Segmental Dyskinesis during Acute Myocardial Ischemia and following Coronary Reperfusion

The effect of alterations of blood pressure and heart rate on segmental dyskinesis induced by coronary artery ligation and the influence of such manipulations on the magnitude of recovery of the dyskinetic segment during subsequent coronary artery reperfusion were evaluated in 77 open-chest dogs. Wall motion was recorded by ultrasound reflected directly from the ischemic myocardial segment. Acute ischemia produced characteristic regional abnormalities in wall motion: aneurysmal bulging occurred during isometric contraction and wall velocity was markedly reduced during ventricular ejection. During 60 minutes of ischemia, a control group of dogs underwent no interventions and showed no further changes in wall motion. Tachycardia induced by atrial pacing during ischemia had no significant effect. Arterial hypertension during ischemia caused a marked reduction in wall velocity when methoxamine was used: 14 ± 2 (SE) mm/sec (ischemia alone) to 6 ± 1 mm/sec (ischemia + drug). In contrast, norepinephrine improved wall velocity: 11 ± 2 mm/sec (ischemia alone) to 25 ± 4 mm/ sec (ischemia + drug). Hypertension caused by infusion of phenylephrine gave intermediate results, as did hypotension induced by either nitroprusside or hemorrhage during the ischemic period. After 60 minutes the drugs were stopped, the coronary ligation released, and the ischemic myocardium reperfused. The relative order of improvement of wall velocity with reperfusion was 11 ± 2 mm/sec (ischemia alone) to 24 ± 3 mm/sec (reperfusion) in the group that received norepinephrine, 12 ± 3 mm/sec to 20 ± 3 mm/ sec in the control group with no intervention during ischemia, 13 ± 2 mm/sec to 20 ± 1 mm/sec in the nitroprusside group, 9 ± 1 mm/sec to 9 ± 2 mm/sec in the phenylephrine group, and 14 ± 2 mm/sec to 12 ± 1 mm/sec in the methoxamine group. The aneurysmal bulging during isometric contraction also was reduced to a greater degree by reperfusion in the group that received norepinephrine during the ischemic period than it was in the groups undergoing other interventions during ischemia. We conclude that drug-induced elevations in arterial blood pressure can have different effects on the dyskinetic motion of acutely ischemic myocardium and on the degree of recovery following reperfusion depending on the particular agent used. A reduction in blood pressure or an increase in heart rate during the period of ischemia has no significant beneficial effect on the recovery of the dyskinesis toward control levels after reperfusion. However, it remains possible that such manipulations over a broader range of pressure and rate or for a longer period of ischemia may have more noticeable effects.