Citations

A simple classification of atrioventricular block, criteria for diagnosis, and suggested therapy are discussed. The differences between Mobitz I and II second-degree A-V block are reviewed. Good management of patients who have bundle-branch or other forms of intraventricular block depends on informed judgment which includes consideration of (1) the effect of intraventricular conduction disturbances on the pumping action of the heart, and (2) the likelihood that a specific intraventricular conduction disturbance will be complicated by complete heart block. Evidence suggests that common forms of intraventricular disturbance, unlike ventricular fibrillation, do not alter significantly the pumping action of the heart. The role of intraventricular conduction disturbances in the genesis of ventricular fibrillation is assessed. We concluded that only when right bundle-branch block is combined with block of the anterior or posterior fascicle of the left bundle branch is complete heart block sufficiently imminent to warrant special concern. If bilateral block is associated with symptoms of episodic severe bradycardia, pacemaker therapy is indicated.

The echocardiographic features of Ebstein's anomaly include a large anterior chamber, paradoxic ventricular septal motion (type B), increased velocity and amplitude of anterior tricuspid leaflet (ATL) motion, and delayed closure of the ATL. This delayed closure has been thought to be secondary to right bundle-branch block (RBBB). We have studied two patients by simultaneous echocardiography and phonocardiography. The findings in both patients were similar. One patient had RBBB and therefore resembles the previously reported patients. However, the other patient had W-P-W preexcitation syndrome, type B, and is reported here in more detail. The ATL closure of this patient was markedly delayed in spite of right ventricular preexcitation. This finding gives further insight into the altered pathophysiology in Ebstein's anomaly and implies that the delayed ATL closure is probably not due to RBBB and may be a specific feature of this anomaly.

The effect of oral aspirin in doses known to influence in vitro platelet aggregation was evaluated in patients undergoing brachial artery catheterization. Neither arterial thrombus formation nor pulse reduction was affected in patients given aspirin when compared to controls. Aspirin in small doses does not decrease the incidence of vascular occlusion after brachial artery catheterization.

Among certain patients with cardiovascular malformations, a common phenomenon is a ventricular septal defect and absence of anatomic origin of the pulmonary arterial supply from the heart. In this situation, true pulmonary arteries may be present or absent. In the latter case, the pulmonary arterial supply comes through bronchial arteries. When true pulmonary arteries are present, the left and right pulmonary arteries either may be in continuity at their origins (confluence) or they may arise from separate sites (nonconfluence). When confluence is present, the two pulmonary arteries may arise either from an atretic pulmonary trunk or from certain forms of persistent truncus arteriosus. Pulmonary atresia may be localized to the proximal end of the pulmonary trunk or diffuse in this vessel. When nonconfluence is present, each pulmonary artery arises separately from one of three possible sources as follows: (1) a form of persistent truncus arteriosus, (2) through ducti arteriosi from the aortic arch system, or (3) through bronchial arteries from the descending aorta.

During cardiac catheterization in nine patients with ventricular septal defect and seven patients with truncus arteriosus, all with severe pulmonary vascular obstructive disease, hemodynamics were compared while they were breathing first room air and then 100% oxygen. Patients with higher pulmonary vascular resistance had higher systemic vascular resistances. With 100% oxygen, pulmonary vascular resistance decreased and systemic vascular resistance increased in both groups. The effect of oxygen was found to be more pronounced on the systemic than on the pulmonary vascular bed in the patients studied. Indicator-dilution dye curves changed and exhibited characteristics of left-to-right shunts in patients with severe pulmonary vascular obstructive disease, as a result solely of an increase in systemic resistance; that is, without a decrease in pulmonary resistance. It is suggested that in patients with severe pulmonary vascular obstructive disease maintenance of an increased systemic resistance is essential to well being and is a factor in longevity. It is also suggested that any transient decrease in systemic resistance in these patients might initiate a vicious cycle leading to sudden death.

Some, but not all, cardiac arrhythmias are related to pathologic lesions of the cardiac conduction system. Common atrial dysrhythmias and first-degree atrioventricular (A-V) block rarely are explained on the basis of anatomic lesions in specific sites of the conduction system or its blood supply. Second-degree A-V block of Mobitz type II, which may be a precursor of complete (third-degree) heart block, commonly is associated with fibrotic lesions of uncertain etiology in the branching part of the bundle of His or the bundle branches. Ischemic lesions are found less often, and other pathologic processes rarely are present. Chronic complete heart block most often results from nonspecific, fibrotic interruption of the distal bundle of His, or of the first parts of the bundle branches after their origins. Ischemic lesions are uncommonly the cause of chronic block. High-grade A-V block complicating acute myocardial infarction may be associated with infarction of the A-V conduction system, but often morphologic evidence of ischemia cannot be identified. Congenital variants in anatomy of the conduction system are responsible for some relatively uncommon arrhythmias.

Five patients have had the common features of pulmonary atresia or severe stenosis associated with a septal defect and a coronary artery-to-pulmonary artery (CA-PA) fistula. Four had pulmonary valvular atresia, and one had severe pulmonary stenosis. In all five, the CA-PA fistula contributed the principal component of the pulmonary blood flow. Cyanosis, continuous murmur, right ventricular hypertrophy, and decreased or normal pulmonary vascularity were frequent clinical manifestations, but angiocardiography was required to establish the diagnosis. The fistula was a side-to-side communication between the left coronary artery and the main pulmonary artery in each of the five patients. The dilated proximal coronary artery connecting the aortic root with the pulmonary artery gave a unique angiocardiographic appearance distinguishing it from truncus arteriosus or aorticopulmonary window. It is suggested that this unique angiocardiographic appearance be called an "aorticopulmonary tunnel." The surgical repair of this anomaly is closely related to that for severe tetralogy of Fallot and should involve a comparable risk and achieve a comparable result.

Cerebral blood flow (CBF) was measured during 28 carotid endarterectomies in 25 patients, by injection of 133 Xe into the exposed internal carotid artery (ICA). Twenty-three patients had episodic cerebral or retinal ischemia and five had neurologic deficits before operation. Initial CBF values were variable. Increases of Pa Co Co2 caused CBF to increase in four of six patients, to increase slightly in one, and to decrease in one. In each of 19 procedures, CBF decreased during surgical occlusion of the ICA, 11 times to less than 30 ml/100 g/min, but absence of postoperative worsening indicated that decreased ICA blood flow is not a major risk of the procedure; embolization from the site of operation may be a greater threat to the patient. CBF increased after 14 endarterectomies, perhaps due to failure of autoregulation or to reactive hyperemia. Measurements of jugular PV o o2 and lactate concentration were of little value.

Cellular energy substrates and metabolites, electrolytes, oxygenation, and acid-base balance, in arterial and coronary sinus blood of seven adult patients who died after valvular replacements, were studied and compared with these measurements from five patients having aortic replacement who survived. Six of the patients were in New York Heart Association class IV. All but one died within 24 hr of acute circulatory failure, with excessive bleeding being a contributing factor. Plasma potassium and osmolality remained higher in the first postoperative hours in nonsurvivors. Ketone bodies, growth hormone, and lactate levels rose precipitously as shock became severe. Increased arterial blood osmolality and potassium, plus a still-rising lactate concentration, were evident 2 hr after operation in patients who died in the next 24 hr. Low cardiac output, hyperosmolality, and the degree of lactic acidosis were the only early changes predicting the fatal outcome.