Myocardial protection in the failing heart: I. Effect of cardioplegia and the beating state under simulated left ventricular restoration

ObjectiveHeart failure was induced by cardiac pacing to evaluate myocardial flow distribution of the open ventricle during delivery of either cardioplegia or in the beating state during simulated left ventricular restoration.MethodsStudies included 5 (pacing-induced) failing pig hearts and 6 control hearts. Pacing-induced cardiac failure reduced fractional shortening by approximately 22%, increased left ventricular end-diastolic diameter by 34%, caused pulmonary hypertension (mean blood pressure increased from 12 to 35 mm Hg), and led to significant ascites. Global and regional coronary blood flow were measured with microspheres during cardiopulmonary bypass at 80 mm Hg perfusion pressure in either vented (collapsed) or open (exposure by traction for left ventricular restoration) left ventricles during continuous perfusion under either beating-heart or cardioplegic conditions.ResultsIn control hearts, venting and exposure ventriculotomy did not affect flow. In failing hearts decompressed by venting, coronary flow was lower during the beating and cardioplegic delivery than during control conditions at the same perfusion pressure of 80 mm Hg. Mean cardioplegic flow during ventricular decompression by venting exceeded beating flow by 97%. Conversely, traction to increase the ventricular radius during exposure ventriculotomy reduced endocardial cardioplegic coronary blood flow by 64% (from 0.97 to 0.59 mL/[min  ·  g]), whereas the beating state raised endocardial flow by 95% (from 0.40 to 0.78 mL/[min  ·  g]). Changing ventricular shape changed coronary vascular resistance in failing hearts during beating or cardioplegic delivery.ConclusionsCoronary blood flow alterations occurred only in failing hearts when geometry was changed from closed to open state. The beating method provided more endocardial flow than cardioplegic delivery during ventricular exposure for restoration. Vascular remodeling raised coronary vascular resistance in failing hearts, thereby requiring higher pressure for similar blood flows.