Swan, H.J.C.

Ventricular performance was assessed before and after angiocardiography in 22 patients with normal left ventricle, mitral stenosis, aortic stenosis, and myocardial disease. The increased circulating blood volume known to occur after angiocardiography is a determinant of the increased ventricular pre-load. The after-load is unchanged. Patients with normal left ventricle and some patients with valve stenosis responded by an increase in the work performed and some had only a minimal or no increase. A group of patients with serious heart disease performed less work. If the ventricular response can be considered on the basis of the Frank-Starling principle, then the abnormal response of such patients is due to an altered length-tension relationship.

Data from 43 patients with common ventricle for whom satisfactory hemodynamic data are available are presented; these form 3.2% of the patients with congenital heart disease studied by means of catheterization at the Mayo Clinic. Selective biplane angiocardiography is essential for diagnosis of common ventricle. Associated cardiovascular anomalies are common, with transposition of the great vessels occurring in 84% of the patients. The right-to-left shunt present in all 43 patients results in desaturation of systemic arterial blood. The common ventricle receives all the systemic and pulmonary venous blood [see table in the PDF file] flows; yet complete mixing is uncommon in this chamber, for it occurred in only 16% of the patients who did not have severe pulmonary stenosis. Fifty-eight per cent had oxygenated blood directed preferentially to the systemic circuit ("favorable streaming"). This occurred most commonly with L-transposition and resulted in a higher oxygen saturation of systemic arterial blood. Obstruction to pulmonary flow (from pulmonary stenosis or pulmonary vascular disease) results in a larger right-to-left shunt and lower oxygen saturation of systemic arterial blood.

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.

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.

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.

The cardiovascular response to angiographic contrast medium was studied in 28 patients undergoing diagnostic angiocardiography under anesthesia. A transient phase of hypotension and tachycardia similar to that described by other authors was noted. Cardiac output was increased initially by 50 per cent and returned to the base line in 20 minutes. Peripheral blood flow increased by 100 per cent, apparently due to the direct effect of the hyperosmotic solution on the vascular smooth muscle. Hemodilution, maximal 2 to 4 minutes after injection of contrast medium, suggested a transient increase in circulating blood volume. Increased ventricular filling pressures, which were thought to be due to hypervolemia, were associated with increased left ventricular stroke work.

Left heart volumes were determined angiographically in 50 subjects of whom 18 had no abnormality of the left heart, 12 had lesions causing pressure overload of the left ventricle, and 20 had lesions causing volume overload of the left ventricle. The left heart volumes were in the normal range in the presence of pressure overload, but, with volume overload, end-diastolic, end-systolic, and atrial volumes were in excess of normal. A linear relationship was demonstrated between end-diastolic and end-systolic volumes, regardless of the pressure load on the ventricle. Thus, for all but one of the cases studied, total left ventricular ejection volume formed a nearly constant proportion of end-diastolic volume.

Eighteen cases of stenosis of the branches of the pulmonary artery, seen at the Mayo Clinic, have been reviewed and subdivided into two main types: Type I, stenosis of the main branches of the pulmonary artery, 11 cases, and type II, stenosis of multiple peripheral branches of the pulmonary arteries, seven cases. Of special interest were two cases in which thrombosis occurred as a complication and one case in which surgical relief of multiple areas of stenosis in the peripheral branches of the pulmonary arteries was accomplished. Unexplained pulmonary hypertension necessitates further investigation, which includes cardiac catheterization for measurement of intracardiac pressure and frequently selective angiocardiography. Main branch or peripheral pulmonary artery stenosis should be suspected when a continuous murmur is heard or when poststenotic dilatations of the pulmonary artery branches or areas of decreased pulmonary vasculature can be perceived in the roentgenogram. Angiocardiography is the only technic that permits detailed anatomic evaluation of the entire pulmonary vasculature, especially in the cases associated with severe infundibular or valvular pulmonic stenosis. Stenosis of the branches of the pulmonary artery must be taken into account, when surgical repair of associated cardiovascular defects is considered. These lesions also might complicate anastomotic procedures involving the pulmonary artery in cyanotic patients.