Karen Rovang

Efficacy and tolerance of high-dose intravenous amiodarone for recurrent, refractory ventricular tachycardia

High-dose intravenous amiodarone was given to 35 patients with recurrent life-threatening ventricular tachycardia (VT) refractory to conventional antiarrhythmic agents. Intravenous amiodarone was given as a 5 mg/kg dose over 30 minutes followed by 20 to 30 mg/kg/day as a constant infusion for 5 days. Twenty-two (63%) patients responded to intravenous amiodarone. All 22 responders received oral amiodarone. Thirteen (59%) continue to receive oral amiodarone after an average follow-up of 19 months, 4 (18%) had sudden cardiac death on oral amiodarone, 2 (9%) died while receiving amiodarone, secondary to left ventricular failure, and 3 (14%) discontinued amiodarone because of side effects. Of the 13 (37%) nonresponders, 10 died in the hospital while receiving intravenous amiodarone, secondary to lethal arrhythmia. Three nonresponders were discharged from the hospital; 2 with automatic cardioverter/defibrillators and 1 receiving a combination of antiarrhythmic agents. Serious adverse events occurred in 13 (37%) patients during intravenous amiodarone therapy. These included hypotension in 8 patients, symptomatic bradycardia in 4 patients and sinus arrest with bradycardia and hypotension in 1 patient. Minor side effects occurred in 23 (66%) patients. In conclusion, high dose intravenous amiodarone is effective in most patients with recurrent, sustained VT but is associated with an unacceptably high incidence of serious adverse events. The optimal dose and duration of intravenous amiodarone for patients with recurrent, refractory sustained VT remain unknown.

The impact of povidone-iodine pocket irrigation use on pacemaker and defibrillator infections

Background: Infection is a devastating complication of permanent pacemakers (PMs) implantable cardioverter defibrillators (ICDs). Many implanting physicians commonly use povidone‐iodine solution to irrigate the device pocket before implanting the device. We sought to assess if such a measure would alter the rate of infection.

Dressler's syndrome complicating radiofrequency ablation of an accessory atrioventricular pathway.

Radiofrequency energy is being used frequently in catheter ablation of accessory pathways. This case reports a patient who underwent radiofrequency ablation that was complicated by the development of Dresslers syndrome.

Lead-induced accumulation of erythrocyte pyrimidine nucleotides in the rabbit

Abstract Rabbits fed lead acetate, 30 mg/kg/day, had a rapid decrease in erythrocyte pyrimidine 5′ nucleotidase (P5N; EC 3.1.3.5) to 38% of control activity by 30 days at which time mean blood lead (Pb B) was 50.2 μg/dl. At 45 days, when Pb B was 45.7 ± 12.2 μg/dl and P5N was at 33% of control activity, red cell uridine-5′-triphosphate (UTP) and cytidine-5′-triphosphate (CTP) increased from trace levels in the controls to 1.48 ± 1.35 nmol UTP/10 9 red blood cells (RBC) and 1.47 ± 1.35 nmol CTP/10 9 RBC. At 60 days, when Pb B was 69.4 ± 21.9 μg/dl and P5N reduced to 24%, UTP was 2.61 ± 1.99 nmol/10 9 RBC and CTP was 3.38 ± 4.15 nmol/10 9 RBC. The purine nucleotides were unchanged. The increases in UTP and CTP antedated basophilic stippling. There was a significant logarithmic correlation of UTP and CTP with Pb B, P5N, and zinc erythrocyte protoporphyrins (protoporphyrin IX). The lag in accumulation of UTP and CTP, coincident with red cell life span, fits the hypothesis that P5N is effectively functional only during reticulocyte maturation when the pyrimidine nucleotides of degraded RNA are being extruded. Accumulation may be enhanced by lead-induced increases in polysome degradation. HPLC assay of UTP and CTP provides a stable index of cumulative lead exposure during the life span of the circulating erythrocytes.

Transesophageal echocardiography before cardioversion of recurrent atrial fibrillation: Does absence of previous atrial thrombi preclude the need of a repeat test?

BACKGROUND Atrial fibrillation (AF) is a recurrent problem that frequently requires repeat cardioversion. Transesophageal echocardiography (TEE) is indicated before cardioversion in patients who are underanticoagulated (warfarin therapy <3 weeks or international normalized ratio [INR] <2.0). It remains uncertain if TEE should be repeated in underanticoagulated patients who had no atrial thrombi detected by previous TEE. Methods and results From January 1996 to June 2001, 76 patients (43 men, 33 women; mean age, 68.8 +/- 10.4 years) who were underanticoagulated and had no atrial thrombi in previous TEE underwent repeat TEE before cardioversion of recurrent AF. The duration of recurrent AF at the time of the second TEE was 5.1 +/- 9.3 months (1 day to 4 years). The underlying diseases included coronary artery disease (n = 30), hypertension (n = 22), valvular heart diseases (n = 8), dilated cardiomyopathy (n = 4), hypertrophic cardiomyopathy (n = 2), and others (n = 10). Eight (10.5%) patients (2 men, 6 women; mean age, 68.6 +/- 6.6 years) were found to have intra-atrial thrombi on the second TEE. Of these 8 patients, 3 had coronary artery disease, 1 had hypertension, 2 had dilated cardiomyopathy, 1 had hypertrophic cardiomyopathy, and 1 had AF of unknown cause. The duration of recurrent AF in patients with and without thrombi was not significantly different (3.6 +/- 4.7 versus 5.3 +/- 9.7 months, P =.22). Of the 8 patients with intra-atrial thrombi on the second TEE, 5 had been taking warfarin for 3 to 4 weeks but had subtherapeutic INR and 3 were taking aspirin only. Compared with patients without intra-atrial thrombi, patients with intra-atrial thrombi had lower ejection fraction (32.5% +/- 18.1% versus 49.9% +/- 14.1%, P =.015), slower left atrial appendage empty velocity (0.22 +/- 0.08 versus 0.41 +/- 0.17 m/s, P <.01), and higher prevalence of spontaneous echo contrast (87.5%) than in patients without intra-atrial thrombi (19.1%, P <.05) but similar left atrial size (49.5 +/- 5.3 versus 47.3 +/- 7.1 mm, P =.15). Cardioversion was cancelled in all patients with atrial thrombi. CONCLUSIONS In underanticoagulated patients, repeat TEE is necessary before cardioversion of recurrent AF even if the previous TEE showed no atrial thrombi.

Effect of estrogen on exercise electrocardiograms in healthy postmenopausal women

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Efficacy and safety of clonazepam in refractory neurally mediated syncope

Neurally mediated syncope is a complex syndrome that is often difficult to manage using currently available treatment strategies. The efficacy and safety of clonazepam was evaluated in 35 patients with refractory neurally mediated syncope. All patients had syncope (n=33) or disabling presyncope (n=2) and a positive head‐up tilt table test (HUTT) despite treatment with one or more of the following therapies: β‐blocker, high‐salt diet, fludrocortisone, elastic compression stockings, and disopyramide. Clonazepam was initiated at 0.5 mg/day and titrated in 0.25–0.5 mg/day increments for symptom control. Early (first 8 weeks) symptomatic response was achieved in 31 of 35 (89%) patients. Early HUTT reverted to negative in 29 of 35 (83%) patients. Two patients discontinued clonazepam during early follow‐up due to side effects. Thirty‐three patients received long‐term clonazepam therapy. Twenty‐five patients had late HUTT with 21 remaining negative. Of the eight patients who did not have late HUTT, one patient discontinued clonazepam prior to HUTT due to side effects. Seven patients refused late HUTT. All seven patients achieved symptomatic control on clonazepam with two requiring dose titration. Of the 21 patients with a negative late HUTT, 18 achieved symptomatic control with two of these patients requiring dose titration. Two patients who had only partial symptom control despite dose titration achieved total symptomatic control with the addition of disopyramide and β‐blockers. Two patients with a negative late HUTT discontinued clonazepam due to side effects. One patient had been symptomatically controlled while the other had recurrent symptoms with dose limiting side effects occurring after clonazepam dose titration. In the 4 patients with a positive late HUTT, 2 patients were symptomatically controlled, 1 patient required combination therapy with a β‐blocker to achieve symptomatic control, and 1 patient discontinued therapy due to side effects. Overall, 29 of 35 (83%) patients continue to receive clonazepam with symptom control. Based on intention‐to‐treat HUTT results, 21 of 35 (60%) patients were responders. Four patients required clonazepam dose titration and three required combination therapy with clonazepam plus disopyramide and/or a β‐blocker to achieve control. Clonazepam was discontinued in 6 patients. 5 for side effects and 1 following a transient ischemic attack. Clonazepam appears to be an effective therapeutic alternative in patients with refractory neurally mediated syncope. Based on our preliminary findings, a placebo controlled evaluation of clonazepam in neurally mediated syncope is warranted.

Warfarin Therapy Initiated before Is More Beneficial Than after Transesophageal Echocardiography Detected Left Atrial Thrombus

Objective: Warfarin anticoagulation significantly reduces the risk of thromboembolism in patients with atrial fibrillation (AF). However, there are many patients with AF who begin anticoagulation only after left atrial thrombus (LAT) is detected by transesophageal echocardiography (TEE). The impact of anticoagulation in these patients has not been clearly described. The purpose of this study was to investigate the incidence of cerebrovascular accident (CVA) among AF patients who began warfarin before LAT was detected by TEE compared to those who began warfarin only after TEE demonstrated LAT and those did not receive warfarin at any point. Method: Of the 90 consecutive AF patients with LAT (male 48, female 42, age 71.5 ± 10.1 years), 49 began warfarin more than 3 weeks before TEE (Group I); 29 began warfarin after TEE (Group II); and 12 did not receive warfarin at all (Group III). Results: The incidence of CVA in Group I (14%, 7/49, prior CVA 5, new CVA after TEE 2) was significantly lower than Group II (45%, 13/29, prior CVA 10, new CVA after TEE 3, P = 0.006) and III (42%, 5/12, prior CVA 3, new CVA after TEE 2, P = 0.047). Patients with persistent LAT had significantly higher incidence (64% vs 23%, P = 0.024) of CVA and lower CVA free survival than those with resolved LAT. Conclusion: The incidence of CVA among AF patients, who began warfarin before LAT detection, is significantly lower than those who began warfarin after LAT detection as well as those who did not receive warfarin at all.

Nifedipine in the Treatment of Hypertensive Episodes in the Coronary Care Unit

The effectiveness of nifedipine for the treatment of acute hypertensive episodes in patients already taking chronic calcium-channel blocker therapy is unknown. We report our experience with 43 consecutive patients who received nifedipine for acute hypertensive episodes in the coronary care unit. Of the 43 patients (24 men, 19 women), 23 (53 percent) were taking chronic (>2 mo) calcium-channel blocker therapy. Nifedipine 10 mg capsules were chewed and swallowed with repeat doses given at hourly intervals if necessary. Target BP was 140/90 mm Hg, which was achieved in 31 of 43 patients (72 percent). In patients already taking calcium-channel blockers, target BP was achieved in 18 of 23 patients (78 percent). Response in patients not taking chronic calcium-channel blockers was observed in 13 of 20 patients (65 percent). Overall, adverse effects occurred in 16 of 43 patients (37 percent): 11 of 23 patients (48 percent) taking calcium-channel blockers, and 5 of 20 patients (25 percent) not taking calcium-channel blockers. Nifedipine is equally effective in lowering BP in patients taking calcium-channel blockers as it is in patients not taking them. Although associated with a higher incidence of adverse effects in patients already taking calcium-channel blockers, these effects were not considered serious. Nifedipine is an effective agent in acute hypertensive episodes, even in patients receiving chronic calcium-channel blocker therapy.

A Wide QRS Tachycardia Inducible Only by Atrial Pacing and Terminable Only by Ventricular Pacing

A 72-year-old, white female with a history of idiopathic dilated cardiomyopathy (left ventricular ejection fraction 30%) was referred for electrophysiological study because of multiple shocks from an implantable cardioverter defibrillator (ICD). She received the ICD for recurrent wide QRS tachycardia associated with syncope, 4 years ago. Before the ICD implantation, she had no inducible tachycardia during the electrophysiological study. She has been on amiodarone therapy (400 mg/day) for recurrent tachycardia for the past 3 years. She has no history of spontaneous polymorphic ventricular tachycardia (VT) or ventricular fibrillation. The patient’s baseline rhythm was sinus, with complete right bundle branch block and an AH interval of 100 ms and HV interval of 58 ms. During the baseline electrophysiological study, no tachyarrhythmias could be induced by different atrial or ventricular stimulation protocols, including standard extrastimulation, short-longshort coupling,1 and burst pacing. Programmed stimulation was then repeated with isoproterenol infusion at 1 μg/minute. A wide QRS tachycardia was then induced reproducibly but only by atrial pacing at a cycle length of 300 ms (Fig. 1A and 1B). One to one atrioventricular activation ratio was observed at the beginning of the induced tachycardia (Fig. 1A). The induced tachycardia could be terminated only by ventricular burst pacing. During the tachycardia, recording from the right ventricular outflow tract showed local activation time ≥ 25 ms after QRS onset. The earliest ventricular activation was found at a site just inferior to the tip of the His bundle catheter and was simultaneous with QRS onset. Radiofrequency current application to that site terminated the tachycardia in about 2 seconds (Fig. 2). The termination was preceded by ventriculoatrial conduction block. After tachycardia termination and during radiofrequency application, the first sinus beat had QRS morphology of typical right bundle branch block, with AH and