Pulmonary valve vegetations detected with echocardiography.

In a patient with pseudomonas endocarditis a pulmonary regurgitant murmur developed. Sequential echocardiography demonstrated the initial absence of vegetations, the evolution of pulmonary valve vegetations with relapse and finally the apperance of vegetations on all cardiac valves. The findings were confirmed at autopsy. Echocardiography, a useful technique for evaluating mitral, aortic and tricuspid vegetations, can also detect pulmonary valve vegetations.

Pathologic correlations in a case of complete heart block with split His potentials resulting from a stab wound of the heart.

A 23 year old previously healthy man was stabbed in the anterior chest. This resulted in a ventricular septal defect and complete atrioventricular (A-V) block. The electrocardiogram revealed complete A-V block with a QRS pattern of right bundle branch block. His bundle recordings 26 days later revealed A-V dissociation with split His potentials (P-H1 interval of 100 msec and H2-V interval of 40 msec). During the study the escape QRS shifted from right to left bundle branch block with H2 potentials still preceding each QRS interval with H2-V intervals of 40 msec. A permanent pacemaker was implanted because of persistent congestive heart failure and bradycardia due to A-V block. The patient subsequently became asymptomatic. He died suddenly 3 1/2 years later. Pathologically there were sizable openings in both the tricuspid and mitral valve substance and a ventricular septal defect involving the pars membranacea and part of the adjacent muscular septum. Serial sections of the conduction system revealed total destruction and fibrous replacement of the bifurcation and beginning of the right and left bundle branches and subtotal fibrous replacement of the branching bundle. Thus, the bifurcation of the bundle of His was totally absent at autopsy despite apparent electrophysiologic evidence of its existence 26 days after the stab wound. A possible explanation for this discrepancy is the subsequent fibrosis of the bifurcation produced by hemodynamic changes at the lower margin of the ventricular septal defect.

Conduction system in a patient with Prinzmetal's angina and transient atrioventricular block.

His bundle recordings obtained during and between attacks of Prinzmetal's variant angina and transient atrioventricular (A-V) block were followed by a comprehensive serial section study of the conduction system in a 33 year old woman. Recordings between attacks showed normal A-H and H-V intervals. During an attack there was block proximal to the His bundle recording site. Pathologic studies revealed severe narrowing of the right coronary artery. Arteriolosclerosis of the heart was diffuse. Insignificant changes were found in the approaches to the A-V node and the A-V node itself. Major changes found in the left bundle branch had no counterpart in the electrocardiogram; the discordance in these findings is discussed.

Significance of A-H interval in patients with chronic bundle branch block. Clinical, electrophysiologic and follow-up observations.

His bundle electrograms were recorded in 308 adults with chronic bundle branch block. The A-H interval was normal in 249 patients and prolonged in 59. Comparison of patients with normal and prolonged A-H intervals revealed a greater incidence of demonstrable organic heart disease in the latter (P less than 0.01). Dyspnea, cardiomegaly and congestive heart failure were more frequent in patients with A-H prolongation. These patients also had longer P-R intervals and atrioventricular (A-V) nodal effective refractory periods, lower paced rates producing second degree A-V block proximal to the His bundle and a greater frequency of H-V prolongation. All patients were prospectively followed up in a conduction disease clinic with mean follow-up periods (+/- standard error of the mean) of 523 +/- 23 and 588 +/- 47 days in the patients with normal and prolonged A-H intervals, respectively. Seven (3 percent) of the patients with a normal A-H interval had A-V block with probable or definite site of block proximal to the His bundle in three and distal to the His bundle in four. In five of the six patients with a prolonged A-H interval who experienced A-V block (10 percent), the probable or definite site of block was proximal to the His bundle. Mortality (both sudden and nonsudden) was not significantly different in the patients with normal and prolonged A-H intervals. In summary, A-H prolongation was associated with increased incidence of organic heart disease and myocardial dysfunction. The risk of development of A-V nodal block was greater in patients with a prolonged A-H interval but appeared to be of minimal clinical significance.

Pulmonary edema due to tetrachloroethylene.

A patient with massive exposure to tetrachloroethylene fumes presented with coma and severe pulmonary edema. Sequential blood gases, chest x-rays, and clinical findings showed dramatic improvement with conventional but aggressive management and the patient recovered completely. There was no evidence of permanent renal, hepatic, or central nervous system damage.

The mitral knock with atrial fibrillation. A possible source of auscultatory confusion.

A 29-year-old woman with atrial fibrillation and severe rheumatic mitral regurgitation initially had a very loud third heart sound with high-frequency components (mitral knock), as well as with a first heart sound of widely varying intensity. After long diastoles a faint first heart sound was heard, with distinct separation from the third heart sound of the preceding cycle; however, on short cycles the loud and high-pitched third heart sound combined with a loud first heart sound to simulate the combination of a first heart sound with an ejection click. Phonoechocardiographic studies clarified the identity of the transients.

Myocardial infarction associated with thyrotoxicosis.

Myocardial infarction occurs rarely with thyrotoxicosis. A 34-year-old woman with thyrotoxicosis sustained a transmural myocardial infarction and subsequently on cardiac catheterization studies had no significant coronary arterial disease but only residual apical wall akinesia. Thyroid hormone may directly influence myocardial oxygen supply and demand and, by some unknown mechanism exclusive of major coronary arterial blood supply, cause a critical imbalance resulting in angina pectoris and myocardial infarction.

Persistence of the third heart sound after resection of the native mitral and tricuspid valves. Evidence against the valvular theory of third sound origin.

A patient is described with severe rheumatic mitral and tricuspid insufficiency in whom both atrioventricular valves with their chordae tendineae and papillary muscles were resected and replaced with Hancock porcine grafts. This would appear to be the second such patient reported and the first described in detail in whom the third heart sound persisted postoperation. This occurrence documents the fact that a third heart sound can occur in the absence of native atrioventricular valve leaflets and the major portions of the subvalvular supporting apparatus, and argues against the theory that the third heart sound is generated by either the valvular leaflets of the subvalvular apparatus.

A midsystolic ejection click.

A patient of faintly marfanoid habitus with left venticular failure, aortic regurgitation, and rate-related left bundle-branch block was found to have a midsystolic click and echocardiographic findings suggestive of mitral valve prolapse; however, the click did not move earlier in systole in response to head-up tilt or atrial pacing. Cardiac catheterization and angiocardiographic studies revealed severe left ventricular dysfunction out of proportion to the moderate amount of aortic regurgitation observed on aortographic study. Mitral valve prolapse was not confirmed by left ventriculographic study. Intracardiac phonocardiographic and catheter-tip manometric studies identified the click as being aortic in origin, ejection in timing, and midsystolic, rather than early systolic, because of delayed aortic valve opening related to left ventricular dysfunction and delay in conduction.

Tuberculous Addison's disease and thyrotoxicosis.

Addison's disease developed in two patients after they had tuberculosis. Thyrotoxicosis subsequently developed. In both cases, the adrenal glands were calcified, suggesting that Addison's disease was tuberculous in origin. Results of tests for antihyroglobulin, antimicrosomal, and adrenal cortex antibodies were normal. These findings do not suggest an autoimmune basis for the occurrence of the two endocrinopathies. The rarity of the simultaneous occurrence of both disorders suggests it to be fortuitous.

Systolic prolapse of the mitral valve in Noonan's syndrome.

A thirty-five-year-old woman with Noonan's syndrome (Turner phenotype with normal chromosome pattern) had mitral valve prolapse and mitral insufficiency associated with the auscultatory findings of a midsystolic click and late systolic murmur. Selective left-ventricular angiocardiography also showed eccentric hypertrophy of the left ventricle. To our knowledge, this is the first reported instance of mitral valve prolapse occurring in association with Noonan's syndrome.

A new method for measurement of sinoatrial conduction time.

This study describes a new method (NM) for estimation of sinoatrial conduction time (SACT), which utilizes constant atrial pacing (AP) instead of the premature atrial beats (PABs) used in the method reported in 1973 by Strauss et al. The SACTs were obtained by both methods in 20 patients. The SACT by the Strauss method (SM) was calculated as A2A3 minus A1A1. The NM consists of high right AP for a train of eight consecutive beats at rates less than or equal to 10 beats/min faster than the sinus rhythm. The interval between the last paced atrial electrogram (Ap) and the first escape atrial electrogram (A) of sinus origin (Ap-A) was measured along with several post pacing sinus cycles. The SACT by the NM was calculated as follows: SACT = Ap-A minus A1A1. The effect of AP at higher rates was also analyzed. In two patients, the SACT with the SM could not be defined, as all the A2A3 intervals were fully compensatory; with the NM the SACT was 217 and 320 msec. In the remaining 18 patients the SACT was obtainable by both methods. With SM, the SACT ranged 105--452 msec (mean 219 +/- 102 SD) and with the NM it was 85--492 msec (mean 201 +/- 112 SD), and the difference was statistically significant (P = 0.0162). The coefficient of correlation between the two methods was r = 0.97. During AP at faster rates, a rate related increment in Ap-A intervals and also post pacing sinus cycles was noted. This study describes a new and simple method for measurement of SACT in man.

Electrocardiographic changes simulating acute myocardial infarction caused by hyperkalemia: report of a patient with normal coronary arteriograms.

A patient is described with severe diabetic ketoacidosis and hyperkalemia who presented with an ECG resembling an acute anterior wall myocardial infarction. Treatment of hyperkalemia resulted in prompt return of the ECG towards normal. Subsequent work-up including exercise testing and selective coronary arteriography ruled out any significant coronary artery disease suggesting that the ECG changes were probably caused by hyperkalemia. While similar changes have rarely been described in the past, this would appear to be the first such case in whom coronary artery disease was ruled out by a negative exercise testing and coronary arteriography.

Proof by catheterization of mitral valvular origin of a systolic click.

A patient with a loud intermittent midsystolic click presented a problem in differential diagnosis between mitral valve prolapse (intracardiac origin of the click) and left pneumothorax (extracardiac origin). External phonocardiography performed at the time of cardiac catheterization revealed that this loud midsystolic click disappeared whenever a catheter was positioned across the mitral valve. It reappeared whenever the catheter was removed from the transmitral position. Selective left ventriculography confirmed the diagnosis of mitral valve prolapse.

Effects of gravitational stresses on mitral valve prolapse. I. Changes in auscultatory findings produced by progressive passive head-up tilt.

The effects of passive head-up tilt on systolic time intervals were assessed in 18 patients with mitral valve prolapse. In addition to causing prolongation of the pre-ejection period and shortening of left ventricular ejection time, this circulatory stress led to progressive shortening of the Q to click interval. In 1 patient, a systolic click became audible which had not been heard in the supine posture. In 7 patients the click disappeared during head-up tilt, usually at 60 degrees or 90 degrees. In 2 patients without a murmur while supine, a mid-late systolic murmur appeared with tilt; 1 of these 2 as well as another patient who had a soft late systolic murmur while supine developed loud systolic whoops at greater angles of tile. The correlations between Q to click interval and aortic valve opening to click interval, and both the angle and the sine of the angle of tilt were highly significant.

Erythrocyte survival in patients with porcine xenograft aortic and mitral valves.

Ten patients with porcine xenograft aortic and mitral valve prostheses were studied three to 36 months (mean 15 months) postoperatively for evidence of hemolysis. Studies included complete blood count, reticulocyte count, red cell indices, percentage of schistocytes on blood smears, bilirubin concentration, lactic dehydrogenase, serum iron, total iron binding capacity, haptoglobin, serum folate and vitamin B12 levels, Coombs' test, methemoglobin reduction test, autologous 51Cr erythrocyte survival, and urinary examination for iron and hemosiderin. All patients were hemodynamically stable. Nine patients had normal valve function and no evidence of hemolysis. One patient with paravalvular aortic regurgitation had mechanical hemolytic anemia with a negative Coombs' test. Porcine valve xenografts do not seem to be associated with hemolysis unless complicated by a paravalvular leak.