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Biomedical subjects

T R Engel

Publications and source records attributed to T R Engel.

At least 37 records · Page 2Linked to original sources
PubMed1983

Effect of procainamide on dispersion of ventricular refractoriness.

Ventricular arrhythmias after Q-T prolongation by drugs could result from a nonhomogeneous increase in refractoriness (dispersion). Dispersion of effective refractory periods (ERP) was measured before and after infusion of 1 g of procainamide using twice-threshold extrastimuli applied in sinus rhythm and with 500 ms ventricular drive cycle length at 3 right ventricular sites (2 patients) or 2 right and 1 left ventricular site (10 patients). Procainamide prolonged ERP. In drive, average ERP was 247 +/- 5 ms (standard error of the mean) before and 277 +/- 7 ms after procainamide (p less than 0.001). The Q-T interval was prolonged by 50 ms in drive (p less than 0.001), but Q-T prolongation did not reflect the increased ERP (r =-0.05). However, procainamide did not alter measured dispersion (54 +/- 16 to 44 +/- 14 ms in sinus, 48 +/- 14 to 47 +/- 13 ms in drive). Polymorphic ventricular tachycardia (VT) was induced in 6 patients in whom drive itself generally failed to reduce dispersion, and failure to induce tachycardia or shorter runs after procainamide was associated with narrowed dispersion. Polymorphic VT was not induced after procainamide in 2 patients with clinical episodes of torsades de pointes caused by type I agents. The mechanism of torsades de pointes was not explained by dispersion of refractoriness or by polymorphic VT initiated by premature beats after a type I drug.

Aged↗
PubMed1983

Atrial coronary angiography, tachyarrhythmias and the Ta segment.

Electrocardiograms and angiograms were reviewed to determine if atrial Ta segment displacements and atrial flutter or fibrillation indicate atrial coronary disease. Atrial circulation was assessed by angiography in 28 patients with chest pain and normal coronary arteries, 29 patients with significant stenosis of at least one major coronary vessel, and 16 with coronary artery disease and atrial flutter or fibrillation. The prevalence of Ta segment displacement was 71% without coronary disease and 79% with coronary disease. There was no relationship between Ta displacement and segmental atrial coronary insufficiency. Among an additional 28 patients with acute transmural myocardial infarction, 79% had equivalent Ta segment displacement. Half of the patients with atrial flutter/fibrillation had significant mitral regurgitation, in contrast to 3% of coronary patients in sinus rhythm (p less than 0.001), but their atrial coronary circulation was not more severely compromised. Thus, Ta segment displacement did not identify atrial coronary disease and was not more frequent during acute myocardial infarction. Abnormal atrial perfusion did not explain Ta segment displacement or atrial flutter/fibrillation.

Atrial Fibrillation↗
PubMed1983

Effect of whiskey on atrial vulnerability and "holiday heart".

Vulnerability to atrial fibrillation and flutter was examined in 11 alcohol abusers who did not have cardiomyopathy or manifest heart failure. Atrial extrastimulation was done with rapid pacing (drive cycle length 500 ms) to facilitate induction of atrial vulnerability, seen in four alcohol abusers. The remaining seven were retested 30 minutes after drinking 60 to 120 ml of 86 proof whiskey (ethanol blood levels were 49 to 101 mg/100 ml but pulmonary capillary wedge pressure remained normal in all) and atrial fibrillation or flutter was induced in three of the drinkers. Three nondrinkers, symptomatic with sinus bradycardia but not in heart failure, were found not to be vulnerable to atrial fibrillation or flutter, but flutter was induced in two of the three after drinking whiskey. Whiskey did not alter atrial functional refractory periods (mean +/- standard error of the mean 297 +/- 14 to 290 +/- 12 ms) or widen the dispersion among three disparate right atrial sites (57 +/- 13 to 47 +/- 12 ms). Thus, whiskey enhanced vulnerability to atrial fibrillation and flutter in patients without heart failure or cardiomyopathy, substantiating the "holiday heart" syndrome.

Adult↗
PubMed1983

Overdrive pacing for ventricular tachyarrhythmias: a reassessment.

Overdrive pacing was used for many years to prevent ventricular tachycardia and there are many reports of its effectiveness. Nevertheless, the use of overdrive pacing for most types of ventricular tachyarrhythmia has been abandoned. One notable exception is torsades de pointes, in which interventions that increase heart rate, including pacing, at least temporarily protect against recurrence. Overdrive may work by narrowing dispersion of ventricular refractoriness, and measurement of the latter could provide a marker to selectively apply overdrive pacing, thus increasing its usefulness.

Cardiac Pacing, Artificial↗
PubMed1983

A case of being scared to death.

A 21-year-old student had generalized tonic-clonic seizures induced by the mental image of human pain. One ictal event occurred while he was listening to a description of suffering, as read from Fox's Book of Martyrs. While again listening to the offending passage during EEG and ECG monitoring, he had 25 s of asystole terminating in electrocerebral silence and a generalized tonic, tonic-clonic seizure. A 24-hour ambulatory monitor recorded episodes of progressive sinus bradycardia concomitant with PR-interval prolongation and Wenckebach atrioventricular block. Sinoatrial conduction times and sinus node recovery times were normal on atrial pacing. Since implantation of a permanent pacemaker, he has been asymptomatic. This patient demonstrates the advantages of reproducing the circumstances associated with an unexplained loss of consciousness while monitoring the EEG and ECG.

Adult↗
PubMed1982

The electropharmacology of acute drug testing using pacemakers.

Acute drug testing in patients is useful to select prophylactic treatment for life-threatening or intractable tachycardias. This is generally done by induction of tachycardias with pacing. Acute studies that depend on temporary insertion of pacing electrodes do not determine efficacy in the same sense as longer term clinical drug trials because of the biased population referred for testing with pacemakers. However, the pharmacologic activity of compounds can be tested in terms of electrical functions such as conductivity and refractoriness not merely of the heart in general, but also of the arrhythmogenic focus. Such data can be directly applied to patients with similar arrhythmias, obviating the confusion often caused by interspecies and disease differences.

Acecainide↗
PubMed1981

Syncope and conduction problems: when is pacing the solution?

SSS is characterized by sinus bradycardia and asystole. Syncope from SSS carries a better prognosis than syncope from heart block. AV node heart block is signaled by P-R prolongation and Wenckebach periodicity. Symptoms vary in severity, with or without syncope. TF heart block is preceded by left-bundle branch block or by right-bundle branch block plus fascicular block. Prognosis for the unpaced patient subject to TF block is grave. The fact that ECGs suggesting sinus bradycardia, P-R prolongation, and bifascicular block (all causes of syncope) are very common among the elderly and usually have an innocent course, increases the difficulty of deciding which patient will benefit from pacing. Certainly a pacemaker should not be inserted because of abnormal ECG alone.

Cardiac Pacing, Artificial↗
PubMed1980

Modification of ventricular tachycardia by procainamide in patients with coronary artery disease.

Fifteen consecutive patients with coronary artery disease had rapid (158 to 272 beats/min) and sustained ventricular tachycardia induced by the extrastimulus technique, and received procainamide infusion. Before the study, all but one patient had severe symptoms with tachycardia, and six had survived apparent sudden death. Procainamide consistently slowed ventricular tachycardia. However, in traditional doses (1 g infusion, plasma concentration greater than 4 micrograms/ml), it prevented induction of ventricular tachycardia in only 2 of the 15 patients. Induction of ventricular tachycardia was facilitated by procainamide in 10 patients. Larger doses of procainamide (plasma concentration 20.2 micrograms/ml +/- 9.7 [mean +/- standard deviation]) prevented induction of ventricular tachycardia in one of eight patients. Rapid ventricular rates (more than 210 beats/min) that were not slowed (by 50 percent or more) after a 1 g infusion of the drug predicted failure of procainamide to prevent ventricular tachycardia. Therefore, procainamide slowed but did not prevent induced ventricular tachycardia in most of these patients with coronary artery disease at risk of sudden death.

Adult↗
PubMed1979

Diagnostic implications of atrial vulnerability.

Extrastimulation in the atrial vulnerable zone may result in atrial fibrillation or flutter (AFF), especially with stimulation of multiple atrial sites. However, the clinical relevance of such vulnerability to AFF is unknown. Therefore, single twice-threshold extrastimuli were applied at three disparate right atrial sites in 45 consecutive unmedicated patients without overt heart failure. Group I consisted of 12 patients with documented spontaneous paroxysms of AFF. AFF was duplicated in 9 to 12 patients using extrastimulation in the vulnerable zone (5 in sinus rhythm, 4 requiring atrial pacing at 120 beats/min). Group II consisted of 33 patients without documented AFF dispite monitoring. Vulnerability to AFF was found in 12 of 33 patients (4 in sinus rhythm, 8 requiring atrial pacing). The duration of induced AFF did not discriminate between the two groups. Among the 12 Group II patients vulnerable to AFF, 3 had rapid palpitations, 2 had undiagnosed rapid tachycardias, 1 had atrial tachycardias and 1 junctional tachycardias. In vulnerable patients, the pause after AFF correlated with the pause after atrial pacing, but only 1 of 11 Group II patients with sick sinus syndrome was vulnerable. Thus, paroxysmal AFF may be duplicated with the extrastimulus technique if sufficient arial sites are stimulated, providing a model for evaluation of these arrhythmias. But atrial vulnerability, even to extrastimulation at normal heart rates, may be seen in patients suspected of atrial tachyarrhythmia in the absence of documented AFF, and does not contribute to the diagnosis of sinoatrial dysfunction.

Atrial Fibrillation↗
PubMed1979

Dispersion of atrial refractoriness in patients with sinus node dysfunction.

Abnormal atrial refractoriness was examined as a cause of atrial fibrillation/flutter (AFF) in patients with bradycardia. Refractory periods at three disparate right atrial sites were compared in 17 patients with sinus node dysfunction (SND) and 16 controls. Atrial pacing shortened refractory periods, but failed to decrease dispersion of refractoriness significantly. During sinus rhythm, duration and dispersion of refractoriness were greater in SND patients than in controls. These differences persisted with atrial pacing. For example, at the paced rate, dispersion of effective refractory periods in SND patients was greater than in controls (62.9 +/- 34 vs 36.6 +/- 21 msec, p less than 0.01). Six SND patients had AFF, but they did not have greater dispersion than other SND patients, or unusually short or long refractory periods. Thus, prolonged and nonuniform refractoriness were features of SND. Abnormal refractoriness in SND reflected atrial disease and persisted with pacing. These abnormalities were not unique to patients with AFF.

Adult↗
PubMed1978

Effect of procainamide on induced ventricular tachycardia.

Ventricular extrastimulation was performed in 11 patients evaluated for chronic recurrent ventricular tachycardia, before and after a 1-gm procainamide infusion. Extrastimulation caused only nonsustained extra beats (less than 4) in 3 patients. Sustained tachycardia was induced in 7 patients in the basal state, of which 6 continued to have inducible tachycardia after procainamide was given (5.2 to 9.8 mg/L). The zone of coupling intervals that initiated tachycardia was unchanged or widened in these 6 patients because ventricular refractoriness was unchanged or because the tachycardia zone shifted to later diastole by an interval at least equivalent to the prolongation of ventricular refractoriness. Post-procainamide tachycardia cycle length was prolonged in all patients, by an average 51 msec. The one patient who responded to procainamide had a shortened ventricular refractory period, but the greatest slowing of tachycardia. Finally, sustained ventricular tachycardia could be induced in the eleventh patient only following procainamide administration, consistent with his clinical history. These results suggest that procainamide often may be ineffective in preventing sustained ventricular tachycardia, and that slowed conduction, rather than prolonged refractoriness, is the basis for the procainamide antiarrhythmic effect. Our data emphasize that antiarrhythmic drug effectiveness be evaluated in terms of effect on sustained arrhythmia rather than suppression of isolated ectopic beats.

Aged↗
PubMed1978

Effects of digitalis on atrial vulnerability.

The effects of digitalis on vulnerability to atrial fibrillation and flutter were assessed in man, using the model of repetitive atrial firing initiated by post-drive atrial extrastimulation. Nine patients without heart failure or significant mitral valve disease were tested before and 30 minutes after the administration of 0.01 mg/kg ouabain. When repetitive firing was manifested by flutter, neither the flutter cycle length nor the interval from the initiating beat to the first flutter beat was consistently altered by ouabain. Repetitive firing was found at the atrial site with the shortest functional refractory period. The vulnerable zone bordered this refractory period. The functional refractory period was lengthened after ouabain, from 231 +/- 13 to 246 +/- 15 msec (mean +/- standard error of the mean) (P less than 0.025). Partly because of prolonged refractoriness, the vulnerable zone was curtailed by ouabain, from 32.2 +/- 5.7 to 9.4 +/- 4.6 msec (P less than 0.001). This result suggests a protective effect of digitalis against atrial fibrillation and flutter independent of its hemodynamic actions.

Adult↗