Abstract. To assess the relation of ventricular arrhythmias to myocardial Ki movement during ischemia, we placed an electrode catheter in the left anterior descending coronary artery for thrombus production in intact anesthetized dogs. 85Kr injections distal to the thrombus permitted serial coronary blood flow measurements. Animals of Group I with a moderate flow reduction exhibited no arrhythmia or myocardial egress of K+. In Group II, marked flow reduction was accompanied by an injury potential and loss of K+ from the ischemic site, before and during ventricular tachycardia.Therapeutic interventions were performed in animals having the same degree of ischemia as Group II. Systemic procaine amide in Group III interrupted the tachycardia and egress of K+, despite persistent ischemia. Group IV did not respond to intracoronary insulin with K+ uptake, as did normal dogs, and progressed to fibrillation. During the production of hyperglycemia in Group V, myocardial loss of Ki ceased with maintenance of sinus rhythm.Hemodynamic factors did not appear to have a major role in the genesis of the arrhythmia.Since intracoronary infusion of Ki in normal dogs similarly altered repolarization and produced fibrillation, it would appear that during ischemia egress of Ki before development of the arrhythmia indicates a major role of the ion in pathogenesis. This view is supported by the myocardial loss of K+ and arrhythmia induced in normal dogs by strophanthidin and by the fact that pharmacologic regulation of K+ loss is associated with correction of the arrhythmia, despite persistence of low blood flow.

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As an approach to delivery of inert gas to the myocardium in the presence of coronary artery obstruction, Kr 85 in saline was injected into a catheter in the coronary venous system of intact anesthetized dogs. Isotope delivered at the level of the great cardiac vein was selectively localized in the region of myocardium subserved by the vein and the left anterior descending artery. Similarly, injection at the coronary sinus level was attended by localization of isotope to the area perfused by the circumflex branch of the left coronary artery. Precordial counting of isotope delivered in this retrograde manner yielded coronary blood flow values that closely corresponded to those derived from coronary arterial injection.Coronary thrombus formation in either of the major left coronary branches was reflected in substantial flow reductions when isotope was delivered via the artery distal to the thrombus. A similar flow decrement was observed when the gas was delivered via the corresponding venous site, while normal blood flow levels were derived from the nonischemic area. Application of the method to detection of coronary arterial obstruction in man is discussed.ADDITIONAL KEY WORDS regional blood flow coronary vein injection of Kr 88 coronary sinus coronary artery thrombosis anesthetized dogs myocardial ischemia great cardiac vein

Seven patients with severe, chronic postmyocardial infarction cardiac failure underwent open intracardiac operation following catheterization and quantitative biplane angiocardiographic studies. Four patients with mitral incompetence had valve replacements; three had dilated mitral rings and did not survive the immediate postoperative period. In contrast, the single surviving patient had papillary muscle dysfunction evident at surgery and had less severe myocardial impairment as indicated preoperatively by a lower end-diastole volume and higher ejection fraction. Three patients demonstrated significant clinical and hemodynamic improvement after resection of a sccared akinetic area of left ventricular myocardium. Although two of the three patients died within the first year of operation, neither died in congestive failure. The results of this study indicate that certain patients with chronic postinfarction heart failure may benefit from surgery.

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