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. 1976 May;53(5):853-9.
doi: 10.1161/01.cir.53.5.853.

Effect of intra-aortic balloon counterpulsation on the motion and perfusion of acutely ischemic myocardium. An experimental echocardiographic study

Effect of intra-aortic balloon counterpulsation on the motion and perfusion of acutely ischemic myocardium. An experimental echocardiographic study

R E Kerber et al. Circulation. 1976 May.

Abstract

The effect of intra-aortic balloon counterpulsation (IABC) on the motion and perfusion of ischemic left ventricular posterior myocardium was studied in 30 open-chest dogs, using ultrasound to register motion and 7-10 mu radioactive microspheres to determine perfusion. Circumflex coronary artery ligation produced acute aneurysmal bulging during isovolumetric contraction and diminished ischemic wall velocity during systolic ejection. Myocardial perfusion was determined in five dogs; perfusion of the area supplied by the ligated coronary artery fell from a control value of 72.9 +/- 13.8 (SE) to 30.0 +/- 2.3 cc/100 g/min (P less than 0.05) at 5 minutes after coronary occlusion. IABC was then administered for one hour, with a fall in aortic systolic pressure (112 +/- 6 to 105 +/- 7 mm Hg, P less than 0.05) and rise in peak aortic diastolic pressure (94 +/- 6 to 102 +/- 7 mm Hg, P less than 0.05). Despite this the ischemic area showed no change in perfusion (measured at the same time): 30.0 +/- 2.3 to 28.0 +/- 2.4 cc/100 g/min. Little change in wall motion occurred: aneurysmal bulging decreased modestly (4.5 +/- 0.3 to 3.6 +/- 0.3 mm, P less than 0.05), but ischemic wall velocity did not increase. After cessation of counterpulsation and one hour of coronary reperfusion aneurysmal bulging disappeared and wall velocity improved. The addition of norepinephrine (eight dogs) or nitroprusside (seven dogs) to intraaortic balloon counterpulsation did not cause a significant further improvement in the response of the dyskinesis during the period of ischemia. We conclude that IABC has little effect on ischemic dyskinesis, probably due to its failure to improve perfusion of the acutely ischemic myocardium.

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