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Biomedical subjects

Z Feliciano

Publications and source records attributed to Z Feliciano.

8 recordsLinked to original sources

Improved survival in patients with nonischemic advanced heart failure and syncope treated with an implantable cardioverter-defibrillator.

The purpose of this study was to assess whether in patients with syncope and heart failure due to nonischemic cardiomyopathy, treatment with an implantable cardioverter-defibrillator (ICD) compared with conventional medical therapy is associated with a reduction in sudden death and total mortality. Patients with advanced heart failure who have syncope have been shown to be at high risk for sudden death. Further risk stratification has been difficult in patients with nonischemic cardiomyopathy in whom inducibility on electrophysiologic study is not predictive of future risk. Of 639 consecutive patients with nonischemic cardiomyopathy referred for heart transplantation, 147 patients with history of syncope and no prior history of sustained ventricular tachycardia or cardiac arrest were identified. Outcomes were compared for the 25 patients managed with an ICD and 122 patients managed with conventional medical therapy. There were no differences in the baseline variables in the 2 groups of patients, including age, ejection fraction, and medical treatments for heart failure, but patients receiving an ICD were more likely to have had nonsustained ventricular tachycardia (56% vs. 15%, p = 0.001). During a mean follow-up of 22 months, there were 31 deaths, 18 sudden, in patients treated with conventional therapy, whereas there were 2 deaths, none sudden, in patients treated with an ICD. An appropriate shock occurred in 40% of the ICD patients. Actuarial survival at 2 years was 84.9% with ICD therapy and 66.9% with conventional therapy (p = 0.04). Thus, in patients with nonischemic cardiomyopathy and syncope, therapy with an ICD is associated with a reduction in sudden death and an improvement in overall survival.

Actuarial Analysis↗

Intradevice interaction in a dual chamber implantable cardioverter defibrillator preventing ventricular tachyarrhythmia detection.

Failure to detect ventricular tachycardia and/or ventricular fibrillation by implantable cardioverter defibrillators (ICDs) is a rare but serious problem. We report a case of failure to detect an episode of induced ventricular tachycardia by a dual chamber ICD, due to abbreviation of ventricular detection window secondary to programmed pacing parameters and a rate-smoothing algorithm. In this patient, the intradevice interaction was corrected by programming rate-smoothing off. This report highlights the potentially lethal consequences of critical timing relationships among the pacing function, arrhythmia detection, and the characteristics of the arrhythmia when using a modern dual chamber ICD. Physicians responsible for patients with ICDs must be aware of such interactions.

Algorithms↗

Comparison of class Ia/Ib versus class III antiarrhythmic drugs for the suppression of inducible sustained ventricular tachycardia associated with coronary artery disease.

Previous studies suggest that class Ia drugs are ineffective in suppression of sustained ventricular tachycardia by programmed stimulation. More favorable results have been described with combinations of Ia and Ib drugs and also with class III antiarrhythmic drugs, but there have been no direct comparisons between these 2 regimens. The present study was undertaken to compare the electrophysiologic efficacy and predictors of success of these 2 regimens in patients with ischemic heart disease and inducible sustained monomorphic ventricular tachycardia. The population consisted of 136 patients with documented coronary artery disease. All had sustained monomorphic ventricular tachycardia inducible during baseline electrophysiologic study and following intravenous procainamide. Follow-up studies were performed with a combination of oral class Ia and Ib or class III antiarrhythmic drugs. A positive response was the inability to induce a sustained ventricular arrhythmia with up to 3 extrastimuli at 2 right ventricular pacing sites. Response rates were 13% for Ia/Ib combination and 19% for class III agents (p = 0.40). Congestive heart failure differentially affected response rates. Only 8% of those responding to Ia/Ib therapy had heart failure compared with 59% of responders to class III (p <0.01). Multivariate analysis identified heart failure (RR 12.2, p = 0.03) as the only parameter with independent predictive value of response to Ia/Ib therapy. These results indicate that congestive heart failure is a potent predictor of a negative response to a combination of class Ia and Ib antiarrhythmic drugs. In this population, class III drugs or nonpharmacologic therapy should be considered as initial treatment.

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The acute hemodynamic effects of right ventricular septal pacing in patients with congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

To assess the hemodynamic effects of right ventricular septal pacing in patients with severe chronic heart failure, we studied 13 patients during intrinsic rhythm and with pacing in the VDD mode at atrioventricular delays of 100 to 200 ms. There was no improvement of any hemodynamic parameter measured with pacing, even in the subgroup of patients with prolonged PR intervals.

Atrioventricular Node↗

Acute electrophysiologic effects of amiodarone in patients with congestive heart failure.

Patients with severe congestive heart failure (CHF) are at increased risk for atrial and ventricular arrhythmias and sudden cardiac death. Amiodarone is generally well tolerated by this population and has a low proarrhythmic potential. Because of its peculiar kinetics, amiodarone requires a prolonged loading period, necessitating lengthy hospitalizations in a monitored setting. This study was planned prospectively to assess the electrophysiologic effects of an abbreviated high-dose oral load of amiodarone in patients with severe CHF and known or suspected life-threatening ventricular arrhythmias. Fifteen patients with stable CHF and known or suspected life-threatening ventricular arrhythmias underwent baseline electrophysiologic study. The study was repeated after administration of oral amiodarone, 50 mg/kg/day for 2 days in 8 divided doses (mean dose 6.9 +/- 0.4 g). After amiodarone administration, there was prolongation in virtually all conduction times and refractory periods. The prolongation of refractoriness was most pronounced in the atrium. Ventricular effective refractory periods demonstrated reverse frequency dependence. We conclude that a brief high-dose oral load of amiodarone is well tolerated by patients with CHF. It has marked and diffuse electrophysiologic actions suggestive of class I and III effects in addition to antiadrenergic and calcium blocking action. These effects are especially pronounced in the atrium.

Administration, Oral↗

Dual-chamber pacing with a short atrioventricular delay in congestive heart failure: a randomized study.

OBJECTIVES: This prospective study assessed the initial hemodynamic effects and long-term clinical benefits of dual-chamber pacing with a short atrioventricular (AV) delay in patients with chronic heart failure who had no traditional indication for pacemaker implantation. BACKGROUND: Dual-chamber pacing with a short AV delay has been proposed as a nonpharmacologic treatment for drug-refractory heart failure. Both initial and long-term hemodynamic as well as functional benefits have been reported. All previous studies have used an AV delay of 100 ms. Despite encouraging results, these previous studies have been anecdotal and uncontrolled. METHODS: This double-blind, randomized, crossover trial included 12 subjects with chronic congestive heart failure despite optimal medical therapy. Patients were required to be in sinus rhythm with no evidence of significant bradyarrhythmias. On the day after implantation of a dual-chamber pacemaker, invasive hemodynamic measurements were made at varying AV delays between 100 and 200 ms. Patients were then randomized to either dual-chamber pacing with a 100-ms AV delay or backup mode (VVI at 40 beats/min). After 4 to 6 weeks, crossover to the other pacing mode was programmed. RESULTS: Hemodynamic measurements on the day after pacemaker implantation demonstrated no benefit of pacing with any AV delay compared with intrinsic conduction. At the optimal AV interval for each patient, neither cardiac output (4.5 +/- 1.5 vs 4.7 +/- 1.6 liters/min [mean +/- SD]) nor wedge pressure (16 +/- 10 vs 17 +/- 8 mm Hg) improved significantly from baseline measurements during intrinsic conduction. The long-term pacing protocol was completed in nine patients. Ejection fraction was 16 +/- 6% with dual-chamber (VDD mode) pacing and 18 +/- 4% in backup mode (p = NS). No patient had an increase in ejection fraction by > or = 5% with VDD pacing, nor did any patient improve in New York Heart Association functional class with short AV delay dual-chamber pacing. Also, there were no significant reductions in body weight or diuretic requirements during this pacing period. CONCLUSIONS: Dual-chamber pacing with a short AV delay does not improve hemodynamic and clinical status or ejection fraction measured on the day after pacemaker implantation in patients with chronic congestive heart failure. Routine use of pacemaker therapy with a short AV delay aas a primary treatment of heart failure in patients without standard arrhythmic indications is unwarranted.

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Pulmonary hypertension decreases the predictive accuracy of echocardiographic clues for cardiac tamponade.

A number of echocardiographic clues of pericardial tamponade have been described, but their accuracy in patients with pulmonary hypertension has not been well elucidated. Four echocardiographic clues of pericardial tamponade, namely, right atrial collapse (RAC), right ventricular diastolic collapse (RVDC), marked (> 40%) respiratory variation in transmitral Doppler flow velocity ("flow velocity paradoxus [FVP]"), and inferior vena cava plethora (IVCP) were prospectively evaluated in 32 patients with large pericardial effusions. Of 12 patients with pulmonary hypertension, 6 had invasively determined evidence of tamponade and 6 did not; of 20 patients without pulmonary hypertension, 11 had tamponade and 9 did not. These echocardiographic clues were evaluated in a blinded fashion. Predictive accuracies for RAC, RVDC, FVP, and IVCP were 75%, 80%, 90%, and 95%, respectively, for the patients without pulmonary hypertension and 67%, 58%, 58%, and 83%, respectively, for the patients with pulmonary hypertension. Although all predictive accuracies were lower in patients with pulmonary hypertension, statistically significant decreased predictive accuracy was found only with FVP (p < 0.05). Interestingly, IVCP had the best predictive accuracy among patients with pulmonary hypertension. Our findings suggest that despite somewhat decreased accuracy in patients with pulmonary hypertension, traditional echocardiographic clues for pericardial tamponade may be useful.

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Overdrive pacing for atrial flutter.

To determine the incidence and predictors of conversion to normal sinus rhythm, a total of 124 procedures using a standard pacing protocol were performed in 101 consecutive inpatients referred for pace termination of atrial flutter. Normal sinus rhythm was achieved in 75 pace termination procedures (60%), including 10 in which atrial fibrillation occurred initially and later converted spontaneously. Sustained atrial fibrillation was provoked in 39 procedures, and atrial flutter persisted in 10. Clinical and laboratory parameters, including use of antiarrhythmic drugs, were not helpful in predicting the outcome of pacing. Of 17 patients undergoing repeat pacing for recurrent flutter, concordant results were obtained in only 4. It is concluded that: (1) overdrive pacing is only a moderately effective means of restoring sinus rhythm in patients with atrial flutter, although some change in rhythm occurs in the vast majority; (2) pacing-induced atrial fibrillation may be unstable and spontaneously converts to sinus rhythm in > 20% of cases; (3) there are no clinically useful predictors of success; (4) antiarrhythmic drugs do not facilitate pacing-induced conversion to sinus rhythm; and (5) failure to convert to sinus rhythm with 1 episode of flutter does not preclude success on subsequent occasions.

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