Thrombolysis in acute myocardial infarction.

RATIONALE M yocardial injury produced by complete coronary occlusion is acutely interrupted only by restoration of coronary flow. Other techniques designed to reduce injury, namely: reduction in myocardial oxygen demand, attenuation of inflammation, increased substrate transport or increased peak diastolic coronary perfusion pressure have been unimpressive, particularly when the occlusion is complete and collateral circulation is poor. However, despite the ability to demonstrate restoration of coronary reflow, most investigators initially had difficulty showing significant preservation ofmyocardial function. It is now generally assumed that this lack of preservation was from mitiating therapy too late from onset ofinfarction. Results of recent studies show streptokinase therapy initiated within three to six hours was associated with limitation of infarct size, reduction in acute mortality and improved ventricular function. Patients receiving streptokinase within the first hour ofonset of infarction had a 50 percent reduction in acute mortality. This information, coupled with the finding that transmural myocardial infarction is nearly always caused by the combination of plaque and an occlusive coronary thrombus, leads to the inescapable conclusion that therapy for transmural infarction with a large area of myocardium at risk should be directed at restoration of coronary flow without delay.