PubMed Health⌕ Search

Biomedical subjects

K E Jochim

Publications and source records attributed to K E Jochim.

8 recordsLinked to original sources

Nucleotide degradation and functional impairment during cardioplegia: amelioration by inosine.

The degradation of adenine nucleotide levels and impairment of functional recovery associated with exposure to hypothermic (20 degrees C) cardioplegia was studied in 84 isolated working rat hearts. After a 1-hour control period, hearts were exposed to 1 hour of cardioplegia that consisted of increasingly longer periods of cardioplegic solution (CPS) infusion (30 seconds and 10, 30 and 60 minutes), followed by increasingly shorter periods of global ischemia (591/2 minutes and 50, 30 and 0 minutes). Hearts were then reperfused for 1 hour with control perfusate, during which recovery of cardiac output was monitored. Additional hearts were freeze-clamped at various points in the protocols to determine adenine nucleotide levels (ATP, ADP, AMP and their sum TAN). Exposure to increasingly longer periods of CPS perfusion resulted in proportionally greater degradation of nucleotides and poorer recovery of cardiac output. Addition of inosine to the recovery perfusate as well as the CPS further improved nucleotide levels and recovery of cardiac output. These results suggest that washout of nucleotide degradation products in the CPS or reperfusion prevents their salvage for nucleotide resynthesis and impairs functional recovery from cardioplegia.

Adenine Nucleotides↗

Electrophysiologic delineation of the intraventricular His bundle in two patients with endocardial cushion type of ventricular septal defect.

Two patients who had an endocardial cushion type of ventricular septal defect underwent electrophysiologic studies for detection of specialized conduction tissue during operative repair. In one patient, with an inferior leftward frontal plane QRS axis on the ECG, we recorded an intraventricular His bundle electrograms from both the anterosuperior and posteroinferior margins of the defect, suggesting dual atrioventricular conduction tracts (branching intraventricular His bundle). These anatomic and electrophysiologic findings may account for the more normally oriented QRS frontal plane axis on the surface ECG of both of these patients and support the hypothesis that the changes observed on the ECGs of patients with the various forms of endocardial cushion defect can be explained by alterations in the anatomic configuration of the specialized atrioventricular conduction tissue.

Bundle of His↗

Effects of methylprednisolone in cardioplegic solution during coronary bypass grafting.

The effects of adding 500 mg. of methylprednisolone to each liter of cardioplegic solution were studied in patients undergoing coronary artery bypass grafts. Patients were randomly assigned to control (12 patients) or steroid-treated groups (10 patients). The cardioplegic solution was identical in the two groups except for the added methylprednisolone. Contractile element velocity (VCE and left ventricular end-diastolic pressure (LVEDP) were recorded immediately before and after perfusion in the operating room. There were no differences between the two groups with respect to these two variables or the postoperative courses. Thus this study fails to demonstrate a beneficial effect of methylprednisolone when added to cardioplegic solutions.

Coronary Artery Bypass↗

Effects of cardioplegic solution on human contractile element velocity.

A technique for measuring the maximum contractile element velocity (Vpm) of the myocardium was developed, verified, and employed in patients to allow accurate intraoperative assessment of the adequacy of myocardial protection. Four groups of patients were studied. Ten patients had coronary artery bypass grafts (CABG) with cardioplegia; 13 had CABG with coronary perfusion, ventricular fibrillation at 28 degrees C, and aortic clamping for distal anastamoses; 6 had aortic valve replacement (AVR) with cardioplegia; and 7 had AVR with coronary perfusion to the beating heart. For cardioplegia, a solution of 5% dextrose in 0.2% saline at 4 degrees C with 25 mEq of potassium chloride and 12.5 gm of mannitol was infused initially, followed by 500 ml every 30 minutes. Clinically all patients did well, and there were no deaths. Patients having CABG with intermittent coronary perfusion during ventricular fibrillation had significant (p less than 0.01) depression of Vpm from 38.3 to 30.8 sec-1 while Vpm in patients having CABG with cardioplegia was unchanged. Patients having AVR with continuous coronary perfusion or with cardioplegia (average anoxia time, 70.4 minutes) had no significant change in Vpm. We conclude that this cardioplegic solution provided adequate protection of myocardial function for up to 105 minutes of continuous aortic clamping in humans. The depression in Vpm observed following CABG with intermittent coronary perfusion is consistent with previous suggestions that this combination is detrimental because of maldistribution of coronary blood flow during ventricular fibrillation.

Aortic Valve↗

Effect of temperature of cardioplegic solution.

This study tests the hypothesis that the efficacy of cardioplegic solution depends upon its chemical constituents rather than on its temperature alone. A standard preparation of right heart bypass in the dog was utilized. Left ventricular function curves were inscribed before and after 1 hour of aortic cross-clamping. No deterioration in function was observed in nonischemic control hearts or in hearts protected with cardioplegic solution consisting of potassium chloride (25 mEq. per liter) and mannitol (12.5 Gm. per liter in 5 percent dextrose and 0.2 percent saline at either 4 degrees C or 28 degrees C. Severe myocardial depression was observed in hearts rendered ischemic for 1 hour at 28 degrees C. without protection and also in hearts perfused with 5 percent dextrose and 0.2 percent saline at 28 degrees C. without the potassium chloride and mannitol. The evidence from this study indicates that cardioplegic solution exerts a protective effect beyond that which is afforded by hypothermia.

Animals↗

Evaluation of myocardial function.

In assessing myocardial contractility one may examine isolated heart muscle, the isolated whole heart in controlled circumstances, or the heart in an intact patient. In each situation a number of different indices of contractility may be recorded, each of which has merit but none of which is perfect. Some reflect events occurring during isometric contraction prior to ejection, such as rate of change in intraventricular pressure, maximum velocity of muscle shortening, and velocity of shortening of contractile elements. Others reflect ejection phenomena such as stroke volume, the Starling curve, and the ejection fraction. None of these indices is entirely independent of preload, afterload, and heart rate, and these factors must be controlled. In the whole heart, especially in a clinical setting, this may be difficult. Many clinical studies of myocardial function fail to recognize the need for controlling these variables and therefore are of limited validity.

Cardiomyopathy, Hypertrophic↗