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.

Fast Fourier transformation of the entire low amplitude late QRS potential to predict ventricular tachycardia.

Signal-averaged electrocardiograms (X, Y and Z leads) were acquired from 24 patients with coronary artery disease and recurrent ventricular tachycardia, 24 control patients with coronary artery disease and 23 normal subjects to assess the discriminant value of fast Fourier transformation of the entire late potential period of the QRS complex. Analysis of the vector magnitude in the temporal domain (25 to 250 Hz bandpass filters) measured high frequency QRS duration, the duration of terminal signals less than 40 microV and the root mean square voltage of the last 40 ms. Late potentials were defined as terminal signals greater than 25 Hz that were less than 40 microV. Analysis in the frequency domain used a 120 ms window that encompassed (had onset with) all of the late potential, but the mean value was first subtracted to eliminate a direct current component. High frequency spectral areas (60 to 120 Hz) and the percent high frequency (100 x [60 to 120 Hz/0 to 120 Hz]) were calculated. Results in both temporal and frequency domains were similar in control patients with coronary artery disease and normal subjects. Patients with ventricular tachycardia had a longer high frequency QRS complex (p less than 0.0001) and longer high frequency terminal signals less than 40 microV (p less than 0.0004), but not significantly lower voltage in the last 40 ms. The most useful temporal domain measurement was high frequency QRS duration (if greater than or equal to 120 ms, odds ratio = 8.2). Patients with ventricular tachycardia had increased high frequency spectral areas (p less than 0.0002) in the late potential, and the percent high frequency was especially increased (p = 0.0000; if percent high frequency greater than 3.1%, odds ratio = 18.4). The odds ratio and the area under the receiver operating characteristic curve were both greater for percent high frequency than for high frequency QRS duration (p less than 0.03). All patients with ventricular tachycardia had a high frequency QRS complex greater than or equal to 107 ms or percent high frequency greater than or equal to 3.1% (sensitivity 100%). For a high frequency QRS complex greater than or equal to 107 ms and percent high frequency greater than or equal to 3.1%, specificity was 96%. Therefore, high frequencies in late potentials, not their duration or reduced voltage, most usefully identify patients with coronary artery disease who are prone to ventricular tachycardia.

Late induction of tachycardia in patients with ventricular fibrillation associated with acute myocardial infarction.

A prospective study was made of 57 asymptomatic patients, 1 to 24 months after acute myocardial infarction, 17 with (Group I) and 40 without (Group II) ventricular fibrillation during the acute event. None of the 57 patients had symptomatic arrhythmias, uncontrolled heart failure or unstable angina. There was no significant difference between the two patient groups in time from acute myocardial infarction, medication used or left ventricular ejection fraction. Repetitive forms of arrhythmia (Lown grade 4) were more prevalent (29 versus 16%, not significant) during 24 hour ambulatory monitoring in patients in Group I (ventricular fibrillation group). Programmed extrastimulation was performed using 1 to 3 twice-threshold, 2 ms decremental extrastimuli delivered during right ventricular drive. Of the 17 patients in Group I, 8 had no induced arrhythmia (less than or equal to 4 extra responses), 4 had nonsustained ventricular tachycardia and 5 had sustained ventricular tachycardia (degenerating into ventricular fibrillation requiring electrical reversion in 4). None of the 40 patients in Group II had induced sustained ventricular tachycardia (p less than 0.005), although 9 had nonsustained ventricular tachycardia. Patients with ventricular fibrillation during acute myocardial infarction may have an increased risk for ventricular tachycardia or ventricular fibrillation that may be exposed by programmed electrical stimulation even when not yet clinically manifest.

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.

Effect of lidocaine on right ventricular muscle refractoriness.

The effect of clinical doses of lidocaine on ventricular refractoriness was investigated in man. Effective refractory period (ERP) and functional refractory period (FRP) were determined in 11 normokalemic patients via a catheter at the right ventricular apex using programmed extra-stimuli and a ventricular electrogram recorded from the pacing catheter. No subject had recent ischemia or infarction. Measurements were repeated after clinical doses of lidocaine that produced therapeutic blood levels. Lidocaine caused no significant change in ERP or FRP during ventricular or atrial drive, or sinus rhythm with unchanged cycle length (CL). During sinus rhythm ERP/CL was unchanged. In 4 of 5 patients, lidocaine did not abolish echo phenomena observed during ventricular drive. This study demonstrates that ventricular refractoriness can be safely measured in man. Clinical doses of lidocaine did not alter right ventricular refractory periods. Lidocaine action is not explained by alteration of ventricular refractoriness, at least in muscle remote from the site of acute infarction.

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.

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.

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.

Pacing-induced angina pectoris and induction of ventricular arrhythmias in coronary artery disease.

Ischemia caused by rapid pacing during electrophysiologic study could facilitate induction of ventricular arrhythmias. The results of extrastimulation were retrospectively analyzed in 32 patients with coronary artery disease (CAD) without a history of symptomatic arrhythmia. These patients were studied at cardiac catheterization for angina pectoris refractory to medical therapy. Eleven patients (group I) had typical angina during trains of rapid right ventricular pacing (repeated trains of 8 stimuli [mean cycle length (CL) 473 +/- 47 ms]) but were asymptomatic during slower trains (CL 800 +/- 100 ms). Twenty-one patients (group II) had no symptoms with either rapid (CL 448 +/- 51 ms) or slow (CL 688 +/- 105 ms) trains, despite comparable left ventricular function, CAD severity and medication. Effective refractory periods (S1S2) after rapid drive were shorter in group I than in group II patients (225 +/- 9 vs 240 +/- 14 ms, p less than 0.002), but refractory periods during slow pacing were similar (251 +/- 12 vs 253 +/- 17 ms, difference not significant). No patient in either group had sustained arrhythmia (more than 15 beats) induced by single and double ventricular extrastimuli, decrementally applied at the right ventricular apex. The number of extra beats provoked in group I when rapid trains caused angina (4.3 +/- 3.6) was similar to that induced by extra-stimulation after slower pacing without angina (4.4 +/- 3.5) and to that obtained with rapid or slow pacing in group II (3.1 +/- 3.3 and 2.8 +/- 2.2).(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Electrophysiologic effects of hydralazine on sinoatrial function in patients with sick sinus node syndrome.

The electrophysiologic effects of hydralazine were evaluated in nine hypertensive patients with sinoatrial dysfunction. Intravenous hydralazine, 0.15 mg/kg, caused no significant reduction in arterial blood pressure. Yet this dose of hydralazine increased heart rate from 61.9 +/- 4.1 beats/min (mean +/- standard error of the mean) to 68.6 +/- 4.9 (P less than 0.001). Sinus nodal recovery time upon termination of atrial pacing shortened from 3,207 +/- 1,098 to 2,064 +/- 573 msec (P less than 0.05) and second escape cycles shortened as well (P less than 0.025). Acceleration of heart rate and abbreviation of recovery time did not closely correlate with change in blood pressure (r = 0.41 and 0.18, respectively). Junctional escape beats became more frequent and junctional escape time shortened from 2,525 +/- 692 to 1,705 +/- 382 msec (P less than 0.05). Sinoatrial conduction time tended to shorten, but a significant change was not observed. Atrial tachyarrhythmias did not occur and atrial refractoriness was unchanged. Thus, a minimal blood pressure response to hydralazine was associated with enhanced automaticity. Hydralazine merits clinical trial for treatment of sick sinus syndrome with concomitant hypertension.

Effect of site of pacing on dispersion of refractoriness.

The variation in dispersion of ventricular refractoriness with different sites of pacing was measured in 11 patients not taking antiarrhythmic drugs. Dispersion of refractoriness between 3 right ventricular sites was determined at constant paced cycle lengths (S1S1). Refractoriness to ventricular extrastimulation (S2) using atrial pacing vs "clinical" pacing (drive or S1 at the right ventricular apex) vs the conventional measurement of dispersion (S1 at the site of S2) was compared. Effective and functional refractory periods (ERP and FRP) were measured from electrograms at the site of application of S2. Dispersion of ERP was always wider using clinical pacing (65.4 +/- 26 ms [+/- standard deviation]) than atrial pacing or traditional drive (20.4 +/- 14 and 19.1 +/- 10 ms, p less than 0.0001). Similarly, dispersion of FRP was greater with clinical pacing (45.0 +/- 35 vs 21.8 +/- 14 and 17.3 +/- 13, p less than 0.011). In 2 patients with left bundle branch block these differences were most striking. Clinical pacing foreshortened FRP relative to ERP (FRP shorter than ERP by an average 12.5 ms at nonapical sites) but this did not induce tachycardias, perhaps because FRP was still longer than the shortest V1V2 achieved conventionally (FRP was longer at nonapical sites than at the apex using clinical pacing, p less than 0.05). With atrial pacing there is less dispersion of refractoriness than with clinical ventricular pacing, although this difference is not appreciated when dispersion is measured in the conventional manner.

Arrhythmias from fiberoptic bronchoscopy.

The electrocardiogram was monitored in 51 patients during fiberoptic bronchoscopic procedures and was compared to recordings made before premedication. Sixteen of the patients had heart disease. During the bronchoscopic procedure, the heart rate increased by 154 "/- 5 percent (+/- SE). The frequency of atrial ectopic beats was minimally increased, by an average 0.15 +/- 0.12 beats per minute (not significant). Ventricular ectopic beats became less frequent during the bronchoscopic procedure (-0.17 +/- 0.41 beats per minute; not significant), and there was no ventricular tachycardia. Frequent ventricular ectopic beats were seen mainly during bronchoscopic procedures in patients with coronary heart disease, but even in this group, ventricular ectopic beats became less frequent than at rest (-1.13 +/- 1.46 beats per minute; not significant). The nearly uniform sinus tachycardia that was observed was well tolerated but could predispose coronary patients to ischemia; however, the fiberoptic bronchoscopic procedure per se does not enhance prior ectopy.

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.

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.

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.

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.