PubMed Health⌕ Search

Biomedical subjects

F E Marchlinski

Publications and source records attributed to F E Marchlinski.

At least 19 recordsLinked to original sources
PubMed1992

Effect of high-current stimulation in patients with sustained ventricular tachycardia rendered noninducible by antiarrhythmic drugs.

Successful antiarrhythmic drug therapy for sustained ventricular tachycardia (VT) is presumed to be related to effects on myocardium within the re-entrant circuit. To test the hypothesis that prevention of VT induction may be related to effects on myocardium other than that directly involved in the tachycardia circuit, high-current stimulation was used to achieve shorter coupling intervals in 22 patients with sustained uniform VT that was rendered noninducible by antiarrhythmic agents during stimulation at twice threshold. Sustained uniform VT was induced in 10 patients in response to high-current stimulation (group 1), including 4 tachycardias with the same morphology observed in the baseline study. There were no inducible arrhythmias in 12 patients (group 2). Patients were receiving several different antiarrhythmic regimens, but there was no particular drug associated with the induction of VT using high-current stimulation. There was no statistically significant difference between groups 1 and 2 in baseline VT cycle length (247 +/- 41 vs 253 +/- 44 ms), drug-induced increase in effective refractory period (20 +/- 15 vs 16 +/- 7%), QRS duration (25 +/- 10 vs 20 +/- 17%) or maximal current strength delivered (10.9 +/- 5.3 vs 9.3 +/- 4.0 mA). There was no significant difference in local activation with high-current stimulation between groups 1 and 2. In conclusion, sustained uniform VT was induced in 45% (10 of 22) of patients whose arrhythmias were rendered noninducible by antiarrhythmic agents during programmed stimulation at twice threshold.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1992

Redefining the role of digoxin in the treatment of atrial fibrillation.

Atrial fibrillation (AF) encompasses a variety of discrete clinical syndromes, including paroxysmal, chronic, acute, and postoperative. Digoxin, long considered the mainstay of therapy for rate control in all types of AF, appears to have only modest electrophysiologic effects, which are mediated primarily by the autonomic nervous system. Digoxin has less potency than the calcium antagonists or beta-blocking drugs with respect to atrioventricular nodal blockade. Although less potent than calcium antagonists or beta-blocking drugs on the atrioventricular node, digoxin provides positive inotropic support, whereas the other 2 agents can suppress left ventricular function. Thus, digoxin is the agent of choice in patients with AF in the setting of significant left ventricular dysfunction. However, in the absence of left ventricular dysfunction, digoxin should be considered second-line therapy for the treatment of all AF syndromes.

Acute Disease↗
PubMed1992

Dissociation of termination and prevention of inducibility of sustained ventricular tachycardia with infusion of procainamide: evidence for distinct mechanisms.

To determine if termination of hemodynamically tolerated, sustained ventricular tachycardia during intravenous infusion of procainamide predicts the success of procainamide therapy in preventing induction of tachycardia, 15 patients with inducible, sustained ventricular tachycardia in the setting of chronic coronary artery disease were studied. Procainamide was infused at a rate of 50 mg/min during ventricular tachycardia until the arrhythmia terminated spontaneously or a total dose of 15 mg/kg was administered. An infusion (2 to 10 mg/min) was given after the loading dose to maintain constant serum drug concentrations after termination of the tachycardia. The infusion of procainamide was well tolerated and resulted in termination of ventricular tachycardia in 14 (93%) of 15 patients after administration of 100 to 1,080 mg (median dose 600 mg). In all patients, programmed ventricular stimulation was repeated immediately after termination of the arrhythmia until ventricular tachycardia was reinitiated or until the stimulation protocol was completed. Of the 14 patients whose ventricular tachycardia terminated during the infusion of procainamide, 1 patient had no inducible sustained tachycardia with repeated programmed stimulation. In the remaining 13 patients, programmed stimulation resulted in initiation of sustained ventricular tachycardia of the same configuration in 7 patients and of a different configuration in 6. In the former 7 patients, the serum procainamide concentration (7.7 +/- 4 vs. 7.4 +/- 3.3 mg/liter, p = NS) and the observed drug effects on the tachycardia cycle length (449 +/- 78 vs. 450 +/- 81 ms, p = NS) and QRS duration (184 +/- 38 vs. 185 +/- 38 ms, p = NS) were similar at the times of termination and reinitiation of ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1992

Acute and chronic cycle length dependent increase in ventricular pacing threshold.

Several factors have been shown to influence ventricular pacing threshold in humans, including pacing lead location (endocardial vs epicardial), lead maturation, and antiarrhythmic agents. To determine whether ventricular pacing rate has a significant influence on acute and chronic pacing thresholds, we measured pacing thresholds in 16 patients receiving an implantable antitachycardia pacemaker cardioverter defibrillator (Cadence). Ventricular pacing thresholds were determined using the device programmer at cycle lengths of 600, 400 and 300 msec at the time of implantation; prior to hospital discharge at 3-14 days; and during follow-up outpatient visits at 6-8 weeks, 3 months, and 6 months to 1 year. Eleven patients had an epicardial lead system and five an endocardial lead system. Eleven patients were being treated with antiarrhythmic drug therapy. Device output ranged from 1-10 V and was adjustable in 1-V increments (pulse width was held constant at 1 msec). A cycle length dependent increase in pacing threshold (defined as a > or = 1-V increase in threshold at 400 or 300 msec relative to 600 msec) was observed in 10/16 patients during 12/72 pacing trials at 400 msec, and in 15/16 patients during 31/67 trials at 300 msec. In trials in which an increase in pacing threshold occurred, the magnitude of the increase at 400 msec relative to 600 msec was only 1 V in all 12 trials, but at 300 msec the increase ranged from 4-9 V in 7/31 (23%) trials.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1992

Electrocardiographically documented unnecessary, spontaneous shocks in 241 patients with implantable cardioverter defibrillators.

The incidence and cause of electrocardiographically documented spontaneous implantable cardioverter defibrillator (ICD) discharges for a rhythm other than ventricular tachycardia (VT) or fibrillation (VF) (unnecessary shocks) were determined in 241 patients who underwent ICD implantation between March 1983 and November 1991. During follow-up of 24 +/- 20 months, 54 of 241 patients (22%) received a total of 132 unnecessary ICD shocks confirmed by Holter or telemetry monitoring or stored electrograms (Egs) from the ICD. The rhythm preceding these unnecessary ICD shocks was atrial fibrillation in 30 patients, sinus or supraventricular tachycardia (SVT) in 11 patients, antitachycardia pacing triggered by atrial fibrillation or SVT resulting in VT in 5 patients, nonsustained VT in 3 patients, and normal sinus or pacemaker rhythm in 10 patients. Unnecessary ICD discharges occurred most frequently during the first week after implantation or generator replacement (18 of 54 patients [33%]). Unnecessary ICD discharges could be documented more often by stored Egs in patients with devices with Eg storage capability (Ventritex Cadence, 19 of 54 patients [35%]) than by Holter or telemetry monitoring in patients with devices without Egs storage capabilities (34 of 193 patients [18%], P < 0.01), despite a shorter mean follow-up duration of 14 +/- 9 months versus 26 +/- 21 months, respectively. Only six of 54 patients (11%) in whom unnecessary ICD discharges occurred had recurrent unnecessary shocks during 22 +/- 20 months of follow-up after treatment directed at the cause of the first episode or device reprogramming to preclude non-VT rhythm detection.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Fibrillation↗
PubMed1992

Failure of defibrillator paddle as mimic for subcutaneous patch lead during nonthoracotomy implantable cardioverter defibrillator lead configuration assessment.

It is a common, although virtually unsubstantiated, practice to assess the efficacy of nonthoracotomy lead systems for implantable cardioverter defibrillators using a defibrillator paddle as mimic for the subcutaneous patch lead. We report a case in which an adequate defibrillation threshold was documented with the nonthoracotomy lead system using a defibrillator paddle but not following implantation of the true subcutaneous patch lead. This case suggests that the substitution of a defibrillator paddle for the subcutaneous patch lead during nonthoracotomy lead system evaluation may have significant limitations in assessing lead configuration efficacy.

Adult↗
PubMed1992

Results of electrophysiological testing and long-term follow-up in patients sustaining cardiac arrest only while receiving type IA antiarrhythmic agents.

UNLABELLED: Therapeutic management of patients sustaining a cardiac arrest while receiving antiarrhythmic agents can be difficult since the role of the drug in possibly facilitating the arrhythmia is often difficult to define. To determine if the response to programmed stimulation could give insight into which patients may have experienced a drug-induced cardiac arrest, we studied 29 patients (61 +/- 9 years) with no prior history of sustained ventricular tachyarrhythmias (VT) who suffered a cardiac arrest only while receiving type Ia antiarrhythmic agents. Patients with documented myocardial infarction, acute ischemia, electrolyte abnormalities, or torsade de pointes were excluded from the study. Twenty-four patients had coronary artery disease with prior myocardial infarction (ejection fraction 28% +/- 9%) and five patients had idiopathic dilated cardiomyopathy (ejection fraction 31% +/- 6%). During baseline electrophysiological testing, 19 patients (66%) had inducible sustained ventricular arrhythmias: uniform VT, n = 14 (group I), polymorphic VT or ventricular fibrillation, n = 5 (group II). Ten patients (group III) had no inducible sustained ventricular arrhythmias. To determine if rechallenge with a type Ia agent could facilitate induction of a sustained ventricular arrhythmia in group III, eight patients underwent ten electrophysiological studies during therapy with either procainamide or quinidine. Only two patients developed sustained VT in response to programmed stimulation. Patients in groups I and II received therapy guided by electrophysiological testing, including antiarrhythmic agents alone (n = 8), subendocardial resection (n = 4), or an implantable cardioverter defibrillator (n = 7). Patients in group III received antiarrhythmic agents empirically (n = 3), or for treatment of atrial tachyarrhythmias (n = 2) or nonsustained VT (n = 1). In addition, four patients in group III received an implantable cardioverter defibrillator. During a mean follow-up of 28 +/- 27 months (range: 1 day-84 months) 13 patients died suddenly or received a defibrillator shock preceded by syncope or presyncope: group I: n = 5; group II: n = 2; group III: n = 6. IN CONCLUSION: (1) most patients sustaining a cardiac arrest only in the presence of type Ia antiarrhythmic agents have inducible sustained VT in the absence of antiarrhythmic agents, and (2) the risk of recurrent VT persists in patients without inducible sustained arrhythmias in the drug-free state, regardless of whether they manifest inducible arrhythmias after rechallenge with a type Ia agent.

Aged↗
PubMed1992

Nonpharmacologic therapy of ventricular arrhythmias.

Since the first attempt at surgical therapy for VT, much progress has been made in developing techniques for both localization of arrhythmogenic regions as well as their removal or alteration. In the setting of previous myocardial infarction, surgery for VT has evolved from an experiment/last resort procedure to the treatment of choice in many cases, yielding complete freedom from arrhythmia recurrence without adjunctive antiarrhythmic drugs in up to three quarters of operative survivors. Remaining issues in this field include (1) further reduction of operative mortality, perhaps by more careful patient selection (and use of alternative forms of therapy in those judged to be too high risk); (2) better and more accurate mapping techniques to enhance the antiarrhythmic efficacy of surgery; and (3) development of more effective procedures to deal with VT in the setting of cardiomyopathy. Judging from the progress made in the last decade and a half in this field, surgery for VT in many pathologic settings may take on a greater role in the future as further refinements in techniques are realized.

Arrhythmias, Cardiac↗
PubMed1991

Arrhythmias induced by device antitachycardia therapy due to diagnostic nonspecificity.

New technology has produced automatic cardioverter-defibrillators capable of delivering antitachycardia pacing, as well as low and high energy shocks and backup bradycardia pacing. These expanded treatment options have led to a wider range of clinical applications for such devices, including the treatment of ventricular tachycardias with longer cycle lengths, which may overlap the cycle lengths of some supraventricular arrhythmias. The diagnostic capability of these devices, although improved, has not advanced sufficiently to ensure reliable discrimination between all supraventricular and ventricular arrhythmias. Two cases are presented in which device-mediated pacing therapy, triggered by supraventricular arrhythmias, induced ventricular tachycardia requiring additional therapeutic intervention. This report illustrates the therapeutic versatility and some of the potential pitfalls, of the recently developed devices and reviews the status of automatic arrhythmia identification technology.

Adult↗
PubMed1991

Usefulness of the electrophysiology laboratory for evaluation of proarrhythmic drug response in coronary artery disease.

Two potential manifestations of proarrhythmic responses to type IA antiarrhythmic agents in the electrophysiology laboratory were evaluated in 122 patients with chronic coronary artery disease and previous myocardial infarction: (1) conversion of uniform nonsustained ventricular tachycardia (VT) into sustained VT after drug administration, and (2) induction of sustained VT by fewer extrastimuli after drug administration. Forty-two patients were evaluated for nonsustained VT. Eighty patients were evaluated for sustained VT: 30 of these had spontaneous sustained VT only while receiving empiric therapy with quinidine or procainamide, whereas the remaining 50 developed spontaneous VT in the absence of antiarrhythmic drugs. All patients underwent programmed stimulation in the baseline state and after procainamide. Four patients had conversion of induced uniform nonsustained VT into the same morphology, but sustained VT after procainamide administration. These responses only occurred in patients evaluated for nonsustained VT. Over 90% of patients presenting with sustained VT had uniform sustained VT induced at the baseline study and after procainamide, regardless of whether the spontaneous arrhythmia occurred only in the presence or absence of antiarrhythmic drugs. There was no significant difference in the change in mode of induction from baseline to procainamide study, regardless of whether patients had developed spontaneous VT only in the presence or absence of antiarrhythmic drugs. One patient with no inducible VT at the baseline study had inducible uniform sustained VT after procainamide administration, and 1 patient with inducible VT at baseline developed spontaneous sustained uniform VT after procainamide administration. Both patients had developed spontaneous sustained VT only while receiving therapy with type IA agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Complexes, Premature↗
PubMed1991

Value of ventricular electrogram recordings in the diagnosis of arrhythmias precipitating electrical device shock therapy.

An antitachycardia pacemaker-cardioverter-defibrillator that is capable of storing ventricular electrograms before and after delivery of device shock therapy was implanted in 16 patients. Three of the patients experienced out-of-hospital device shock therapy preceded by minimal symptoms. Although limitations of electrogram analysis exist and are discussed, careful analysis and registration of electrograms during all supraventricular and ventricular rhythms observed during in-hospital testing served as an important reference for subsequent arrhythmia diagnosis. By analyzing the electrogram rate and RR interval stability and configuration, a definitive diagnosis was established in all three patients (atrial fibrillation, polymorphic ventricular tachycardia and rate-sensing lead disruption, respectively). Thus, the ability to store ventricular electrograms before shock therapy represents a major advance in the management of patients who receive an electrical device to treat ventricular tachyarrhythmia.

Adult↗
PubMed1991

Characterization of spontaneous termination of sustained ventricular tachycardia associated with coronary artery disease.

To characterize the change in cycle length and QRS morphology before spontaneous termination of sustained ventricular tachycardia (VT), electrocardiograms were recorded and VT cycle length measured for the periods 31 to 21 and 11 to 1 beats before termination in 55 episodes from 28 patients with coronary artery disease. Beats 31 to 21 were designated as a period of stable arrhythmia and served as a reference for changes occurring just before termination. Forty-four episodes of VT occurred in the setting of antiarrhythmic drug therapy; 11 episodes occurred in patients not treated with antiarrhythmic drugs. Variability in cycle length was indexed by the standard deviation of the mean cycle length and by the percentage of consecutive cycles varying by greater than or equal to 40 ms (% greater than or equal to 40 ms). There was greater variability just before termination (standard deviation of the mean cycle length, 25.8 ms; % greater than or equal to 40 ms, 16.7%) than during the stable period (standard deviation of the mean cycle length, 8.5 ms; % greater than or equal to 40 ms, 5.4%; p less than 0.001 for both). This was true irrespective of antiarrhythmic drug use, although the differences in the standard deviation of the mean cycle length for beats 11 to 1 and for beats 31 to 21 were greater for the antiarrhythmic drug group (29.6 vs 8.9 ms, p less than 0.001) than for the group not receiving antiarrhythmic drugs (11.0 vs 6.7 ms, difference not significant). No specific patterns of cycle length variability characteristic of VT termination were found.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Which cardiac disturbances should be treated with digoxin immune Fab (ovine) antibody?

Digoxin excess can produce characteristic bradyarrhythmias, tachyarrhythmias, and hyperkalemia. The bradyarrhythmias, which consist of disturbances in conduction and block at the level of the atrioventricular and sinus nodes, are mediated by a direct and vagotonic effect. The vagotonic effect of excess digoxin may also result in a marked slowing of the sinus rate in the setting of severe toxicity. Digoxin increases automatic and triggered electrical activity in atrial muscle, His-Purkinje system, and ventricular muscle, which predisposes to tachycardias. Many of the tachyarrhythmias are relatively specific for the toxic effects of digoxin. Atrial tachycardias with variable atrioventricular block, accelerated junctional rhythms (especially in the setting of atrial fibrillation), and fascicular tachycardias are characteristic digoxin toxic rhythms. Digoxin-specific antibody fragments should be considered the treatment of choice for any digoxin toxic arrhythmia associated with hemodynamic compromise or the threat of hemodynamic compromise. Hyperkalemia, when due to acute severe digoxin toxicity, is also an appropriate indication for digoxin-specific Fab fragment therapy. When assessing the risk:benefit ratio for using digoxin-specific Fab fragment therapy, one needs to determine, in addition to the electrocardiographic manifestations and patient's hemodynamic status (1) the severity of toxicity, as indexed by the amount ingested and/or the serum digoxin concentration; (2) the expected time course for reversal of toxicity, which is usually determined by the status of renal function; (3) the need for digoxin to provide ventricular rate control or improved ventricular contractility and therapeutic alternatives to digoxin; (4) the presence of a strong allergy history; (5) the presence of such factors as increased age and severity of heart disease that may predispose to digoxin toxicity.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1991

Paced beats following single nonsensed complexes in a "codependent" cardioverter defibrillator and bradycardia pacing system: potential for ventricular tachycardia induction.

Patients with implantable defibrillators often require bradycardia pacemakers. Adverse interactions between separate defibrillator and bradycardia pacing units have occurred, including failure to detect ventricular fibrillation due to persistent bradycardia pacing during the arrhythmia. A device with combined bradycardia pacing and antitachycardia therapy capability may obviate adverse device interactions. We describe a previously unrecognized phenomenon that may occur in a combined device when the algorithms for sensing bradycardia and tachycardia are "codependent"; that is, the circuitry for brady- and tachyarrhythmia detection relies on the same automatic gain sense amplifier. Three of 37 patients in whom the device was implanted had ventricular tachycardia initiated when bradycardia pacing stimuli were delivered by the device after probable nonsensed sinus beats. In each case, nonsensed beats appeared to have a markedly diminished amplitude, occurred after ventricular premature depolarizations that produced large amplitude electrograms, and had an electrogram morphology that matched that of sinus rhythm. In each case, the bradycardia pacing interval was at least 1,200 msec (range 1,200 to 1,714 msec). In two of the three patients, large amplitude ventricular premature depolarizations or nonsustained ventricular tachycardia caused an adjustment of the gain control that potentiated the failure to sense the subsequent lower amplitude signal. In all three patients, the induced arrhythmia was rapidly terminated by pacing or cardioversion. Decreasing the bradycardia pacing interval by 110-514 msec has prevented recurrence during short-term follow-up. Our findings suggest that codependent bradycardia and antitachycardia devices may have their own unique potential difficulties in adapting to rapid changes in rate and signal amplitude.

Aged↗
PubMed1991

Differences in electrophysiological substrate in patients with coronary artery disease and cardiac arrest or ventricular tachycardia. Insights from endocardial mapping and signal-averaged electrocardiography.

BACKGROUND: Many studies have combined patients with hemodynamically well-tolerated ventricular tachycardia (VT) and those with cardiac arrest (CA) as a single, homogenous group. Recent studies suggest that these two groups have different electrophysiological substrates and responses to therapy. Most of these studies, however, enrolled patients with a variety of cardiac diagnoses. METHODS AND RESULTS: We used signal-averaged electrocardiography (SAECG) and endocardial catheter mapping to define the electrophysiological substrate in patients with coronary artery disease and VT or CA and correlate the results of the two methods. We also examined the usefulness of SAECG in CA patients to differentiate those with inducible arrhythmias from those who are noninducible. VT patients were more likely to have had a prior myocardial infarction (p = 0.0005) and to have inducible arrhythmias (p = 0.0001) than were CA patients. The induced arrhythmias in patients who presented with VT was VT in more than 90% of cases, whereas in CA patients, polymorphic ventricular tachycardia (PMVT) accounted for one third of induced arrhythmias. Mean filtered QRS duration was longer (135 versus 120 msec) and the terminal QRS voltage was smaller (20 versus 34 microV) in VT than in CA patients (p less than 0.01). Sixty-three percent of CA patients and 87% of VT patients had abnormal SAECG (p = 0.001). VT patients had more extensive endocardial abnormalities and more abnormal (53% versus 40%, p = 0.002), fractionated (8% versus 3%, p = 0.02), late (17% versus 8%, p = 0.0003), and late abnormal or fractionated (14% versus 4%, p = 0.0001) sites than CA patients. VT patients had a greater duration of the longest electrogram (129 versus 109 msec, p = 0.0006) and total endocardial activation time (68 versus 54 msec, p = 0.009). Among CA patients, those with induced VT had more extensive substrate than did those with induced PMVT and were similar to VT patients with induced VT. Among CA patients, the trend for more patients with inducible VT (77%) or PMVT (55%) than noninducible patients (47%) to have an abnormal SAECG did not reach statistical significance (p = 0.14). The positive and negative predictive values of an abnormal SAECG were 77% and 44%, respectively. CONCLUSIONS: VT patients have more extensive endocardial substrate than CA patients, which translates into greater and more frequent SAECG abnormalities. Among CA patients, there are significant differences in substrate between patients with induced VT and those with induced PMVT. SAECG is not useful in differentiating CA patients who have inducible VT or PMVT from those who do not.

Coronary Disease↗
PubMed1990

Cycle-length response of ventricular tachycardia associated with coronary artery disease to procainamide and amiodarone.

We undertook this study to determine if the cycle-length response of ventricular tachycardia (VT) to procainamide and amiodarone is similar in the individual patient. We enrolled 40 patients with uniform, monomorphic VT at a baseline, drug-free electrophysiologic study, after procainamide infusion and during oral amiodarone therapy. We found a significant correlation (p less than 0.01) between VT cycle-lengths on the 2 agents as well as the percent change in cycle length from baseline. Only 60% of the patients exhibited VT rates within 10% between the 2 agents. Importantly, less than 20% of patients had further slowing of the VT rate (greater than 10% slowing) during amiodarone therapy as compared to procainamide. Thus, although the cycle-length response of VT to procainamide correlates with the cycle-length response to amiodarone, 40% of patients have a disparate response (greater than 10% difference in cycle length) to the 2 agents; additional slowing of VT rates in response to amiodarone beyond that seen with procainamide is unlikely. These results have important implications regarding the institution of amiodarone therapy and the need for repeat electrophysiologic testing during amiodarone therapy.

Amiodarone↗