Continuity of Myocardial Stunning— Latent Myocardial Damage After Coronary Occlusion

Summary

In order to investigate the contrinuity of myocardial stunning, the pre-stage of manifest myocardial stunning or latent myocardial damage was studied in 20 anesthetized, open-chest dogs. Myocardial contractile function (percent of systolic shortening:%SS) was evaluated by sonocrystals. Myocardial tissue PCO₂, pH, and extracellular K⁺ concentration (K⁺ _e) were measured in the middle layer of myocardium. Epicardial surface ECG (AC-and DC-coupled) were recorded. A 2-min occlusion of the left anterior descending coronary artery (LAD) was used as a tool for analyzing latent myocardial damage after reperfusion. During occlusion,%SS, PCO₂, pH, and K⁺ _e were observed in ischemic myocardium. There were no differences in these variables between the first 2-min occlusion (T-l) and the second 2-min occlusion (T-2) which was done 110min after T-l. Therefore, these two occlusions affected the ischemic myocardium almost identically in this situation.

For investigating the effects of brief ischemia on myocardium, 5-min LAD occlusion was introduced 15min after T-l. Although%SS seemed to be completely recovered 90 min after reperfusion, early contractile failure in%SS was observed during T-2. The R wave amplitude during T-2 showed earlier progression of the first decrease phase and reduced the rise of the second increase phase. Also, during T-2, ST deviation in the ECG was reduced, and PCO₂, pH, and K⁺ _e were decreased. Then, metabolic damage was latently continued for 90min after reperfusion.

It is concluded that a 5-min coronary occlusion causes latent myocardial dysfunction and latent metabolic damage even after 90min of reperfusion. This latent myocardial damage of myocardial function and metabolism may be quite important as a pre-stage of manifest myocardial stunning.