular paced rhythm and ST-segment elevation in lead aVR. In the context of symptoms of an ACS, and widespread ST depression, ST elevation in aVR suggests proximal LAD or left main disease and should be regarded as a STEMI equivalent. If the initial ECG is normal, and there is a high clinical suspicion of ongoing MI, serial ECGs should be performed at 5 to 10 minute intervals and optimally continuous ST segment monitoring should be performed. ECGs should be obtained every 6 to 8 hours in all other patients until an established diagnosis has been made. Patients who present with a history consistent with acute myocardial ischaemia and have an ECG with new or presumed new LBBB should be classified and managed as a STEMI. The absence of ST elevation or a new LBBB pattern does not exclude the presence of epicardial coronary artery occlusion, but the benefit of reperfusion has not been demonstrated among these patients. Cardiac biomarkers Blood samples for measurement of troponin levels, which are the preferred cardiac markers,10 should be obtained within 10 minutes of presentation. Class I; Level of Evidence C Measurement should be repeated 3 hours later and again if prolonged recurrent ischaemia occurs. Decisions on immediate management of STEMI should not await biomarker results. Class I; Level of Evidence C High sensitivity (hs) troponins are detected in many individuals and for the diagnosis of MI a \u2265 50% change (rise and/or fall) above the 99th/% is required at low levels (e.g. hsTroponin T \u226515-50 ng/L) and a \u226520% change with higher levels e.g.>50 ng/L hsTroponin T.11,12 Troponins (which are specific cardiac markers), may be elevated in conditions other than an MI.13,14 CKMB should not be measured if troponin assays are available. Other blood tests Blood should also be obtained for full blood count, electrolytes, glucose, renal function, liver functions and lipids. A chest X-ray should be performed, but in the absence of clinical features suggesting aortic dissection or other differential diagnoses, not before initiation of treatment. Acute echocardiography Acute echocardiography may be a useful adjunct when the diagnosis of MI is uncertain but must not delay primary PCI or administration of fibrinolytic therapy in clear cases. Class I; Level of Evidence C Regional wall motion abnormalities occur within minutes following coronary occlusion and their presence supports but is not specific for the diagnosis of MI. Echocardiography may also suggest alternative diagnoses such as pulmonary embolism, pericardial effusion, myocarditis and aortic dissection. The absence of wall-motion abnormalities excludes major MI. Echocardiography should be performed early in patients with shock and is useful in the detection and assessment of complications such as ventricular septal defect, sub acute rupture and LV thrombus. . Computed tomographic angiography In the emergency setting, the role of computed tomographic (CT) scanning should be confined to the differential diagnosis of acute aortic dissection or pulmonary embolism. Management Pre-hospital Pre-hospital triage has been one of the biggest advances in the management of STEMI and is strongly recommended as a critical factor in reducing times to reperfusion.Class I; Level of Evidence C Availability of automated external defibrillators is a key factor in increasing survival. Class I; Level of Evidence C Patients presenting at locations requiring transport times to the nearest hospital of greater than 45 minutes,15 and \u2018first medical contact to device time\u2019>120 minutes, should be considered for administration of pre-hospital fibrinolysis. Class I; Level of Evidence B Fibrinolytic therapy should be administered in patients without contraindications (see Table 8), if there are trained medical or paramedical staff able to interpret ECGs on-site (or able to transmit the ECG for interpretation)16,17 and trained in how to administer fibrinolytic therapy. Bolus thrombolytic agents (TNK or r-PA) should be administered together with aspirin and enoxaparin (see doses below). Class I; Level of Evidence B Monitoring Continuous ECG monitoring should be performed from first medical contact in all patients with suspected MI Class I; Level of Evidence B 12-lead ECGs should be recorded to assess ST segment recovery. This is recommended to be performed at 60 minutes after start of fibrinolytic infusion. Failure of reperfusion is defined as <50% ST segment resolution Adjunctive therapies for all patients Oxygen should be administered to patients who are breathless, hypoxic (saturations <93%), or who have heart failure or cardiogenic shock. Oxygen may be harmful if saturations are>93%. Oxygen may increase afterload via arterial vasoconstriction. A recent Cochrane analysis showed increased mortality with oxygen therapy.18 Sublingual GTN and morphine or fentanyl should be administered for pain relief (observe BP and RR). IV antiemetics should be given with morphine (metoclopramide 10 mg or cyclizine 25 mg). Aspirin All patients should immediately receive aspirin 150-300 mg which should be chewed if enteric-coated and 75-150 mg continued indefinitely (if there are no contraindications).Class I; Level of Evidence A This recommendation is based on the collaborative meta-analysis of randomised trials of antiplatelet therapy showing no relation of dose with efficacy19 and information from other studies showing increased bleeding with increasing aspirin doses.20 Table 1. Pre-hospital therapies Table 2. Emergency Department therapies Reperfusion therapy Urgent reperfusion of the ischaemic myocardium by restoration of flow in the occluded epicardial coronary artery is the primary therapeutic goal in patients with STEMI who present \u2264 12 hours of symptom onset. If reperfusion therapies are initiated early after symptom onset, the infarctions are smaller, complications are reduced and survival is greater.21 When epicardial flow is restored within 30 minutes of occlusion infarction may be aborted. Reperfusion can be achieved using a strategy of primary PCI, fibrinolysis or a pharmacoinvasive approach. Primary angioplasty is superior to fibrinolytic therapy in reducing mortality, reinfarction, and stroke. Therefore the preferred reperfusion strategy for STEMI is primary angioplasty if performed by an experienced team. Class I; Level of Evidence A However there may be situations where fibrinolytic therapy is appropriate such as treatment within 1 hour of symptom onset when outcomes with fibrinolytic therapy may be similar to those achieved with primary angioplasty. Table 3. Primary angioplasty compared with fibrinolytic therapy Primary PCI preferred Fibrinolytic therapy preferred Primary PCI capable catheterisation laboratory available (door-to-balloon time <90 minutes) Primary PCI capable catheterisation laboratory not available Appropriate operator and team experience Transfer for PCI not possible \u2264120 min Duration of symptoms \u22651 hour Duration of symptoms <1 hour (and delay to laboratory) Cardiogenic shock Difficult vascular access Contraindications to fibrinolysis (Table 8) Primary PCI should be performed in patients with STEMI and cardiogenic shock or acute severe heart failure, irrespective of time delay from MI onset22-24 Class I; Level of Evidence: B Reperfusion therapy is reasonable for patients with STEMI and symptom onset within the prior 12 to 24 hours who have clinical and/or ECG evidence of ongoing ischaemia. Primary PCI is the preferred strategy in this population. Class I; Level of Evidence C Reperfusion therapy with primary PCI may be considered in stable patients presenting 12-24 hours after symptom onset. Class IIa; Level of Evidence B Primary angioplasty The catheterisation laboratory staff should be notified by a single call,25 preferably while the patient is enroute to hospital, laboratory staff should aim to arrive in the catheterisation laboratory within 20 min of being contacted. On arrival at hospital, the patient should be taken to the catheterisation laboratory as soon as catheterisation laboratory staff are available. Class IIa; Level of Evidence B Table 4. Primary angioplasty: exclusion criteria Frailty, comorbidities, procedural risk, ability to benefit, and patient preferences must be taken into account. Class I; Level of Evidence C There should be no age criteria. Peripheral vascular disease, inability to lie flat (patients can be intubated), renal impairment and severe respiratory disease are not exclusions. Table 5. Angiography and PCI Intra-aortic balloon pumping Routine use of Intra-aortic balloon pumping IABP (in patients without shock) is not recommended. Class III; Level of Evidence A The Counterpulsation to Reduce Infarct Size Pre-PCI-Acute MI (CRISP AMI) trial showed no benefit of routine insertion of an IABP in patients with anterior MI without shock,26 and showed increased bleeding, which is consistent with previous data regarding the role of IABPs in patients with acute MI without cardiogenic shock.27 Aspiration thrombectomy Aspiration thrombectomy may be considered in patients undergoing primary PCI.28-33 Class IIb, Level of Evidence B One single-centre randomised trial, the Thrombus Aspiration during Percutaneous coronary intervention in Acute myocardial infarction (TAPAS) trial,31,32 showed improvement in indices of myocardial reperfusion (ST-segment resolution and myocardial blush) with routine use of manual thrombus aspiration before a balloon or a stent was introduced into the coronary artery. One-year follow-up showed a reduction in mortality with thrombus aspiration as a secondary endpoint. In the TASTE (Thrombus Aspiration in ST-Elevation Myocardial Infarction in Scandinavia) trial 7244 patients were randomised to receive thrombus aspiration. Thrombus aspiration resulted in no difference in 30-day mortality; 2.8% vs 3.0% or other efficacy or safety endpoints. Long-term follow-up is awaited.33 Stenting Stenting is recommended over balloon angioplasty alone. Class I; Level of Evidence A Drug eluting stents are be preferred, according to standard PCI guidelines. Class IIa, Level of Evidence A Bare-metal stents should be considered in patients with high bleeding risk, inability to comply with 6 months of dual antiplatelet therapy (DAPT), or anticipated invasive or surgical procedures in the next 6 months. Culprit vessel or multivessel PCI PCI of non-culprit lesions may be considered in patients with cardiogenic shock Class IIa; Level of Evidence B and persistent ischaemia after PCI of the culprit lesion. PCI of the non-culprit lesions at the time of primary PCI may also be considered in stenosis of>50%. Class IIb; Level of Evidence B34-39.In the PRAMI (Preventive Angioplasty in Acute Myocardial Infarction) trial39 246 patients with PCI of the non-infarct culprit lesions> 50% resulted in a reduction in the endpoint of cardiovascular death, MI or refractory angina at 23 months; HR 0.35; 95% CI 0.21 - 0.58; p<0.001. There was a trend for cardiac death to be reduced; HR 0.34; 95% CI 0.11 - 1.08; p=0.07. P2Y12 inhibitors Ticagrelor Administration of ticagrelor is the preferred P2Y12 inhibitor and should be given at presentation in all patients with STEMI undergoing primary PCI, with a 180 mg loading dose, even in patients who have already received clopidogrel, and then 90 mg bid for a year. Class I; Level of Evidence B Ticagrelor should be stopped 5 days prior to surgery. This recommendation is based on one trial, the PLATelet inhibition and patient Outcome (PLATO) trial, where there was a 22% (1.4% absolute) reduction in total mortality with a significant 16% (1.9% absolute) reduction in CV death, MI and stroke with diverging event curves up to 12 months. There was an increase in non CABG-related PLATO defined major bleeding (4.5%vs 3.8%, p=0.03)40 Contraindications are those on dialysis, those with \u2265 moderate liver dysfunction, those with severe lung disease, and those with advanced conduction system disease (\u2265 Mobitz type 2). Prasugrel Prasugrel (60 mg loading dose, then 10 mg daily) can be considered for patients who are not receiving a P2Y12 inhibitor (safety of switching is not well defined) and in diabetes, where a larger effect was shown in the Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel (TRITON) trial41,42 unless patients have had a previous stroke, transient ischaemic attack, <60 kg, or are at high bleeding risk. Class I; Level of Evidence B Prasugrel is funded by PHARMAC for 7 days after STEMI and for patients who have undergone drug eluting stent implantation, angioplasty or had a bare metal stent implanted in the previous 4 weeks and are clopidogrel-allergic or have experienced stent thrombosis whilst on clopidogrel. Prasugrel should be stopped 7 days prior to surgery. Clopidogrel Clopidogrel should be considered for use in patient cohorts with contraindications to ticagrelor and prasugrel and in patients at very high bleeding risk. In general clopidogrel should not be used unless ticagrelor or prasugrel are not available or these drugs have to be stopped for a major side effect. Class I; Level of Evidence C Antithrombotic therapy with primary PCI Unfractionated heparin (UFH) Class I; Level of Evidence C or bivalirudin Class I; Level of Evidence B can be used for primary PCI. In the absence of a single trial showing benefit enoxaparin is not recommended. There have been no placebo-controlled trials evaluating UFH in primary PCI but there is a large body of experience with this agent. One large open-label trial demonstrated the superiority of bivalirudin over the combination of UFH+GP IIb/IIIa inhibitor,43 with the benefit being driven by a marked reduction in bleeding. There was also decreased thrombocytopaenia. There was an increase in stent thrombosis in the first 30 days in the bivalirudin arm. The reduction in all cause and cardiovascular mortality at 30 days, was maintained up to 3 years.43 In the EUROMAX (European Ambulance Acute Coronary Syndrome Angiography) trial pre-hospital administration of bivalirudin in 2218 patients with STEMI reduced major bleeding by 47%; 2.6% vs 6.0%; p<0.001.44 There was no difference in death. There was an increase in stent thrombosis within 24 hours (1% vs 0.2%; p=0.007). Unfractionated heparin dosing With GP IIb/IIIa receptor antagonist planned: 50-to 70 -U/kg IV bolus. With no GP IIb/IIIa receptor antagonist planned: 70-to 100 -U/kg bolus. Bivalirudin dosing Bivalirudin: 0.75-mg/kg IV bolus, then 1.75-mg/kg/h infusion with or without prior treatment with UFH. Reduce infusion to 1 mg/kg/h with estimated creatinine clearance <30 mL/min. A bolus only can be given if the procedure is expected to be <1 hour. Bivalirudin is preferred over UFH in patients at high risk of bleeding. Class I; Level of Evidence C Glycoprotein IIb/IIIa inhibitors with primary PCI Routine upstream administration of IIb/IIIa inhibitors is not recommended for PCI and stenting. Class III; Level of Evidence B IIb/IIIa inhibitors (eptifibatide Class IIB; Level of Evidence B or abxicimab Class IIB; Level of Evidence A are recommended to be considered to be given selectively when there is angiographic thrombus, embolism or slow flow. Class II; Level of Evidence B High bolus dose tirofiban can be given upstream and has shown benefit 45,46 but is no longer funded by PHARMAC. IC rather than i.v. administration of GP IIb/IIIa inhibitors has been tested in several small studies with variable results.47 In the Intracoronary Abciximab Infusion and Aspiration Thrombectomy in Patients Undergoing Percutaneous Coronary Intervention for Anterior ST Segment Elevation Myocardial Infarction (INFUSE-AMI) trial comparing IC abxicimab versus no abxicimab there was a reduction in infarct size as measured by magnetic resonance imaging (MRI).30 In the large Abciximab Intracoronary versus Intravenous Drug Application 4 in STEMI (AIDA-4) trial there was a significant reduction in heart failure at 90 days but not at 12 months (p=0.07) with IC versus IV abxicimab.48 There was no reduction in the primary composite of death, reinfarction and heart failure at one year. There have been no trials of IC IIb/IIIa administration versus placebo for poor coronary flow, distal embolisation or large thrombus burden. There has been no evidence of harm with IC administration. It is recommended that IC administration and continuing IV administration be given for 18-24 hours in these circumstances. Class IIa; Level of Evidence C Dosing Abciximab: 0.25-mg/kg IV bolus, then 0.125 mcg/kg/min (maximum 10mcg/min). IC abxicimab 0.25-mg/kg bolus. Eptifibatide: (double bolus): 180-mcg/kg IV bolus, then 2 mcg/kg/min; a second 180-mcg/kg bolus is administered 10 minutes after the first bolus. In patients with creatinine clearance <50 mL/min the infusion should be reduced by 50%. The boluses can be given IC. PCI of a non-infarct artery before hospital discharge PCI is indicated in a non-infarct artery at a time separate from the primary PCI if recurrent ischaemia occurs at rest or on mild to moderate exercise, Class I; Level of Evidence C, and is reasonable in patients with inducible ischaemia on non-invasive testing or decreased fractional flow reserve <0.80. Class IIa; Level of Evidence B Table 6. Time targets for primary PCI Table 7. Audit of primary PCI All aspects of delay should be audited with regular feedback to all parties involved. Fibrinolytic therapy Fibrinolytic therapy is recommended within 12 hours of onset of ischaemic symptoms in patients without contraindications or primary PCI cannot be performed by an experienced team within 120 minutes of first medical contact. Class I; Level of Evidence A Choice of fibrinolytic In the absence of contraindications (Table 8) a fibrin specific agent (tPA, TNK, r-PA) is most ef

Summary

Abstract

The New Zealand branch of the Cardiac Society of Australia and New Zealand have produced guidelines on the randomisation of acute coronary symptoms since 2005. These have been developed by clinicians throughout New Zealand with the aim to improve quality of care. They focus on the most effective strategies based on evidence from clinical trials. The evidence is graded and the recommendations are patient focused. Patients should be informed of the risks and benefits of treatment and share in decision making.

Aim

Method

Results

Conclusion

Author Information

ST-Elevation Acute Coronary Syndrome Guidelines Group (refer to Appendix 1), The New Zealand Branch of The Cardiac Society of Australia and New Zealand, Wellington

Acknowledgements

We are extremely grateful to Charlene Nell for excellent secretarial assistance.

Correspondence

Professor Harvey White, Green Lane Cardiovascular Service, Auckland City Hospital, Private Bag 92024, Victoria St West, Auckland 1142, New Zealand. Fax: +64 (0)9 6309915;

Correspondence Email

HarveyW@adhb.govt.nz

Competing Interests

Nil

- ST-Elevation Acute Coronary Syndrome Guidelines Group and the New Zealand Branch of the Cardiac Society of Australia and New Zealand. ST-elevation myocardial infarction: New Zealand management guidelines. N Z Med J. 2005;118(1223):1-21. Chew DP, Aroney CN, Aylward PE, et al. 2011 Addendum to the National Heart Foundation of Australia/Cardiac Society of Australia and New Zealand Guidelines for the management of acute coronary syndromes (ACS) 2006. Heart Lung Circ. 2011;20(8):487-502. O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127(4):529-55. Steg PG, James SK, Atar D, et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2012;33(20):2569-619. Macfarlane PW. Age, sex, and the ST amplitude in health and disease. J Electrocardiol. 2001;34 Suppl:235-41. White HD, Chew DP. Acute myocardial infarction. Lancet. 2008;372(9638):570-84. Wong CK, White HD. Patients with circumflex occlusions miss out on reperfusion: How to recognize and manage them. Curr Opin Cardiol. 2012;27(4):327-30. Jain S, Ting HT, Bell M, et al. Utility of left bundle branch block as a diagnostic criterion for acute myocardial infarction. Am J Cardiol. 2011 Apr 15;107(8):1111-6. Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. N Engl J Med. 1996;334(8):481-7. The Joint European Society of Cardiology/American College of Cardiology Committee. Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction. J Am Coll Cardiol. 2000;36(3):959-69. 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Glossary ACS Acute coronary syndromes ACE Angiotensin converting enzyme AF Atrial fibrillation AMI Acute myocardial infarction ARB Angiotensin receptor blocker BP Blood pressure CABG Coronary artery bypass grafting CCU Coronary care unit CPR Cardiopulmonary resuscitation CKMB Creatine kinase MB fraction DAPT Dual antiplatelet therapy ED Emergency department EF Ejection fraction GTN Glyceryl trinitrate IRA Infarct related artery IC Intracoronary IV Intravenous LV Left ventricular LDL Low density lipoprotein LBBB Left bundle branch block MI Myocardial infarction PCI Percutaneous coronary intervention r-PA Reteplase SC Subcutaneous SL Sublingual STEMI ST-elevation myocardial infarction TIMI Thrombolysis in myocardial infarction TNK Tenecteplase TPA Tissue plasminogen activator UFH Unfractionated heparin Purpose These guidelines apply to the management of patients with ST-elevation myocardial infarction (STEMI) and are an update from the 2005 guidelines.1 They have been developed by representatives of all major New Zealand hospitals including general cardiologists, invasive cardiologists, non-invasive cardiologists, emergency department physicians and experts in rehabilitation and nursing (Appendix 1). The purpose of these guidelines are to provide a summary of the most up-to-date New Zealand2 and overseas evidence as well as recommendations of recent European Society of Cardiology (2012) and US (2013)3,4 guidelines and to make recommendations based on the evidence that will lead to the best outcomes for patients with STEMI in New Zealand. The guidelines are recommended for all health providers who care for patients with STEMI. For a detailed description of the levels of evidence cited in these guidelines, please see Appendix 2. These guidelines are intended for best clinical practice. Treatments and approaches need to be modified according to individualised assessment of patients risk and likelihood to benefit as well as patient preferences. Where doctors or hospitals are not able to meet the guidelines because of resource constraints it is important that there is documentation of communication between doctors and managers clearly defining the clinical implications of any resource shortages. Management ST segment elevation on the electrocardiogram (ECG) persisting for \u226520 minutes in the context of an acute coronary syndrome (ACS) is indicative of an occluded epicardial artery. Included within this subset are those patients presenting with presumed new left bundle branch block pattern on the ECG. When patients first present with ischaemic symptoms (chest pain or a surrogate such as shortness of breath) lasting \u226520 minutes, or syncope, their management (Figure 1) depends on whether ST elevation or presumed new onset (left bundle branch block) LBBB is present on the ECG or not. If the symptoms are \u2264 12 hours, urgent reperfusion with fibrinolysis, or catheter-based reperfusion is mandatory (Appendix 2). Good nursing care is a very important component of the care of patients with STEMI. Figure 1. STEMI algorithm Diagnosis The diagnosis of STEMI is defined as new ST elevation at the J point in at least 2 contiguous leads using the cut points defined below or presumed new LBBB. Investigations ECGs An ECG should be performed <10 minutes of presentation and reviewed immediately on first assessment. Class I; Level of Evidence B The ECG criteria eligibility for reperfusion are new ST elevation at the J point in two contiguous leads. Sex differences require different cut-points for women, since J point elevation in healthy women in leads V2 and V3 is less than in men.5,6 The following cut-points should be used: \u22652 mm in men>40 years,>2.5 mm in men <40 years, or \u22651.5 mm in women in leads V2-V3, and/or \u22651 mm in other leads. ST elevation may be observed in other conditions, such as acute pericarditis, LBBB, Brugada syndrome, stress cardiomyopathy and early re-polarization pattern. Supplemental leads, as well as serial ECG recordings, should always be considered in patients that present with ischaemic chest pain and a non-diagnostic initial ECG.7 Circumflex occlusion with ECG evidence of ischaemia in the left circumflex territory of the infero-basal wall of the LV is often overlooked. With an infero-basal MI due to circumflex artery occlusion there may be marked ST segment depression in leads V1 to V4 associated with tall R waves and upright T waves in the right precordial leads (V1 to V3). The best leads for recording circumflex territory ischemia are the posterior leads in the fifth interspace; V7 at the left posterior axillary line, V8 at the left midscapular line, and V9 at the left paraspinal border. These leads should be recorded when there is a high clinical suspicion for circumflex occlusion e.g.: ST segment depression in leads V1-3 or ongoing ischaemic symptoms or haemodynamic instability and a normal ECG. Class IIa; Level of Evidence C Patients are eligible for reperfusion if ST elevation is>0.5 mm. Right ventricular leads (V3R & V4R) reflect the free wall of the right ventricle and should be recorded in patients with inferior infarction. If there is ST elevation>0.5mm, (>1 mm in men <30 years) this is diagnostic of RV infarction. Class IIa; Level of Evidence C Often patients with new LBBB may not have an acute thrombotic occlusion and the diagnosis of MI is more difficult in the presence of LBBB.8,9 However, concordant ST-segment elevation or a previous ECG may be helpful to determine the presence of an acute MI in this setting. The Sgarbossa criteria define 3 criteria for diagnosing acute MI during LBBB. The 2 criteria with independent diagnostic value were concordant ST elevation>1mm (i.e., ST elevation with positive QRS complex) and precordial V1-3 ST depression>1 mm, a third criterion of discordant ST elevation>5 mm was suggestive but not diagnostic of acute MI. Patients with old LBBB, with ST elevation changes as above, and a good ischaemic history should have acute angiography. Atypical ECG presentations that require consideration for urgent reperfusion include ventricular paced rhythm and ST-segment elevation in lead aVR. In the context of symptoms of an ACS, and widespread ST depression, ST elevation in aVR suggests proximal LAD or left main disease and should be regarded as a STEMI equivalent. If the initial ECG is normal, and there is a high clinical suspicion of ongoing MI, serial ECGs should be performed at 5 to 10 minute intervals and optimally continuous ST segment monitoring should be performed. ECGs should be obtained every 6 to 8 hours in all other patients until an established diagnosis has been made. Patients who present with a history consistent with acute myocardial ischaemia and have an ECG with new or presumed new LBBB should be classified and managed as a STEMI. The absence of ST elevation or a new LBBB pattern does not exclude the presence of epicardial coronary artery occlusion, but the benefit of reperfusion has not been demonstrated among these patients. Cardiac biomarkers Blood samples for measurement of troponin levels, which are the preferred cardiac markers,10 should be obtained within 10 minutes of presentation. Class I; Level of Evidence C Measurement should be repeated 3 hours later and again if prolonged recurrent ischaemia occurs. Decisions on immediate management of STEMI should not await biomarker results. Class I; Level of Evidence C High sensitivity (hs) troponins are detected in many individuals and for the diagnosis of MI a \u2265 50% change (rise and/or fall) above the 99th/% is required at low levels (e.g. hsTroponin T \u226515-50 ng/L) and a \u226520% change with higher levels e.g.>50 ng/L hsTroponin T.11,12 Troponins (which are specific cardiac markers), may be elevated in conditions other than an MI.13,14 CKMB should not be measured if troponin assays are available. Other blood tests Blood should also be obtained for full blood count, electrolytes, glucose, renal function, liver functions and lipids. A chest X-ray should be performed, but in the absence of clinical features suggesting aortic dissection or other differential diagnoses, not before initiation of treatment. Acute echocardiography Acute echocardiography may be a useful adjunct when the diagnosis of MI is uncertain but must not delay primary PCI or administration of fibrinolytic therapy in clear cases. Class I; Level of Evidence C Regional wall motion abnormalities occur within minutes following coronary occlusion and their presence supports but is not specific for the diagnosis of MI. Echocardiography may also suggest alternative diagnoses such as pulmonary embolism, pericardial effusion, myocarditis and aortic dissection. The absence of wall-motion abnormalities excludes major MI. Echocardiography should be performed early in patients with shock and is useful in the detection and assessment of complications such as ventricular septal defect, sub acute rupture and LV thrombus. . Computed tomographic angiography In the emergency setting, the role of computed tomographic (CT) scanning should be confined to the differential diagnosis of acute aortic dissection or pulmonary embolism. Management Pre-hospital Pre-hospital triage has been one of the biggest advances in the management of STEMI and is strongly recommended as a critical factor in reducing times to reperfusion.Class I; Level of Evidence C Availability of automated external defibrillators is a key factor in increasing survival. Class I; Level of Evidence C Patients presenting at locations requiring transport times to the nearest hospital of greater than 45 minutes,15 and \u2018first medical contact to device time\u2019>120 minutes, should be considered for administration of pre-hospital fibrinolysis. Class I; Level of Evidence B Fibrinolytic therapy should be administered in patients without contraindications (see Table 8), if there are trained medical or paramedical staff able to interpret ECGs on-site (or able to transmit the ECG for interpretation)16,17 and trained in how to administer fibrinolytic therapy. Bolus thrombolytic agents (TNK or r-PA) should be administered together with aspirin and enoxaparin (see doses below). Class I; Level of Evidence B Monitoring Continuous ECG monitoring should be performed from first medical contact in all patients with suspected MI Class I; Level of Evidence B 12-lead ECGs should be recorded to assess ST segment recovery. This is recommended to be performed at 60 minutes after start of fibrinolytic infusion. Failure of reperfusion is defined as <50% ST segment resolution Adjunctive therapies for all patients Oxygen should be administered to patients who are breathless, hypoxic (saturations <93%), or who have heart failure or cardiogenic shock. Oxygen may be harmful if saturations are>93%. Oxygen may increase afterload via arterial vasoconstriction. A recent Cochrane analysis showed increased mortality with oxygen therapy.18 Sublingual GTN and morphine or fentanyl should be administered for pain relief (observe BP and RR). IV antiemetics should be given with morphine (metoclopramide 10 mg or cyclizine 25 mg). Aspirin All patients should immediately receive aspirin 150-300 mg which should be chewed if enteric-coated and 75-150 mg continued indefinitely (if there are no contraindications).Class I; Level of Evidence A This recommendation is based on the collaborative meta-analysis of randomised trials of antiplatelet therapy showing no relation of dose with efficacy19 and information from other studies showing increased bleeding with increasing aspirin doses.20 Table 1. Pre-hospital therapies Table 2. Emergency Department therapies Reperfusion therapy Urgent reperfusion of the ischaemic myocardium by restoration of flow in the occluded epicardial coronary artery is the primary therapeutic goal in patients with STEMI who present \u2264 12 hours of symptom onset. If reperfusion therapies are initiated early after symptom onset, the infarctions are smaller, complications are reduced and survival is greater.21 When epicardial flow is restored within 30 minutes of occlusion infarction may be aborted. Reperfusion can be achieved using a strategy of primary PCI, fibrinolysis or a pharmacoinvasive approach. Primary angioplasty is superior to fibrinolytic therapy in reducing mortality, reinfarction, and stroke. Therefore the preferred reperfusion strategy for STEMI is primary angioplasty if performed by an experienced team. Class I; Level of Evidence A However there may be situations where fibrinolytic therapy is appropriate such as treatment within 1 hour of symptom onset when outcomes with fibrinolytic therapy may be similar to those achieved with primary angioplasty. Table 3. Primary angioplasty compared with fibrinolytic therapy Primary PCI preferred Fibrinolytic therapy preferred Primary PCI capable catheterisation laboratory available (door-to-balloon time <90 minutes) Primary PCI capable catheterisation laboratory not available Appropriate operator and team experience Transfer for PCI not possible \u2264120 min Duration of symptoms \u22651 hour Duration of symptoms <1 hour (and delay to laboratory) Cardiogenic shock Difficult vascular access Contraindications to fibrinolysis (Table 8) Primary PCI should be performed in patients with STEMI and cardiogenic shock or acute severe heart failure, irrespective of time delay from MI onset22-24 Class I; Level of Evidence: B Reperfusion therapy is reasonable for patients with STEMI and symptom onset within the prior 12 to 24 hours who have clinical and/or ECG evidence of ongoing ischaemia. Primary PCI is the preferred strategy in this population. Class I; Level of Evidence C Reperfusion therapy with primary PCI may be considered in stable patients presenting 12-24 hours after symptom onset. Class IIa; Level of Evidence B Primary angioplasty The catheterisation laboratory staff should be notified by a single call,25 preferably while the patient is enroute to hospital, laboratory staff should aim to arrive in the catheterisation laboratory within 20 min of being contacted. On arrival at hospital, the patient should be taken to the catheterisation laboratory as soon as catheterisation laboratory staff are available. Class IIa; Level of Evidence B Table 4. Primary angioplasty: exclusion criteria Frailty, comorbidities, procedural risk, ability to benefit, and patient preferences must be taken into account. Class I; Level of Evidence C There should be no age criteria. Peripheral vascular disease, inability to lie flat (patients can be intubated), renal impairment and severe respiratory disease are not exclusions. Table 5. Angiography and PCI Intra-aortic balloon pumping Routine use of Intra-aortic balloon pumping IABP (in patients without shock) is not recommended. Class III; Level of Evidence A The Counterpulsation to Reduce Infarct Size Pre-PCI-Acute MI (CRISP AMI) trial showed no benefit of routine insertion of an IABP in patients with anterior MI without shock,26 and showed increased bleeding, which is consistent with previous data regarding the role of IABPs in patients with acute MI without cardiogenic shock.27 Aspiration thrombectomy Aspiration thrombectomy may be considered in patients undergoing primary PCI.28-33 Class IIb, Level of Evidence B One single-centre randomised trial, the Thrombus Aspiration during Percutaneous coronary intervention in Acute myocardial infarction (TAPAS) trial,31,32 showed improvement in indices of myocardial reperfusion (ST-segment resolution and myocardial blush) with routine use of manual thrombus aspiration before a balloon or a stent was introduced into the coronary artery. One-year follow-up showed a reduction in mortality with thrombus aspiration as a secondary endpoint. In the TASTE (Thrombus Aspiration in ST-Elevation Myocardial Infarction in Scandinavia) trial 7244 patients were randomised to receive thrombus aspiration. Thrombus aspiration resulted in no difference in 30-day mortality; 2.8% vs 3.0% or other efficacy or safety endpoints. Long-term follow-up is awaited.33 Stenting Stenting is recommended over balloon angioplasty alone. Class I; Level of Evidence A Drug eluting stents are be preferred, according to standard PCI guidelines. Class IIa, Level of Evidence A Bare-metal stents should be considered in patients with high bleeding risk, inability to comply with 6 months of dual antiplatelet therapy (DAPT), or anticipated invasive or surgical procedures in the next 6 months. Culprit vessel or multivessel PCI PCI of non-culprit lesions may be considered in patients with cardiogenic shock Class IIa; Level of Evidence B and persistent ischaemia after PCI of the culprit lesion. PCI of the non-culprit lesions at the time of primary PCI may also be considered in stenosis of>50%. Class IIb; Level of Evidence B34-39.In the PRAMI (Preventive Angioplasty in Acute Myocardial Infarction) trial39 246 patients with PCI of the non-infarct culprit lesions> 50% resulted in a reduction in the endpoint of cardiovascular death, MI or refractory angina at 23 months; HR 0.35; 95% CI 0.21 - 0.58; p<0.001. There was a trend for cardiac death to be reduced; HR 0.34; 95% CI 0.11 - 1.08; p=0.07. P2Y12 inhibitors Ticagrelor Administration of ticagrelor is the preferred P2Y12 inhibitor and should be given at presentation in all patients with STEMI undergoing primary PCI, with a 180 mg loading dose, even in patients who have already received clopidogrel, and then 90 mg bid for a year. Class I; Level of Evidence B Ticagrelor should be stopped 5 days prior to surgery. This recommendation is based on one trial, the PLATelet inhibition and patient Outcome (PLATO) trial, where there was a 22% (1.4% absolute) reduction in total mortality with a significant 16% (1.9% absolute) reduction in CV death, MI and stroke with diverging event curves up to 12 months. There was an increase in non CABG-related PLATO defined major bleeding (4.5%vs 3.8%, p=0.03)40 Contraindications are those on dialysis, those with \u2265 moderate liver dysfunction, those with severe lung disease, and those with advanced conduction system disease (\u2265 Mobitz type 2). Prasugrel Prasugrel (60 mg loading dose, then 10 mg daily) can be considered for patients who are not receiving a P2Y12 inhibitor (safety of switching is not well defined) and in diabetes, where a larger effect was shown in the Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel (TRITON) trial41,42 unless patients have had a previous stroke, transient ischaemic attack, <60 kg, or are at high bleeding risk. Class I; Level of Evidence B Prasugrel is funded by PHARMAC for 7 days after STEMI and for patients who have undergone drug eluting stent implantation, angioplasty or had a bare metal stent implanted in the previous 4 weeks and are clopidogrel-allergic or have experienced stent thrombosis whilst on clopidogrel. Prasugrel should be stopped 7 days prior to surgery. Clopidogrel Clopidogrel should be considered for use in patient cohorts with contraindications to ticagrelor and prasugrel and in patients at very high bleeding risk. In general clopidogrel should not be used unless ticagrelor or prasugrel are not available or these drugs have to be stopped for a major side effect. Class I; Level of Evidence C Antithrombotic therapy with primary PCI Unfractionated heparin (UFH) Class I; Level of Evidence C or bivalirudin Class I; Level of Evidence B can be used for primary PCI. In the absence of a single trial showing benefit enoxaparin is not recommended. There have been no placebo-controlled trials evaluating UFH in primary PCI but there is a large body of experience with this agent. One large open-label trial demonstrated the superiority of bivalirudin over the combination of UFH+GP IIb/IIIa inhibitor,43 with the benefit being driven by a marked reduction in bleeding. There was also decreased thrombocytopaenia. There was an increase in stent thrombosis in the first 30 days in the bivalirudin arm. The reduction in all cause and cardiovascular mortality at 30 days, was maintained up to 3 years.43 In the EUROMAX (European Ambulance Acute Coronary Syndrome Angiography) trial pre-hospital administration of bivalirudin in 2218 patients with STEMI reduced major bleeding by 47%; 2.6% vs 6.0%; p<0.001.44 There was no difference in death. There was an increase in stent thrombosis within 24 hours (1% vs 0.2%; p=0.007). Unfractionated heparin dosing With GP IIb/IIIa receptor antagonist planned: 50-to 70 -U/kg IV bolus. With no GP IIb/IIIa receptor antagonist planned: 70-to 100 -U/kg bolus. Bivalirudin dosing Bivalirudin: 0.75-mg/kg IV bolus, then 1.75-mg/kg/h infusion with or without prior treatment with UFH. Reduce infusion to 1 mg/kg/h with estimated creatinine clearance <30 mL/min. A bolus only can be given if the procedure is expected to be <1 hour. Bivalirudin is preferred over UFH in patients at high risk of bleeding. Class I; Level of Evidence C Glycoprotein IIb/IIIa inhibitors with primary PCI Routine upstream administration of IIb/IIIa inhibitors is not recommended for PCI and stenting. Class III; Level of Evidence B IIb/IIIa inhibitors (eptifibatide Class IIB; Level of Evidence B or abxicimab Class IIB; Level of Evidence A are recommended to be considered to be given selectively when there is angiographic thrombus, embolism or slow flow. Class II; Level of Evidence B High bolus dose tirofiban can be given upstream and has shown benefit 45,46 but is no longer funded by PHARMAC. IC rather than i.v. administration of GP IIb/IIIa inhibitors has been tested in several small studies with variable results.47 In the Intracoronary Abciximab Infusion and Aspiration Thrombectomy in Patients Undergoing Percutaneous Coronary Intervention for Anterior ST Segment Elevation Myocardial Infarction (INFUSE-AMI) trial comparing IC abxicimab versus no abxicimab there was a reduction in infarct size as measured by magnetic resonance imaging (MRI).30 In the large Abciximab Intracoronary versus Intravenous Drug Application 4 in STEMI (AIDA-4) trial there was a significant reduction in heart failure at 90 days but not at 12 months (p=0.07) with IC versus IV abxicimab.48 There was no reduction in the primary composite of death, reinfarction and heart failure at one year. There have been no trials of IC IIb/IIIa administration versus placebo for poor coronary flow, distal embolisation or large thrombus burden. There has been no evidence of harm with IC administration. It is recommended that IC administration and continuing IV administration be given for 18-24 hours in these circumstances. Class IIa; Level of Evidence C Dosing Abciximab: 0.25-mg/kg IV bolus, then 0.125 mcg/kg/min (maximum 10mcg/min). IC abxicimab 0.25-mg/kg bolus. Eptifibatide: (double bolus): 180-mcg/kg IV bolus, then 2 mcg/kg/min; a second 180-mcg/kg bolus is administered 10 minutes after the first bolus. In patients with creatinine clearance <50 mL/min the infusion should be reduced by 50%. The boluses can be given IC. PCI of a non-infarct artery before hospital discharge PCI is indicated in a non-infarct artery at a time separate from the primary PCI if recurrent ischaemia occurs at rest or on mild to moderate exercise, Class I; Level of Evidence C, and is reasonable in patients with inducible ischaemia on non-invasive testing or decreased fractional flow reserve <0.80. Class IIa; Level of Evidence B Table 6. Time targets for primary PCI Table 7. Audit of primary PCI All aspects of delay should be audited with regular feedback to all parties involved. Fibrinolytic therapy Fibrinolytic therapy is recommended within 12 hours of onset of ischaemic symptoms in patients without contraindications or primary PCI cannot be performed by an experienced team within 120 minutes of first medical contact. Class I; Level of Evidence A Choice of fibrinolytic In the absence of contraindications (Table 8) a fibrin specific agent (tPA, TNK, r-PA) is most ef

Summary

Abstract

The New Zealand branch of the Cardiac Society of Australia and New Zealand have produced guidelines on the randomisation of acute coronary symptoms since 2005. These have been developed by clinicians throughout New Zealand with the aim to improve quality of care. They focus on the most effective strategies based on evidence from clinical trials. The evidence is graded and the recommendations are patient focused. Patients should be informed of the risks and benefits of treatment and share in decision making.

Aim

Method

Results

Conclusion

Author Information

ST-Elevation Acute Coronary Syndrome Guidelines Group (refer to Appendix 1), The New Zealand Branch of The Cardiac Society of Australia and New Zealand, Wellington

Acknowledgements

We are extremely grateful to Charlene Nell for excellent secretarial assistance.

Correspondence

Professor Harvey White, Green Lane Cardiovascular Service, Auckland City Hospital, Private Bag 92024, Victoria St West, Auckland 1142, New Zealand. Fax: +64 (0)9 6309915;

Correspondence Email

HarveyW@adhb.govt.nz

Competing Interests

Nil

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