We studied the individual and combined effects of extracellular acidosis and increases in extracellular potassium on action potential characteristics and conduction in order to gain a better understanding of the effects of acute ischemia. At each level of potassium between 2.7 and 17 mm, acidosis induced by increasing Pco2 (respiratory acidosis) and by decreasing HCO3- (metabolic acidosis) decreased resting membrane potential, the maximum rate of rise of the action potential upstroke (Vmax), and slowed conduction. Metabolic acidosis consistently and significantly lengthened the steady state action potential duration whereas respiratory acidosis did not. Respiratory acidosis caused changes in resting membrane potential, Vmax, and conduction velocity; which occurred more rapidly and were of greater magnitude than the changes induced by metabolic acidosis. The changes in Vmax induced both types of acidosis were due to a change in the resting membrane potential-Vmax relationship as well as to the changes in the resting membrane potential. The conduction slowing induced by acidosis was greater when potassium was 9 and 13 mM than when potassium was 5.4 mm. Our results suggest that acidosis causes important changes in the electrophysiological properties of ventricular fibers and that many of the known electrophysiological effects of acute ischemia can be mimicked by the combined effects of extracellular acidosis and an increase in extracellular potassium.

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A case of acute myocardial infarction associated with primary coronary dissection was followed up angiographically. A 46-year-old woman complained of chest oppression. Electrocardiogram on admission showed ST-segment elevation in V1-5. Urgent coronary angiography was performed under a diagnosis of acute anterior myocardial infarction, and showed a significant stenosis with multiple filling defects in segments 7-8 (99% with severe delay) in the left anterior descending artery. There was no organic lesion in the right coronary artery. Intracoronary thrombolytic therapy was unsuccessful, and thereafter she was treated with aspirin, warfarin and isosorbide dinitrate. Coronary angiography performed 1 month later revealed a long dissection with double lumens in segments 7-8. The septal branches emerged from the smaller lumen. Two months later, the 2 lumens were almost equal in size. These findings indicated that coronary dissection produced a false lumen with an entry in segment 7 and a reentry in segment 8, and that the false lumen was responsible for the greater flow. Four months later, the flow in the true lumen had improved remarkably while that in the false lumen had almost disappeared. She remained in stable condition during the follow-up period of 4 months.

Since it is very rare that cardiac tamponade due to myocardial rupture caused by infective endocarditis, occurs we are reporting this case. A 62 year old man, who had underlying diseases of pneumoconiosis and hypertensive heart disease, visited Chikuho Rosai Hospital complaining of chest oppression and general fatigue on Feb. 7, 1987. He was diagnosed as having ischemic heart disease by electrocardiogram. Two days later, he suddenly had chills and a fever, and the laboratory data showed leukocytosis and a positive C-reactive protein (CRP). The echo cardiogram showed mitral regurgitation (MR) and aortic regurgitation (AR), but neither vegetation nor pericardial effusion was observed. On Feb. 16, he was admitted with shock, and he died the next day. The blood cultures grew gram-positive cocci, respectively. From the clinical symptoms, chest roentgenogram and electrocardiogram, we suspected a cardiac tamponade. On autopsy findings, though coronary arteries were intact, the aortic valves had severe valvular adhesions, calcifications and hypertrophies. The rupture hole was observed in the left ventricles, which was just under the aortic valve through the pericardiac space. It seemed that he died of a cardiac tamponade due to the outflow of blood from this hole. On histopathologic findings of the cardiac wall, gram-positive cocci and many of neutrophils were observed.

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