Relationship between epicardial ST-segment elevation and myocardial ischemic damage after experimental coronary artery occlusion in dogs.

Abstract

A B S T R A C T The relationship between early and late epicardial electrocardiographic changes as well as those in regional myocardial blood flow (MBF) and the severity of myocardial damage was determined in 12 anesthetized dogs with left anterior descending coronary artery ligation. Radioactive microspheres (15 ,um) were used to measure regional MBF at 15 min (early) and 24h (late) after coronary occlusion. Severity of myocardial damage was assessed by the extent of myocardial creatine phosphokinase depletion 24 h after coronary ligation. There was a close linear correlation between myocardial creatine phosphokinase activity and regional MBF both early (r = 0.93, 2P < 0.001) and late (r = 0.88, 2P < 0.001). An inverse but less precise relationship existed between acute epicardial ST-segment elevation and early (r = -0.41, 2P < 0.001), or late (r = -0.35, 2P < 0.05) regional MBF. Similarly, a weak correlation was found between myocardial creatine phosphokinase (IU/mg protein) at 24 h and early epicardial ST (millivolt) elevation (r = -0.36, 2P < 0.02). In the center zones of the infarct with MBF 1/10 of normal, about 35% of the areas with normal QRS width had no epicardial ST-segment elevation 15 min after coronary occlusion. About 44% of the areas which An abstract embodying the results was presented at the 48th Annual Scientific Meeting of the American Heart Association, Anaheim, Calif., November 1975 and has been published as an abstract in Circulation. 51, 52: II-6, (1975 developed pathological Q-waves in the electrocardiogram at 24 h had no ST elevation 15 min after coronary ligation. Late evolution of abnormal Qwaves occurred almost invariably in areas in which the early MBF was reduced to less than 50% of normal and in areas which subsequently had myocardial creatine phosphokinase levels reduced to less than 60%o of normal. After coronary occlusion, the severity of the ultimate myocardial damage, which was directly proportional to the degree of reduction in MBF, was therefore not reliably predicted by the early epicardial ST-segment elevation. The data obtained in these studies suggest the need for caution in the use of acute ST-segment elevation as a predictive index of the extent or severity of myocardial ischemic damage.

Functional characterization of left ventricular segmental responses during the initial 24 h and 1 wk after experimental canine myocardial infarction.

“…For group 1 segments resting function was depressed significantly below control levels between 1 to 3 h post-LAD occlusion. Significant increases in NET occurred at each infusion rate (7,14, and 27 pLg/min) at 1, 2, 4, and 6 h postocclusion, and at 7 and 27 jig/min at 8 h. No significant increases occurred at 24 h postocclusion. For group 2, resting function was significantly depressed below control levels at each time period after occlusion (NET = 33±4 at 5 min postocclusion).…”

“…Histochemical (9), metabolic (10), electrocardiographic (11)(12)(13)(14), rheological (15,16), enzymatic (6), scintigraphic (17), and histologic (18) studies of jeopardized zones of myocardium have been carried out in experimental animals. However, the relationship between these parameters of ischemic injury and the segmental contractile properties of ventricular myocardium is unresolved.…”

Inhalation of concentrated ambient air particles exacerbates myocardial ischemia in conscious dogs.

“…The degree of ischemic injury produced during brief coronary artery occlusion is reflected by changes in the magnitude of ST-segment elevation as well as the overall duration. Several investigators have demonstrated that ST-segment elevation measured early after coronary artery occlusion correlates with reductions in myocardial blood flow (Heng et al 1976;Irvin and Cobb 1977;Kjekshus et al 1972;Wégria et al 1949) and cellular damage as estimated by myocardial creatine phosphokinase activity (Heng et al 1976;Maroko et al 1971). It is now postulated that ST-segment changes are caused by intracellular electrical potential differences between normal and ischemic myocytes during different phases of the cardiac cycle.…”

A solid angle analysis of the epicardial ischemic TQ-ST deflection in the pig. A theoretical and experimental study.

“…" 12 as well as by data from Cohen and Kirk 13 and Heng et al 14 Holland applied the solid angle theory to the electrical events resulting from transmembrane potential alterations within the ischemic tissue and suggested that factors other than the extent of the ischemic region (e.g., geometry of the ischemic zone, degree of alteration of action potential morphology, changes in intra-and extracellular conductivity) are influential in determining the extent, polarity, and magnitude of the resulting TQ-ST deflection.…”