Objective: To describe the contemporary management and outcomes of patients presenting with ST‐segment‐elevation myocardial infarction (STEMI) in Australia.
Design, participants and setting: Observational analysis of data for patients who presented with suspected STEMI and enrolled in the Australian Acute Coronary Syndrome Prospective Audit from 1 November 2005 to 31 July 2007.
Main outcome measures: Factors associated with use of reperfusion therapy and timely use of reperfusion therapy, and the effects of reperfusion on mortality.
Results: In total, 755 patients had suspected STEMI. Median time to presentation was 105 minutes (IQR, 60–235 minutes). Reperfusion therapy was used in 66.9% of patients (505/755), and timely reperfusion therapy in 23.1% (174/755). Thombolysis was administered in 39.2% of those who received reperfusion therapy (198/505), while 60.8% (307/505) received primary percutaneous intervention. Cardiac arrest (OR, 2.83; P = 0.001) and treatment under the auspices of a cardiology unit (OR, 2.14; P = 0.02) were associated with use of reperfusion therapy. A normal electrocardiogram on presentation (OR, 0.42; P = 0.01), left bundle branch block (OR, 0.18; P = 0.001), acute pulmonary oedema (OR, 0.34; P < 0.01), history of diabetes (OR, 0.54; P < 0.01), and previous lesion on angiogram of > 50% (OR, 0.51; P = 0.001) were associated with not using reperfusion. Inhospital mortality was 4.0% (30/755), mortality at 30 days was 4.8% (36/755), and mortality at 1 year was 7.8% (59/755). Receiving reperfusion therapy of any kind was associated with decreased 12‐month mortality (hazard ratio [HR], 0.44; 95% CI, 0.25–0.78; P < 0.01). Timely reperfusion was associated with a reduction in mortality of 78% (HR, 0.22; P = 0.04). There were no significant differences in early and late mortality in rural patients compared with metropolitan patients (P = 0.66).
Conclusion: Timely reperfusion, not the modality of reperfusion, was associated with significant outcome benefits. Australian use of timely or any reperfusion remains poor and incomplete.
The generation of thrombin and the formation of platelet rich intra-coronary thrombus in response to atherosclerotic plaque rupture is pathognomonic of acute coronary syndromes. An understanding of the process of thrombin generation and the unique relationship between the structure and function of thrombin is essential to developing more effective anti-thrombotic strategies than the use of standard unfractionated heparin in the acute coronary syndromes. The mechanisms of action of heparin, low molecular weight heparins (LMWHs) and the newer direct anti-thrombins, recombinant hirudin and Hirulog, are reviewed. Evidence from the currently available phase 2 and 3 trials of these drugs regarding their efficacy in the acute coronary syndromes is also reviewed.
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