Citations

The results of complete repair of double-outlet right ventricle with pulmonic stenosis in 22 Mayo Clinic patients were analyzed. The overall mortality rate was 32%. Since 1960, the mortality rate has been reduced to 16%. Anomalies of the distribution of the right coronary artery, a second ventricular septal defect of the atrioventricular canal type, and significant residual pulmonic stenosis were associated with a higher mortality rate. The difficulties in the diagnosis of this uncommon condition are emphasized. Complete repair is best carried out after the patient is 4 years old. A systemic-to-pulmonary arterial shunt is the procedure of choice for those who are younger than this. In the occasional patient with anomalous distribution of the right coronary artery which precludes adequate relief of the pulmonic stenosis, use of an aortic homograft from the right ventricle to the pulmonary artery should be considered.

The ability of a left ventricular balloon pump to provide support of the circulation when myocardial function had been severely impaired was examined in six dogs. When the unassisted damaged left ventricle could not maintain systemic blood flows adequate for survival, left ventricular balloon pumping resulted in peripheral blood flows which ranged from 37 to 77 ml/min/kg. These balloon-generated blood flows have been maintained for periods up to three hours. Assist of the circulation by balloon pumping was accompanied by an increase in systemic arterial blood pressure and a decrease in left atrial end-diastolic pressure. The effectiveness of left ventricular balloon pumping was reduced in hypovolemia and in the presence of ventricular extrasystolic beats. Left ventricular balloon pumping was not effective in generating a sustained peripheral flow of blood when the heart was fibrillating.

The results of complete repair of double-outlet right ventricle without pulmonic stenosis in 18 Mayo Clinic patients are analyzed; the over-all operative mortality rate was 22%. Pulmonary vascular obstructive disease and a second ventricular septal defect of the atrioventricular canal type were associated with a higher mortality rate. The difficulties in the diagnosis of this uncommon condition are emphasized. Patients with double-outlet right ventricle without pulmonic stenosis should have complete repair early in life before the onset of severe pulmonary vascular obstructive disease-the only specific contraindication to operation. Pulmonary artery banding may be preferable as a first-stage palliative procedure in infants less than six months old who do not respond to medical therapy.

Flow-directed catheters recorded serial changes in mean pulmonary artery pressure (PA) every 4 to 6 hours in 25 patients during the first 4 or 5 days following acute myocardial infarction. On the basis of the PA on admission, patients were divided into three groups. Patients in group 1 had normal PA (10-20 mm Hg) and maintained a stroke volume index (SVI)>35 ml/min/m 2 , a pulmonary artery oxygen saturation (MVSO 2 )>70%, and a normal cardiac index, arterial oxygen saturation, p H, and P CO CO2 . They developed only minor arrhythmias, no heart failure, and none died. Group 3 consisted of one patient with abnormally low PA (<10 mm Hg) who was hypovolemic. Group 2, those patients with elevated PA (>20 mm Hg) who maintained this elevation over the first 48 hours of monitoring, or showed progressive elevation prior to this, had SVI<35 ml/min/m 2 , MVSO 2 <70%, cardiac index<3 liters/min/m 2 , arterial desaturation, and respiratory alkalosis. They demonstrated clinical evidence of heart failure, had major arrhythmias, and 25% died. Three patients with elevated PA on admission spontaneously returned this pressure to normal over the first 48 hours of monitoring. Each of these patients maintained normal hemodynamics and had a good prognosis. PA was always elevated prior to the usual clinical signs of left ventricular failure. We conclude that PA provides a reliable early objective measure of left ventricular failure and is, therefore, an excellent guide to therapy.

One hundred sixty-nine patients underwent replacement of the aortic valve with an aortic valve homograft; of these patients 17 had concomitant commissurotomy or annuloplasty for an associated mitral valve lesion. Homografts were prepared by sterilization with beta-propiolactone solution and stored in Hanks' solution, or were prepared by sterilization with irradiation and stored at -70 C. Operative mortality was 5.3%. Thirty (19%) of the 160 surviving patients had an aortic diastolic murmur at the time of hospital dismissal, and five of these patients had hemodynamically significant homograft incompetence. For 156 patients, follow-up was longer than 6 months; among the 147 patients who survived operation, there were 12 late deaths. Eighty-four per cent (132) of these 156 patients were alive and well 6 to 54 months after operation. Six patients have required reoperation for valve incompetence. An aortic diastolic murmur was present in 43% of patients. Five patients had significant valve incompetence; four of these patients are markedly improved over their preoperative status. Thromboembolism has been a rare complication despite the fact that anticoagulant therapy was not used. Late calcification of the homograft valve has been noted in only one patient.

Four cases of ventricular septal defect and ventricular aneurysm after myocardial infarction are reported. The clinical findings and surgical results in these four cases and in eight previously reported patients with this combination of complications are summarized. Resection of the ventricular aneurysm and closure of the ventricular septal defect appear indicated, both on theoretical grounds and in view of the excellent results observed in six patients who underwent combined repair. In one of our patients, closure of the ventricular septal defect and resection of the ventricular aneurysm were possible with only a single suture line, as these defects were anatomically contiguous.

Left ventricular hemodynamics at rest and during supine exercise were studied before and 1 year after internal mammary artery implantation in 24 patients with severe coronary artery disease and angina pectoris and in five similar patients before and after 1 year of medical treatment. In the surgical group, 14 had evidence of one or more implants providing collaterals to coronary arteries, and 10 had no evidence of collaterals from the implant. Only two patients, both with functioning implants, showed a return to normal of left ventricular end-diastolic pressure at rest and during exercise. There was no correlation between clinical improvement and hemodynamics at the time of the postoperative study. It is concluded that left ventricular hemodynamics may return to normal after internal mammary artery implantation but this was uncommon in the present study.

Serial histologic sections of the atrioventricular (A-V) conduction system were studied in four hearts with persistent common A-V canal, and the anatomic findings were related to the abnormal ECG patterns. Two hearts were examples of the partial form and two of the complete form of A-V canal. The major anatomic abnormalities were: (1) postero-inferior displacement of the A-V node; (2) relatively short distances between the A-V node and the origin of the left bundle branching; (3) marked posteroinferior displacement of the left bundle branching system; and (4) relative hypoplasia of the anterior (superior) left bundle branches. The anatomic configuration of the A-V conduction system in A-V canal could result in relatively early impulse propagation to the posterior aspect of the ventricular septum as suggested by reported electrophysiologica studies. The anatomic findings are considered to be related closely to the known ECG patterns of A-V canal.

Simultaneously recorded standard electrocardiograms (ECG) and Frank vectorcardiograms (VCG) were correlated with the coronary arteriograms and the left ventriculograms of 210 patients. Quantitative criteria were applied to ECG measurements made by manual technics and to VCG measurements obtained by computer technics. As the extent of significant arteriographic disease increased, the frequency of ECG and VCG evidence of "definite" myocardial infarction (MI) increased. The VCG was diagnostic of MI in a greater number of patients than the ECG (50 versus 39, P < 0.01) and excelled in the detection of multiple areas of infarction in a greater number of patients (13 versus six, P < 0.05). This increased sensitivity was gained in anterior, inferior, and true posterior infarcts. Excluding patients with myocardiopathy, all MIs diagnosed from the VCG and all but one from the ECG were associated with significant arteriographic disease in the distribution of the predicted nutrient artery. Quantitative VCG analysis appears superior to the usual ECG analysis in the accurate detection of MI. When MI is diagnosed by either technic, significant associated coronary artery disease can be anticipated in a predictable anatomic distribution.

Ten patients with the electrocardiographic diagnosis of atrial flutter were investigated by exploration with electrodes within the esophagus and the right atrium. The records obtained were studied in regard to the timing of the intrinsic deflection and the contour of the atrial waves, as recorded at various sites. In four patients, atrial activation progressed in sequence cephalad in the left atrial wall and caudad in the right atrium. This process continued through two thirds of the total atrial cycle, favoring "circus movement" as the underlying mechanism. In six other patients, activation was believed to originate low in the left atrium, with simultaneous spread of excitation of both atrial walls in a general cephalad direction and terminating within the first half (usually the first third) of the atrial cycle. This pattern is compatible with, but not conclusive of, an ectopic focal mechanism. Serial records in one patient are presented in which transformation of one type into a second type of atrial flutter is suggested. It is likely that at least two mechanisms are present in human atrial flutter.