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1 Department of Medical Research, St. Joseph Hospital, Burbank, California, and Instituto National de Cardiologia, Mexico, D.F.
Left ventricular failure was reproduced in dogs with open chest and closed pericardium in two ways: a) by overloading the heart, the resulting rise of LVDP being manifested electrocardiographically by evidence of injury to the subepicardial layers of LV wall: the elevations of R-ST segments being proportional to the magnitude of LVDP. This type of heart failure was not considered to leave residual injury because coronary flow and myocardial oxygen consumption returned to normal when the work of the heart was returned to control levels; b) by decreasing the perfusion pressure in the left coronary tree, the ECG revealing consecutive states of subendocardial ischemia, subendocardial injury, subendocardial injury plus subepicardial ischemia, and subepicardial injury. This typical ECG sequence changed simultaneously with increases of LVDP and of the acidity of coronary venous blood. After periods of "coronary insufficiency," physiologic, but not electrocardiographic, variables remained abnormal for prolonged periods.
Key Words: acute heart failure heart failure and ECG heart failure and myocardial metabolism myocardial metabolism and ECG coronary insufficiency and ECG
Submitted on February 11, 1965
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