Effects of Intraaortic Balloon Counterpulsation on the Severity of Myocardial Ischemic Injury following Acute Coronary Occlusion

Abstract

The effects of intraaortic balloon counterpulsation (IABC) on the magnitude and severity of myocardial ischemic injury were studied in 19 dogs following acute coronary occlusion and in two patients with cardiogenic shock. In the experimental group, epicardial electrocardiograms were taken from 10-14 sites on the anterior surface of the left ventricle following occlusion of the left anterior descending coronary artery or its apical branch. The average S-T-segment elevation (ST) was used as an index of the magnitude of myocardial ischemic injury. In six dogs, two successive 20-min occlusions were performed, and IABC was started prior to the second occlusion. ST 15 min following occlusion decreased from 3.3 + 0.9 mv after the control occlusion to 1.4 0.4 mv (P < 0.01) after the occlusion with IABC. In three dogs in which the occlusion was maintained and IABC initiated 30 min later, ST decreased from 1.2 to 0.6 mv. In six dogs in which IABC was started 3 hours after occlusion, it induced a reduction of ST from 4.2 1.1 to 2.8 1.0 mv (P < 0.01). In four dogs, ischemic injury was augmented by isoproterenol infusion (0.25 ,ug/kg/min), and while continuing the infusion IABC was initiated. It reduced ST from 8.0 + 1.9 to 5.7 1.8 mv (P < 0.05). Thus, IABC reduced the magnitude and extent of myocardial ischemic injury after experimental coronary occlusion, both when IABC was employed prior to, and 3 hours following, coronary occlusion. IABC was also effective in reducing myocardial ischemic injury which had been increased by isoproterenol infusion. Employing a noninvasive technic, which utilizes 35 electrodes on the thorax, the effects of IABC were examined in two patients with cardiogenic shock associated with acute myocardial infarction. Preliminary observations in these patients confirmed the experimental results indicating that IABC reduced myocardial ischemic injury.

Reduction by Cobra Venom Factor of Myocardial Necrosis after Coronary Artery Occlusion

“…In these experimental studies, myocardial damage was reduced with agents aimed at decreasing myocardial oxygen consumption (5-9), at increasing coronary flow either directly by reperfusion (10,11) or indirectly by enhancing collateral flow (5,6,12), by enhancinig anaerobic metabolism (13), and by the administration of hyaluronidase (14) and hydrocortisone (15). The application ofthese principles to the therapy of patients with acute myocardial infarction using some of these interventions seems to confirm these experimenital conclusions (4,6,(16)(17)(18)(19)(20)(21).…”

“…After dissolving 1 g of venom in 65 ml sodium phosphate buffer, 0.03M, pH 7.4 at 37°C, the sample is applied to a 2.5 x 40-cm column of equilibrated DEAE-cellulose. The nionbound proteins, mostly phospholipase, are washed through at 50 ml/h for [16][17][18] h. A linear salt gradient to 0.5 M NaCl is then begun, and the anticomplementary peak is concentrated and applied to a G-200 column in isotonic saline phosphate buffer, pH 7.4. The final peak is a homogenous band on polyacrylamide electrophoresis (34) (Fig.…”

Protection of ischemic myocardium by whole-body hypothermia after coronary artery occlusion in dogs

“…Since an imbalance between oxygen supply and demand in the ischemic tissue results in myocardial necrosis, interventions that improve this balance could significantly reduce the size of an infarct. Thus, beta-adrenergic blockade with propranolol [1], intra-aortic balloon counterpulsation [19], and nitroglycerin [3] have been shown to decrease ischemic injury following coronary artery occlusion. In the present study, whole body hypothermia appeared to decrease the extent of ischemic injury produced by either 5 or 10 hours of coronary occlusion.…”

Initial experience with transluminal recanalization of the recently occluded infarct‐related coronary artery in acute myocardial infarction — Comparison with conventionally treated patients

“…A number of clinical (2 I, 32, 58), pathologic-anatomical (6,18) and experimental findings (45,48,53) indicate that the extent of myocardial injury can be limited by collateral flow. Therapy with nitrates and IABP could have been an additional factor limiting infarct size (5,7,12,17,20,25,31,33,34,43,50,51,56). On the other hand, there were col-laterals to the infarct area in 6 of the 9 patients during the acute stage of infarction.…”