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The risk of sudden cardiac death from ventricular fibrillation can be reduced by access to and use of a defibrillator. Coronary care ambulances with skilled paramedical staff have saved many lives since their introduction to Australia in the late 1960s.² Increasingly, strategic placement of semi-automatic defibrillators -- for example, in large passenger aircraft and football stadiums -- is being considered, to further improve out-of-hospital survival. Once the patient reaches hospital, modern reperfusion strategies such as thrombo lysis and acute angioplasty can save lives, limit myocardial damage and reduce subsequent cardiac disability.^3,4

Improved understanding of myocardial infarction from angiographic and postmortem studies has reaffirmed that most cases are indeed due to coronary thrombosis. The need to achieve coronary reperfusion as early as possible has long been recognised from pathophysiological studies and clinical trial experience.^3,4 Since the mid 1980s, thrombolytic therapy has been studied in over 200 000 patients,³ and a recent overview has shown very clearly that streptokinase and recombinant tissue plasminogen activator (t-PA) are effective thrombolytic agents in acute myocardial infarction. Their appropriate use in patients with suspected myocardial infarction can save 20-30 lives per 1000 patients treated over the first 35 days,³ and there is the prospect of even better outcomes with new thrombolytic agents. More recently, reperfusion with acute coronary angioplasty has been shown to be equivalent to thrombolysis in most centres and to have superior outcomes in some centres, particularly those with a high level of expertise and readily available angioplasty services.⁴ The use of intracoronary stents adjunctive to angioplasty may improve even further the early outcome, with a reduced risk of late restenosis.

The average loss of life per hour of delay of thrombolytic therapy is 1.6 lives per 1000 patients treated.³ The myocardial infarction triage and intervention trial in Seattle demonstrated even more accurately the importance of urgent treatment in the first hour.⁵ For patients surviving to hospital and being treated within 70 minutes of symptom onset, the 28-day mortality rate was 1.2% and only 5% of the left ventricular mass was infarcted; those treated later than 70 minutes had a mortality rate of 8.7% and 11% of myocardium was infarcted. These benefits were demonstrated with thrombolytic regimens now known to achieve early patency and restoration of normal coronary blood flow in less than half the patients treated. With the more aggressive reperfusion strategies now available the prospects are even brighter. The first hour after the onset of coronary thrombosis is indeed the "golden hour" of opportunity for preserving heart muscle and saving lives.

Given what can be achieved with early treatment, the reluctance of patients who suffer a heart attack to present to hospital is disappointing. Previous Australian studies^8,9 have shown avoidable delays in presentation of up to several hours from the onset of symptoms. In this issue of the Journal Dracup and colleagues provide further evidence of this risk-taking behaviour -- they report an unusually long median delay of 6.4 hours, even longer than the approximately two-hour delay reported by Leitch et al.⁸ in a Sydney-based study in 1989 and the approximately 1.2-hour delay found by Bett et al.⁹ in a study of 22 centres in 1988-89. The difference is probably partly due to differences in the definition of time of onset. Dracup et al. report the duration from onset of the first symptoms until hospital presentation, whereas Leitch et al. reported the time of onset of the symptom which initiated action until hospital presentation⁸ (which does not take into account the duration of any preceding intermittent symptoms), and Bett et al. reported the time from onset of the symptom which initiated action to when "help was first sought"⁹ (as opposed to hospital presentation). Thus, the latter studies would be expected to give a shorter average interval than that reported by Dracup et al.

It is noteworthy that Dracup et al. conducted their study before the May 1996 Heart Foundation Heart Week campaign, which emphasised how to recognise symptoms of heart attack, with posters and television commercials depicting squeezing chest pain as a python-like grip, and the need for early action by patients suffering symptoms of a heart attack. Dracup et al. found that the patients who recognised their symptoms as cardiac in origin had only one-third the response time of those who did not. It would be interesting to see if a follow-up study showed any effect of the 1996 campaign.

Although the complex human response to chest pain is more likely to be instinctive rather than knowledge-based,⁹ Dracup and colleagues provide further useful insight into factors that cause delay. The independent predictors of delay were educational status (slower response times in less educated patients), a desire not to cause trouble, failure to recognise symptoms as being cardiac in origin, and an intermittent pattern of symptoms. The message for future public education campaigns is clear -- publicise the symptoms of a possible heart attack, emphasise the importance of reporting them (no-one ever died of embarrassment), and ensure that the message is aimed at all educational levels. The message for health professionals is especially clear -- a third of patients reported that they learnt about heart attack symptoms from a health professional. Doctors and nurses dealing with existing heart patients or those with substantial risk factors for myocardial infarction have many opportunities to educate patients about heart attack symptoms and to give clear instructions on how -- and why -- they should summon an ambulance and get to a hospital fast.

Paul E Langton
Cardiology Research Fellow, Sir Charles Gairdner Hospital, Perth, WA

Peter L Thompson
Clinical Professor, Department of Cardiovascular Medicine, Sir Charles Gairdner Hospital, Perth, WA

1. Tunstall-Pedoe H, Kuulasmaa K, Amouzel P, et al. Myocardial infarction and coronary deaths in the World Health Organization MONICA project. Circulation 1994; 90: 563-612.
2. O'Rourke MF. Acute myocardial infarction: prehospital coronary care. In: Thompson PL, editor. Coronary care manual. London: Churchill-Livingstone, 1997: 429-433.
3. Fibrinolytic Therapy Trialists Collaborative Group. Fibrinolytic therapy -- indications in suspected acute myocardial infarction. Lancet 1994; 343: 311-322.
4. Ryan TJ, Anderson JL, Autman EM, et al. ACC/AHA Guidelines for the management of patients with acute myocardial infarction: executive summary. Circulation 1996; 94: 2341-2350.
5. Weaver WD, Cerqueria M, Hallstrom AP, et al. for the MITI project group. Prehospital-initiated v. hospital-initiated thrombolytic therapy. The myocardial infarction triage and intervention (MITI) trial. JAMA 1993; 270: 1211-1216.
6. DeVreede JJM, Gorgels AP, Verstraaten GMP, et al. Did prognosis after myocardial infarction change during the past 30 years? J Am Coll Cardiol 1991; 18: 698-706.
7. Jamrozik K, Broadhurst R, Parsons RW, et al. Ten year trends in medical management and case fatality in acute myocardial infarction [abstract]. J Am Coll Cardiol 1996; 27: 278A.
8. Leitch JW, Birbara T, Freedman B, et al. Factors influencing the time from onset of chest pain to arrival at hospital. Med J Aust 1989; 150: 6-8.
9. Bett N, Aroney G, Thompson PL. Impact of a national education campaign to reduce patient delay in possible heart attack. Aust N Z J Med 1993; 23: 157-161.

Reprints: Dr P E Langton, Sir Charles Gairdner Hospital, Verdun Street, Nedlands, WA 6009.