Daniel J. Goodman

Arrhythmias in patients with mitral valve prolapse.

Resting ECGs, exercise treadmill tests and 24-hour ambulatory ECGs were recorded and analyzed in 24 unselected patients with mitral valve prolapse. Arrhythmias were frequent. There were three distinct groups of patients, defined on the basis of total number of premature ventricular contractions (PVCs) during the 24 hours: there were no PVCs in 25%, infrequent PVCs in 25%, and frequent PVCs in 50%. Complex ventricular arrhythmias, including ventricular tachycardia in five patients, were found almost exclusively in the group with frequent PVCs. Fifteen of the 24 patients demonstrated atrial premature contractions (APCs) during the 24 hours. Complex atrial arrhythmias were found among patients with infrequent, as well as those with frequent, APCs. Supraventricular tachycardia was detected in seven of these patients. The incidence of PVCs decreased during sleep in 58% of the patients, increased in 17%, and showed no change in 25%. The incidence of APCs decreased during sleep in 67% of the patients and showed no change during sleep in 33%. A poor correlation was found between symptoms recorded in patient diaries and changes noted on 24-hour ECG recordings. The peak PVCs/15 min and peak APCs/15 min during a 24-hour period of monitoring was found to be an excellent guide to the total number of PVCs and APCs occurring during that period. This permits an accurate prediction of the total number of PVCs in 24 hours after performing an exact PVC count on only 15 minutes of ECG data. Finally, the 24-hour ambulatory ECG was more sensitive than the treadmill test and both were superior to the 12-lead ECG for detecting arrhythmias in these patients.

Effect of Nitroprusside on Left Ventricular Dynamics in Mitral Regurgitation

In order to evaluate the circulatory action of vasodilator therapy in patients with significant mitral regurgitation, sodium nitroprusside was infused intravenously in 14 patients who had mitral regurgitation due to a variety of causes. In 13 of these patients, valvular insufficiency had been present for several years. The mean arterial pressure fall from 88 ± 1.2 to 71 ± 2.1 mm Hg was accompanied by a significant decrease in pulmonary artery pressure (from 27.4 ± 2.7 to 19.1 ± 2.4 mm Hg), pulmonary artery wedge v wave (from 31.7 ± 3.3 to 17.0 ± 1.9 mm Hg), and left ventricular end-diastolic pressure (from 16.7 ± 1.6 to 9.3 ± 1.2 mm Hg). In 10 patients significant decreases in angiographic end-diastolic volumes (from 196 ± 10 to 177 ± 10 ml) and end-systolic volumes (from 90 ± 10 to 77 ± 9 ml) were accompanied by slight decreases in the total stroke volume and slight increases in the ejection fraction. The improved forward stroke volume index (from 27 ± 3.0 to 33 ± 2.1 ml) was due to a very significant reduction in the regurgitant fraction (from 57 ± 6 to 42 ± 6%). Nitroprusside, therefore, has beneficial hemodynamic effects in patients with chronic mitral regurgitation.

Echocardiographic features of primary pulmonary hypertension

Abstract Echocardiograms were recorded in nine patients with primary pulmonary hypertension proved at cardiac catheterization. A reduced diastolic slope of the anterior mitral valve leaflet, simulating mitral stenosis but with normal motion of the posterior leaflet, was observed in all patients. Other features found included a large right ventricular dimension (nine patients), a small left ventricular dimension (three patients), a thick interventricular septum (six patients), systolic mitral leaflet prolapse (four patients) and abnormal septal motion (four patients). The last feature was most probably due to secondary tricuspid or pulmonic insufficiency, or both. The finding of a decreased mitral valve slope, often used as a criterion for mitral stenosis, should not be accepted alone as proof of mitral stenosis; the posterior mitral valve leaflet echo must be carefully searched for and identified. This echo is often difficult to identify, but the normal motion of this structure found in all patients excludes the diagnosis of mitral stenosis as a cause for the pulmonary hypertension.

Propranolol for patients with mitral valve prolapse

This study evaluates propranolols effect on symptoms, arrhythmias, and exercise tolerance in 16 patients with mitral valve prolapse. Three patients (19 per cent) experienced symptomatic deterioration with propranolol therapy, seven (44 per cent) were unchanged, and six (37 per cent) noted an over-all symptomatic improvement, primarily due to a reduction in palpitation. Symptomatic improvement continues in these six patients an average of 12.5 months after beginning propranolol therapy. Treatment with propranolol alleviated chest pain in only two of eight patients and it did not improve the ability to perform treadmill exercise. Fatigue did not improve, and in three patients appeared for the first time during propranolol therapy. Premature ventricular contractions were reduced by at least 75 per cent in five of nin patients (56 per cent), and paroxysmal ventricular tachycardia was eliminated in three of four patients. We conclude that propranolol is not uniformly effective in patients with mitral vale prolapse. A trial of propranolol may be instituted fro patients with mitral valve prolapse who have severe symptoms and/or arrhythmias, but the drug should only be continued in those who demonstrate clinical and/or antiarrhythmic response.

Echocardiographic Criteria in the Diagnosis of Idiopathic Hypertrophic Subaortic Stenosis

Echocardiography has proven to be a useful technique in the diagnosis and assessment of therapy in idiopathic hypertrophic subaortic stenosis (IHSS). Asymmetric septal hypertrophy has been described as the pathognomonic anatomic marker of the disease. A characteristic systolic anterior motion of the anterior mitral valve leaflet has been detected in the presence of hemodynamically significant subaortic left ventricular outflow obstruction. An echocardiographic quantification of the outflow gradient (the obstruction index) has been derived previously.Four patients were studied by ultrasound at the time of cardiac catheterization. All four demonstrated systolic anterior motion of the anterior mitral leaflet in the absence of a resting gradient. In three of the four, the calculated obstruction index predicted hemodynamically significant resting gradients. All four patients were shown to have labile gradients with provocative maneuvers. A fifth patient with abnormal systolic anterior motion demonstrated a close correlation between the obstruction index and resting gradient; however, symmetric hypertrophy of the septum and left ventricular posterior wall was detected by ultrasound. Therefore, the abnormal mitral valve pattern may be seen in the absence of a resting gradient and symmetric left ventricular hypertrophy may exist in the presence of IHSS.

Effect of digoxin on atioventricular conduction. Studies in patients with and without cardiac autonomic innervation.

The effect of digoxin on atrioventricular (a-v) conduction was compared in five patients with an intact cardiac autonomic nervous system (Group I) and seven patients who had undergone cardiac transplantation (Group II), in whom we have previously shown the transplanted heart to be completely denervated. Small decreases in the atrial effective refractory period (ERP) (from 262 plus or minus 12 to 254 plus or minus 11 msec) and atrial functional refractory period (FRP) (from 304 plus or minus 12 msec) were observed in Group I patients after digoxin, but these changes were not significant. However, significant increases in the A-V nodal ERP (from 315 plus or minus 18 msec to 351 plus or minus 17 msec, P less than 0.05), and A-V nodal FRP (from 426 plus or minus 42 to 460 plus or minus 46 msec, P less than 0.01) were produced by digoxin and were unrelated to changes in cycle length. In Group II patients with denervated hearts, changes in atrial ERP (from 246 plus or minus 4 to 243 plus or minus 6 during spontaneous sinus rhythm; from 204 plus or minus 10 to 216 plus or minus 8 msec during atrial pacing) and atrial FRP (from 311 plus or minus 12 to 316 plus or minus 11 msec during spontaneous sinus rhythm; from 254 plus or minus 12 to 260 plus or minus 10 msec during atrial pacing) were not significant. However, in contrast to the Group I patients, the digoxin-induced changes in A-V nodal ERP (from 280 plus or minus 22 to 297 plus or minus 18 msec during atrial pacing) and FRP (from 368 plus or minus 18 to 377 plus or minus 18 msec during spontaneous sinus rhythm; from 334 plus or minus 13 to 346 plus or minus 16 msec during atrial pacing) were also statistically insignificant. Our results demonstrate that the electrophysiologic effects of digoxin on atrioventricular conduction in man are most marked in the atrioventricular node and are dependent on cardiac innervation

Ventricular Systolic Septal Thickening and Excursion in Idiopathic Hypertrophic Subaortic Stenosis

Abstract Asymmetric septal hypertrophy has been described as the pathognomonic abnormality in idiopathic hypertrophic subaortic stenosis. It has been suggested that the ventricular septum is hyperc...

Sinus node function in the denervated human heart. Effect of digitalis.

Evaluation of sinus node function was performed in 5 patients with an intact cardiac autonomic nervous system (group I), and in 8 patients with a transplantated, denervated heart (group 2). After baseline data were recorded, the electrophysiological studies were repeated in all group I patients and in 6 of the 8 group 2 patients, 45 to 60 minutes after the administration of digoxin 1.25 mg intravenously. Baseline cycle length, sinus node recovery time, and sinoatrial conduction time were significantly shorter in the transplanted heart than in those with intact autonomic innervation, but correction of the sinus node recovery time and sinoatrial conduction time for heart rate abolished these differences. Digoxin produced a small increase in cycle length, sinus node recovery time, and sinoatrial conduction time which did not reach statistical significance in this small study group of patients with innervated hearts. In the denervated, transplanted patients, no change in cycle length occurred after digoxin in any patient. The sinus node recovery time was unaffected by glycoside administration in 3 of 6 patients, while the sinoatrial conduction time was unchanged in 4 of 6. In one group 2 patient, digoxin produced first degree sinoatrial node exit block, and in a second patient, 2:1 sinoatrial nodal exit block developed. The mechanisms responsible for these effects in the denervated heart are not clear.

Electrophysiologic Findings in Patients With Idiopathic Hypertrophic Subaortic Stenosis

Thirteen patients with catheterization-proved idiopathic hypertrophic subaortic stenosis underwent intracardiac electrophysiologic study. There was a large incidence of arrhythmias and a strikingly large incidence of conduction system abnormalities among these patients. The P-A and A-H intervals were normal in all patients. Atrial pacing resulted in Mobitz type 1 block proximal to the His bundle at an abnormal rate (less than 140/min) in 2 of 12 patients (17 percent). H-V intervals were prolonged (greater than 50 msec) in 10 of 12 patients (83 percent) and were greater than 60 msec in 7 patients (58 percent). The atrial effective refractory period was prolonged in 3 of 12 patients and was markedly prolonged in 1 of them. Effective refractory period of the atrioventricular (A-V) node, determined in five patients, was prolonged in three. Dual responses of the A-V node to atrial extrastimuli were found in seven patients. Dual A-V nodal repsonses were evoked with propranolol in three patients and persisted in the other four patients with dual responses despite propranolol administration.

The effect of cycle length on cardiac refractory periods in the denervated human heart

We have previously demonstrated that the transplanted human heart is functionally denervated. With the use of the extra stimulus technique during His bundle electrocardiography, refractory periods of the arterioventricular (A-V) conduction system were determined at several heart rates after pacing-induced changes in cycle length in eight patients who had previously undergone cardiac transplantation. Shortening of the cycle length was accompanied by a decrease in both the effective and functional refractory periods of the atrium. No consistent change in A-V nodal effective refractory period or functional refractory period could be demonstrated. Because A-V conduction was limited at shorter cycle lengths by the functional refractory periods of the atrium and A-V node, bundle branch refractory periods could be determined in three patients only at the longest cycle length studied. In four of the eight patients, atrial arrhythmias were produced at short cycle lengths with the introduction of early atrial extra stimuli. This may be due to a lack of vagal innervation of the atrium. These results contribute to our understanding of atrial arrhythmias.