Citations

At the Mayo Clinic, four patients were seen in whom a ventricular septal defect (VSD) of the atrioventricular (A-V) canal type was associated with an angle of nearly 90° between the intact atrial septum and the ventricular septum. The right atrium overrode the ventricular septum and communicated with both ventricles. A complex, straddling right A-V valve had some attachments in the left ventricle and resembled the common A-V valve of persistent common A-V canal. In three of the patients, a congenital mitral valve deformity also existed. Mild cyanosis probably is not a contraindication to surgical repair in such patients because right atrial blood may enter the left ventricle directly.

The morphology of the sinus and atrioventricular (A-V) nodes of human hearts was studied and connecting pathways between these nodes were sought. The cells of both nodes differed from ordinary atrial and ventricular myocardium in respect to size, shape, number, and arrangement of cytoplasmic organelles. Using the criteria of fiber-to-fiber connection, shown by means of serial histological sectioning, this study confirmed previous reports of three pathways between the sinus and A-V nodes in the human heart. It was not required that these pathways be composed of classic Purkinje-type fibers, though many of the fibers did possess some of the features of Purkinje fibers. While recent evidence reveals that specialized atrial pathways do demonstrate increased conduction velocity, their prime functional significance may be in the facilitation of orderly atrial depolarization, the maintenance of sinus node control of ventricular depolarization under various physiological conditions, and the provision of an orderly "input" into the A-V node, a tissue generally acknowledged to have a low margin of safety.

A patient with an atrial septal defect, paroxysmal tachycardia, and the Wolff-Parkinson-White syndrome (type B) had epicardial exploration to determine the nature of the excitation anomaly. Right bundle-branch block in association with the WPW syndrome (type B) was evidenced by the late activation (0.12 sec) of the epicardium over the outflow tract of the right ventricle. Early activation of the base of the right ventricle (near the atrioventricular groove at the right border of the heart) was interpreted as indicating an actively conducting atrioventricular muscle bridge (bundle of Kent) in this region. During paroxysms of tachycardia, the ventricular area excited much later than when sinus mechanism was present, and the adjacent right atrium was excited in sequence. This sequence supported the concept of a circus movement, that is, movement from atrium to ventricle via atrioventricular bundle (His) and ventricle to atrium via a muscle bridge (Kent). Injection of procaine into the base of the right ventricle abolished the pre-excitation of the ventricle.

Experience with 110 separate periods of transvenous cardiac pacing by means of a catheter-electrode in 91 patients has been reviewed. Indications for the use of the catheter-electrode included (1) complete heart block with and without Adams-Stokes syndrome, (2) other arrhythmias with and without cardiogenic syncope, (3) malfunction of previously implanted permanent pacemaker units, and (4) need for pacing during general surgical procedures in patients with a variety of rhythm disturbances. A case illustrating the combined use of drug therapy and catheter-electrode pacing in controlling paroxysmal ventricular tachycardia is presented. Only six deaths occurred in spite of the serious heart disease in all 91 patients in this series. Two were related to complications of temporary transvenous intracardiac pacing. The major complications associated with the procedure included perforation of the heart, bacteremia, acute myocardial infarction, cephalic vein phlebitis, and ventricular tachyarrhythmia. Minor problems were primarily related to equipment failure or positional difficulties with the catheter-electrode and were usually of no serious consequence.

Two cases in which large intramural ventricular cardiac fibromas were successfully removed from children are reported. In one the fibroma was principally septal, and in the other it lay in the free wall of the left ventricle. These are the second and third such operations reported. A review of these two cases plus 34 other reported cases of cardiac fibroma indicates that a primary mural tumor of the heart should be suspected in patients, particularly children, with unexplained cardiac failure, unexplained cardiac dysrhythmia, intracardiac calcifications, irregular shadows on roentgenograms, or unexplained newly developing cardiac symptoms and murmurs. Angiocardiography is the best way of confirming the diagnosis. In view of the potential hazard of these tumors, their surgical removal should be undertaken, and this experience indicates that even very large and extensive intramural ventricular tumors may be removed successfully.

The ratio of the mean systolic transaortic valvular gradient to the mean systolic left ventricular pressure times 100 yields a percentage that represents the portion of left ventricular pressure-volume work per stroke lost because of outflow-tract obstruction. The percentage of the left ventricular stroke work loss and the area of the aortic orifice have been estimated in 49 patients with aortic valvular stenosis and two open-chest dogs with varying degrees of supravalvular aortic constriction. Left ventricular stroke work loss of 30% or greater was associated with calculated aortic valve areas of 1.0 cm 2 (or 0.60 cm 2 /m 2 ) or less. These values are representative of serious obstruction to left ventricular outflow, that is, approximately 75% or greater reduction of normal orifice size. The calculation of the percentage of left ventricular stroke work loss, besides being simple, is based upon the most reliable measurements obtainable at left heart catheterization, that of the pressure pulses.

The first 50 cases at the Mayo Clinic of insertion of an aortic valvular homograft after excision of the aortic valve are reported. The hospital mortality rate was 6%. An aortic diastolic murmur was noted in 17% of the surviving patients just prior to their dismissal from the hospital. In none was there evidence of hemodynamically significant aortic valvular incompetence. At follow-up examination 3 to 12 months postoperatively, an aortic diastolic murmur was audible in 44% of the traced patients. Only one patient had hemodynamically significant aortic valvular incompetence. The patients were not given anticoagulant therapy, and there were no thromboembolic complications.

The incidence of thromboembolism after insertion of prosthetic cardiac valves is related to the type of prosthesis and in the cases reviewed here was highest for the ball-valve prosthesis. The risk of thromboembolism was studied by constructing actuarial curves showing the proportion of patients with embolism at increasing time intervals postoperatively. Such curves for the patients studied suggest that the risk of thromboembolism diminishes with time, particularly by the third postoperative year. The risk was remarkably similar for patients having aortic, mitral, and multiplevalve replacements, being 15% for the first 6 postoperative months, another 8% for the next 6 months, and another 20% for the next 2 years. Emboli lodged in cerebral, coronary, renal, and other sites in these patients in diminishing frequency. The risk of fatality averaged 15%. None of the nonfatal embolisms resulted in significant continuing disability, save for 7% of the cerebral embolisms. A beneficial effect of anticoagulation was demonstrated for patients having replacement of the aortic valve with a ball-valve prosthesis, particularly when this treatment was carefully controlled. In the latter group, the risk of thromboembolism was less than 5% 2 years postoperatively.

The effect of the mitral Starr-Edwards ball-valve prosthesis on cardiac function was investigated in the dog. Fifteen dogs were studied for the first 48 hours after replacement of the mitral valve (the chordae tendineae [see Figure in the PDF file] had been totally resected, partially resected, or preserved). The cardiac output and left atrial pressure were similar in these three groups of animals and in two animals subjected to sham operation. Ten dogs (five with intact chordae and five with excised chordae) were studied two months after the insertion of a Starr-Edwards prosthesis. In these animals normal hemodynamic values were obtained at rest and during infusion of acetylcholine, except for a marked (liastolic gradient across the prosthesis, which developed at high cardiac output and heart rate. Six dogs were able to complete a standard test of substantial, unrestrained, graded exercise and gave a normal heart rate response. Heart rate increased and was maintained during maximal efforts, to levels of about 300 beats/min, demonstrating that heart rate need not be a limit of cardiac performance. No evidence of left ventricular dysfunction or of a decrement in cardiac performance could be demonstrated in dogs early or late after replacement of the mitral valve with a Starr-Edwards prosthesis. The presence or absence of chordae tendineae was irrelevant to cardiac performance.