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Biomedical subjects

F E Marchlinski

Publications and source records attributed to F E Marchlinski.

At least 181 records · Page 10Linked to original sources
PubMed1985

Use of programmed electrical stimulation to predict sudden death after myocardial infarction.

The use of programmed ventricular stimulation to identify patients at risk for sudden cardiac death following myocardial infarction has not yet been firmly established. The repetitive ventricular response following extrastimuli does not appear to be useful in identifying patients at risk and should not be used to guide antiarrhythmic therapy. Similarly, the response to single and/or double ventricular extrastimuli delivered at twice diastolic threshold from a single right ventricular site during normal sinus rhythm and ventricular pacing also does not appear to be helpful in identifying patients at risk for life-threatening ventricular arrhythmias. A more vigorous stimulation protocol that involves more than one right ventricular site and increased current strength may be necessary to elicit a predictive electrophysiologic response. The need for a more vigorous stimulation is suggested by two preliminary studies. Confirmation of initial reports is necessary. The predictive value of the response to programmed ventricular stimulation must be compared with other noninvasive and invasive measurements of left ventricular dysfunction and the degree of spontaneous ventricular ectopy to determine its superiority or to ascertain multiple variables that can be used together to identify those patients most likely to die suddenly after myocardial infarction. Stimulation protocols used during programmed stimulation must have sufficient sensitivity without sacrificing specificity. A concerted effort using uniform stimulation protocols in large numbers of patients is essential to resolve this important clinical problem.

Cardiac Pacing, Artificial↗
PubMed1984

Repetitive, monomorphic ventricular tachycardia: clinical and electrophysiologic characteristics in patients with and patients without organic heart disease.

The clinical and electrophysiologic characteristics of 6 patients who had repetitive monomorphic ventricular tachycardia (VT) after a remote myocardial infarction (group A) were compared with those of 22 patients who had this arrhythmia without structural heart disease (group B). VT had a right bundle branch block morphologic pattern in 5 of 6 group A patients and a left bundle branch block morphologic pattern in all group B patients. Endocardial catheter activation mapping was performed in 4 group A patients and in 9 group B patients during VT. In all group A patients, the site of VT origin was on the border of the previous infarction; in all group B patients VT originated at the right ventricular outflow tract. Pacing and programmed stimulation induced VT in 5 of 6 group A patients and 7 of 22 group B patients (p = 0.03). Isoproterenol infusion provoked VT in 4 group A patients and 9 group B patients. Type I antiarrhythmic agents suppressed VT in 4 group A patients and in 14 group B patients, whereas propranolol suppressed VT in 3 of 3 group A patients tested and in 12 of 20 group B patients. Verapamil suppressed spontaneous VT in 1 group A patient and in 4 group B patients. During a mean follow-up of 19 months for group A and 40 months for group B, no patient had died suddenly or had cardiac arrest.

Adolescent↗
PubMed1984

Timing of the right ventricular apical electrogram during sustained ventricular tachycardia: relation to surface QRS morphology and potential clinical implications.

To evaluate the timing of the right ventricular (RV) apical electrogram in relation to the QRS complex during ventricular tachycardia (VT), 94 episodes of sustained uniform VT were analyzed in 56 patients. The timing of the RV apical electrogram varied and could be recorded from 33 ms before to 180 ms (mean 77 +/- 44 ms) after the onset of the QRS complex. The timing of the RV apical electrogram, expressed both as an absolute value and as a percentage of a QRS width, was significantly different when right bundle branch block (BBB) morphology VT (95 +/- 37 ms) and left BBB morphology VT (40 +/- 341) were compared (p less than 0.001). The timing of the RV apical electrogram, expressed as a percentage of the QRS width, was significantly different when VT with different axes were compared in the right BBB VT group (p less than 0.01). A left BBB VT, as compared to a right BBB VT, predicted an RV apical electrogram occurring in the first 35% of the QRS with a sensitivity of 74%, a specificity of 91%, and a positive predictive value of 84%. Right BBB VT with a right and inferior axis were usually associated with the latest occurring RV apical electrogram. A right BBB VT with a right and inferior axis predicted an RV apical electrogram inscribed in the latter half of the QRS with a sensitivity of 65%, a specificity of 84% and a positive predictive value of 80%.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1984

Atrial conduction: effects of extrastimuli with and without atrial dysrhythmias.

The effects of cycle length and stimulation site on intraatrial conduction and refractoriness were evaluated in patients with and without atrial flutter (AFI) or fibrillation (AF) using the extrastimulus technique. Nineteen patients with spontaneous sustained AFI or AF were compared with 19 control patients. Programmed stimulation was performed at the right atrium and coronary sinus at drive cycle lengths of 600 and 450 ms. The atrial effective refractory period was similar in the patients with atrial dysrhythmias and the control group. The right atrial effective refractory period at a drive cycle length of 600 ms was significantly shorter in patients with AF (211 ms) than in patients with AFI (235 ms, p = 0.05). The conduction time of late (coupling intervals more than 50% of the drive cycle length) premature impulses was similar in the patients with atrial dysrhythmias and the control group. However, early extrastimuli (coupling intervals less than 50% of the drive cycle length) at a drive cycle length of 600 ms produced significantly more intraatrial conduction delay in the patients with atrial dysrhythmias than in the control patients. At a drive cycle length of 450 ms, similar delays in intraatrial conduction occurred in the patients with and without atrial dysrhythmias because of an increase in the maximal-observed intraatrial conduction delay in the control patients. This study shows that delay in conduction of early premature atrial stimuli at a drive cycle length of 600 ms is a marker of patients with spontaneous AFI and AF.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Discordant results of programmed ventricular stimulation at different right ventricular sites in patients with and without spontaneous sustained ventricular tachycardia: a prospective study of 56 patients.

Programmed ventricular stimulation (PVS) was prospectively performed in 56 consecutive patients from both the right ventricular (RV) apex and the RV outflow tract. Thirty-seven patients had documented clinical sustained ventricular tachycardia (VT) and 19 patients had no sustained spontaneous VT in the absence of antiarrhythmic drugs. The sensitivity of VT induction was 65% from the RV apex, 76% from the RV outflow tract and was 89% with combined stimulation at both RV sites. The specificity from the RV apex, the RV outflow tract and both sites combined was 100%. When sustained VT was induced from both sites (51%), it was usually of the same morphologic characteristics, axis and cycle length. When sustained VT was induced at 1 site and nonsustained VT at the second site, the morphologic characteristics or axis usually differed. Of patients who had VT induced at both RV sites during the baseline study 37% had VT rendered noninducible during treatment with conventional antiarrhythmic agents. No patients whose VT was induced at only 1 RV site responded to conventional drugs. We conclude that programmed ventricular stimulation at a second RV site is frequently helpful in the evaluation of VT. Inducibility at only 1 of 2 RV sites predicts a poor response to conventional antiarrhythmic drugs.

Adult↗
PubMed1984

Prognostic factors in nonsustained ventricular tachycardia.

Electrophysiologic studies were performed in 83 consecutive patients with spontaneous nonsustained ventricular tachycardia (VT). VT was inducible in 52 patients (nonsustained VT only in 37 patients, nonsustained and sustained VT in 13 and sustained VT only in 2). During a follow-up of 3 to 111 months (mean 33), 10 patients died suddenly, 5 with coronary artery disease (CAD) and 5 with dilated cardiomyopathy. All patients with sudden death had an ejection fraction less than or equal to 0.40. Sudden death occurred in 4 of 15 patients with inducible sustained VT, 2 of 37 patients with only nonsustained VT and 4 of 31 patients without inducible VT. One patient with dilated cardiomyopathy and VT inducible only by isoproterenol died suddenly. Three of 5 patients with CAD who had sudden death had had inducible sustained VT, but 3 of 5 patients with cardiomyopathy who had sudden death had no inducible VT. Multivariate analysis revealed that patients with inducible sustained VT or an ejection fraction less than or equal to 0.40 had a 3-fold increased risk of sudden death, and patients with both factors had a 7-fold increased risk of sudden death. This study demonstrates that patients with nonsustained VT with an ejection fraction greater than 0.40 have an uncomplicated course; however, noninducibility does not predict such a course, particularly in patients with cardiomyopathy. The most powerful predictor of risk for sudden cardiac death is a left ventricular ejection fraction less than or equal to 0.40, but the presence of inducible sustained VT is an independent risk factor for sudden death.

Adolescent↗
PubMed1984

Electropharmacology of nonsustained ventricular tachycardia: effects of class I antiarrhythmic agents, verapamil and propranolol.

Forty-seven patients with spontaneous and inducible nonsustained ventricular tachycardia (VT) underwent serial electrophysiologic studies to evaluate the effects of antiarrhythmic agents on inducible arrhythmias, the role of electrophysiologic testing in the evaluation of pharmacologic therapy for these arrhythmias, and potential mechanisms underlying these arrhythmias. Type I antiarrhythmic agents prevented induction of VT by programmed stimulation in 18 of 37 patients and by isoproterenol in 9 of 11 patients. Verapamil and propranolol did not prevent or alter the mode of induction of VT by programmed stimulation, nor did they slow the induced tachycardias. Propranolol prevented induction of VT by isoproterenol in all 14 patients tested. Type I antiarrhythmic agents converted nonsustained into sustained VT in 2 of 37 patients. Inducible VT was prevented in 88% of patients without underlying heart disease, in contrast to only 38% of patients with associated cardiac disease (p less than 0.02). This study demonstrates that electrophysiologic studies may be used to identify antiarrhythmic agents with both beneficial and potentially harmful effects in patients with nonsustained VT. The responses of inducible tachycardias to antiarrhythmic agents in this group of patients with spontaneous nonsustained VT are similar to those previously observed in patients with sustained VT. Finally, the results suggest that VT induced by isoproterenol may frequently respond to type I antiarrhythmic agents in addition to beta blockers.

Anti-Arrhythmia Agents↗
PubMed1984

Electrophysiologic effects of intravenous metoprolol.

We evaluated the electrophysiologic effects of intravenous metoprolol, a selective beta-1-blocking agent, in 12 patients. Electrophysiologic parameters were measured during the control period, immediately following, and 4 to 6 hours after infusion of 0.15 mg/kg. Metoprolol serum concentration was serially measured in 6 of the 12 patients. Immediately after metoprolol infusion, the sinus cycle length increased by 20% from 738 +/- 166 msec to 885 +/- 181 msec (p less than 0.01), AH interval during sinus rhythm increased by 34% from 83 +/- 27 msec to 112 +/- 37 msec (p less than 0.01), and antegrade atrioventricular (AV) nodal Wenckebach cycle length increased by 20% from 360 +/- 188 msec to 432 +/- 199 msec (p less than 0.01). Sinus node recovery time and sinoatrial conduction time did not become abnormally prolonged in any patient. His-Purkinje conduction was unaltered. High atrial and ventricular refractory periods were modestly increased (less than 15 msec); the increase in refractoriness reached statistical significance when repeat measurements were made at 4 to 6 hours. No adverse effects were noted. Metoprolol serum concentration at the time of peak measured electrophysiologic effect was 54.6 +/- 15.2 ng/ml. We conclude that at this dose, intravenous metoprolol significantly prolongs sinus cycle length and AV nodal conduction, may modestly increase atrial and ventricular refractoriness, and appears to have electrophysiologic potency similar to propranolol. It is well tolerated following intravenous administration and may be of particular value in the acute treatment of supraventricular tachycardia when beta-receptor selectivity is desired.

Adult↗
PubMed1984

Prognosis in patients with intra-Hisian conduction disturbances.

Intra-Hisian delay is usually associated with fascicular conduction abnormalities. We report our experience in 23 patients who had intra-Hisian delay as their only conduction defect. First-degree intra-Hisian delay (His bundle deflection greater than or equal to 30 msec) was present in 17 patients, 5 of whom also had split His potentials. Three of these patients received permanent pacemakers, all of whom had a history of syncope. Higher degrees of intra-Hisian delay were observed either spontaneously or in response to atrial pacing in 6 patients. Five of these patients were treated with permanent pacing, 4 of whom had symptomatic bradyarrhythmias and/or syncope. No patient has had a recurrence of symptoms following pacemaker insertion during the mean 31-month follow-up. No patient with first-degree intra-Hisian delay not receiving a pacemaker developed symptomatic bradyarrhythmias or syncope during a mean follow-up of 21 months.

Adult↗
PubMed1984

Comparative electrophysiologic effects of intravenous and oral procainamide in patients with sustained ventricular arrhythmias.

Thirty-three patients with sustained ventricular arrhythmias underwent electrophysiologic testing after intravenous and again after oral procainamide administration. Two groups were identified: group 1 included 15 patients with concordant serum procainamide concentrations with less than a 3 micrograms/ml difference after intravenous (mean 8.6 +/- 2.7) and oral (mean 8.8 +/- 2.7) procainamide administration, with mean N-acetylprocainamide concentrations of 1.0 +/- 0.6 and 6.2 +/- 2.8 micrograms/ml, respectively. Group 2 included 18 patients with discordant serum procainamide concentrations after intravenous (mean 9.5 +/- 5.9 micrograms/ml) and oral (mean 14.1 +/- 5.2 micrograms/ml) procainamide, with mean N-acetylprocainamide concentrations of 0.9 +/- 0.5 and 10.7 +/- 5.7 micrograms/ml, respectively. In group 1, response to programmed stimulation was the same after intravenous and oral procainamide administration, with no inducible ventricular arrhythmia in 5 of 15 patients. In group 2, 3 of 18 patients had no inducible arrhythmia after intravenous compared with 7 of 18 patients after oral procainamide administration. There was a different response to programmed stimulation after oral compared with intravenous procainamide in 6 of 18 patients in group 2 but in none of 15 patients in group 1 (p = 0.02). The effective procainamide concentration was greater than the ineffective concentration in five of the six patients with a discordant response, and the effective route of administration was oral in five of the six patients. The change in ventricular refractoriness in group 1 was similar after intravenous (28 +/- 23 ms) and oral (29 +/- 19 ms) procainamide, whereas in group 2, refractoriness was increased more after oral (33 +/- 21 ms) than intravenous (20 +/- 17 ms) procainamide administration and paralleled the difference in procainamide concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Acecainide↗
PubMed1984

Limited role of intravenous propafenone hydrochloride in the treatment of sustained ventricular tachycardia: electrophysiologic effects and results of programmed ventricular stimulation.

The electrophysiologic effects and response to programmed ventricular stimulation of intravenous propafenone, an experimental antiarrhythmic agent, were studied in a group of 14 patients with both clinical and induced sustained ventricular tachycardia. Twelve of the 14 patients had not responded to conventional antiarrhythmic drug therapy. Propafenone had no significant effect on sinus cycle length (836 +/- 170 ms before and 750 +/- 124 ms after propafenone), P wave duration (108 +/- 24 ms before and 106 +/- 23 ms after propafenone) or PR interval (181 +/- 45 ms before and 194 +/- 53 ms after propafenone). QRS duration and ventricular effective refractory periods increased significantly (109 +/- 20 to 130 +/- 21 ms and 235 +/- 24 to 256 +/- 19 ms, respectively). Ventricular tachycardia remained inducible or occurred spontaneously in 13 of 14 patients after propafenone administration. Neither mode of initiation nor mode of termination of ventricular tachycardia was predictably altered. Additional forms of ventricular tachycardia were seen in six patients. Cycle length of ventricular tachycardia was 303 +/- 73 ms before and 346 +/- 143 ms after propafenone (p = NS). In conclusion, intravenous propafenone does not significantly affect sinus rate, intraatrial conduction or atrioventricular conduction. Ventricular refractoriness and intraventricular conduction are prolonged. The mode of initiation, mode of termination and ventricular tachycardia cycle length are not predictably altered, but ventricular tachycardia occasionally occurs spontaneously after propafenone. Intravenous propafenone rarely prevents induction of ventricular tachycardia in patients with sustained ventricular tachycardia refractory to conventional antiarrhythmic agents.

Anti-Arrhythmia Agents↗
PubMed1984

Medical versus surgical treatment of tachydysrhythmias.

Traditionally, surgical therapy for tachydysrhythmias has been reserved for drug-refractory cases. Accordingly, there has been no study comparing medical with surgical therapy in similar groups of patients. Recent developments in surgical therapy for supraventricular and ventricular tachydysrhythmias have resulted in lower morbidity and mortality with good surgical success. In most patients with the Wolff-Parkinson-White syndrome, accessory pathway division can be performed with very low mortality and high chance for success, obviating the need for lifelong drug therapy. Similarly, in patients with life-threatening ventricular tachydysrhythmias, several operative techniques including the encircling endocardial ventriculotomy and subendocardial resection offer an alternative to therapy which often requires frequent dosing with one or more medications, each associated with a significant incidence of adverse effects. These newer operative techniques for both supraventricular and ventricular tachydysrhythmias are challenging the widely held concept that surgery should be reserved only for patients with drug-refractory tachydysrhythmias.

Anti-Arrhythmia Agents↗
PubMed1984

Role of triple extrastimuli during electrophysiologic study of patients with documented sustained ventricular tachyarrhythmias.

Electrophysiologic studies were performed in 172 consecutive patients for evaluation of documented sustained ventricular tachyarrhythmias. One hundred thirteen patients presented with sustained ventricular tachycardia that was hemodynamically stable, and 59 patients presented with cardiac arrest. Seventy-one patients without previously documented or suspected ventricular arrhythmias were also studied to determine the specificity of our electrophysiologic study protocol. The stimulation protocol included single, double, and triple right ventricular extrastimuli and rapid ventricular pacing at multiple cycle lengths performed at one or more right ventricular sites. Stimulation was performed at one or more left ventricular sites in patients with documented spontaneous arrhythmias when right ventricular programmed stimulation failed to induce sustained ventricular tachycardia. Ventricular tachyarrhythmias were induced in 110 (97%) of the patients who presented with sustained ventricular tachycardia, in 48 (81%) of the patients who presented with cardiac arrest, and in 28 (40%) of the patients without documented spontaneous arrhythmias. Right ventricular triple extrastimuli induced tachycardia in 22% of patients who presented with sustained ventricular tachycardia vs 46% of those who presented with cardiac arrest (p less than .001). Left ventricular stimulation was required for tachycardia induction in 3% of patients with stable tachycardia vs 19% of those with cardiac arrest (p less than .01). Triple extrastimuli induced 57% of tachycardias in the 28 patients without spontaneous arrhythmias, and virtually all of these tachycardias were polymorphic and nonsustained. The cycle lengths of tachycardias induced in each group by double and triple extrastimuli were similar, but the tachycardias induced in patients with cardiac arrest were significantly faster than those induced in the ventricular tachycardia group (mean cycle length 218 vs 291 msec, p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Endocardial activation of left bundle branch block.

Endocardial catheter mapping was performed in 18 patients with left bundle branch block (LBBB). Four patients had no organic heart disease (group I), six had cardiomyopathy (group II), and eight had coronary artery disease and previous infarction (group III). Twelve patients had one septal site of left ventricular endocardial breakthrough, while six had two left ventricular endocardial breakthrough sites, with one site always being septal. There was no significant difference among the groups with respect to time of left ventricular breakthrough (group I, 44 msec after the onset of the QRS complex; group II, 58 msec; and group III, 51 msec). Total left ventricular endocardial activation time was significantly longer in group III (119 msec) than group I (81 msec; p less than .05) and group II (61 msec; p less than .001). Duration of total right ventricular endocardial activation was 36 msec (seven patients). The final site of right ventricular activation was at 44 msec after the onset of the QRS complex. We conclude that (1) right ventricular activation occurs before initiation of left ventricular activation in patients with LBBB, (2) left ventricular endocardial activation in patients with LBBB most likely occurs as a result of right-to-left transseptal activation, (3) left ventricular endocardial activation sequence in patients with LBBB is heterogeneous, and (4) patients with coronary artery disease and LBBB have significantly longer total left ventricular endocardial activation times than patients with no organic heart disease or those with cardiomyopathies.

Adult↗