Citations

Records of 273 cases of ventricular septal defect from five participating institutions were studied. Insignificant hemodynamic disturbance (Roger's) was found in 11 per cent, moderate to large left-to-right shunts in 55 per cent, and severe pulmonary vascular disease ("Eisenmenger's") in 8 per cent. Because of insufficient data, 26 per cent of the cases were not classified hemodynamically. Thus, a spectrum of severity ranging from mild to severe was noted. There was evidence of congestive heart failure in infancy in 78 cases and a significant mortality occurred in this group, whether treatment was medical (mortality, 27 per cent) or surgical (mortality, 46 per cent). Six patients had hemodynamic evidence of severe progressive pulmonary vascular disease, three when they were less than 8 years old. Correlations of hemodynamic severity with clinical symptoms, roentgenographic findings, and electrocardiographic changes were reasonably good at the extreme ends of the severity spectrum but only fair in the middle range. Over-all mortality was high (28 per cent) for the 163 patients treated surgically, but mortality was also high (18 per cent) for the 110 patients treated medically. Ten of the 20 deaths in the medical group occurred in patients who had had congestive heart failure in infancy. Further study of the natural history of ventricular septal defect is clearly indicated for establishment of improved criteria for selection of cases for operation.

The pathogenesis of certain types of focal cerebral ischemia, particularly episodes of focal cerebrovascular insufficiency, is not fully understood. Atherosclerosis, a relatively static process, commonly occurs without producing any neurologic phenomena. However, such episodes rarely occur in cerebral vascular systems unaffected by atherosclerosis. Atherosclerosis plus some transitory pathophysiologic event would explain the clinical events. A list of such events includes vasospasm, transitory systemic hypotension, kinking and external compression of vessels, transitory hypoglycemia, temporary shunts, and thrombosis and multiple emboli. The roles of polycythemia and anemia are mentioned. Evidence is presented that incriminates thrombosis or embolus formation (or both) as the process, secondary to atherosclerosis or associated with atherosclerosis, that produces the focal cerebral ischemia.

Renal performance of seven patients undergoing replacement of the aortic valve was investigated. The initial portion of cardiopulmonary bypass was characterized by low arterial blood pressure and anuria. With a subsequent rise in arterial pressure during bypass, urine flow suddenly increased in five patients. In two patients urine flow did not resume until immediately after cardiopulmonary bypass. The high rate of urine flow at these times is thought to be partially due to a glucose-induced osmotic diuresis. The glomerular filtration rate (inulin clearance) and the effective renal plasma flow (PAH clearance) fell with induction of anesthesia and opening of the chest, but there was no further drop in these functions as a result of total body perfusion. Urine osmolality fell significantly during and immediately after cardiopulmonary bypass. The changes in urine osmolality are thought to be due in part to the osmotic diuresis and in part to a temporary reduction in the renal medullary hyperosmolality secondary to hemodynamic changes. All of the alterations in renal function were reversible in the patients studied.

Sixteen patients with diffuse hypertrophic subaortic stenosis have been treated surgically. Thirteen of 14 patients undergoing excision of hypertrophied muscle from the left ventricular outflow tract via left ventriculotomy or aortotomy have survived. Operation has provided excellent symptomatic relief, associated with eradication or significant reduction of the systolic pressure gradient between the left ventricle and the aorta while the patient is at rest. Operation is recommended for those patients with this disease who are experiencing significant and limiting symptoms related to obstruction of the left ventricular outflow tract.

Cardiac output was determined by the indicator-dilution technic with injection of indicator into the ascending aorta, left ventricle, and pulmonary artery in 13 cases of mitral incompetence and in 15 control cases (normal or mild valvular obstruction). The ascending aortic dye curve is not involved in mitral incompetence in its primary circulation and was used for comparison. In normal subjects, there is no significant difference between the cardiac output obtained by injection of indicator into the ascending aorta and the left ventricle. The cardiac output obtained from indicator-dilution curves affected by mitral regurgitation in its primary circulation is underestimated by approximately 20 per cent. The effects of the coronary recirculated indicator particles on the disappearance slope would best explain the discrepancy. Even in the normal circulation, the inclusion of the coronary recirculated particles leads to a small underestimation of the cardiac output when the indicator is injected into the pulmonary artery.

Between 1945 and 1961 50 patients with aortic dissection were seen at the Mayo Clinic. Survival information for prognostic purposes was available in 40 patients and revealed that more than half of the patients were dead within a week. Of 15 patients who survived the acute phase (2 weeks) more than half were dead within a year. The cause of death was determined by necropsy in 24 patients and 22 died of external rupture of the dissecting aneurysm. In 11 patients a site of re-entry in the dissection was found and in all of these patients external aortic rupture had occurred also. The surgical approach to the treatment of aortic dissection is discussed in the light of these findings. The relationship of the location of the primary tear, blood pressure, and the age of the patient to prognosis is reviewed.

A total of 131 patients with the partial form of common atrioventricular canal were operated on between March, 1955 and January, 1964. The over-all hospital mortality rate was 3.8%; no deaths occurred in patients who had no or only mild incompetence of the mitral valve. Permanent heart block has not occurred in the last 93 cases. Results have been good in general, although there is evidence of residual mitral valve incompetence in many patients. In the few who had severe incompetence at the mitral valve before repair, the results have been considerably less satisfactory than in the group as a whole; therefore, further work is needed on this aspect of the problem.

Of the 614 open-heart operations performed at the Mayo Clinic for acquired aortic valvular disease, 130 were performed on patients who also required repair of other valves. Review of the remaining 484 operations resulted in the following observations. Operation for acquired aortic valvular disease may now be accomplished with a hospital mortality rate of 4%. The incidence of late death and failure of patients to improve has averaged 44% for previously employed techniques of valvular repair. Failure of the valve or prosthesis to function properly was the most common cause of late failure after operations in which these earlier methods were used. In the 138 more recent cases, in which operations employing the aortic ball valve (Starr-Edwards prosthesis) were used, the incidence of late failure has been reduced to 14%, and failure of the prosthesis to function properly has not yet occurred in the absence of infection. Late bacterial endocarditis and thromboembolism were the most serious problems associated with use of the ball-valve prosthesis. In contrast with the late results of the former techniques, use of the ball valve has resulted in improvement for 79% of the patients; in the great majority of these there has been a dramatic return to normal living. Despite the highly satisfactory results of current methods, the fact that 14% of patients have already died after an initially successful operative result, and that another 12% have suffered complications causing their late result to be less than totally satisfactory, indicates that the policy of recommending for operation only those patients who have significant and progressive cardiac disability should be continued.

The effect of valvular insufficiency on left ventricular volumes was studied by an angiographic method in 37 patients. Ejection of the additional volume load imposed by valvular insufficiency was achieved by an increase in end-diastolic volume and not by increasing the proportion of end-diastolic volume ejected. Of the 37 patients, 16 (43 per cent) had a significant reduction in the fraction of end-diastolic volume ejected per beat. These patients performed significantly less stroke work from a given end-diastolic fiber length (end-diastolic volume) than did the others and evidence is presented that they had impaired myocardial function. An index of myocardial contractility is derived which relates stroke work to end-diastolic volume. The magnitude of left ventricular volumes is determined in part by the severity of the volume load but a further increase in volume without necessarily a further increase in ejection occurs in those patients with impaired myocardial function. Valvular insufficiency is quantitated from the difference between left ventricular ejection volume determined angiographically and forward stroke volume determined from indicator-dilution curves. The results show good agreement with subsequent surgical findings in the 15 patients who underwent operation.