Enzymatic estimation of infarct size. Thrombolysis induced its demise: will it now rekindle its renaissance?

I nfarct size was central to the major thrust of cardiac research in the 1970s and as such occupied center stage as the culprit to be conquered by interventions designed to cardioprotect and limit myocardial damage (infarct size). Myocardial infarction, with its consequent necrosis, was the leading cause of death and came under intense attack with infarct size posing as the surrogate villain. Investigators were unified in their attack on infarct size, namely, that its course must be charted, the extent of damage quantified, and ultimately therapy designed for its elimination. Studies demonstrated that the evolution of myocardial infarction is a dynamic process and that its rate of evolution, as well as the ultimate extent of damage, could be favorably modified.1,2 Quantitative histologic estimates of infarct size were regarded as the only gold standard but obviously were not possible in patients surviving acute myocardial infarction. Attempts to quantitate