Long-term cardiac arrest by cardioplegic coronary perfusion (author's transl)

Abstract

The Mg++ aspartate-procaine-cardioplegia has been proven in animal experiments as well as from 1970 til 1975 in more than 1000 open-heart-procedures by a myocardial temperature of 32 degrees C and aortic crossclamping time up to 40 minutes superior to all other known procedures of cardiac preservations. To guarantee a safe myocardial protection of the arrested heart for a remarkable longer period of total ischemia, we further developed the cardioplegic technique in the animal lab, and use it now clinically. The arrest is induced by cardioplegia (Mg++ aspartate-procaine), than the arrested heart is cooled down to 15-20 degrees C by cardioplegic coronary perfusion maintaining the oxidative metabolism. The perfusion is stopped. The begin of ischemia is still under normal ATP-levels and continuous cardioplegia. 1. Crossclamping of the aorta; 2. cardioplegic induced cardiac arrest by Mg++ aspartate-procaine (Kirsch); 3. Surface cooling of the heart; 4. Coronary perfusion by hypothermic cardioplegic solution (8-10 min, flow 80-120 ml/min, perfusion pressure maximal 30 mmHg). Perfusate: O2-saturated, erythrocyte free, 6% hydroxyethyl starch solution added 2 mM Mg++ aspartate, 4 mM procaine, 50 mM Na+, 5 mM K+, 0,5 mM Ca++, 25 mM HCO3-, 10 mM glucose, 200 mM mannitol, 250 mg/l 6-methylprednisolone. 84 patients (29 ACVB; 55 valve replacements); crossclamping time: 71 min (SD 22); total time of ischemia: 57 min (SD 18; max 96, min. 27 min); reperfusion time restoring normal excitation-contraction of the heart: 3 min (SD 2); weaning off bypass: 23 min (SD 14). Hemodynamic 12 h postop.: SO2 venous 76% (SD 6). No sympathicomimetics were used. Only 30% of myocardial ATP is splitted after 120 min of cardiac arrest. Electron microscopic findings show only small, reversible alterations of fine structure.