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C I Haffajee

Publications and source records attributed to C I Haffajee.

At least 19 recordsLinked to original sources
PubMed2000

Antiarrhythmic agents and proarrhythmia.

The Vaughn Williams classification divides antiarrhythmic agents into four groups according to their effects on various ion channels. Class I agents block sodium channels and are subdivided into three groups. The use of class Ia agents is gradually on the decline, secondary to lack of a favorable risk/benefit ratio. Class Ib agents include lidocaine, which is extensively used for the acute treatment of ventricular tachyarrhythmias. Class Ic drugs are not advisable for patients with structural cardiac abnormalities secondary to a high risk of proarrhythmia. They are mainly used for supraventricular tachyarrhythmias. beta blockers form class II. Class III agents, such as amiodarone and sotalol, prolong action potential duration and repolarization and are among the most widely used antiarrhythmics. They are the subject of active research, and newer agents are being developed. Calcium-channel blockers are grouped under class IV. Digoxin and adenosine have unique antiarrhythmic properties, which can be useful in the management of selected patients. All antiarrhythmic drugs have the potential to provoke arrhythmias and, therefore, should be used with caution. The risk of proarrhythmia is increased in patients with abnormal cardiac substrate, with electrolyte abnormalities, and during drug initiation. Correction of electrolyte imbalance and prevention of bradycardia while the drug is metabolized and/or excreted are the cornerstones of proarrhythmia management.

Amiodarone↗
PubMed1996

Effects of oral propafenone on defibrillation and pacing thresholds in patients receiving implantable cardioverter-defibrillators. Propafenone Defibrillation Threshold Investigators.

OBJECTIVES: The effects of propafenone, a predominantly class IC antiarrhythmic drug, on defibrillation and pacing thresholds were evaluated in patients undergoing cardioverter-defibrillator implantation. BACKGROUND: Previous studies have shown that the class IC agents encainide and flecainide may increase the energy requirements for pacing and defibrillation. Animal studies with propafenone have shown inconsistent results regarding its effect on defibrillation energy requirements. This report investigated the effects of propafenone on defibrillation and pacing thresholds in humans. METHODS: After cardioverter-defibrillator implantation, 47 patients were enrolled in a double-blind, three-way parallel, randomized trial of 450 mg/day (Group 1) or 675 mg/day (Group 2) of oral propafenone or placebo (Group 3) for 3 to 7 days. Predischarge defibrillation and pacing thresholds after treatment were compared with baseline thresholds obtained at implantation. RESULTS: There was no statistically significant difference between implantation and predischarge defibrillation thresholds in the three groups (Group 1: [mean +/- SE] 11.0 +/- 1.3 vs. 12.1 +/- 1.5 J; Group 2: 11.5 +/- 1.1 vs. 13.6 +/- 1.3 J; Group 3: 12.5 +/- 1.2 vs. 13.3 +/- 1.6 J), and no significant difference between treatment groups was found with a 0.86 power to detect a 5-J difference between groups. Paired pulse width pacing thresholds at 2.8 V were compared in 14 patients. A small increase of 0.02 ms was noted at predischarge testing in patients treated with propafenone and placebo. CONCLUSIONS: Short-term oral propafenone (450 and 675 mg/day) does not significantly affect defibrillation or pacing thresholds. Concomitant use of propafenone in patients with implantable cardioverter-defibrillators with recurrent ventricular or atrial tachyarrhythmias should not interfere with proper device function.

Administration, Oral↗
PubMed1993

Sudden death in idiopathic dilated cardiomyopathy: role of ventricular arrhythmias.

Sudden cardiac death (SCD) is associated with idiopathic congestive cardiomyopathy (IDCM) and most commonly is due to ventricular tachyarrhythmias. The recurrence rate of SCD in the absence of specific therapy is thought to be around 20%-30% per year. Asymptomatic and symptomatic ventricular arrhythmias are common in patients with IDCM and the direct causal link of such arrhythmias with SCD in IDCM patients remains to be established. Furthermore, therapy directed at suppressing these ventricular arrhythmias has not been shown to decrease the incidence of SCD. Various approaches such as ambulatory monitoring, electrophysiological testing, signal-averaged electrocardiogram, and hemodynamics have met with variable success in identifying patients prone to SCD. Additionally, therapeutic approaches to prevent SCD in IDCM patients have produced equivocal results. This article reviews the published studies addressing the causal link of ventricular arrhythmias to sudden death in patients with IDCM and the attempts to decrease the incidence of sudden.

Arrhythmias, Cardiac↗
PubMed1989

Clinical experience in seventy-seven patients with the automatic implantable cardioverter defibrillator.

Seventy-seven patients with drug-refractory sustained ventricular tachycardia (VT) (28 patients) or ventricular fibrillation (VF) (49 patients) underwent implantation of an automatic cardioverter defibrillator (AICD). The 67 men and 10 women, with a mean age of 60 +/- 12 years (range 18 to 79), had coronary artery disease (60 patients), idiopathic cardiomyopathy (eight patients), mitral valve prolapse (four patients), hypertensive heart disease (one patient), Ebstein's anomaly (one patient), long QT syndrome (one patient), and primary electrical disease (two patients). The mean left ventricular ejection fraction was 35 +/- 16% (range 10% to 75%). Sustained VT/VF was induced in 64 patients (83%) at baseline electrophysiologic testing. A mean of 4.1 +/- 1.3 antiarrhythmic drugs failed to control the arrhythmia. Associated surgery at AICD implantation included coronary artery bypass in 19 patients, coronary bypass with aneurysmectomy in six patients, and aneurysmectomy alone in one patient. Five patients had only prophylactic patches implanted during aneurysmectomy or coronary bypass and the AICD device was subsequently implanted under local anesthesia to prevent arrhythmia recurrence or to control persistently inducible VT. Operative mortality was 2.6% with two deaths from intractable VF. Fifty-two patients (69%) continued receiving antiarrhythmic drugs to suppress spontaneous VT. During a mean follow-up of 15 +/- 13 months (range 1 to 63), six patients died: two suddenly due to probable pulse generator failure (greater than 2 years old), one of acute myocardial infarction, two of heart failure, and one of respiratory failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1988

The relation of the kinetics of pirmenol to its antiarrhythmic efficacy.

In a single-blind study the multiple oral dose kinetics of pirmenol were related to its efficacy in eight patients with frequent (mean, 631; range, 167-1374 beats/hour) premature ventricular contractions (PVC). Oral pirmenol was started at 100 mg bid for 48 hours and increased to 150 mg bid in six patients to obtain more than 70% suppression of PVC counts. Efficacy was achieved without side effects. Pirmenol decreased heart rate but not PR interval, QRS duration, or QTc interval. Peak plasma levels after the first 100-mg dose occurred at 1 to 3 hours and ranged from 0.6 to 1.9 micrograms/mL. Plasma elimination half-life ranged from 9.7 to 31 hours (mean, 18.3). From 67.4 to 171.3 mg pirmenol (mean, 102.3 mg) were recovered in the urine in 48 hours after the last dose. Cumulative excretion in divided urine collections was consistent with a mean elimination half-life of 15 to 20 hours. The pharmacokinetics of pirmenol support oral twice-daily administration. The minimum PVC suppressing plasma level is between 0.5 and 1.5 micrograms/mL.

Aged↗
PubMed1988

Long-term outcome following programmed electrical stimulation in patients with high-grade ventricular ectopy.

To determine if programmed electrical stimulation (PES) could be utilized to identify patients with high-grade ventricular ectopy at low- or high-risk for sudden cardiac death, we performed PES in 40 patients with high-grade ventricular ectopy refractory to conventional antiarrhythmic agents. Twenty-one patients had a previous myocardial infarction, five had cardiomyopathy, six had hypertension, three had valvular heart disease and five had no known structural heart disease. The mean age was 50 years (range, 18 to 76). During programmed ventricular stimulation, eight patients had inducible sustained (more than 30 seconds) monomorphic ventricular tachycardia (Group I) but in 32 patients sustained ventricular tachycardia was not inducible (Group II). None of the five patients without structural heart disease were inducible while seven out of 21 (33%) patients with previous myocardial infarction had inducible ventricular tachycardia (VT). Antiarrhythmic therapy was instituted in patients with inducible VT; patients without inducible VT did not receive antiarrhythmic agents. In Group I, seven of the eight patients are alive (mean follow-up, 16 months) and in Group II, 28 of the 32 patients are alive (mean follow-up, 17 months). None of the five deaths were sudden. We conclude that in the absence of antiarrhythmic therapy, the incidence of sudden cardiac death is very low in patients with high-grade ventricular ectopy who do not have inducible monomorphic ventricular tachycardia during programmed ventricular stimulation.

Death, Sudden↗
PubMed1988

The efficacy, electrophysiologic and electrocardiographic effects of intravenous pirmenol, a new class I antiarrhythmic agent, in patients with ventricular tachycardia: comparison with procainamide.

UNLABELLED: The electrophysiologic and electrocardiographic effects of intravenous pirmenol were compared with intravenous procainamide in 17 patients with symptomatic ventricular tachycardia. Pirmenol was found to prolong the PR interval, the QRS duration, the QTc interval, the HV interval, the atrial effective refractory period, and the ventricular effective refractory period. The sinus cycle length decreased following pirmenol administration. The sinus node recovery time, the PA interval, the AH interval, the Wenckebach cycle length, and the AV nodal ERP were unchanged. In patients whose ventricular tachycardias remained inducible on pirmenol, the cycle length was significantly prolonged compared to baseline. These changes were similar to those seen following the administration of procainamide. All 17 patients had sustained ventricular tachycardia inducible during programmed ventricular stimulation in the baseline state. In four patients the ventricular tachycardia was suppressed with both primenol and procainamide. In the remaining 13 patients ventricular tachycardia remained inducible on procainamide. Of these 13 patients, an additional two patients had their ventricular tachycardias rendered noninducible on pirmenol. IN CONCLUSION: (1) the electrophysiologic and electrocardiographic effects of pirmenol are similar to those of procainamide; (2) although ventricular tachycardia inducibility following procainamide was similar to that of pirmenol, an occasional patient with ventricular tachycardia inducible on procainamide had ventricular tachycardias suppressed on pirmenol.

Administration, Oral↗
PubMed1987

Electrophysiologic predictors of long-term clinical outcome with amiodarone for refractory ventricular tachycardia secondary to coronary artery disease.

Fifty-four patients with a previous myocardial infarction and drug-refractory symptomatic ventricular tachycardia (VT) were treated with amiodarone on a long-term basis (range 6 to 54 months, mean 26) irrespective of the results of programmed ventricular stimulation, which was performed after high-dose oral amiodarone loading for more than 4 weeks. VT was rendered noninducible in 6 of 54 patients (11%) taking oral amiodarone. During a mean follow-up of 32 months, these 6 patients remained free of VT or sudden cardiac death. Forty-eight patients (89%) continued to have VT inducible by programmed ventricular stimulation. However, they could be separated into 2 groups: VT-modified (20 patients) and VT-unchanged (28 patients). In the VT-modified group, the induced VT with amiodarone was slowed or rendered nonsustained, and only 3 of 20 (15%) patients during a mean follow-up of 23 months had well tolerated VT recurrences. In the VT-unchanged group, 16 of 28 patients (57%) had recurrences of VT or ventricular fibrillation during a mean follow-up of 24 months. Sudden cardiac death occurred in 6 of these 16 patients. Thus, programmed ventricular stimulation in patients with VT taking long-term amiodarone may have prognostic implications.

Adult↗
PubMed1987

Outcome after cardiac arrest during acute myocardial infarction.

A community-wide study of acute myocardial infarction (AMI) was conducted in all 16 acute-care general hospitals in the Worcester, Massachusetts, metropolitan area during the years 1975, 1978, 1981 and 1984. The in-hospital and long-term prognoses of 667 patients with AMI complicated by cardiac arrest (CA) was compared with that of 2,596 AMI patients without CA. The incidence of CA complicating AMI was similar (21%) during each of the 4 study years. Among patients with AMI who had CA, 36% had CA within the first day of hospitalization and 48% within the first 2 days. The in-hospital case-fatality rate was much higher for AMI patients with CA (78%) than for those without CA (4%) (p less than 0.001). For patients discharged alive from the hospital, a trend toward a higher mortality rate was seen at 1 and 2 years after hospital discharge for patients with CA; however, long-term survival rates were not significantly different between AMI patients with and without CA. When time of occurrence of CA relative to in-hospital survival was examined, patients with early CA (within 1 day or within 2 days of hospital admission) had a significantly greater in-hospital survival (39% and 34%) than did those with late CA (after 1 day or after 2 days) (13% and 12%). Similarly, patients discharged from the hospital after early CA had a significantly better chance of long-term survival than patients discharged after late CA.

Aged↗
PubMed1987

Clinical pharmacokinetics of amiodarone.

This article attempts to provide an overview of the present knowledge of the pharmacokinetics of amiodarone and how this relates to the clinical usage of oral amiodarone. It is apparent that wide gaps still exist in our knowledge of amiodarone's pharmacokinetics in humans and the best fit for the observations following a single oral dose and chronic dosing is that of a three compartment model with body tissues acting as a large reservoir of the drug; hence the very large volume of distribution (greater than 5001). It remains unclear as to exactly when steady state is achieved except that full clinical efficacy for ventricular tachyarrhythmias may take several weeks following high oral dosing (about 15g). The drug's bioavailability is modest (approximately 40%) and excretion is minimal via the hepatic route. It is extensively metabolised in all tissues to desethylamiodarone, whose antiarrhythmic properties remain to be elucidated. This metabolite is found to parallel amiodarone's concentration in serum but its concentration is variable in tissues. The liver shows the highest, and body fat the lowest concentrations of desethylamiodarone. The minimal effective serum concentration has not been established with certainty, and the unique pharmacokinetics of this agent has made it difficult to perform dose-response studies, especially in life threatening arrhythmias. Similarly, the toxic serum concentrations have not been established though it appears that a higher incidence of side effects occurs if serum concentrations exceed 2.5 mg/l during chronic (steady state) therapy.

Amiodarone↗
PubMed1986

Amiodarone for refractory atrial fibrillation.

Atrial fibrillation (AF) is a difficult arrhythmia to manage with antiarrhythmic agents. Amiodarone is highly effective in restoring and maintaining normal sinus rhythm in patients with AF. However, the mechanism and predictors of efficacy for amiodarone in treating AF have not been adequately addressed. Various measures of success or failure of amiodarone therapy were examined in 68 patients who had paroxysmal or chronic, established AF refractory to conventional antiarrhythmic agents. The patients were 25 to 75 years old (mean 59) and mean follow-up was 21 months (range 3 to 56). Maintenance amiodarone dosages were 200 to 400 mg/day. Overall, amiodarone therapy was effective long term in 54 of the 68 patients (79%). Left atrial diameter, age, gender and origin of AF were not helpful in predicting success or failure of amiodarone therapy. The presence of chronic AF for longer than 1 year was an adverse factor in maintaining normal sinus rhythm (p = 0.007), although the success rate even in this group was relatively high (57%). Thirty-five percent of the patients had adverse effects, which precluded long-term therapy with amiodarone in 10%.

Adult↗
PubMed1986

Electrophysiologic and clinical factors influencing response to class IA antiarrhythmic agents in patients with inducible sustained monomorphic ventricular tachycardia.

Clinical and electrophysiologic data from 51 consecutive patients with sustained monomorphic ventricular tachycardia inducible during programmed ventricular stimulation were evaluated to determine what variables predict the response to intravenous class IA antiarrhythmic agents. All patients received acute drug testing in the electrophysiologic laboratory with either intravenous procainamide or intravenous quinidine. Ventricular tachycardia suppression was achieved in 9 out of 51 patients (18%). The age, gender, left ventricular ejection fraction, baseline right ventricular effective refractory period, baseline HV interval, and baseline ventricular tachycardia cycle length were not predictive of ventricular tachycardia suppression with intravenous procainamide or quinidine during programmed ventricular stimulation. The degree of prolongation of the right ventricular effective refractory period after drug administration did not predict success or failure to suppress inducible ventricular tachycardia. The degree of prolongation of the HV interval was also not predictive. In addition, the degree of prolongation of the right ventricular effective refractory period or the HV interval did not predict the change in the ventricular tachycardia cycle length after drug administration in patients who remained inducible. These data indicate that the response to class IA antiarrhythmic agents in patients with inducible sustained monomorphic ventricular tachycardia cannot be predicted on the basis of various clinical and electrophysiologic parameters.

Arrhythmias, Cardiac↗
PubMed1986

Sudden cardiac death in a southeast Asian immigrant: clinical, electrophysiologic, and biopsy characteristics.

The syndrome of sudden cardiac death in southeast Asians has only recently been given attention in the American medical literature. This case report describes a patient who presented with this rare syndrome. The physical examination, Holter monitor, 2-D echocardiogram, exercise treadmill test, radionuclide ventriculogram, coronary angiography, and endomyocardial biopsy were all normal. Programmed ventricular stimulation reproducibly induced sustained polymorphic ventricular tachycardia. Oral procainamide, oral quinidine and oral quinidine plus propranolol were not successful in suppressing inducible polymorphic ventricular tachycardia. The arrhythmia remained inducible after six weeks of oral amiodarone therapy. However, he has no clinical recurrences while on amiodarone after one year of follow-up.

Adult↗
PubMed1986

A theoretically and practically more effective method for interruption of ventricular tachycardia: self-adapting autodecremental overdrive pacing.

The efficacy and safety of a new antitachycardia pacing technique, self-adapting decremental overdrive pacing, was assessed in patients with clinical ventricular tachyarrhythmias who underwent programmed ventricular stimulation and serial drug testing. The three phases of this study involved a learning/experience phase, followed by intrapatient comparison of decremental overdrive pacing with conventional antitachycardia pacing modalities of overdrive burst ventricular pacing, and diastolic scanning with single (S2) and double (S2S3) ventricular extrastimuli. The final phase involved an intrapatient comparison of automated decremental overdrive pacing with overdrive burst ventricular pacing in patients with ventricular tachycardia (VT) cycle lengths of 280 msec or greater. Decremental overdrive pacing was superior to overdrive burst pacing and diastolic scanning (S2S3 and S2) (83% vs 38%, 50%, 9%) in patients with VT cycle lengths of 280 msec or greater. Automated decremental overdrive pacing as applied in the final phase was the most efficacious modality, terminating 92% of VT episodes compared with 56% for overdrive burst pacing in the same patients.

Adult↗
PubMed1985

Temporary cardiac pacing: modes, evaluation of function, equipment, and trouble shooting.

Artificial cardiac pacing has become a sophisticated therapeutic and diagnostic tool in the management of arrhythmic cardiac emergencies. Major innovations have occurred in the last three decades since the advent of temporary pacing, and today, pacing can be effected "physiologically" in both chambers. This has been the result of improved venous access techniques, technologic improvements in electrode design, and the development of sophisticated external pulse generators. It has become clear that ventricular pacing alone does not improve the hemodynamic derangement consequent upon ventricular bradycardia and AV dyssynchrony. The restoration of AV synchrony either by atrial pacing preceding ventricular events or by ventricular pacing at a defined AV delay following a sensed atrial event (P wave) can often reverse the hemodynamic derangement and result in both extension of life and more rapid reversal of the clinical compromise in certain cases of acute heart block. Temporary pacing has always been used for bradyarrhythmias, but more recently, antitachycardia pacing is being utilized increasingly in the acute care setting.

Cardiac Pacing, Artificial↗