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Biomedical subjects

C D Swerdlow

Publications and source records attributed to C D Swerdlow.

At least 55 records · Page 3Linked to original sources
PubMed1988

Effect of flestolol on ventricular rate during atrial fibrillation in Wolff-Parkinson-White syndrome.

The ultrashort-acting beta blocker flestolol was studied during atrial pacing and atrial fibrillation (AF) in 10 patients with Wolff-Parkinson-White syndrome. Flestolol was given as a 100-micrograms/kg bolus followed by a 10-micrograms/kg/min infusion for 15 minutes. The drug did not alter the antegrade effective refractory period of the accessory pathway or the atrial paced cycle length at which block occurred in the accessory pathway. After flestolol, the percent of preexcited QRS complexes during AF increased (60 +/- 10 vs 87 +/- 5%, p = 0.01). Despite this, the ventricular rate slowed, with increases in mean RR interval (382 +/- 20 vs 416 +/- 22 ms, p = 0.02) and in the shortest interval between preexcited QRS complexes (251 +/- 18 vs 270 +/- 17 ms, p less than 0.01). The effect of isoproterenol 3 to 5 micrograms/min was studied in 5 patients. During atrial pacing, isoproterenol decreased the antegrade refractory period and the atrial paced cycle length of block in the accessory pathway (p less than or equal to 0.05). During AF, it decreased the percent of preexcited QRS complexes, mean RR interval and shortest interval between preexcited QRS complexes (p less than 0.05). Flestolol reversed the effects of isoproterenol both during atrial pacing and AF. Thus, flestolol does not alter conduction over the accessory pathway during atrial pacing, but during AF it slows conduction over the accessory pathway and prevents isoproterenol-mediated increases in ventricular rate. This suggests that in patients with Wolff-Parkinson-White syndrome sympathetic stimulation after the onset of AF enhances conduction over the accessory pathway and is an important determinant of ventricular rate.

Adrenergic beta-Antagonists↗
PubMed1988

Prognostic significance of arrhythmia inducibility or noninducibility at initial electrophysiologic study in survivors of cardiac arrest.

The value of arrhythmia inducibility or noninducibility at initial electrophysiologic study to predict the likelihood of arrhythmia recurrence was assessed in 150 consecutive survivors of cardiac arrest. Ventricular tachycardia (greater than or equal to 6 beats) or ventricular fibrilation was induced in 113 patients (75%); ventricular arrhythmia could not be induced in 37 patients (25%). During follow-up of a mean of 16 months (range 1 to 72), there were 65 arrhythmia recurrences, 34 of them fatal, in 58 patients. Multivariate regression analysis showed that inducibility at initial study of ventricular tachycardia or ventricular fibrilation was an independent predictor of total arrhythmia recurrence (p less than 0.0001) and fatal arrhythmia recurrence (p = 0.02). At 1 year, 25 +/- 5% of patients with an inducible arrhythmia had a fatal arrhythmia recurrence compared with only 4 +/- 4% of patients without (p = 0.003). The nature of the inducible arrhythmia had no additional predictive value. Inducibility or noninducibility of ventricular arrhythmias at initial electrophysiologic study is a powerful, independent predictor of subsequent arrhythmia recurrence in survivors of cardiac arrest. Patients without inducible arrhythmias have a low frequency of fatal arrhythmia recurrence.

Arrhythmias, Cardiac↗
PubMed1988

Strength-interval relation for ventricular functional refractoriness.

Successful initiation and termination of presumed reentrant ventricular tachycardia frequently depends on the ability to deliver closely coupled impulses to the region of the tachycardia origin. To evaluate systematically the relative influence of local latency and large-scale conduction delay in limiting the delivery of closely coupled impulses, the strength-interval relation of the effective refractory period (RP), and the local and remote functional RP in 35 patients at paced cycle length of 500 ms were measured. The pacing threshold was less than or equal to 0.25 mA in all patients. The drive-train (S1) and the extrastimulus (S2) were applied from the same site, the right ventricular (RV) apex, in 25 patients, and from separate sites (RV apex and RV outflow tract) in 10 patients. The effect of procainamide (plasma concentration 10.1 +/- 2.3 micrograms/ml) on the strength-interval relations in 10 patients was also assessed. Although effective RP decreased significantly with each successive increase in current strength (p less than 0.001), local functional RP decreased only up to current strength of 4 mA, and remote functional RP decreased only up to 2 mA. Procainamide shifted the effective RP and local and remote functional RP strength-interval curves uniformly to the right without altering their relation. These data indicate that large-scale conduction delay provides the principal limitation for using increasing current strengths of a single extrastimulus to initiate or terminate ventricular tachycardia.

Adult↗
PubMed1988

Pharmacodynamics of procainamide in patients with ventricular tachyarrhythmias.

The onset and offset of the electropharmacologic effect of procainamide was studied in nine patients with ventricular arrhythmias. Procainamide was given at a constant infusion rate of 0.27 +/- 0.05 mg/kg/min for 50 to 60 minutes to an average total dose of 15.5 +/- 4.4 mg/kg. The QRS interval (used as an index of electropharmacologic effect) at a paced cycle length of 500 ms, and the plasma procainamide concentration were measured simultaneously every 5 minutes during infusion and at frequent intervals for up to 4 hours during a washout period. The average peak plasma concentration was 15.8 +/- 9.6 micrograms/ml and the average maximum QRS interval prolongation was 23.9 +/- 6.8% from baseline. The temporal and static plasma concentration-effect relationships were evaluated by pharmacodynamic modeling and linear regression. For six patients, there was a minimal (less than 2 minutes) delay in the plasma concentration-effect relationship, and the data fit a linear relationship with an average slope of 3.2 +/- 1.1 msec/microgram/ml. For the other three patients, there was a significant delay (3, 10, and 18 minutes respectively) in the plasma concentration-effect relationship. In most patients, the electropharmacologic effect of procainamide is rapid and proportional to plasma concentration; but in a minority of patients, significant delay occurs and could influence the results and interpretation of electropharmacologic studies.

Adult↗
PubMed1988

Long-segment coronary ulcerations in survivors of sudden cardiac death.

Angiographically irregular coronary stenoses usually represent plaque rupture with or without superimposed thrombi. Long-segment coronary stenoses with diffuse irregularities (type IIB morphology) have been shown to be more prevalent than focal irregular lesions (type IIA morphology) in survivors of cardiac arrest without acute myocardial infarction. To further understand the pathogenetic importance of type IIB morphology, the clinical and angiographic characteristics in 59 such patients were analyzed. Type IIB lesions accounted for 63% of all type II lesions. Type IIB patients were older than type IIA patients (p less than 0.05). There was a tendency for type IIB morphology to be associated with more extensive disease than other types of lesion morphology (p less than 0.10). Type IIB morphology probably reflects more advanced atherosclerosis. Platelet microemboli may precipitate spasm and/or acute ischemic ventricular tachyarrhythmias. It is possible that long-segment coronary ulcerations are associated with a higher risk for local coronary thromboembolism, and hence with sudden death, than focal lesions.

Aged↗
PubMed1988

Angiographic coronary morphology in survivors of cardiac arrest.

Autopsy studies in victims of sudden coronary death revealed intramyocardial platelet aggregates with microscopic myonecrosis downstream from ruptured atherosclerotic plaques. Ruptured plaques usually manifest angiographically as irregularly bordered (type II) lesions. To investigate the possible pathogenic role of ruptured plaques in arrhythmic death, we analyzed clinical, angiographic, and electrophysiologic data from 49 survivors of cardiac arrest without acute myocardial infarction. All patients had greater than or equal to 50% stenoses of greater than or equal to one coronary artery; 16 had type II morphology, and 33 did not. Type II morphology was more prevalent in patients without inducible sustained monomorphic ventricular tachycardia (11 of 22 or 50%) than in those with it (five of 27 or 19%), p less than 0.05, and patients without akinetic or dyskinetic segments (eight of 14 or 57%) than in those with them (eight of 34 or 24%), p less than 0.06. Thus type II morphology is more prevalent in patients without a demonstrable anatomic and/or electrophysiologic substrate for reentrant ventricular tachycardia, indirectly implicating ruptured plaques in the pathogenesis of cardiac arrest in this subset of patients.

Aged↗
PubMed1988

Tocainide for drug-resistant sustained ventricular tachyarrhythmias.

Eighty-two patients with drug-resistant ventricular tachycardia or fibrillation were treated with oral tocainide. Treatment in 54 patients, all with inducible ventricular tachycardia or fibrillation at baseline electrophysiologic testing, was based on the results of invasive electrophysiologic testing. Twenty-eight additional patients with frequent spontaneous ventricular tachycardia or no inducible arrhythmia during electrophysiologic testing were treated on the basis of the findings of electrocardiographic (ECG) Holter monitoring. Tocainide was effective in 7 (13%) and partially effective in 5 (8%) of the 54 patients in the electrophysiologic study group and was effective in 17 (61%) of the 28 patients in the ECG monitoring group. History of previous myocardial infarction and failure of response to lidocaine correlated with failure to respond to tocainide. Side effects were common both during initial therapy and during long-term treatment and necessitated discontinuation of tocainide therapy in 17% of the patients. At a mean follow-up period of 14 months, 13 patients are still receiving tocainide and are arrhythmia-free. In conclusion, the usefulness of oral tocainide in the management of drug-refractory sustained ventricular tachycardia or fibrillation is limited because of its low effectiveness and frequent side effects.

Anti-Arrhythmia Agents↗
PubMed1988

Clinical predictors of arrhythmia inducibility in survivors of cardiac arrest: importance of gender and prior myocardial infarction.

Clinical characteristics that correlate with arrhythmia inducibility were determined in 150 consecutive survivors of cardiac arrest. All underwent electrophysiologic study with a uniform protocol when they were not receiving antiarrhythmic drugs. A ventricular tachyarrhythmia (sustained monomorphic ventricular tachycardia, ventricular fibrillation or nonsustained ventricular tachycardia) was induced in 113 patients (75%). The strongest correlates of inducing a tachyarrhythmia were male gender (p less than 0.0001) and a history of prior myocardial infarction (p less than 0.0001). Induction of sustained monomorphic tachycardia alone was also strongly related to gender and prior infarction; in particular, none of 26 women without prior infarction had induction of sustained monomorphic ventricular tachycardia. Among patients with induced sustained tachyarrhythmias, those with induced monomorphic ventricular tachycardia were distinguished from those with induced ventricular fibrillation in they were more likely to have coronary artery disease (p = 0.0001), healed myocardial infarction (p = 0.0002), left ventricular aneurysm (p = 0.0007) and ventricular tachycardia documented at the time of cardiac arrest (p = 0.02). Other variables showing significant correlations with arrhythmia inducibility were ejection fraction, documentation of ventricular tachycardia at the time of cardiac arrest and presence of an intraventricular conduction delay. However, stepwise logistic regression identified male gender and healed myocardial infarction as the only independent predictors of arrhythmia inducibility. On the basis of these two variables alone, arrhythmia inducibility or noninducibility could be correctly predicted in 89% of the patients in this series.

Arrhythmias, Cardiac↗
PubMed1988

Cycle length dependence of human action potential duration in vivo. Effects of single extrastimuli, sudden sustained rate acceleration and deceleration, and different steady-state frequencies.

Using a new method for long-term recording of monophasic action potentials from the human heart, we studied in 17 patients the effects on ventricular action potential duration (APD) of three clinically pertinent cycle length perturbations: (1) single extrastimuli, (2) abrupt sustained rate acceleration and deceleration, and (3) different steady-state cycle lengths. Results were: (a) APD after single extrastimuli at progressively longer cycle lengths were related to the extrastimulus cycle length with a biphasic electrical restitution curve which after an initial steep rise and a subsequent transient descent rose again more gradually to a plateau at cycle lengths above 800-1,000 ms. (b) After a sustained step decrease in cycle length, the first APD shortened abruptly while final steady-state adaptation required up to several minutes. The transition between the rapid and slow phase of APD change was characterized by a variable alternans of APD which correlated inversely with the preceding diastolic interval. (c) In the steady state, APD correlated linearly with cycle length, increasing an average of 23 ms per 100 ms cycle length increase (r = 0.995). The divergence between steady-state and non-steady-state APD, and the slowness of steady-state adaptation, are important factors to be considered in clinical electrophysiologic studies and in rate correction algorithms of APD or QT intervals, respectively.

Action Potentials↗
PubMed1987

Electrophysiology and antiarrhythmic efficacy of intravenous pirmenol in patients with sustained ventricular tachyarrhythmias.

We assessed the electrophysiologic effects and antiarrhythmic efficacy of intravenous pirmenol in 15 patients who had spontaneous and induced sustained ventricular tachyarrhythmias. At a plasma concentration of 2.29 +/- 0.75 micrograms/ml, pirmenol decreased sinus cycle length by 11 +/- 13%, increased QRS, QTc, and HV intervals by 14 +/- 12%, 13 +/- 12%, and 22 +/- 28%, respectively, and increased atrial and ventricular effective refractory periods (ERP) by 20 +/- 14% and 7 +/- 8%, respectively. There was a greater increase in QRS duration during ventricular tachycardia and ventricular pacing than during sinus rhythm (p less than 0.005). By electropharmacologic testing, pirmenol was judged effective in six patients (40%) and was proarrhythmic in one (6%). In the nine patients in whom pirmenol was judged ineffective, the cycle length of induced VT increased by 36 +/- 15% and the associated mean arterial pressure increased by 21 +/- 14 mm Hg. The only side effects were mild hypotension and mild nausea in one patient each. Intravenous pirmenol has type IA electrophysiologic effects. It can be administered safely to patients with sustained ventricular tachyarrhythmias and is as effective as approved antiarrhythmic drugs when assessed by electropharmacologic testing.

Adult↗
PubMed1987

Long-term follow-up after surgical correction of Wolff-Parkinson-White syndrome.

The long-term efficacy of surgical correction of Wolff-Parkinson-White syndrome was evaluated in 45 consecutive patients. Before surgery, 42 patients had reciprocating tachycardia and 12 had atrial fibrillation. The principal operative procedure was endocardial incision in 42 patients, endocardial cryoablation in 2 patients and epicardial cryoablation without dissection of the atrioventricular (AV) fat pad in 1 patient. Two patients had perioperative complications. One patient had bleeding that necessitated reoperation, and one had a right cerebral stroke with subsequent clearing of neurologic deficit. At postoperative electrophysiologic study, only the patient who underwent epicardial cryoablation had conduction over an accessory connection. Two others had intermittent delta waves in the early postoperative period but no accessory connection conduction at electrophysiologic study. During a mean follow-up of 3.1 years, the patient with ineffective cryoablation had recurrent orthodromic tachycardia, and one other patient had late recurrence of delta waves without arrhythmias. Four other patients had frequent palpitation, which was caused by premature ventricular complexes in three and sinus tachycardia in one. Seventeen patients had occasional "skipped beats" without recurrence of tachyarrhythmias. Twelve of 13 patients whose arrhythmias limited employment before surgery returned to work after surgery. By actuarial analysis at 1, 2 and 3 years, all patients were alive and 98% were free from tachyarrhythmias. Surgical correction of Wolff-Parkinson-White syndrome provides excellent long-term results with low morbidity. Patients who are disabled by arrhythmias return to work after successful surgery. Delta waves may persist or recur without return of arrhythmias. Minor postoperative episodes of palpitation are common and do not correlate with tachyarrhythmias.

Endocardium↗
PubMed1987

Differential electrophysiologic properties of decremental retrograde pathways in long RP' tachycardia.

Long RP' supraventricular tachycardias (SVT) often demonstrate both slow and decremental conduction properties in the retrograde pathway of the reentrant circuit. The electrophysiologic properties of these pathways are poorly understood. We studied 10 patients with long RP' SVT (RP'/RR, 0.52 to 0.71); five had the unusual form of atrioventricular nodal reentry (fast-slow) and five patients had accessory AV pathways with slow, decremental retrograde conduction properties. During SVT, the effects of intravenous adenosine (37.5 to 150 micrograms/kg), which increases potassium current (iK) in supraventricular tissue and hyperpolarizes membrane potential toward Ek (-90 mV), and the response to slow-inward channel blockade with verapamil (0.10 to 0.20 mg/kg iv) were evaluated. Adenosine and verapamil has similar effects in the presence of fast-slow AV nodal reentry since both agents terminated SVT by producing block in the retrograde slow AV nodal pathway. In contrast, adenosine and verapamil had differential effects on retrograde conduction in decremental accessory pathways. Adenosine terminated all episodes of SVT in the retrograde decremental pathway, whereas verapamil had a direct effect on this tissue in only two of five patients. Decremental retrograde accessory pathways can therefore demonstrate at least two types of electrophysiologic responses. Pathways that respond only to adenosine-induced hyperpolarizing K+ current likely comprise depressed fast-Na+ channel tissue, i.e., partially depolarized (greater than -60 to -70 mV) atrial tissue. In contrast, decremental accessory pathways that respond to both modulation of the slow-inward calcium current and K+ conductance have pharmacologic properties similar to those of the AV node and may represent more completely depolarized atrial fibers with resting membrane potentials of -60 mV or less.

Adenosine↗
PubMed1987

Determinants of induced sustained arrhythmias in survivors of out-of-hospital ventricular fibrillation.

We prospectively studied 196 consecutive survivors of out-of-hospital ventricular fibrillation (VF) not associated with acute myocardial infarction and 46 consecutive, control patients without prior ventricular arrhythmias. Programmed stimulation included two extrastimuli (S3 protocol) in all patients and three extrastimuli (S4 protocol) in the last 140 study patients and in all control patients. Sustained ventricular tachycardia (VT) or VF was not induced in any control patient. In study patients, logistic regression identified two independent predictors of induced, sustained VT for both S3 and S4 protocols: prior spontaneous, sustained VT (37 patients; p less than or equal to .001) and prior myocardial infarction (113 patients; p = .005). With the S3 protocol, sustained VT was induced in 54% of patients with both prior myocardial infarction and prior sustained VT vs 4% without either; with the S4 protocol, sustained VT was induced in 91% vs 13%, respectively. Eighty-three percent of induced VT episodes had a cycle length less than 300 msec, and all required termination by cardioversion or pacing. VF was induced only in survivors of out-of-hospital VF without prior, spontaneous, sustained VT (S3 protocol, 9%; S4 protocol, 24%) but not in study patients with prior sustained VT (S3, p = .10; S4, p = .05) or control patients (S3, p = .06; S4, p = .01). The mean coupling intervals of extrastimuli that induced VF were not significantly different from the intervals that induced sustained VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1987

Summation and inhibition by ultrarapid train pacing in the human ventricle.

Trains of ultrarapid stimuli that begin late in the refractory period have been reported both to produce early single captures to terminate tachyarrhythmias and to inhibit the response to subsequent threshold stimuli. To determine which characteristics of trains facilitate capture and which enhance inhibition, we compared the right ventricular strength interval relationship for single extrastimuli (S2) with that for 100 Hz trains with a duration of 100 msec in 29 patients. Pulse frequency was varied in 12 patients (50, 100, and 200 Hz) and train duration (50, 100, and 150 msec) was varied in 11 patients; the effect of procainamide (10.1 +/- 2.3 micrograms/ml) was assessed in 10 patients. Relative to S2, 100 Hz trains with a duration of 100 msec prolonged the effective refractory period (ERP) at low current strength (inhibition), but shortened the ERP at high-current strength (summation): at 0.5 mA, the train ERP was 47 +/- 6 (SEM) msec longer than the S2 ERP (p less than .001); at 16 mA it was 12 +/- 1 msec shorter (p less than .001). Trains prolonged the functional refractory period (FRP) slightly at low currents (13 +/- 3 msec, p = .001 at .05 mA), but did not shorten FRP significantly at high currents (2 +/- 2 msec, p = NS at 16 mA) because of increased stimulus-response latency. Inhibition increased with increasing pulse frequency (p less than .001), increasing train duration (p less than .001), and procainamide (p less than .01). Summation increased with increasing pulse frequency (p less than .001), but not increasing train duration or procainamide, suggesting that inhibition and summation depend on different electrophysiologic mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Determinants of prognosis in ventricular tachyarrhythmia patients without induced sustained arrhythmias.

We studied 59 patients with sustained ventricular tachycardia (VT) or ventricular fibrillation in whom programmed stimulation induced 15 or fewer repetitive ventricular complexes. During follow-up of 2.2 +/- 1.5 years, 13 patients had an arrhythmia recurrence and seven died suddenly. At 1, 2, and 3 years, the actuarial incidence of arrhythmia recurrence was 15 +/- 5%, 17 +/- 5%, and 23 +/- 6%, and that of sudden death was 6 +/- 4%, 15 +/- 6%, and 21 +/- 8%. Prior myocardial infarction (MI) was the only independent predictor of arrhythmia recurrence (p less than 0.02) and sudden death (p = 0.05): at 2 years, 36 +/- 12% of 18 patients with MI and 8 +/- 4% of 41 patients without MI had arrhythmia recurrence, and 24 +/- 12% with MI and 3 +/- 3% without MI died suddenly. None of the nine patients with greater than or equal to 70% coronary stenosis but no MI had arrhythmia recurrence after anti-ischemic therapy. Possible arrhythmia-precipitating conditions were present during all arrhythmias in 14 patients, but did not predict freedom from arrhythmia recurrence (p = 0.52) or sudden death (p = 0.81). The maximum number of induced ventricular complexes did not predict arrhythmia recurrence or sudden death: for patients with 0 to 2, 3 to 5, and 6 to 15 induced complexes, the 2-year incidence of arrhythmia recurrence was 16 +/- 7%, 15 +/- 10%, and 18 +/- 10%; for sudden death, it was 9 +/- 6%, 0 +/- 0%, and 14 +/- 9%. In this group of patients, prior MI predicted arrhythmia recurrence and sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Clinical electrophysiology of flestolol, a potent ultra short-acting beta blocker.

We measured the electrophysiologic effects of flestolol, an ultra short-acting beta blocker, in 15 patients at two infusion rates: a 45 micrograms/kg loading dose followed by a 5 micrograms/kg/min infusion and a 60 micrograms/kg loading dose followed by a 10 micrograms/kg/min infusion. Electrophysiologic measurements were made after 15 minutes at each infusion rate (plasma concentrations 46 +/- 11 and 94 +/- 23 ng/ml). Flestolol produced dose-dependent effects on the sinus node, the atrioventricular (AV) node, and right ventricular refractoriness, whereas atrial refractoriness and infranodal conduction were unchanged. At the 10 micrograms/kg/min dose, flestolol prolonged sinus cycle length by a mean of 20% (p = 0.0001), corrected sinus node recovery time by 42% (p = 0.02), AH interval by 21% (p = 0.0001), AV node effective refractory period by 28%, AV node Wenckebach cycle length by 30% (0.0001), and right ventricular effective refractory period by 5% (p = 0.03). A significant concentration-effect relationship (p less than or equal to 0.03) was present for all variables which had significant dose-effect relationships. No patient developed hypotension, bradyarrhythmias, or other toxicity. Sinus cycle length decreased linearly with time in the post infusion period (r = 0.99); by 30 minutes post infusion, measured electrophysiologic variables had returned to control values and flestolol plasma concentration had decreased to 4 +/- 2 ng/ml. Flestolol's electrophysiologic effects are similar to those of other beta blockers. In doses up to 10 micrograms/kg/min, it is safe in selected patients, has rapid onset and offset of action, and does not cause acute rebound.

Adrenergic beta-Antagonists↗
PubMed1986

Septal origin of sustained ventricular tachycardia in a patient with right ventricular outflow tract obstruction after correction of tetralogy of Fallot.

Right ventricular hypertension and ventricular arrhythmias are risk factors for sudden death after correction of tetralogy of Fallot, but sustained ventricular tachycardia has been reported only in patients without residual hemodynamic abnormalities. A patient with right ventricular hypertension and hypotensive ventricular tachycardia tolerated the arrhythmia better after relief of right ventricular outflow tract obstruction. This case provides insight into the relationship between hemodynamic abnormalities and the clinical consequences of arrhythmias. To our knowledge, it is the first report of ventricular tachycardia originating in scar adjacent to the ventricular septal defect patch after correction of tetralogy of Fallot.

Adolescent↗