Complete occlusion of the infarct-related coronary artery is a frequent finding soon after Q-wave (transmural) myocardial infarction. We performed coronary arteriography to study the frequency of total coronary occlusion and of angiographically visible collateral vessels in 341 patients within one week of non-Q-wave myocardial infarction. In this cross-sectional study, 192, 94, and 55 patients underwent coronary arteriography within 24 hours of peak symptoms, between 24 and 72 hours after peak symptoms, and between 72 hours and seven days after peak symptoms, respectively. In the three groups, total occlusion of the infarct-related vessel was found in 26 percent (49 of 192), 37 percent (35 of 94), and 42 percent (23 of 55) of the patients, respectively (P less than 0.05). The presence of visible collateral vessels increased in parallel: 27 percent (52 of 192), 34 percent (32 of 94), and 42 percent (23 of 55), respectively (P less than 0.05). The frequency of subtotal occlusion (i.e., greater than or equal to 90 percent stenosis) decreased inversely: 34 percent (65 of 192), 25.5 percent (24 of 94), and 18 percent (10 of 55), respectively (P less than 0.05). Thus, in contrast to Q-wave infarction, total coronary occlusion of the infarct-related vessel is infrequently observed in the early hours of non-Q-wave infarction, but it increases moderately in frequency over the next several days. These cross-sectional data suggest that non-Q-wave infarction may be related to a preserved but marginal blood supply, which sufficiently disrupts the relation between the supply of and the demand for myocardial oxygen to cause tissue necrosis.

The hemodynamic effect of varying heart rate was studied in eight patients with aortic regurgitation. At the subjects' resting sinus rhythm and at a higher heart rate induced with right atrial pacing, left ventricular and aortic pressures and Fick cardiac outputs (FCO) were measured, and left ventricular biplane angiocardiograms were performed. Left ventricular volumes and left ventricular minute flow (LVMF) were determined from the angiograms. Regurgitant flow was quantitated by subtracting the FCO from LVMF. Increased heart rate produced highly significant reductions in the left ventricular end-diastolic pressure (LVEDP), left ventricular end-diastolic volume, and stroke volume. End-diastolic circumferential stress (EDCS) and enddiastolic load (EDL) were abnormally high at resting sinus rhythm and were markedly decreased with increased heart rate. FCO increased, but no significant changes were observed in either the LVMF or the regurgitant flow per minute.Bradyeardia in aortic regurgitation may cause pulmonary congestion secondary to high LVEDP and may accelerate left ventricular dilatation secondary to markedly elevated EDCS and EDL. The possible benefits of preventing bradyeardia in aortic regurgitation by chronic demand pacing is currently being tested.

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