Estimation of Infarct Size in Man and its Relation to Prognosis

Abstract

SUMMARYInfarct size was assessed quantitatively in 33 patients with acute myocardial infarction with a new technic based on analysis of serial serum creatine phosphokinase (CPK) changes to determine its relationship to prognosis. We have recently measured infarct size in the conscious dog with this method which takes into account CPK distribution space, fractional disappearance rate, proportion degraded in myocardium, and proportion released into the circulation, and we have validated the method by measurement of myocardial CPK depletion in the same animals. In the present study, CPK activity (determined spectrophotometrically) and isoenzyme profiles (assayed electrophoretically) were measured in patient serum samples obtained every 2 hours. Infarct size was estimated by mathematical analysis of serial CPK changes utilizing the method previously developed in the conscious dog model. CPK isoenzyme profiles demonstrated prominent anodal bands, absent from normal serum, indicating that enzyme elevations reflected CPK released from heart rather than skeletal muscle. In 19 class I-II survivors (New York Heart Association) estimated infarct size was 31 + 4 CPK-gram-equivalents (CPK-g-Eq). It was significantly larger (P < 0.01), 103 +-14, in nine patients who died and in four class III or IV survivors (91 8). Estimation of cumulative infarct size differentiated patients with electrocardiographic changes and clinical sequelae from complications such as pericarditis from those patients with extension of infarction. Thus, infarct size can be assessed quantitatively in patients with acute myocardial infarction and provide a useful diagnostic and prognostic index based on the extent of myocardial damage.

Noninvasive quantitation of myocardial infarction with technetium 99m pyrophosphate.

“…Such quantitation of infarction could be of critical importance in determining patient prognosis and in guiding therapy. 20 It has been shown that CPK depletion is propor- farction in the heart at postmortem examination. Most important, it was also possible to predict the area and weight of infarction in the living animal.…”

Angiogenesis induced by hepatocyte growth factor in non-infarcted myocardium and infarcted myocardium: up-regulation of essential transcription factor for angiogenesis, ets

“…Taken together, overexpression of HGF might enhance angiogenesis in myocardial infarction. Since the size of myocardial infarction correlates closely with mortality and residual impairment of function in survivors, 36 a therapy targeted at promoting collateral formation would decrease the size of chronic myocardial infarction. Indeed, the beneficial effect of HGF gene transfer was also reported by Ueda et al 37 They demonstrated that transfection of HGF gene into transplanted hearts resulted in the attenuation of reperfusion injury.…”

Size and transmural extent of first-time reperfused myocardial infarction assessed by cardiac magnetic resonance can be estimated by 12-lead electrocardiogram

“…The incidence and prognosis of heart failure and ventricular arrhythmias after acute coronary occlusion are related to myocardial infarction (MI) size (1)(2)(3)(4). The transmural extent of MI has been shown to be related to probability of functional recovery after acute revascularization (5).…”