Critical Analysis of Intra-aortic Balloon Counterpulsation and Transapical Left Ventricular Bypass in the Sufficient and Insufficient Circulation

Summary

Reduction of cardiac work/oxygen consumption (LVQO₂) may be beneficial in diminishing ischemic damage after myocardial infarction (MI). This study compares intra-aortic balloon pumping (IABP) and transapical left ventricular bypass (TALVB) to a specially developed method of LV assistance, i.e. transapical left ventricular bypass with complete LV-decompression (TALVB/TD), a) in the sufficient circulation of swine for effectiveness in actively reducing myocardial oxygen requirements and b) in the insufficient circulation for effectiveness in improving circulatory dynamics, to reduce gross size and to prevent morphological damage in myocardial infarction in swine.

Thirty-four pigs (17-29 kg) had standardized general anesthesia.

a) In 10 of these animals LVQO₂ was determined by measuring left coronary artery blood flow (LCBF) electromagnetically, blood samples for O₂-content were taken from the aorta and the coronary vein draining the LV. Cardiac work/oxygen consumption was related, during variable degrees of IABP assist and during total bypass, with graded reduction of LV pressure work, culminating in complete LV decompression (LV press.max. permanently below 8 mmHg).

b) Twenty-four pigs underwent ligation of the LAD distal to the first diagonal branch and were divided into 4 groups. Six pigs served as controls. Starting 45 minutes after ligation 6 had 24-hour treatment with IABP, 6 had 24-hour TALVB and 6 animals were treated with TALVB/TD.

Heart rate, central venous, pulmonary artery, aortic and left ventricular pressures and cardiac output were recorded prior to ligation and at 1/2, 1, 2, 3, and 24 hours. At 24 hours myocardial infarct size (MIS) was quantitated in g infarct per 100 g left ventricular and septal mass, and infarcted areas were examined histologically.

a) In the sufficient circulation, heart rate, cardiac output, mean aortic, pulmonary artery, and central venous pressures were not significantly changed by IABP, TALVB, and TALVB/TD assist. During IABP (1:1), LVQO₂ was decreased only 2.8%, LCBF was increased 4.4%, which is not significantly different from controls. Total LV bypass decreased LCBF 8.3% and LVQO₂ 18.1%, total LV bypass with complete LV decompression reduced LCBF 31% and LVQO₂ 60.4% from control values.

b) MI reduced mean aortic pressure (24.5%) and cardiac output (47.5%) significantly (p < .05). Confirmed in switchon/switch-off studies, IABP increased mean aortic pressure and cardiac output 4% to 9%. TALVB displaced 70% to 100% of the LV volume work, LV decompression was seen in 5 of the 6 TALVB animals (LVP syst. = AOP -11 mmHg). Transapical left ventricular bypass with a complete LV decompression immediately took over 100% LV volume work and complete LV decompression was achieved during the whole period of circulatory assist. All methods of circulatory assist were equally effective in improving circulatory dynamics.

With IABP, MIS was insignificantly reduced 15.5% (p >.3). However, with TALVB and TALVB/TD, MIS was reduced significantly by 28.5% and/or 30% (p <.03). Histologically the examination of infarcted zones showed nearly complete ischemic damage to muscle fibers in controls, IABP and TALVB animals, whereas there was only discrete damage in the muscle fibers of TALVB/TD treated hearts.

These data indicate that circulatory assistance without left ventricular decompression has minimum effect on myocardial oxygen utilization, and assist devices which do not decompress the left ventricle will not adequately reduce left ventricular oxygen requirements. Despite significant hemodynamic improvement IABP cannot effectively reduce myocardial infarct size. Transapical left ventricular bypass, i.e. reducing LV volume work, is necessary to significantly reduce myocardial infarct size. The histological results indicate that total left ventricular bypass with total LV decompression, besides reducing myocardial infarct size significantly, is capable of preventing morphological damage within the infarcting areas.

Key words

Mechanical circulatory assist - Myocardial oxygen consumption - Myocardial infarct size - Myocardial infarction morphology