Massive Destruction of the Myocardium of the Canine Right Ventricle

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Abstract
Myocardial damge, (80% of total right ventricular muscle) was produced by injection of vinyl acetate into the right coronary arterial system and injection or ligation of other coronary arteries supplying the right ventricle. Thirteen animals were observed from 8 to 390 days after operation. Three animals with marked insufficiency of the tricuspid valve were observed for 150 days after valve lesion was produced. Immediately following damage to right ventricle there was an elevation of end diastolic pressure in the right and left ventricles and of mean pressure in the right atrium, thoracic venae cavae and abdominal vena cava. There was a substantial reduction in the mean pressure difference between pulmonary artery and right ventricle due to the rise in right ventricular mean pressure. Similar but more marked pressure changes resulted from tricuspid valve insufficiency. Here the most marked immediate rises in mean and pulse pressure were noted in the right atrium and vena cava. These immediate pressure changes after damage to the right ventricular myocardium were either maintained or slightly augmented with time. In 1 animal a marked progressive rise in right ventricular systolic pressure was noted, and necropsy disclosed the presence of marked pulmonic and subpul-monic stenosis. Marked ascites was recorded in 2 of the 13 animals with right ventricular damage and in all 3 animals with tricuspid insufficiency. With one exception, no reduction in exercise ability was noted. In the exception, a systolic murmur became evident 5 months after operation, followed by ascites and a progressive reduction in exercise tolerance. At necropsy marked pulmonic stenosis was demonstrated. Atrioventricular nodal rhythm with retrograde P wave was present in 18 of 25 dogs for periods from 1 hour to 11 days after the injection of the right coronary arterial system. In 11 of these, the P wave was abnormal following return of sinus rhythm. Marked elevation of the S-T in leads aVR and aVL and right precordial leads, accompanied by S-T depression in leads I, II, III and aVF and left precordial leads, was noted immediately following right ventricle damage. A similar but less prominent change of P-Q segment level was recorded. The heavy scarring of the tissue around the atrioventricular orifice and the wirelike effect of the injected right coronary artery produced a tricuspid insufficiency which in some measure caused the rise in right atrial and venae cavae pressure. The cause of the continued ability of the severely damaged right ventricle to maintain an adequate output both under conditions of rest and exercise was not finally determined but appeared to reside in the still viable muscle elements of its myocardium. With the passage of time there was hypertrophy of this marginal area of right ventricular muscle sufficient in 1 instance to maintain flow in the presence of severe pulmonic stenosis. The view is expressed that, both in the resting state and during exercise, an adequate transfer of blood from the systemic venous circulation to the lungs can be achieved by a very small fraction of functional right ventricular muscle.