Citations

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.

The morphology of the atrioventricular (A-V) conduction system was studied by serial histologic section in two cases of tricuspid atresia type IB (without transposition of the great arteries, with subpulmonary stenosis). The A-V node was adjacent to the central fibrous body, and its location was indicated by a "dimple" in the floor of the right atrium. The left bundle branches originated unusually close to the nodal-bundle junction. The right bundle branch was markedly elongated in its course to the right septal endocardium. It was situated along the inferior aspect of the channel-like ventricular septal defect as it traversed the septum. The early origin of the left bundle branches and the markedly elongated course of the right bundle branch were such that, theoretically, abnormal spread of the activation wave might result.

Obstructive pulmonary vascular disease (PVD) was evaluated in lung sections taken at autopsy in 53 patients with complete transposition of the great arteries. Twentythree had intact ventricular septa and 30 had ventricular septal defects. Children of similar age and associated defects had widely differing degrees of PVD and presented a spectrum of disease. In a small number of patients, the presence of pulmonic stenosis (congenital or acquired by pulmonary artery banding in infancy), a small ventricular septal defect, or a large atrial septal defect was not protective against the development of severe PVD. The findings of this study demonstrate the need for thorough hemodynamic evaluation of patients with complete transposition of the great arteries prior to repair by present technics. In addition, operation should probably be performed as soon as technically feasible.

Total daily bile acid excretion was measured in 10 patients with primary hypercholesteremia and in nine patients with combined hypercholesteremia and hypertriglyceridemia by using 14 C-labeled cholic acid and 3 H-labeled chenodeoxycholic acid. The average bile acid excretion by the patients with primary hypercholesteremia was 282 mg/day; that by the patients with combined hypercholesteremia and hypertriglyceridemia, 1,094 mg/day. These findings suggest a fundamental difference in cholesterol metabolism in these two types of hyperlipidemia.

During pregnancy, when surgically reparable heart disease can no longer be medically manged, open- or closed-heart surgery is the procedure of choice without prior therapeutic abortion. Cyanotic congenital heart disease in a pregnant patient when completely correctable surgically may be an indication for surgery in itself. Available data suggest that pregnancy per se does not increase the maternal risk of heart surgery with use of extracorporeal circulation. Fetal mortality in our series was 33%.

Postoperative embolism occurred in 35 of 546 patients traced for 2 to 15 years after surgical repair of uncomplicated ASD. A total of 58 embolic episodes occurred, resulting in the death of 11 of these 35 patients. The incidence of embolism was not significantly related to the technique used for surgical repair. Six of the nine patients who had had a preoperative embolism also had an embolism in the postoperative period. The most significant factors associated with an increased risk of postoperative embolism were increased age of the patient, atrial fibrillation, and pulmonary hypertension, all of which are interrelated: seventy-seven per cent (27/35) of patients having a postoperative embolism had either atrial fibrillation or pulmonary hypertension, and 77% (27/35) of patients with postoperative embolism were more than 40 years old at the time of the first embolism. Because actuarial analysis suggests that 30% of patients more than 40 years of age who have atrial fibrillation after repair of ASD may have an embolism within 10 years postoperatively, continuation of anticoagulation therapy indefinitely in these patients is suggested. The highest risk of embolism occurs in the early postoperative period, suggesting the advisability of anticoagulation therapy for all adult patients during convalescence.

Mitral valve function was assessed by roentgen videodensitometry. Mitral reflux was rare when single ventricular ectopic systoles were produced by electronic stimulation of the right or left ventricle at various times in the cardiac cycle. It was also rare during the compensatory pause after the ectopic systole or with the following postectopic systole. Recurrent ventricular ectopic systoles interposed once per cycle were associated with minor reflux when introduced in mid-cycle. Such extrasystoles occurred late enough in the cardiac cycle for the ventricle to relax after the primary systole and for the mitral valve to open before the extrasystole. The extrasystolic contractions were, however, weak and incapable of opening the aortic valve. When interposed early in the cardiac cycle, extrasystolic potentiation of the primary ventricular contraction occurred, and no or minimal mitral reflux was observed.

Complete surgical correction of transposition of the great arteries associated with subvalvular pulmonary stenosis carries a high mortality rate. A new surgical technique that achieves redirection of the ventricular outflows and relieves pulmonary stenosis by bypassing it, was successfully used to repair complete transposition of the great arteries associated with ventricular septal defect (VSD) and valvular and subvalvular pulmonary stenosis in a 14½-year-old patient. The repair consists of (1) division of the pulmonary artery, the cardiac end of which is oversewn, (2) repair of the VSD with a patch in such a way as to connect the left ventricle with the aorta, and (3) reconstruction of the pulmonary artery with an aortic homograft, including the aortic valve, which is anastomosed between the distal end of the pulmonary artery and the right ventricle. A review of the cases in which the current techniques were used indicates that the location and nature of the obstruction in the left ventricular outflow tract defies successful repair in most instances. Localized ridges and diffuse hypoplastic outflow tracts are recognized causes of obstruction, but anomalies of the mitral valve commonly contribute to or are the primary cause of subvalvular obstruction.