Publication | Open Access
Estimation of Infarct Size in Man and its Relation to Prognosis
707
Citations
11
References
1972
Year
Heart FailureSerial Cpk ChangesCerebrovascular DiseaseCardiovascular FunctionCoronary Artery DiseaseAcute Myocardial InfarctionThrombosisClinical InjuryNeurologyPublic HealthCardiologyAtherosclerosisCardiovascular ImagingMyocardial InfarctionMedicineCerebral Blood FlowInfarct SizeEpidemiologyCardiac PathologyCardiovascular DiseasePhysiologyStroke-related ConditionCpk ActivityCardiovascular PharmacodynamicsStrokeEmergency MedicineAnesthesiology
The method for measuring infarct size, validated in conscious dogs by accounting for CPK distribution, fractional disappearance, myocardial degradation, and release into circulation, has been established. The study quantified infarct size in 33 acute myocardial infarction patients using serial serum creatine phosphokinase (CPK) analysis to evaluate its prognostic significance. CPK activity and isoenzyme profiles were measured every two hours, and infarct size was estimated by mathematical analysis of serial CPK changes using the previously developed dog‑model method. Infarct size ranged from 31 ± 4 CPK‑gram‑equivalents in survivors to 103 ± 14 in non‑survivors, and its estimation differentiated patients with complications from those with infarction extension, confirming it as a useful diagnostic and prognostic index.
Infarct 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.
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