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Thrombolytic therapy of acute myocardial infarction
Insights
Thrombotic coronary artery occlusion causes heart attacks. Streptokinase infusion can dissolve clots, potentially improving heart function if given early, though its full benefit is still under study.
Area of Science:
- Cardiology
- Vascular Medicine
- Pharmacology
Background:
- Thrombotic coronary artery occlusion, often due to atherosclerotic plaque rupture, is the primary cause of acute myocardial infarction.
- Myocardial necrosis begins within 40 minutes of coronary occlusion and progresses over several hours.
Purpose of the Study:
- To evaluate the efficacy and safety of streptokinase therapy for acute myocardial infarction.
- To determine the optimal timing and route of administration for thrombolytic therapy.
Main Methods:
- Intracoronary infusion of streptokinase to achieve thrombolysis.
- Comparison of intracoronary versus intravenous (IV) streptokinase administration.
- Assessment of left ventricular function, ECG, and enzyme markers post-treatment.
Main Results:
- Intracoronary streptokinase achieved thrombolysis in up to 80% of patients.
- Early reperfusion (within 4-6 hours, potentially up to 18 hours) showed a small increase in late left ventricular function.
- High-dose IV streptokinase is easier to administer but potentially less effective than the intracoronary route.
Conclusions:
- Intracoronary streptokinase may benefit selected acute myocardial infarction patients in specialized centers.
- Further research and larger trials are needed to define the ultimate role and benefit of thrombolytic therapy.
- Future thrombolytic agents may offer safer and more effective early IV therapy for myocardial infarction and related conditions.
Abstract:
Thrombotic coronary artery occlusion is now recognized as the usual cause of acute myocardial infarction. The thrombus usually forms at the site of intimal disruption over an atherosclerotic plaque. Following coronary occlusion, myocardial necrosis begins within 40 minutes in the subendocardium and progresses outward toward the epicardium over the next several hours. The intracoronary infusion of streptokinase will produce lysis of the occluding thrombus in up to 80% of patients. It appears that reperfusion with streptokinase in the first few hours following the onset of the myocardial infarction produces a small increase in late left ventricular function, though ECG and enzyme evidence of acute myocardial infarction are not prevented. The improvement in left ventricular function is variable from patient to patient and has not been demonstrated in all the randomized studies to date. The time limit for myocardial salvage may not be the same in all patients. The greatest benefit is probably achieved with reperfusion in the first 4-6 hours, although some benefit may occur as late as 18 hours after the onset of infarction. Many patients who receive intracoronary infusion of streptokinase develop a systemic lytic state, though serious bleeding complications in carefully selected patients are infrequent. High-dose IV streptokinase is easier, cheaper, and quicker to initiate than intracoronary streptokinase but is probably less effective than the intracoronary route in producing rapid lysis of the occluding coronary thrombus. The optimal dose and rate of administration of IV streptokinase have not been determined. The final role and ultimate benefit of thrombolytic therapy of myocardial infarction have not yet been determined, but some of the issues may be clarified by the larger randomized trials now under way. It appears, at present, that the use of intracoronary streptokinase may have a role in the treatment of selected patients with acute myocardial infarctions in institutions with the facilities and the personnel necessary to perform this procedure safely. In the future, thrombolytic therapy may also have a place in the treatment of selected patients with unstable angina and post-myocardial infarction angina. The future availability of more selective thrombolytic agents may make the early IV therapy of myocardial infarction a safer, more effective option and expand the indications for thrombolytic therapy.