Citations

Introduction of a cardiac catheter into the pulmonary artery from the right heart is not possible in a substantial proportion of patients with transposition of the great vessels. It is necessary to obtain the pulmonary artery pressure and oxygen saturation value to evaluate the degree of pulmonary stenosis and the pulmonary vascular resistance. Twenty-three patients are described in whom this was accomplished by percutaneous suprasternal puncture. There was no mortality and there were no significant complications. The technique appears to be safe and reliable.

Measurements of flow and pressures related to the left heart were made on 21 patients immediately prior to and at intervals of 2 and 4 minutes after angiocardiography. These patients had normal mitral valves (group 1), mitral incompetence (group 2), or mitral stenosis (group 3). There was an increase in left ventricular end-diastolic pressure accompanied by an increase in "pulmonary artery wedge" (PA wedge) pressure in all patients. Patients with mitral valve disease generally develop higher PA wedge pressures; those with mitral stenosis develop, in addition, significantly increased mean diastolic and end-diastolic gradients across the mitral valve. These increased gradients in mitral stenosis are due to increased flow across the mitral valve, which results from a combination of increased cardiac output and decreased diastolic filling time. Diagnostic angiocardiography affords an opportunity of observing the effects of valve lesions at a higher flow rate and is particularly useful in those patients with normal PA wedge pressure and small gradients initially.

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.