Robert L. Reis

Effects of Coronary Blood Flow and Perfusion Pressure on Left Ventricular Contractility in Dogs

The effects of changes in coronary blood flow and coronary artery pressure on left ventricular (LV) contractility were determined in 18 animals. Dogs on cardiopulmonary bypass provided isovolumetric LV contractions during controlled perfusion of the coronary circulation. Coronary venous efflux, myocardial oxygen consumption, peak LV pressure, LV dp/dt, and the force-velocity relations of the LV were determined at normal and at “supernormal” levels of flow and pressure. Coronary vasodilatation was obtained with nitroglycerine, permitting independent variation of flow and pressure. Augmenting flow by increasing pressure increased LV contractility, as reflected by increases in peak LV pressure, dp/dt max, peak wall tension, and maximal measured contractile element velocity. Increased contractility appeared to be primarily due to increased flow, rather than to pressure, as an increase in flow without an increase in pressure produced similar changes, and decreases in pressure at constant flow did not change maximal measured contractile element velocity or dp/dt max, although some decrease in peak LV pressure and wall tension did occur. These data suggest that coronary flow is an independent determinant of the contractile state of myocardium, and that an increase in flow in excess of that required to supply metabolic demands augments myocardial contractility.

Angina Pectoris: Pathophysiology, Evaluation, and Treatment

Abstract Accurate assessment of the effects and mechanisms of action of any intervention altering exercise performance of patients with angina pectoris caused by coronary artery disease requires us...

Deterioration of Myocardial Function Following Aorto-Coronary Bypass Operation

Twenty-two patients underwent cardiac catheterization before and an average of five months after aorto-coronary bypass operation (ACBO). Two groups were examined: 10 patients with all grafts patent, and 12 patients with one or more grafts occluded. All patients improved symptomatically, regardless of graft patency. However, in the occluded group, left ventricular end-diastolic pressure (LVEDP) increased (4.4 ± 2.2 mm Hg, P < 0.05), stroke volume index fell (9.8 ± 3.1 ml/m2, P < 0.05), ejection fraction decreased (10 ± 4%, P < 0.05), and left ventricular stroke work index fell (12 ± 3 g-m/m2, P < 0.01).Qualitative analysis of segmental left ventricular contractility was performed. Of 28 segments supplied by patent grafts, six improved and nine deteriorated. Of 22 segments supplied by occluded grafts, none improved and eight deteriorated. Frequently no angiographically demonstrable basis for the segmental deterioration was evident.We concluded that while ACBO may appreciably benefit severely symptomatic patients, our results do not substantiate the claim that ACBO should be recommended when the primary surgical goal is preservation or enhancement of myocardial function.

Congenital Fixed Subvalvular Aortic Stenosis: An Anatomical Classification and Correlations with Operative Results

Detailed assessments were carried out before and after operation in 33 consecutive patients with congenital fixed subvalvular aortic stenosis. Effective relief of obstruction to left ventricular outflow can be accomplished at minimal risk in patients with discrete subaortic stenosis, but a pressure gradient may persist after operation because of secondary hypertrophic obstruction which resolves with time. Tunnel subaortic stenosis is characterized by a diffusely narrowed left ventricular outflow tract. When an intraventricular pressure gradient was present in such patients, good but not complete relief of obstruction was achieved. In tunnel deformities with a gradient at the valve or annulus and in subaortic stenosis produced by mitral valve anomalies, operative intervention was ineffective.

Saphenous vein bypass grafts: Long-term patency and effect on the native coronary circulation

The long-term durability of saphenous vein bypass grafts and their effect on existing intrinsic coronary artery disease remain ill defined. Therefore, sequential catheterization studies were performed in patients selected for study solely on the basis of documentation of a patent graft at an earlier study performed three to nine months postoperatively; at that time 29 patent grafts were demonstrated in 20 patients. Fifteen to 36 months postoperatively (average 22 months), 27 grafts were unchanged, 1 manifested minimal luminal irregularities and 1 was occluded. In one additional patient, studied 4 months and 4 1/2 years postoperatively, the graft was widely patent and had good distal runoff at the second study. Sequential coronary arteriograms revealed that progression of disease to complete occlusion occurred in 24 percent of vessels with severe lesions proximal to a patent graft, whereas progression of disease distal to a graft anastomosis was uncommon. Of 25 vessels not receiving grafts, disease progressed in 5 (20 percent). Grafts that are patent 3 months after operation appear to remain patent for at least 2 to 3 years, and their presence does not unduly accelerate the disease process involving the native coronary arteries.

Effects of Induced Ventricular Fibrillation on Ventricular Performance and Cardiac Metabolism

The effects of induced ventricular fibrillation on ventricular performance and cardiac metabolism were studied in dogs. When ventricular fibrillation was induced by a brief 7.5-v a-c stimulus and allowed to persist spontaneously for one hour, no significant effects on subsequent cardiac function were apparent. An increase in myocardial oxygen consumption and a decrease in coronary vascular resistance occurred during the period of fibrillation.When ventricular fibrillation was maintained by constant a-c stimulation, however, immediate and significantly deleterious effects on cardiac performance resulted. Coronary vascular resistance rose; myocardial oxygen consumption increased, but the increase was significantly less than in animals in which fibrillation persisted without electrical stimulation. Anerobic glycolysis ensued, leading to lactate accumulation in coronary venous blood.The small a-c current used to maintain ventricular fibrillation impairs oxygen utilization, interferes with oxygen availability, and has a markedly deleterious effect on cardiac performance. A more satisfactory method of dependably maintaining the heart in ventricular fibrillation is needed before induced ventricular fibrillation can be safely employed to arrest cardiac contraction for prolonged periods during open cardiac operations.

The pharmacological basis of coronary and systemic vasodilator actions of diazepam (Valium)

1 The effects of α and β‐adrenoceptor blockade, depletion of catecholamine stores, vagotomy, atropine, and ganglionic blockade on diazepam‐induced vasodilatation were investigated in forty‐six anaesthetized dogs. 2 Coronary blood flow was measured by timed collections of coronary venous efflux from fibrillating, decompressed ventricles; coronary and systemic vascular resistances were determined during total cardiopulmonary bypass under conditions of normothermia and constant aortic (coronary artery) pressure. 3 No significant alteration in the vasodilatation produced by diazepam was observed following either vagotomy or α‐adrenoceptor blockade; partial inhibition of vasodilatation occurred after β‐adrenoceptor blockade or catecholamine depletion, and nearly total inhibition was observed after small doses of atropine or ganglion‐blocking agents. 4 The results suggest that diazepam may act as a specific ganglion‐stimulant, causing active sympathetic and cholinergic vasodilatation.

Hemodynamic Studies in Patients with 2M and 3M Starr-Edwards Prostheses: Evidence of Obstruction to Left Atrial Emptying

The hemodynamic findings in 28 patients with small (2M uncovered, 2M and 3M covered) Starr-Edwards mitral prostheses are compared with the findings in 12 patients with larger (3M and 4M uncovered) prostheses. Although most patients with the smaller prostheses evidenced both clinical and hemodynamic improvement after operation, the majority continued to have a significant left atrial-left ventricular pressure gradient and an elevated left atrial pressure at rest. During exercise the gradient increased, and left atrial pressure was abnormally elevated in each patient. The hemodynamic findings were decidedly less satisfactory in patients with smaller prostheses than in patients in whom it had been possible to insert larger prostheses. It is concluded that the major site of obstruction to left atrial emptying in patients with smaller prostheses is the small primary orifice of the prosthesis present at the time of insertion. Further narrowing of the primary or secondary orifices by thrombus and/or tissue ingrowth probably contributes to the obstruction in some patients.

Primary Myxoma of the Right Ventricle* Clinical, Hemodynamic and Angiographic Findings Before and Following Operative Treatment

Abstract A patient is described in whom a myxoma originated within the cavity of the right ventricle. The tumor, which caused severe right ventricular outflow obstruction, was successfully excised. The results of pre- and postoperative clinical, hemodynamic and angiographic assessments, and the operative methods are presented. From the findings in this patient, and those in nine others described in the literature, certain conclusions are presented concerning the natural history and clinical manifestations of this unusual cardiac malformation, and the role and results of operative treatment are discussed.

Coronary vasodilatation following diazepam (Valium)

1 . The effects of diazepam (Valium) on coronary and systemic vascular resistance were studied in anaesthetized dogs on cardiopulmonary bypass under conditions of constant heart rate and aortic pressure. 2 . Pharmacological doses of diazepam uniformly produced coronary vasodilation lasting 30 min; systemic vascular resistance also decreased, but to a lesser degree. 3 . When coronary blood flow was maintained constant at physiological levels, diazepam produced no changes in left ventricular contractility, as assessed by peak LV isovolumetric pressure, dp/dt max, force‐velocity, and length‐tension relations, whereas previous experiments had demonstrated a positive inotropic effect in a similar preparation in which coronary blood flow was responsive to alterations in coronary vascular resistance. 4 . In five dogs, complete separation of the coronary and systemic circulations was accomplished by a double pump‐oxygenator system; direct intracoronary administration of diazepam produced coronary vasodilatation, but coronary pressure and flow were not altered by administration of diazepam to the systemic circulation. 5 . It is concluded that diazepam augments myocardial contractility by increasing coronary blood flow. This relationship is independent of extracardiac humoral mechanisms, and appears to require the delivery of diazepam to the coronary circulation.