John F. Sanfelippo

Comparative survival after permanent ventricular and dual chamber pacing for patients with chronic high degree atrioventricular block with and without preexistent congestive heart failure

To determine whether survival after permanent ventricular demand (VVI) pacing differs from survival after permanent dual chamber (DVI or DDD) pacing in patients with chronic high degree atrioventricular (AV) block (Mobitz type II or trifascicular block), 132 patients who received a VVI pacemaker (Group 1) and 48 patients who received a DVI or DDD pacemaker (Group 2) were followed up for 1 to 5 years. There was no significant difference in sex distribution, mean age or incidence of coronary heart disease, hypertension, valvular heart disease, diabetes mellitus, stroke or renal failure between Groups 1 and 2. Overall, the predicted cumulative survival rate at 1, 3 and 5 years was 89, 76 and 73%, respectively, for Group 1 and 95, 82 and 70%, respectively, for Group 2. In patients with preexistent congestive heart failure, the predicted cumulative survival rate at 1, 3 and 5 years was 85, 66 and 47%, respectively, for Group 1 (n = 53) and 94, 81 and 69%, respectively, for Group 2 (n = 20). The 5 year predicted cumulative survival rate was significantly lower in Group 1 patients with preexistent congestive heart failure than in Group 2 patients with the same condition (p less than 0.02). There was no significant difference in 5 year cumulative survival rate between Groups 1 and 2 for patients without preexistent congestive heart failure. The results suggest that permanent dual chamber pacing enhances survival to a greater extent than does permanent ventricular demand pacing in patients with high degree AV block and preexistent congestive heart failure.

Comparative survival following permanent ventricular and dual-chamber pacing for patients with chronic symptomatic sinus node dysfunction with and without congestive heart failure

To determine whether survival following permanent ventricular demand pacing differs from survival following permanent dual-chamber pacing in patients with symptomatic sinus node dysfunction (unexplained sinus bradycardia, subsidiary rhythms, sinus arrest, sinoatrial block, or the bradycardia/tachycardia syndrome), we followed 79 patients who received a VVI pacemaker (group 1) and 49 patients who received a DVI or DDD pacemaker (group 2) for 1 to 5 years. There was no significant difference in sex distribution, mean age, or the incidence of coronary heart disease, hypertension, valvular heart disease, diabetes mellitus, stroke, or renal failure between groups 1 and 2. Overall, the predicted cumulative survival rates at 1, 3, and 5 years were 89%, 82%, and 74%, respectively, for group 1 and 94%, 86%, and 78%, respectively, for group 2. In patients with preexistent congestive heart failure (CHF), predicted cumulative survival rates at 1, 3, and 5 years were 78%, 69%, and 57%, respectively, for group 1 (n = 23) and 90%, 83%, and 75%, respectively, for group 2 (n = 16). Five-year predicted cumulative survival was significantly lower in group 1 patients with CHF than in group 2 patients with CHF (p less than 0.03). There was no significant difference in 5-year cumulative survival rates between groups 1 and 2 in patients without CHF. The results suggest that permanent dual-chamber pacing enhances survival to a greater extent than permanent ventricular demand pacing in patients with chronic symptomatic sinus node dysfunction and CHF.

Difficulty of extraction of chronically implanted tined ventricular endocardial leads

The dislodgment rate of permanent pacing ventricular and atrial endocardial leads has significantly decreased with the incorporation of tines as a fixation device. In contrast, transvenous manual extraction of chronically implanted endocardial leads is, at times, clinically indicated, particularly when pacemaker system infection is present. The success rate of such extraction attempts for ventricular endocardial leads over the past 5 years was reviewed. Extraction was usually successful (six of seven attempts) in patients with silicone rubber nontined (or short-tined) older ventricular endocardial leads (Group A). However, in patients with newer urethane long-tined ventricular endocardial leads (Group B), extraction was unsuccessful in three of four attempts. Because of entrapment of the distal electrode tip in the right ventricular apex, manual traction of these leads resulted in permanent conductor material stretching with resultant urethane insulator material breakage in the region of the joints with proximal and distal electrodes. The one successful extraction in Group B was technically difficult and appeared to create a significant risk of intracardiac lead separation. This experience indicates that with improved pacemaker lead design decreased lead dislodgment has been obtained at the cost of increased difficulty of ventricular endocardial lead extraction. Such difficulty should be anticipated when a clinical decision is made to attempt to extract the new urethane long-tined ventricular leads.

Sensitivity and specificity of two-dimensional echocardiographic signs of mitral valve prolapse

The sensitivity and specificity of previously described 2-dimensional echocardiographic signs of mitral valve prolapse (MVP) were assessed in 70 patients with MVP and in 100 normal control subjects. Specificity of individual signs was uniformly high, ranging from 88% for excessive motion of the posterior mitral ring to 100% for several signs including systolic arching in the parasternal long-axis view, excessive posterior coaptation and diastolic doming of the anterior mitral leaflet. Sensitivity of individual signs was low to moderate, ranging from 1% for whip-like motion of both mitral leaflets to 70% for excessive posterior coaptation of the mitral leaflets in the apical 4-chamber view. The highest sensitivity value (87%) was associated with the presence of systolic arching of 1 or both mitral leaflets in the parasternal long-axis view or systolic bowing of 1 or both mitral leaflets in the apical 4-chamber view or excessive posterior coaptation of the mitral leaflets or a combination. This increase in sensitivity was achieved without sacrificing specificity (97%). Thus, the individual 2-dimensional echocardiographic signs tested possess uniformly high specificity, but only low to moderate sensitivity; however, sensitivity can be markedly enhanced without sacrificing specificity by using selected combinations of echocardiographic signs.

Anomalous Right Coronary Artery Arising from the Midportion of the Left Anterior Descending Coronary Artery—Case Reports

Although coronary artery anomalies are detected during 0.8-1.2% of routine adult cardiac catheterizations, anomalies of the right coronary artery are relatively uncommon and are generally of no clinical significance. This report focuses, however, on 2 patients whose RCA originated from the midportion of the left anterior descending artery, an anomaly with potentially important clinical implications, which are explored.

Observer variation in the echocardiographic diagnosis of mitral valve prolapse

To assess inter- and intraobserver variation in the echocardiographic diagnosis of mitral valve prolapse, three independent observers analyzed M-mode echocardiograms (n = 80) and two-dimensional echocardiograms (n = 65) of patients with a mobile midsystolic click with or without a late or holosystolic murmur. In addition, a control group of 100 normal echocardiograms were interspersed among the echocardiograms of patients with mitral valve prolapse and were then interpreted. Each of the three observers analyzed all M-mode and two-dimensional echocardiograms initially and then 2 weeks later for the presence or absence of mitral valve prolapse. M-mode echocardiographic criteria for mitral valve prolapse consisted of late systolic posterior motion (greater than or equal to 3 mm) of one or both mitral leaflets or holosystolic hammocking (greater than or equal to 3 mm) of one or both mitral leaflets. Two-dimensional echocardiographic criteria for mitral valve prolapse consisted of: posterior systolic arching of one or both mitral leaflets in the parasternal long-axis view, and/or posterior systolic bowing of one or both mitral leaflets in the apical four-chamber view posterior to the plane of the mitral anulus, and/or excessive posterior coaptation of the mitral leaflets in either view flush with or posterior to the plane of the mitral anulus. There was insignificant observer variation both in the M-mode and two-dimensional echo groups, as determined using Cochrans Q test.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of beta blockade with betaxolol on left ventricular systolic function in chronic stable angina pectoris and left ventricular dysfunction

To assess the effect of beta blockade on left ventricular (LV) performance in patients with LV dysfunction and stable angina pectoris, 18 subjects taking a placebo followed by incremental doses of the cardioselective beta-adrenergic blocking agent betaxolol (5, 10, 20, 40 and 80 mg/day) were studied. The study ended with the achievement of optimal clinical beta blockade (heart rate at rest 50 to 60 beats/min, a 20% or smaller increase in heart rate during stage 1 of symptom-limited treadmill exercise using the modified Bruce protocol). Optimal clinical beta blockade produced a decrease in mean frequency of angina, from 6.8 +/- 1.7 to 0.7 +/- 0.8 episodes per week (p less than 0.0005) and an increase in mean treadmill exercise capacity, from 3.1 +/- 1.7 to 7.7 +/- 2.8 minutes (p less than 0.0005). LV systolic function was assessed at rest and during symptom-limited exercise with radionuclide left ventriculography. Mean LV ejection fraction (EF) during therapy with placebo was 39 +/- 7% at rest and 40 +/- 8% at peak exercise. Mean LVEF during optimal clinical beta blockade was 43 +/- 11% at rest and 45 +/- 10% at peak exercise. Neither of these changes was statistically significant. No patient had clinical or radiographic signs of LV failure. The results suggest that optimal clinical beta blockade with betaxolol, in doses sufficient to significantly reduce the frequency of angina and improve exercise capacity in patients with stable angina pectoris and mild to moderate LV systolic dysfunction, does not cause significant deterioration of LV systolic function or produce LV failure.

Efficacy of Betaxolol in the Treatment of Stable Exertional Angina Pectoris: A Dose-Ranging Study

To assess the efficacy of oral betaxolol in the treatment of stable exertional angina pectoris and to determine the relationship between betaxolol doses/serum concentrations and clinical/hemodynamic responses the authors studied 24 patients prior to and following stepwise administration of 5, 10, 20, 40, and 80 mg doses. The major endpoint for the study was the achievement of clinical beta blockade (heart rate 50-60 beats/min and ≤ 20% rise in treadmill stage I heart rate). Betaxolol produced a decrease in mean angina pectoris frequency from 6.6 ± 1.9 episodes/week with placebo to 0.2 ± 0.5 episode/week during clinical beta blockade (p < 0.00005). Mean treadmill exercise time increased from 3.1 ± 1.7 min with placebo to 7.3 ± 2.3 min with doses sufficient to reduce angina pectoris frequency ≥ 75% (p < 0.00005) and to 8.0 ± 2.3 min during clinical beta blockade (p < 0.00005). The mean doses of betaxolol required to produce a ≥ 75% decrease in angina pectoris frequency and clinical beta blockade were 12 ± 5 mg (range 5-40 mg) and 28 ± 29 mg (range 5-80 mg) respectively. Mean serum concentrations associated with these clinical endpoints were 23.8 ± 9.7 ng/mL and 59.7 ± 54.0 ng/mL respectively. The results indicate that betaxolol, in widely ranging doses, is highly effective in reducing angina pectoris frequency and improving exercise capacity in patients with stable exertional angina pectoris.

Limitations of Echocardiography in the Diagnosis of Left Atrial Myxoma: A Case Report

The classical echocardiographic features of left atrial myxoma are quite dis tinctive but do not comprise the full spectrum of abnormalities encountered. This case demonstrates atypical echocardiographic features of left atrial myx oma that initially obscured the correct diagnosis. Our findings underscore the potential limitations of echocardiography in the diagnosis of left atrial myxoma.