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.

Analysis of ambulatory electrocardiograms in 15 patients during spontaneous ventricular fibrillation with special reference to preceding arrhythmic events.

Fifteen patients sustained ventricular fibrillation during ambulatory electrocardiographic recording in a period of 3.5 years over which time 16,500 ambulatory electrocardiograms were analyzed (prevalence = 0.09% or 1/1,100). Eight patients died, and seven survived cardiopulmonary resuscitation. Quantitative analysis of hourly ventricular arrhythmias prior to ventricular fibrillation revealed an increased frequency of premature ventricular beats and ventricular tachycardia, especially in the 2 hours immediately before ventricular fibrillation. Ventricular fibrillation was initiated by ventricular tachycardia in all 15 cases. These runs of ventricular tachycardia were characterized by their unusual length (mean = 560 +/- 536 beats) and their rapid rate (241 +/- 45 beats/min). Although an R on T premature ventricular beat initiated ventricular tachycardia and ventricular fibrillation occasionally, the mean prematurity index of the initiating premature ventricular beat was not early (mean = 1.27 +/- 0.28). QT prolongation was present in only 3 of the 15 patients (mean QTc interval = 0.42 +/- 0.06). Left ventricular dysfunction (mean left ventricular ejection fraction = 34.9 +/- 9.9%) and coronary artery disease were nearly always present. The cardiac medications most frequently associated with these patients at the time of ventricular fibrillation were digitalis and quinidine.

Importance of pacing site in entrainment of ventricular tachycardia.

Transient entrainment by pacing has been demonstrated during various tachyarrhythmias, including ventricular tachycardia. A patient is described who had two morphologically distinct forms of sustained ventricular tachycardia induced by programmed stimulation. Entrainment of both configurations of ventricular tachycardia was demonstrated. Evidence for entrainment included the presence of different degrees of fusion between paced and ventricular tachycardia complexes at different pacing cycle lengths, and the observation that the last entrained beat was always unfused and identical in configuration to the ventricular tachycardia complexes. Termination of ventricular tachycardia only occurred at pacing cycle lengths at which there was loss of fusion. Catheter endocardial mapping suggested a septal origin of both configurations of ventricular tachycardia. Demonstration of entrainment was dependent on pacing site, being seen only during pacing in the ventricle opposite from that showing earliest activation during ventricular tachycardia. Thus, when attempting to entrain ventricular tachycardia, multiple pacing sites in both ventricles should be used.

Permanent triggered antitachycardia pacemakers in the management of recurrent sustained ventricular tachycardia.

Permanent pacemakers capable of triggered ventricular stimulation were implanted in 28 patients with a history of sustained ventricular tachycardia or fibrillation. Noninvasive programmed ventricular stimulation was performed on 125 occasions during follow-up periods ranging from 1 to 25 months and was used to assess the efficacy of antiarrhythmic drug therapy, drug or dosage changes and left ventricular endocardial resection. Drug or dosage changes based on noninvasive programmed ventricular stimulation were made in 19 of the 28 patients. In addition, 126 episodes of spontaneous sustained ventricular tachycardia were terminated noninvasively in nine patients. It is concluded that a permanent pacemaker capable of triggered ventricular stimulation is useful in patients with ventricular tachycardia or fibrillation that is difficult to control.

Specialized delivery systems for intravenous nitroglycerin. Are they necessary?

Nitroglycerin is absorbed in vitro into polyvinyl chloride tubing, and it has been recommended that nitroglycerin be administered intravenously through specialized polyethylene infusion sets. To determine if tubing type is essential to achieve physiologic effectiveness, we studied dose responses to intravenous nitroglycerin in 15 patients with heart failure using standard polyvinyl chloride tubing in seven (group 2) and special polyethylene infusion sets in seven (group 1) (one patient was excluded from analysis because of technical difficulties). We monitored heart rate, blood pressure, right atrial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, and cardiac output. Cardiac index, systemic and pulmonary vascular resistance, triple index, rate pressure product, stroke volume, stroke volume index, and stroke work index were calculated. Baseline and treatment measurements were obtained from five to 15 minutes after the infusion of 10, 20, 40, and 80 micrograms of nitroglycerin per minute. Over-all, systolic blood pressure decreased (p less than 0.05) about 8 percent and mean blood pressure approximately 12 percent, mean pulmonary artery pressure and mean pulmonary capillary wedge pressure decreased 30 to 40 percent, and the decline in mean right atrial pressure was 35 percent of baseline (all p less than 0.05). Heart rate and cardiac index did not change (p greater than 0.05). Pulmonary vascular resistance decreased slightly (p = 0.07) and systemic vascular resistance significantly (p less than 0.05). When the two groups were compared physiologic changes were virtually identical (p less than 0.05). Two-way analysis of variance for baseline corrected data proved no differences between tubing sets (p less than 0.05), but the infusion concentration rate was highly related to response (p = 0.0001). A significant (p less than 0.05) decrease in mean blood pressure and mean right atrial pressure was noted at lower dose rates (20 micrograms per minute and 40 micrograms per minute, respectively) in group 1. Beneficial hemodynamic effects in heart failure patients can, then, be predicted to occur at 80 micrograms per minute infusion rates; these responses seem independent of the type of infusion tubing system employed. Additionally, when patients given intravenous nitroglycerin for various reasons were followed for 48 hours, the majority receiving infusions via polyvinyl chloride tubing (group 2) did not require dosage adjustments. Also, at lower flow rates, more solution than calculated may be delivered when polyethylene tubing infusion sets are employed with volumetric infusion pumps.

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.

Termination of sustained ventricular tachycardia by external noninvasive pacing.

Cardiac pacing has proven useful in the termination of sustained ventricular tachycardia (VT). In this study, the effectiveness of external noninvasive temporary pacing was compared with traditional endocardial burst ventricular pacing for the termination of sustained and hemodynamically stable VT. In 14 patients, 16 VT morphologies induced by programmed right ventricular extrastimulation were reproducibly terminated by endocardial burst pacing (3 to 9 complexes). VT cycle lengths averaged 392 +/- 97 ms (standard deviation) and ranged from 300 to 690 ms. The endocardial burst pacing cycle length used to terminate VT averaged 298 +/- 93 ms (range 220 to 600 ms). External burst pacing terminated 14 of 16 VT morphologies (88%). The pacing cycle length used to terminate these 14 VTs averaged 282 +/- 44 ms. The number of ventricular captures ranged from 5 to 20 beats. Failure to terminate 2 VT morphologies probably represented a failure of the device to capture the ventricle. Acceleration of VT occurred in 1 patient with burst external noninvasive pacing. These observations suggest that external burst pacing may be an effective means of terminating sustained VT in some patients.

Cost-effective management of acute atrial fibrillation: role of rate control, spontaneous conversion, medical and direct current cardioversion, transesophageal echocardiography, and antiembolic therapy.

Management strategies for the acute treatment of atrial fibrillation (AF) include: (1) the use of intravenous drugs for rate control, (2) drug termination, or (3) direct current (DC) cardioversion. Delays in cardioversion can promote atrial remodeling and add thromboembolic risk. Rate control awaiting spontaneous or pharmacologic conversion may be a cost-effective strategy in patients presenting with recent onset of symptoms. Early DC cardioversion can be cost-effective and minimize antiembolic therapy issues in the acute setting. In patients presenting with AF of unknown or >48 hours' duration, rate control and therapeutic warfarin for 3-4 weeks followed by medical or DC cardioversion is standard practice. However, delays in conversion promote atrial remodeling that makes restoration of sinus rhythm more difficult and increases the likelihood of postcardioversion AF recurrence. Transesophageal echocardiography can identify patients at low risk for a cardioversion-related embolic event and allows cardioversion to be performed earlier, thereby minimizing atrial remodeling.

Acute treatment of atrial fibrillation: spontaneous conversion rates and cost of care.

Acute treatment of atrial fibrillation is costly although spontaneous conversion rates are high. We reviewed 114 patients admitted to our inpatient service via the emergency department with a principal diagnosis of atrial fibrillation and found the spontaneous conversion rate was 50% in 48 hours, the average length of stay was 3.9 +/- 5.2 days, and the average cost was $6,692 +/- $4,928.

Prospective comparison of right and left ventricular stimulation for induction of sustained ventricular tachycardia.

Thirty-eight patients who had sustained monomorphic ventricular tachycardia (VT) or sudden cardiac death underwent programmed ventricular stimulation. To assess the relative efficacy of right and left ventricular (RV and LV) stimulation, a tandem protocol with 1 to 4 extrastimuli and burst pacing was used. Each step of the protocol was performed in a rotating sequence at the RV apex, basal RV septum and LV apex. Sustained VT was induced from the RV apex in 26 patients, right ventricle (either site) in 27, and LV apex in 24, and spontaneous VT was reproduced from those sites in 11, 14 and 12 patients, respectively. In the 23 patients who had sustained VT induced from both ventricles, RV stimulation always required fewer or the same number of extrastimuli for induction. At every stage of the protocol, the cumulative yield of sustained VT was consistently greater from the right ventricle than from the left ventricle. After delivering 4 extrastimuli and burst pacing, LV stimulation only increased the yield of sustained VT by 1 patient, and spontaneous VT by 3 patients. Inducibility or noninducibility in the right ventricle generally predicted the same outcome in the left ventricle. Previously undocumented VT or ventricular fibrillation was induced from the right ventricle in 19 patients and from the left ventricle in 13. Thus, LV stimulation was less efficacious than RV stimulation. LV stimulation increased the yield over RV stimulation only minimally and did not reduce the number of extrastimuli required to induce sustained VT.

Electrophysiologic evaluation of pirmenol for sustained ventricular tachycardia secondary to coronary artery disease.

The efficacy and electrophysiologic effects of pirmenol were evaluated in 21 patients with a history of sustained ventricular tachycardia (VT) and coronary artery disease. Intravenous pirmenol (0.7- to 1.1-mg/kg bolus, followed by a 35- to 40-micrograms/kg/min infusion) significantly prolonged the PR, QRS, QT and corrected QT intervals, HV interval and right ventricular effective refractory period, and shortened the sinus cycle length and atrioventricular nodal block cycle length. All 21 patients had inducible VT (20 sustained, 1 nonsustained) during programmed stimulation in the control state. After intravenous pirmenol, 5 patients (24%) no longer had inducible VT. In those in whom VT was still inducible, the VT cycle length was prolonged significantly. The 5 patients who responded to intravenous pirmenol were given oral pirmenol (200 to 250 mg every 8 hours) for 1 to 3 days and retested with programmed stimulation. In 4 of these 5, VT could not be induced with oral pirmenol administration; in 1 patient sustained VT was induced and pirmenol therapy was discontinued. Oral pirmenol suppressed recurrent VT during a follow-up of 315 +/- 133 days in 4 patients. However, pirmenol therapy was discontinued in 2 patients because of possible deleterious effects (worsened heart failure in 1 patient and elevated liver function test results in 1). Thus, pirmenol, a type IA antiarrhythmic drug, had an overall efficacy of approximately 19% in patients with sustained VT secondary to coronary artery disease.

Effect of increased current, multiple pacing sites and number of extrastimuli on induction of ventricular tachycardia.

Reproduction of spontaneously occurring ventricular tachycardia (VT) and induction of previously undocumented VT were studied prospectively in 98 patients: 48 with documented sustained VT or ventricular fibrillation, 25 with nonsustained or exercise-induced VT, and 25 with no documented VT. Patients received 1 to 4 ventricular extrastimuli and ventricular burst pacing at 2 right ventricular (RV) sites, first at twice late diastolic threshold, and then at 10 mA using a prospective, tandem study design. Spontaneously occurring VT was reproduced in 37 of 48 patients (77%) at twice late diastolic threshold and in 1 other patient (2%) at 10 mA. VT was reproduced at both RV sites in 17 of 48 patients (35%) and at 1 site in 20 of 48 patients (42%) at twice late diastolic threshold. A previously undocumented VT was induced in 7 of 25 patients (28%) with no documented VT at twice diastolic threshold and 14 of 25 patients (56%) at 10 mA. A previously undocumented VT was induced in 33 of 73 patients (45%) with a history of sustained or nonsustained VT at twice late diastolic threshold and in 47 of 73 patients (64%) at 10 mA. In patients with documented sustained VT, the use of up to 4 ventricular extrastimuli at multiple RV sites increases the sensitivity of the test. In patients without documented VT, the induction of previously undocumented VT with more than 3 ventricular extrastimuli limits the specificity of the test. Increased current provides only a slight advantage over 4 ventricular extrastimuli at twice late diastolic threshold in terms of reproduction of spontaneously occurring VT, but leads to a marked increase in induction of previously undocumented VT.

Induction of clinical ventricular tachycardia using programmed stimulation: value of third and fourth extrastimuli.

Initiation of ventricular tachycardia (VT) by right ventricular extrastimulation was analyzed in 142 consecutive patients, 53 with electrocardiographically documented episodes of spontaneous VT or ventricular fibrillation (VF) and 68 with no spontaneous VT or VF; 21 patients with a history of sudden death but no documented arrhythmia were excluded from further analysis. All patients received 1 to 4 extrastimuli (S2, S3, S4 and S5) during pacing at fixed cycle lengths of 600 or 500 msec at 1 or 2 right ventricular sites. Clinical VT was reproduced by extrastimulation in 28 of 43 patients (65%) with sustained VT and in 0 of 10 patients with nonsustained VT. Clinical VT was induced by S2 or S3 in 16 patients and by S4 or S5 in 12 patients. Ventricular burst pacing reproduced clinical VT in 3 other patients. Nonclinical VT, which was most often polymorphic and nonsustained, was induced in 24 of 121 patients (20%), in 11 by S2 or S3 and in 13 by S4 or S5. Ventricular burst pacing induced nonclinical VT in 4 other patients. In patients with spontaneous sustained VT, the use of S4 and S5 in the right ventricle increases the yield of inducible clinical VT compared with use of S2 and S3 alone, but at a cost of increased induction of nonclinical VT. Frequent induction of nonclinical VT limits the interpretation of the results of such stimulation in patients without previously documented VT.

Observations on carotid sinus hypersensitivity from direct intraneural recordings of sympathetic nerve traffic.

In summary, we studied 4 patients with mixed-type CS hypersensitivity. We demonstrated that CS massage rapidly inhibits sympathetic nerve activity and decreases heart rate. Arterial pressure starts to decline abruptly with complete sympathetic withdrawal, but the nadir is delayed, suggesting that arterial dilation is not instantaneous. Arterial pressure rebounds slowly, suggesting a latency between the neural reflex and vascular compliance. Pacing had little effect on preventing hypotension in these patients. Our data support the concept that sympathetic withdrawal is responsible for the vasodilatory component seen with CS syncope.

Effect of bradycardia on dispersion of ventricular refractoriness.

The effect of bradycardia on dispersion of ventricular refractoriness was evaluated. Refractory periods were measured at 3 right ventricular sites in 16 patients with severe bradycardia (average heart rate 39 +/- 5 beats/min) and were compared with those measured in 11 control subjects, (average heart rate 72 +/- 12 beats/min). Patients with bradycardia had significantly longer effective (377 +/- 36 ms) and functional (421 +/- 39 ms) refractory periods (ERP and FRP) than control subjects (ERP 296 +/- 25 ms, FRP 346 +/- 18 ms) (p less than 0.001). However, dispersion of refractoriness was similar in the 2 groups. Dispersion of ERP was 43 +/- 38 ms and FRP was 48 +/- 35 ms in patients with bradycardia. In control subjects dispersion of ERP was 37 +/- 12 ms, and FRP was 36 +/- 20 ms. Pacing of 120 beats/min significantly decreased ERP and FRP in both groups. Pacing shortened dispersion significantly in control subjects. In patients with bradycardia, pacing failed to significantly decrease dispersion. Compared with control subjects with normal heart rates, patients with bradycardia have longer absolute refractory periods but do not have significantly increased dispersion of refractoriness. Single and double, twice threshold ventricular extrastimuli (S2 and S3) failed to induce ventricular tachycardia in any patient during bradycardia. Bradycardia alone does not appear to be a factor in the induction of ventricular tachyarrhythmias.

Conduction system abnormalities in symptomatic mitral valve prolapse: an electrophysiologic analysis of 60 patients.

This study examined the site of atrioventricular (AV) block in mitral valve prolapse (MVP). Sixty symptomatic patients with MVP underwent electrophysiologic study; 49 had documented arrhythmias and 28 had syncope. Eight patients had spontaneous second- or third-degree AV block and 10 had chronic bundle branch block. Electrophysiologic study revealed abnormal sinus node function in 8 patients, prolonged HV interval in 10, intra-Hisian delay in 9, and functional bundle branch block in 15. Dual AV nodal pathways were demonstrated in 24 patients. Comparison with 101 similarly symptomatic patients without MVP revealed a greater prevalence of dual AV nodal pathways in the MVP patients. Infranodal conduction abnormalities and dual AV nodal pathways are frequently revealed by electrophysiologic testing in symptomatic patients with MVP.

Clinical suppression of refractory ventricular tachycardia with oral bretylium not predicted by electrophysiologic drug testing.

We report the findings in a patient in whom intravenous bretylium was the only effective agent to suppress refractory ventricular tachycardia and ventricular fibrillation. After attempts to switch the patient to amiodarone and bethanidine (an oral analogue of bretylium) caused proarrhythmic effects, he was successfully converted to oral therapy with bretylium. Electrophysiologic testing was not predictive of the clinical response from oral bretylium. To our knowledge, this is the first report of a proarrhythmic effect from bethanadine and it suggests a divergence in the actions of various class 3 antiarrhythmic agents.

Rapid attenuation of response to nifedipine in primary pulmonary hypertension.

In a 22-year-old woman with primary pulmonary hypertension resistant to all previous attempts to reduce the pulmonary vascular resistance, there was dramatic improvement after the first dose of nifedipine, 20 mg po, which was not sustained with subsequent doses. While there was a persistent reduction in systemic vascular resistance, the initial drug-related reduction in pulmonary vascular resistance was progressively attenuated with the subsequent four doses of nifedipine, 20 mg.

Acute myocarditis in fulminant systemic sclerosis.

Myositis and myocarditis have been reported in progressive systemic sclerosis, and these patients have had favorable therapeutic responses to intravenous pulse methylprednisolone. Thus far, premortem biopsy documentation of myocarditis and myocardial fibrosis has not been reported in such patients. We report the case of a patient with subacute congestive heart failure six months after she developed Raynaud's phenomenon. Clinical examination was typical of scleroderma but there was no proximal muscle weakness. She had elevated creatine kinase and MB-creatine kinase and laboratory evidence of hypothyroidism. Echocardiogram demonstrated four-chamber dilatation and severe left ventricular dysfunction. Cardiac catheterization revealed normal epicardial coronary arteries and severely decreased cardiac index. A skin biopsy specimen of the forearm was consistent with diffuse systemic sclerosis, and an endomyocardial biopsy specimen demonstrated mild fibrosis and lymphocytic infiltrate. Her heart failure initially improved with digoxin, furosemide, and enalapril. She also received L-thyroxine and intravenous methylprednisolone. The heart failure progressed over the next six weeks and she died. Patients with scleroderma and new-onset heart failure may have acute myocarditis.

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.