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Biomedical subjects

A N Munsif

Publications and source records attributed to A N Munsif.

11 recordsLinked to original sources
PubMed1997

Risk stratification and clinical outcome of minimally symptomatic and asymptomatic patients with nonsustained ventricular tachycardia and coronary disease: a prospective single-center study.

The Multicenter Automatic Defibrillator Implantation Trial (MADIT) showed improved survival with defibrillator therapy but was restricted to coronary artery disease patients with nonsustained ventricular tachycardia (NSVT) and inducible nonsupressible VT. The outcome of patients without inducible VT or inducible but suppressed VT still remains unclear. We performed risk stratification at electrophysiologic (EP) study in 111 consecutive unselected patients with nonsustained VT and coronary artery disease and randomized them to drug or device therapy. Follow-up on selected therapy was 1-71 (mean 27 +/- 20) months. Of 111 patients, 39 patients (35%) had inducible sustained VT at baseline EP study and were stratified to a "higher" risk group (group 1) for sudden death. In 9 of these patients (group 1A), sustained VT was suppressed with class IA antiarrhythmic drugs; in the remaining 30 patients (group 1B) sustained VT was not suppressed with class IA antiarrhythmic drugs. The other 72 of 111 patients (65%) had no inducible sustained VT at EP study and were stratified to a "lower"-risk group (group 2) for sudden death. Mean LVEF in group 1 was 30 +/- 10% versus 37 +/- 9% in group 2 (p = 0.001). Selected therapy in group 1 was an implantable cardioverter defibrillator (16 patients) or guided drug therapy (electrophysiologically guided class I antiarrhythmic drugs = 7 patients; Holter-guided class III antiarrhythmic drugs = 16 patients). In group 2, empiric drug therapy included beta blockers in 29 patients or Holter-guided class III antiarrhythmic drugs in 17 patients, with no antiarrhythmic drug therapy being administered in 26 patients. Mean LVEF tended to be lower in patients receiving class III antiarrhythmic drug therapy (34 +/- 12%) than in patients receiving beta blockers (40 +/- 10%, p = 0.06). Three-year total survival was comparable in group 1 (70%) and in group 2 (81%), but sudden cardiac death mortality tended to be lower in group 1 versus group 2 (0 vs 9%, p = 0.09). Patients receiving class III antiarrhythmic therapy had significantly higher 3-year all cause (40%, p = 0.04) and sudden death (25%, p = 0.06) mortality than patients receiving beta blockers (17% and 8% respectively) or no antiarrhythmic drug therapy (4% and 0%, respectively). The following conclusions can be drawn from this analysis: (1) Electrophysiologically guided drug therapy and implantable defibrillators can minimize the risk of sudden cardiac death in patients with coronary artery disease and inducible sustained VT stratified to higher risk of sudden death. A comparable outcome with respect to sudden death prevention in drug-suppressed or drug-refractory patients suggests limited prognostic benefit of class IA drug testing. (2) Lower-risk patients with severely depressed LVEF and minimal or no symptoms do not have a favorable outcome with respect to sudden and all-cause mortality on Holter-guided class III drug therapy. However, asymptomatic patients with mildly depressed left ventricular function have low sudden death event rates on beta blocker or no antiarrhythmic drug therapy.

Aged↗
PubMed1997

Low-energy endocardial defibrillation using dual, triple, and quadruple electrode systems.

The feasibility of achieving both universal application of nonthoracotomy leads and low (< or = 15 J) defibrillation energy requirements by optimizing lead system configuration for use with low-output (<30 J) biphasic shock pulse generators was examined. Sixteen patients (mean age 62 +/- 8 years and mean left ventricular ejection fraction of 38 +/- 15%) were included in the study. All patients had either experienced syncope with induced ventricular tachycardia (n = 4) or had documented sustained ventricular tachycardia (n = 7) or ventricular fibrillation (n = 5). Defibrillation threshold testing was performed in 2 stages on different days in these patients. In the first stage, 2 defibrillation catheter electrodes were positioned in the right ventricle and superior vena cava with an axillary cutaneous patch. Fifteen-joule, 10- and 5-J biphasic shocks were delivered across 3 different electrode configurations-right ventricle to superior vena cava, right ventricle to axillary patch, right ventricle to a combination of superior vena cava and axillary patch. In the second stage, an 80-ml can electrode was added subcutaneously in a pectoral location to the previous leads. Configurations compared were the right ventricle to pectoral can, and right ventricle to an "array"-combining superior vena cava, can, and axillary patch leads. The defibrillation threshold was determined using a step-down method. In stage 1, mean defibrillation threshold for the right ventricle to axillary patch (12.7 +/- 5.9 J) and right ventricle to superior vena cava plus axillary patch (9.8 +/- 5.2 J) configurations was lower than the right ventricle to superior vena cava configuration (14.2 +/- 6.4 J, p <0.05). In stage 2, the defibrillation was higher for the right ventricle to pectoral can (9.2 +/- 5.1 J) configuration compared with the right ventricle to the array (5.6 +/- 3.6 J, p < or =0.05). The right ventricle to array had the lowest defibrillation threshold, whereas the right ventricle to pectoral can was the best dual electrode system. Low-energy endocardial defibrillation (< or =10 J) was feasible in 72% of tested patients with > 1 electrode configuration at 10 J, whereas only 53% of successful patients could be reverted at >1 electrode configuration at 5 J (p <0.05). Reduction in maximum pulse generator output to < or =25 J using these electrode configurations with bidirectional shocks is feasible and maintains an adequate safety margin.

Aged↗
PubMed1997

Acute effects of dual-site right atrial pacing in patients with spontaneous and inducible atrial flutter and fibrillation.

OBJECTIVES: We tested the ability of dual-site right atrial pacing to prevent atrial fibrillation (AF) or atrial flutter induced by single-site atrial pacing and correlated its efficacy with clinical patient characteristics, atrial activation times and refractory periods. BACKGROUND: Prevention of recurrent AF with long-term dual-site right atrial pacing has been demonstrated in our previous studies. However, the mechanism of antiarrhythmic benefit is unclear. METHODS: Using standard electrophysiologic methods, baseline electrocardiographic and electrophysiologic measurements (mean +/- SD) were obtained. Programmed atrial stimulation was performed for AF or atrial flutter induction. Atrial pacing was performed at two drive cycle lengths (600 and 400 ms) and followed by one to three atrial extrastimuli at one to four pacing sites in the right atrium. In patients with inducible AF or atrial flutter, reinduction was then attempted during a dual-site atrial pacing drive train. This was achieved by simultaneously pacing at the high right atrium and coronary sinus ostium at an identical rate to the baseline stimulation, with the atrial extrastimuli being delivered at the pacing site responsible for the initial AF episode initiation. RESULTS: Twenty patients (10 men, 10 women, mean [+/- SD] age 64 +/- 16 years) with symptomatic AF (n = 10) or atrial flutter (n = 10) were studied. There was a significant abbreviation of the P wave duration to 103 +/- 17 ms with dual-site pacing compared with sinus rhythm (120 +/- 12 ms, p = 0.005) and high right atrial pacing (121 +/- 17 ms, p = 0.005). This was also associated with a characteristic change in P wave configuration with an inferior and leftward axis shift. The effective refractory period at the high right atrium remained unchanged with dual-site atrial pacing compared with single-site high right atrial pacing. Sixteen patients had inducible AF or atrial flutter and could be tested after dual-site atrial pacing. The induced atrial tachyarrhythmia was suppressed in nine patients (56%), who had either induced AF (n = 5) or atrial flutter (n = 4). The difference in the effective refractory period between the high right atrium and the coronary sinus ostium pacing sites was significantly greater (33 +/- 12 ms) in patients with suppression of atrial tachyarrhythmia with dual-site atrial pacing compared with patients without suppression (15 +/- 13 ms, p = 0.001). P wave abbreviation did not correlate with arrhythmia suppression. There was no correlation between suppression of inducible AF or atrial flutter and demographic or clinical patient characteristics. CONCLUSIONS: Dual-site right atrial pacing from the high right atrium and coronary sinus ostium can suppress inducible AF or atrial flutter elicited after single-site high right atrial pacing in selected patients. Acute suppression is more likely in patients with greater dispersion of right atrial refractoriness between these two sites.

Adult↗
PubMed1997

Evaluation of a programming algorithm for the third tachycardia zone in a fourth-generation implantable cardioverter-defibrillator.

The clinical efficacy of electrical algorithms for termination of slow ventricular tachycardia (VT) and ventricular fibrillation (VF) in implantable cardioverter-defibrillators (ICDs) is well established. Such algorithms have not been equally well defined for fast VT reversion. We report the testing of a prospectively designed algorithm for ICDs to treat fast VT that is inherently less responsive to antitachycardia pacing than slow VT. Fourth-generation ICD devices were programmed to three prospectively defined tachycardia detection zones as follows: cycle lengths < or = 260 ms for VF, 270-330 ms for fast VT, and > 330 ms for slow VT. The initial selected therapy for the VF zone was a high-energy biphasic shock (> 15 J), while a 3- or 5-J biphasic shock was usually administered for fast VT, and antitachycardia pacing was initially attempted for slow VT. Initial therapy was followed by backup therapy with high-energy shocks. Twenty-eight patients, 24 of whom were males, all with organic heart disease, with a mean age of 65 +/- 9 years, received either a Medtronic 7219D (23 patients), 7219C (2 patients), 7218SP1 (2 patients), or 7218C (1 patient) ICD with a nonthoracotomy lead system. The defibrillation threshold was 10 +/- 5 J. At predischarge electrophysiologic testing, a single 3- or 5-J shock terminated all episodes of fast VT tested. During a follow-up of 18 +/- 9 months, there were four nonarrhythmic deaths. Fourteen patients (50%) had a total of 21 VF, 44 fast VT, and 202 slow VT episodes. Twenty-three of 24 (96%) VF, 33 of 39 (84%) fast VT, and 193 of 202 (95.5%) slow VT episodes were terminated with the first delivered therapy in each therapy algorithm (p = NS). The overall efficacy of the entire electrical therapy algorithm was 100% for VF, 100% for fast VT, and 98% for slow VT episodes (p = NS). No patient experienced syncope or presyncope during fast VT or VF in this study. We conclude that a third detection and therapy zone can be successfully programmed in ICDs to define a range of fast VT episodes that can be effectively terminated with lower energy cardioversion shocks with comparable success and freedom from arrhythmic symptoms to electrical therapies used for slow VT and VF.

Aged↗
PubMed1997

Effects of high-frequency atrial pacing in atypical atrial flutter and atrial fibrillation.

Atypical atrial flutter has, hitherto, been relatively refractory to termination by rapid atrial pacing. High-frequency pacing (HFP) in the atrium, for termination of atrial flutter or atrial fibrillation (AF), and the electrophysiologic effects related to it have not been examined. We examined the clinical efficacy, safety, and electrophysiologic mechanisms of HFP using 50-Hz bursts at 10 mA applied at the high right atrium in patients with atypical atrial flutter (group 1) or AF (group 2), using a prospective randomized study protocol. Four burst durations (500, 1000, 2000, and 4000 ms) were applied at the high right atrium repetitively in random sequence in 22 patients with spontaneous atrial flutter or AF. Local and distant right and left atrial electrogram recordings were analyzed during and after HFP. HFP resulted in local and distant right and left atrial electrogram acceleration in 8 of 10 patients (80%) in group 1 but caused less frequent local atrial electrogram acceleration (6 of 12 patients) and no distant atrial electrogram effects in group 2 (p < .05 versus group 1). The HFP protocol was effective in arrhythmia termination in 6 of 10 patients in group 1 but in no patient in group 2 (p < .05 versus group 1). Standard HFP protocol applied at the high right atrium can frequently alter atrial activation in both atria and can terminate atypical atrial flutter. Efficacy in AF is limited, probably due to limited electrophysiologic actions beyond the local pacing site.

Adult↗
PubMed1997

The role of pacemaker therapy in the prevention of atrial fibrillation.

Atrial fibrillation (AF) has been recognized, with increasing concern, as a potentially disabling illness, occurring either as a symptom of many cardiac diseases or as an isolated disorder. It can independently contribute to mortality and morbidity and may have serious prognostic importance in acute or chronic cardiac disease. In patients with symptomatic drug refractory atrial fibrillation, ventricular rate control by atrioventricular nodal ablation or modification commonly results in pacemaker implantation. The concept of AF prevention by pacemaker therapy has been introduced in patients with bradycardia-tachycardia syndrome or vagally mediated bradycardia-dependent AF. In patients with sick sinus syndrome, atrial pacing has proved to be more effective than VVI pacing in maintaining the electrical stability of the atrium in long-term follow up. Recently, the development of new techniques of atrial pacing employing pacing at two atrial sites may improve the effectiveness of the AF prevention by pacemaker therapy. Dual-site right atrial pacing using overdrive stimulation activates simultaneously the high right atrium and the left atrium via the ostium of the coronary sinus. Two main mechanisms have been proposed to explain the favourable effect of this technique. One is the suppression of atrial premature beats initiating AF by the overdrive pacing. The second is the alteration of atrial activation pattern by preexcitation of the area of the coronary sinus ostium which permits earlier recovery of excitability in sites of atrial conduction delay. The combination of drug therapy and pacing is essential for effective AF control. We have hitherto studied 30 patients with single- and dual-site pacing. Single-site pacing was performed at the high right atrium or coronary sinus ostium. The dual-site pacing mode increased the arrhythmia-free intervals, decreased patients' arrhythmia-related symptoms and anti-arrhythmic drug use as compared to the period preceding institution of pacing and incrementally over conventional high right atrial pacing alone. A multicentre randomized trial, Dual-site Atrial Pacing for Prevention of Atrial Fibrillation (DAPPAF), evaluating three pacing modes (dual-site, single-site and support pacing), is now in progress.

Atrial Fibrillation↗
PubMed1996

Prevention of recurrent atrial fibrillation with chronic dual-site right atrial pacing.

OBJECTIVES: We investigated 1) the feasibility, safety and efficacy of multisite right atrial pacing for prevention of atrial fibrillation (AF); and 2) the ability of atrial pacing in single- and dual-site modes to increase arrhythmia-free intervals in patients with drug-refractory AF. BACKGROUND: We recently developed and applied a novel technique of dual-site right atrial pacing in an unselected group of consecutive patients with AF requiring demand pacing. A prospective crossover study design was used to evaluate single- and dual-site right atrial pacing modes. METHODS: The frequency of AF during the 3 months before pacemaker implantation was analyzed. Consecutive consenting patients underwent insertion of two atrial leads and one ventricular lead with a DDDR pulse generator. Patients were placed in a dual-site pacing mode for the first 3 months and subsequently mode switched to single site pacing for 3 months. Mode switching was repeated at 6-month intervals thereafter. RESULTS: Atrial pacing resulted in a marked decline in AF recurrences (p < 0.001). During dual-site pacing with an optimal drug regimen, there was no AF recurrence in any patient compared with five recurrences in 12 patients during single-site pacing (p = 0.03). The mean (+/-SD) arrhythmia-free interval before pacing (14 +/- 14 days) was prolonged with dual- (89 +/- 7 days, p < 0.0001) and single-site pacing (76 +/- 27 days, p < 0.0001). Symptomatic AF episodes showed a declining trend during dual- and single-site pacing compared with those during the preimplantation period (p = 0.10). Mean antiarrhythmic drug use for all classes declined from 4 +/- 1.9 drugs before implantation to 1.5 +/- 0.5 (p < 0.01) drugs after implantation. Twelve (80%) of 15 patients remained in atrial paced rhythm at 13 +/- 3 months. CONCLUSIONS: We conclude that multisite right atrial pacing is feasible, effective and safe for long-term application. Atrial pacing significantly prolongs arrhythmia-free intervals in patients with drug-refractory paroxysmal AF. Dual-site right atrial pacing may offer additional benefits and should be considered either as the primary mode or in patients unresponsive to single-site pacing.

Adult↗
PubMed1996

New generations of implantable pacemaker defibrillators for ventricular and atrial tachyarrhythmias.

Implantable defibrillation devices have now been extensively applied to patients requiring cardioversion and defibrillation of sustained ventricular tachyarrhythmias. The focus of new developments is in improving technology, achieving physiologic operation in the atrium and ventricle, seeking new indications and identifying patient populations amenable to this therapy. Ventricular application technology is focusing on simplifying and improving robustness of lead systems yet seeking lower defibrillation thresholds. Dual chamber pacing, sensing and defibrillation are being developed. New populations for ventricular application include non-sustained ventricular tachycardia patients with coronary artery disease, dilated cardiomyopathy at risk for sudden death, long QT syndrome, pediatric patients with risk of sudden death and high risk postoperative coronary bypass patients. New applications include atrial defibrillation combined with atrial pacing in future devices. These devices are planned to have capabilities of ventricular defibrillation as a backup to address proarrhythmia concerns. It can be anticipated that implantable cardioverter defibrillator devices will be used for arrhythmia reversion in an expanding group of patients in the future.

Arrhythmias, Cardiac↗
PubMed1989

Efficacy of nadolol alone or in combination with a type IA antiarrhythmic drug in sustained ventricular tachycardia: a prospective study.

We examined the clinical efficacy and safety of intravenous nadolol acutely, as well as chronic nadolol alone or combined with a type IA antiarrhythmic drug in 19 patients with sustained ventricular tachycardia and heart disease, mean age 62 +/- 15 years, and mean left ventricular ejection fraction 39 +/- 8%. Patients underwent electrophysiological studies in the drug-free state (control), after intravenous nadolol (dose = 0.05 mg/kg), and oral nadolol (dose = 80 mg/day) for 5 days alone or in combination with a type IA antiarrhythmic drug. Electrocardiographic and electrophysiological effects as well as ventricular tachycardia induction at electrophysiological study were analyzed. Long-term therapy with oral nadolol alone or in combination with a type IA antiarrhythmic drug was evaluated in responders. Intravenous nadolol prolonged RR and QRS intervals but had no effect on PR and QTc intervals. Oral nadolol alone tended to prolong RR intervals (P = 0.08). Oral nadolol with type IA antiarrhythmic drug prolonged RR and QTc intervals (P less than 0.001). The mean right ventricular effective refractory period tended to prolong after intravenous nadolol alone (from 251 +/- 29 to 263 +/- 25 msec, P = 0.08). Oral nadolol and type IA antiarrhythmic drugs did not prolong right ventricular effective refractory period (P = 0.3). Eighteen patients had inducible sustained ventricular tachycardia at control electrophysiological study. After intravenous nadolol, ventricular tachycardia was no longer inducible in seven patients. Ventricular tachycardia did not recur and remained noninducible in two of six patients who tolerated oral nadolol alone. Mean right ventricular effective refractory period prolonged from baseline values (from 249 +/- 30 to 271 +/- 30 msec, P less than 0.02) in patients who became noninducible on intravenous nadolol. In patients who remained inducible, mean right ventricular effective refractory period remained unchanged (from 253 +/- 29 to 258 +/- 22 msec, P greater than 0.2). In nonresponders to intravenous or oral nadolol, oral nadolol, and type IA antiarrhythmic drug suppressed ventricular tachycardia induction in two of ten patients. During follow-up, three patients continued on oral nadolol alone (one patient) or oral nadolol and type IA antiarrhythmic drug (two patients). Adverse effects resulting in nadolol discontinuation occurred in five patients. Therefore, we concluded that intravenous nadolol is effective in acute suppression of inducible ventricular tachycardia in selected patients. Oral nadolol alone or in combination with type IA antiarrhythmic drug is infrequently effective and poorly tolerated by this patient population. In addition, electrophysiological studies on intravenous nadolol do not predict the outcome of oral nadolol therapy.

Anti-Arrhythmia Agents↗
PubMed1989

Seizure propensity with imipenem.

Five patients with seizures related to imipenem administration are described. The potential of imipenem therapy to cause seizure was further studied in a mouse model and compared with the potential for seizure with penicillin and cefotaxime therapy. Penicillin caused ataxia and seizure at a mean mouse serum level of 5800 microns/mL, cefotaxime at 3400 microns/mL, and imipenem at a much lower serum concentration of 1900 microns/mL. The potent activity of imipenem therapy against bacteria, allowing for a clinical dose of only 2 g/d, is unfortunately offset by its higher propensity to induce neurologic symptoms in humans and mice at much smaller doses than would therapy with penicillin G or the cephalosporins, such as cefotaxime.

Aged↗