Richard G. Trohman

Role of prophylactic anticoagulation for direct current cardioversion in patients with atrial fibrillation or atrial flutter

The need for prophylactic anticoagulation to prevent embolism before direct current cardioversion is performed for atrial fibrillation or atrial flutter is controversial. To examine this issue further, a retrospective review was undertaken to assess the incidence of embolic complications after cardioversion. The review involved 454 elective direct current cardioversions performed for atrial fibrillation or atrial flutter over a 7 year period. The incidence rate of embolic complications was 1.32% (six patients); the complications ranged from minor visual disturbances to a fatal cerebrovascular event. All six patients had atrial fibrillation, and none had been on anticoagulant therapy (p = 0.026). The duration of atrial fibrillation was less than 1 week in five of the six patients who had embolic complications. Baseline characteristics of patients with a postcardioversion embolic event are compared with those of patients who did not have an embolic event. There was no difference in the prevalence of hypertension, diabetes mellitus or prior stroke between the two groups, and there was no difference in the number of patients who were postoperative or had poor left ventricular function. Left atrial size was similar between the two groups. No patient in the embolic group had valvular disease. No patient with atrial flutter had an embolic event regardless of anticoagulant status; therefore, anticoagulation is not recommended for patients with atrial flutter undergoing cardioversion. Prophylactic anticoagulation is pivotal in patients undergoing elective direct current cardioversion for atrial fibrillation, even those with atrial fibrillation of less than 1 weeks duration.

Interference in Implanted Cardiac Devices, Part I

Sensing intrinsic cardiac electrical activity is essential for the function of pacemakers and implantable cardioverter defibrillators (ICDs). Examples of undesired triggering or inhibition of pacemaker output by extraneous signals were identified early after the introduction of noncompetitive, “ demand” pacemakers. Hermetic shielding in metal cases, filtering, and interference rejection circuits, together with a preference (much more marked in the United States 1 than in Europe 2 ) for bipolar sensing, made contemporary pacemakers and ICDs relatively immune to electromagnetic energy sources in homes and workplaces. Sources of electromagnetic interference (EMI) remained ubiquitous in the medical environment. However, they were predictable and avoidable. New technologies that use more of the electromagnetic spectrum (i.e., wireless telephones, electronic article surveillance [EAS] devices) have rekindled interest in EMI risks for patients with implanted cardiac devices. Although these technologies do not constitute a major public health threat, adverse interactions can occur. The counterpart to EMI is electromagnetic compatibility, a science aimed at avoiding interference potential by adding shielding or redesigning circuits against specific EMI sources. There are three essential elements to any electromagnetic compatibility problem. There must be an electromagnetic source, a receptor or victim (in our case the implanted cardiac device) that cannot function properly due to the electromagnetic phenomenon, and a path between them that allows the source to interfere with the receptor. Each of these three elements must be present, although they may not be readily identified in every situation. Identifying at least two of these elements and eliminating (or attenuating) one of them generally solves electromagnetic compatibility problems. Collaboration among industry, physicians, regulatory agencies, and consumer groups will hopefully achieve full compatibility between implanted devices and other technologies. This will require adoption of international standards establishing the upper limit of permissible field intensities for the whole electromagnetic spectrum. Implanted devices should not react to fields below this limit; more intense fields will be prohibited. This two-part review discusses EMI with implanted cardiac devices. The first part of the review addresses general concepts and specific sources of EMI in everyday life and the workplace. The second part focuses on medical sources of EMI, highlighting preventive measures.

Chronic atrial fibrillation and stroke in paced patients with sick sinus syndrome. Relevance of clinical characteristics and pacing modalities.

BACKGROUND The goal of the report was to study the long-term incidence and the independent predictors for chronic atrial fibrillation and stroke in 507 paced patients with sick sinus syndrome, adjusting for differences in baseline clinical variables with multivariate analysis. METHODS AND RESULTS From 1980 to 1989, we implanted 376 dual-chamber, 19 atrial, and 112 ventricular pacemakers to treat patients with sick sinus syndrome. After a maximum follow-up of 134 months (mean: 59 +/- 38 months for chronic atrial fibrillation, 65 +/- 37 months for stroke), actuarial incidence of chronic atrial fibrillation was 7% at 1 year, 16% at 5 years, and 28% at 10 years. Independent predictors for this event, from Coxs proportional hazards model, were history of paroxysmal atrial fibrillation (P < .001; hazard ratio [HR] = 16.84), use of antiarrhythmic drugs before pacemaker implant (P < .001; HR = 2.25), ventricular pacing mode (P = .003; HR = 1.98), age (P = .005; HR = 1.03), and valvular heart disease (P = .008; HR = 2.05). For patients with preimplant history of paroxysmal atrial fibrillation, independent predictors were prolonged episodes of paroxysmal atrial fibrillation (P < .001; HR = 2.56), long history of paroxysmal atrial fibrillation (P = .004; HR = 2.05), ventricular pacing mode (P = .025; HR = 1.69), use of antiarrhythmic drugs before pacemaker implant (P = .024; HR = 1.71), and age (P = .04; HR = 1.02). Actuarial incidence of stroke was 3% at 1 year, 5% at 5 years, and 13% at 10 years. Independent predictors for stroke were history of cerebrovascular disease (P < .001; HR = 5.22), ventricular pacing mode (P = .008; HR = 2.61), and history of paroxysmal atrial fibrillation (P = .037; HR = 2.81). CONCLUSIONS Development of chronic atrial fibrillation and stroke in paced patients with sick sinus syndrome are strongly determined by clinical variables and secondarily by the pacing modality. Ventricular pacing mode predicts chronic atrial fibrillation in patients with preimplant paroxysmal atrial fibrillation but not in those without it.

Radiofrequency catheter ablation for management of symptomatic ventricular ectopic activity

OBJECTIVES This study assessed the useful role of intracardiac mapping and radiofrequency catheter ablation in eliminating drug-refractory monomorphic ventricular ectopic beats in severely symptomatic patients. BACKGROUND Ventricular ectopic activity is commonly encountered in clinical practice. Usually, it is not associated with life-threatening consequences in the absence of significant structural heart disease. However, frequent ventricular ectopic beats can be extremely symptomatic and even incapacitating in some patients. Currently, reassurance and pharmacologic therapy are the mainstays of treatment. There has been little information on the use of catheter ablation in such patients. METHODS Ten patients with frequent and severely symptomatic monomorphic ventricular ectopic beats were selected from three tertiary care centers. The mean frequency +/- SD of ventricular ectopic activity was 1,065 +/- 631 beats/h (range 280 to 2,094) as documented by baseline 24-h ambulatory electrocardiographic (ECG) monitoring. No other spontaneous arrhythmias were documented. These patients had previously been unable to tolerate or had been unsuccessfully treated with a mean of 5 +/- 3 antiarrhythmic drugs. The site of origin of ventricular ectopic activity was accurately mapped by using earliest endocardial activation time during ectopic activity or pace mapping, or both. RESULTS During electrophysiologic study, no patient had inducible ventricular tachycardia. The ectopic focus was located in the right ventricular outflow tract in nine patients and in the left ventricular posteroseptal region in one patient. Frequent ventricular ectopic beats were successfully eliminated by catheter-delivered radiofrequency energy in all 10 patients. The mean number of radiofrequency applications was 2.6 +/- 1.3 (range 1 to 5). No complications were encountered. During a mean follow-up period of 10 +/- 4 months, no patient had a recurrence of symptomatic ectopic activity, and 24-h ambulatory ECG monitoring showed that the frequency of ventricular ectopic activity was 0 beat/h in seven patients, 1 beat/h in two patients and 2 beats/h in one patient. CONCLUSIONS Radiofrequency catheter ablation can be successfully used to eliminate monomorphic ventricular ectopic activity. It may therefore be a reasonable alternative for the treatment of severely symptomatic, drug-resistant monomorphic ventricular ectopic activity in patients without significant structural heart disease.

Cardiac arrest in an adolescent with atrial fibrillation and hypertrophic cardiomyopathy

A 15 year old youth, who presented with out-of-hospital cardiac arrest due to documented ventricular fibrillation, was found to have nonobstructive hypertrophic cardiomyopathy. Electrophysiologic study demonstrated inducible sustained atrial fibrillation with a rapid ventricular response. This rhythm, associated with hypotension and evidence of myocardial ischemia, spontaneously degenerated into ventricular fibrillation. No ventricular arrhythmias were inducible by programmed ventricular stimulation. Therapy with metoprolol and verapamil slowed the ventricular rate during atrial fibrillation and maintained hemodynamic stability, both during follow-up electrophysiologic study and during a subsequent spontaneous episode.

Cardiac pacing: the state of the art

Permanent cardiac pacing remains the only effective treatment for chronic, symptomatic bradycardia. In recent years, the role of implantable pacing devices has expanded substantially. At the beginning of the 21st century, exciting developments in technology seem to happen at an exponential rate. Major advances have extended the use of pacing beyond the arrhythmia horizon. Such developments include dual-chamber pacers, rate-response algorithms, improved functionality of implantable cardioverter defibrillators, combinations of sensors for optimum physiological response, and advances in lead placement and extraction. Cardiac pacing is poised to help millions of patients worldwide to live better electrically. We review pacing studies of sick-sinus syndrome, neurocardiogenic syncope, hypertrophic obstructive cardiomyopathy, and cardiac resynchronisation therapy, which are common or controversial indications for cardiac pacing. We also look at the benefits and complications of implantation in specific arrhythmias, suitability of different pacing modes, and the role of permanent pacing in the management of patients with heart failure.

Amiodarone prophylaxis reduces major cardiovascular morbidity and length of stay after cardiac surgery: a meta-analysis.

Context Tachyarrhythmias are common after heart surgery and are associated with increased morbidity. Contribution This meta-analysis of 10 randomized, double-blind trials involving 1744 patients undergoing open-heart surgery found that, compared with placebo, amiodarone reduced atrial and ventricular arrhythmias, stroke, and length of hospital stay. Side effects included nausea and bradycardia that was not always deemed clinically important. Cautions Trial participants did not always receive prophylaxis with -blockers. Dosages and timing of amiodarone and length of follow-up varied across studies. Implications Amiodarone may benefit some patients undergoing heart surgery. We now need trials of prophylaxis with both -blockers and amiodarone. The Editors Atrial fibrillation and atrial flutter are common after cardiac surgery. Studies have estimated their incidence to be as high as 40% to 60% after coronary artery bypass grafting or cardiac valve surgery (1, 2). These arrhythmias most often develop between the second and fifth postoperative day (3), with a peak incidence in the first 2 to 3 days (4). Atrial fibrillation and atrial flutter increase the occurrence of postoperative stroke (4), perioperative myocardial infarction, heart failure, and readmission to the intensive care unit (and reintubation) (5); length of stay; and total cost of hospitalization (6, 7). Recent data suggest that atrial fibrillation and atrial flutter are independent risk factors for inpatient and long-term mortality after open-heart surgery (8). Amiodarone has complex pharmacokinetics and pharmacodynamics. Although it is categorized as a VaughnWilliams class III agent, amiodarone combines anti-adrenergic effects (9) with sodium-, calcium-, and potassium-channel blocking properties (10). Striking pharmacologic and therapeutic differences between short-term and long-term administration are not readily accounted for by plasma, tissue, or membrane levels of drug. The most rapid electrophysiologic effects of amiodarone are prolongation of AV nodal refractoriness and conduction time. These effects probably result from calcium-channel blockade and noncompetitive -receptor antagonism. Sinus bradycardia develops more gradually as a function of time while receiving a constant dose (11). Short-term amiodarone administration also blocks sodium channels (making the threshold voltage for activation more positive), thereby reducing automaticity (ectopic triggers) and prolonging conduction velocity (length of the tachycardia cycle) (12-14). Amiodarone may also reduce automaticity by decreasing the recruitment of voltage-dependent inward current (the pacemaker current) during spontaneous depolarization, reducing the slope of phase 4 of the action potential (14). Long-term therapy (weeks to months) results in prolongation of atrial and ventricular effective refractory periods because of potassium blockade (11, 15). Clinical trials of varying size and design have evaluated the efficacy of amiodarone in reducing the incidence of atrial fibrillation and atrial flutter after cardiac surgery (16-22). No prospective studies have intentionally been powered to detect decreases in major cardiovascular morbidity or mortality. Current American College of Cardiology/American Heart Association/European Society of Cardiology guidelines recommend -blocker therapy for all patients (without contraindications) before cardiac surgery and reserve therapy with amiodarone for patients at increased risk for postoperative atrial fibrillation and atrial flutter (those with a history of atrial fibrillation, left atrial enlargement, or valvular heart disease) (23). We performed a meta-analysis to compare the effect of treatment with amiodarone or placebo on the incidence of atrial fibrillation and atrial flutter, the incidence of major cardiovascular morbidity (ventricular tachycardia or fibrillation, stroke, or myocardial infarction), length of stay, and death. Subgroup analyses were done to compare patients who began amiodarone prophylaxis up to 13 days before surgery with those who received amiodarone intraoperatively or immediately postoperatively, and patients who received oral amiodarone with those who received intravenous amiodarone. Methods Literature Search We conducted this review in accordance with recommendations put forth by the QUOROM Group (24). We searched the English-language and nonEnglish-language literature by using MEDLINE, EMBASE, and CINAHL databases and the Cochrane Central Register of Controlled Trials from the earliest searchable dates through February 2005. Search terms were atrial fibrillation, amiodarone, and surgery. We also searched the bibliographies of published reviews but excluded unpublished data. Data Collection Inclusion criteria for the meta-analysis were established before the literature search. Studies had a randomized, controlled, double-blind design to compare amiodarone with placebo; included patients who underwent coronary artery bypass grafting or cardiac valve surgery (or both); measured the occurrence of atrial fibrillation, atrial flutter, or supraventricular tachycardia as a primary outcome; and clearly described drug administration, comorbid conditions, the risk profile of study cohorts, study design, and methods. One author screened titles and abstracts before manuscript retrieval. Three authors read all retrieved manuscripts and made the final decision on which studies met the inclusion criteria. All data were abstracted independently and in duplicate by 2 of the authors by using a standardized data collection form. Discrepancies in the data abstracted were resolved by consensus among all authors. We assessed reported randomization methods and completeness of follow-up but avoided use of a formal or aggregated score for quality assessment because such use can produce inconsistent results (25). Statistical Analysis Incidences of atrial fibrillation, atrial flutter, stroke, ventricular tachycardia or fibrillation, myocardial infarction, and death were treated as dichotomous variables. Summary effects for the dichotomous variables were calculated as relative risks. Length of stay was treated as a continuous variable. The summary effect for data on length of stay was calculated as the weighted mean difference. Data on length of stay were included in calculating the summary effect only if both the mean and standard deviation were specified. We pooled data by using the DerSimonianLaird random-effects model (26). Statistical heterogeneity for all variables was assessed by using the I2 measure because this measure is independent of the number of studies that are pooled and of the effect-size metric (27). To assess for possible publication bias, we used the test proposed by Egger and colleagues (28), which provides an assessment of funnel-plot asymmetry (expressed as a P value) by applying an inverse-variance weighted approach. For each variable, studies were assigned a MantelHaenszel weight that was directly proportional to the sample size and inversely proportional to the variance of each study. For subgroup analysis, studies were organized into 2 categories according to when amiodarone or placebo was initially administered. Studies were categorized as preoperative if administration of amiodarone or placebo began before surgery or perioperative if drug or placebo was administered during or immediately after surgery. To compare the efficacy of oral versus intravenous administration of amiodarone, we excluded trials in which both routes were used. Publication bias was assessed by using StatsDirect software, version 2.3.1 (StatsDirect Ltd., Sale, United Kingdom). All other statistical calculations were performed by using Review Manager (RevMan) statistical software, version 4.2.7 for Windows (The Cochrane Collaboration, Oxford, United Kingdom). Continuous data are expressed as the mean and standard deviation, unless otherwise specified. A 2-sided P value less than 0.05 was considered significant. Role of the Funding Source We received no intramural or extramural funding for this study. Results Figure 1 shows the trial selection process. Searches identified 1989 potentially relevant citations. Of these, we considered and retrieved 17 citations for possible inclusion in the meta-analysis (16-22, 29-38). We excluded 4 studies because they were not double-blind (16-18, 22), 1 because it compared amiodarone with propranolol rather than placebo (19), 1 because the characteristics of the participants and details of the study methods were not provided (20), and 1 because the amiodarone regimen (a single oral dose of 1.2 g) differed markedly from those used in other studies (21). Figure 1. Flow diagram of study selection. Table 1 provides information on the patients and design of the included studies. One thousand seven hundred forty-four patients were included. In 4 studies, amiodarone or placebo was administered before surgery. In 6 studies, therapy was given during or immediately after surgery. Five studies included patients who underwent coronary artery bypass grafting only, and 5 included patients who had coronary artery bypass grafting or valve surgery. All patients received at least 2 g of amiodarone by the second postoperative day. Amiodarone was administered orally in 5 studies, intravenously in 2 studies, and both orally and intravenously in 3 studies. Eight studies reported ventricular tachycardia and fibrillation, 8 reported stroke, and 4 reported myocardial infarction. Follow-up data were limited to inpatient stay for all studies except that by Giri and associates (34), which included information on death at 30 days. No study included in our analysis gave data on adequacy of patient follow-up (dropout rate). Table 1. Randomized, Controlled Trials Included in the Meta-Analysis Table 2 shows medical and surgical data for the included patients. The mean patient age was 64.4 years, and the mean left ventricular ejection fraction was 0.49

Clinical performance of the implantable cardioverter defibrillator: electrocardiographic documentation of 101 spontaneous discharges.

Records of 105 patients, who received an automatic implantable Cardioverter defibrillator (AICD), were studied to investigate the causes of spontaneous AJCD discharges and to correlate the symptoms with the arrhythmias triggering AJCD discharges. During a follow‐up period of 13 ± 8 months, 46/105 (44%) patients had 566 spontaneous AICD discharges. A total of 101 discharges were documented with Holter monitoring in 23 patients. In this study group, there were 8 (8%) AICD discharges for 5 episodes of ventricular fibrillation, and 68 (67%) discharges for 63 episodes of sustained ventricular tachycardia. Patients lost consciousness in all episodes of ventricular fibrillation, but were symptomatic prior to only 36 (53%) discharges in ventricular tachycardia. Non‐sustained ventricular tachycardia persisting for a period of 7,5 ± 2 seconds resulted in 20 AICD discharges; patients were symptomatic prior to 13 (65%) discharges. Supraventricular tachycardias triggered three discharges. One patient had two spurious discharges during sinus rhythm. In conclusion, most of the spontaneous AICD discharges were appropriate for the detected rhythms, but only clinically appropriate for the management of arrhythmias in 75% of the cases. A significant portion of the patients with sustained or nonsustained ventricular tachycardias triggering AICD discharges were asymptomatic prior to discharge, which requires further assessment of the physiology of the arrhythmia as a component of the detection algorithm.

Narrative review: Electrocution and life-threatening electrical injuries.

Patients who experience electrical shock, including being struck by lightning, sustain a wide spectrum of injuries with unique pathophysiologic characteristics that require special management. We review the physics and mechanisms of tissue damage, typically encountered injuries, and the prognosis of patients with severe injuries. Epidemiology It is estimated that approximately 1000 people die of exposure to electricity annually in the United States (1, 2). The age distribution of patients who are electrocuted is bimodal; the first peak occurring in children younger than 6 years of age, and the second occurs in persons in young adulthood (3, 4). Electrocution in children usually occurs at home. Most deaths in adults due to electrocution are work related, and electrocution is a frequent cause of occupation-related death. Miners and construction workers account for most of these cases, with rates of 1.8 to 2.0 deaths per 100000 workers (5). Patients surviving electrical shock represent 3% of approximately 100000 patients admitted to specialized burn units annually (6). Physics Electricity is defined as the flow of electrons across a potential gradient from high to low concentration. This potential difference, expressed in voltage (V), represents the force driving the electrons. The amount or volume of electrons that flow along this gradient is called current and is measured in amperes (I). The impedance to flow is described as resistance (R). Ohms law expresses the relationship among these factors as I = V/R (Figure 1). Using this equation, it is easy to see that current is directly proportional to voltage and inversely proportional to resistance. In alternating current, the direction of electron flow changes rapidly in a cyclic fashion, for example, standard household current of 110 V flows at 60 cycles per second (60 Hertz [Hz]). Direct current, on the other hand, flows constantly in 1 direction across the potential. Examples of entities that produce or carry direct current include batteries, automobile electrical systems, high-tension power lines, and lightning. Figure 1. Ohms and Joules laws. The primary determinant of damage caused by direct effects of electricity is the amount of current flowing through the body, which can potentially lead to fatal arrhythmias or apnea. Additional factors that determine damage include voltage, resistance, type of current, current pathway, and duration of contact with an electrical source (7). Joules law describes the relationship of 3 of the aforementioned factors, with thermal energy generated as follows: Energy (thermal) = I2RT, with T representing the time of current flow. This equation demonstrates the relationship of the squared function of current and time and resistance to the amount of thermal energy delivered, which leads to tissue damage. Tissues that have a higher resistance to electricity, such as skin, bone, and fat, tend to increase in temperature and coagulate. Nerves and blood vessels that have low resistance to electricity (I = V/R) conduct electricity readily. The skin has a wide range of resistance to electricity and plays the crucial role of gatekeeper when the body is exposed to electricity. Dry skin, which has a higher resistance to electricity than moist skin, may have extensive superficial tissue damage but may limit conduction of potentially harmful current to deeper structures (8). Moist skin receives less superficial thermal injury but allows more current to pass to deeper structures, resulting in more extensive injury to internal organs. Mechanism of Injury Electrical shocks of 1000 V or more are classified as high voltage (9). Thus, low-voltage electrical shocks are less than 1000 V. Although this classification appears to be somewhat arbitrary, voltage is often the only variable known with certainty after exposure to electricity and therefore is the most reasonable marker for categorizing electrical shocks. High-voltage electrical shocks are expected to result in more severe injury per time of exposure. Typical household electricity has 110 to 230 V, and high-tension power lines have voltages of more than 100000 V. Lightning strikes are can produce 10 million V or more (8). There are 4 causes of electrocution: 1) direct effect of current on body tissues, leading to asystole, ventricular fibrillation, or apnea; 2) blunt mechanical injury from lightning strikes, resulting in muscle contraction or falling; 3) conversion of electrical energy to thermal energy, resulting in burns; and 4) electroporation, defined as the creation of pores in cell membranes by means of electrical current (10). Unlike thermal burns, which cause tissue damage by protein denaturation and coagulation, electroporation disrupts cell membranes and leads to cell death without clinically significant heating. This form of injury occurs when high electrical field strengths (defined as volts per meter) are applied (11). Direct current causes a single muscle contraction, often throwing the person receiving the electrical shock away from the source of electricity. Alternating current is considered more dangerous than direct current because it can lead to repetitive, tetanic muscle contraction. In the case of contact between the palm and an electrical source, alternating current can cause a hand to grip the source of electricity (because of a stronger flexor than extensor tone) and lead to longer electrical exposure. The amount of alternating current needed to cause injury varies with the frequency of the current. Skeletal muscles become tetanic at lower frequencies, ranging from 15 to 150 Hz (8, 12). Household electricity (60 Hz) is particularly arrhythmogenic and may lead to fatal ventricular arrhythmias. Alternating current is the most frequent cause of electrocution. Typical Injuries Skin Burn injuries are categorized into 4 groups: electrothermal burns, arc burns, flame burns, and lightning injuries. We discuss the last in greater detail in the section titled Special Circumstances. Electrothermal burns are the classic injury pattern and create a skin entrance and exit wound. Regardless of the mechanism involved, wounds due to exposure to electricity can be classified as partial-thickness, full-thickness, or skin burns involving deeper subcutaneous tissue. High-voltage injuries commonly produce greater damage to deeper tissues, largely sparing the skin surface. Thus, using estimation of surface burns to guide therapy may lead to critical errors because minor superficial injury may be associated with massive coagulation necrosis of deeper tissue (13, 14). Respiratory Respiratory arrest immediately following electrical shock may result from inhibition of the central nervous system respiratory drive, prolonged paralysis of respiratory muscles, tetanic contraction of respiratory muscles, or a combined cardiorespiratory arrest secondary to ventricular fibrillation or asystole. In the last case, respiratory arrest may persist after restoration of spontaneous circulation, presumably because of the inherent automaticity of cardiomyocytes, which cause quicker recovery of cardiac function. If respiratory arrest is not corrected promptly by ventilation, secondary hypoxic ventricular fibrillation may occur (15). Parenchymal lung damage is rarely seen in patients who have experienced electrocution or received an electrical injury. Cardiovascular Cardiac effects of electrical shock can be divided into arrhythmias, conduction abnormalities, and myocardial damage. The last category can be further separated into injury due to direct electricity exposure and secondary myocardial injury due to induced ischemia. These effects are not mutually exclusive. Arrhythmias Sudden cardiac death due to ventricular fibrillation is more common with low-voltage alternating current, whereas asystole is more frequent with electric shocks from direct current or high-voltage alternating current (16, 17). Experimental studies show alternating current to be more hazardous than direct current applied at the same voltage. In a dog model, ventricular fibrillation occurred 9 times more often with alternating current than with direct current shocks. Of interest, at voltages ranging between 50 to 500 V, the incidence of ventricular fibrillation was inversely proportional to voltage and the occurrence of ventricular tachycardia and atrial fibrillation were directly proportional to voltage (16). Potentially fatal arrhythmias are more likely to be caused by horizontal current flow (hand to hand); current passing in a vertical fashion (from head to foot) more commonly causes myocardial tissue damage (1820). Survivors of electrical shock frequently experience some form of subsequent arrhythmia (10% to 46%) (17, 21, 22). The most common arrhythmias are sinus tachycardia and premature ventricular contractions, but ventricular tachycardia and atrial fibrillation have been reported (17, 2123). Most arrhythmias occur soon after the electrical shock, but delayed ventricular arrhythmias (noted up to 12 hours following an incident) may occur (24). Most patients not experiencing sudden cardiac death have nonspecific STT-wave abnormalities on 12-lead electrocardiography (ECG) that usually resolve spontaneously (25, 26). Patients without ECG changes on presentation are unlikely to experience life-threatening arrhythmias (22). Conduction Abnormalities Sinus bradycardia and high-degree atrioventricular block have been reported following electrical shocks. Electrical injury caused by alternating current seems to have a predilection for the sinoatrial and atrioventricular nodes (27). The reason for this vulnerability is unclear. It has been hypothesized that the sinoatrial- and atrioventricular-node ion channels are the easiest to disrupt and that ischemia and infarction in the right coronary artery distribution (running closest to the chest surface and supplying both nodes) make the nodes more vulnerable to electrical current. Some of th

Is hospital admission for initiation of antiarrhythmic therapy with sotalol for atrial arrhythmias required?: yield of in-hospital monitoring and prediction of risk for significant arrhythmia complications

OBJECTIVES We sought to determine the yield of in-hospital monitoring for detection of significant arrhythmia complications in patients starting sotalol therapy for atrial arrhythmias and to identify factors that might predict safe outpatient initiation. BACKGROUND The need for hospital admission during initiation of antiarrhythmic therapy has been questioned, particularly for sotalol, with which proarrhythmia may be dose related. METHODS The records of 120 patients admitted to the hospital for initiation of sotalol therapy were retrospectively reviewed to determine the incidence of significant arrhythmia complications, defined as new or increased ventricular arrhythmias, significant bradycardia or excessive corrected QT (QTc) interval prolongation. RESULTS Twenty-five patients (20.8%) experienced 35 complications, triggering therapy changes during the hospital period in 21 (17.5%). New or increased ventricular arrhythmias developed in 7 patients (5.8%) (torsade de pointes in 2), significant bradycardia in 20 (16.7%) (rate <40 beats/min in 13, pause >3.0 s in 4, third-degree atrioventricular block in 1, permanent pacemaker implantation in 3) and excessively prolonged QTc intervals in 8 (6.7%) (dosage reduced or discontinued in 6). Time to the earliest detection of complications was 2.1 +/- 2.5 (mean +/- SD) days after initiation of sotalol, with 22 of 25 patients meeting criteria for complications within 3 days of monitoring. Baseline electrocardiographic intervals or absence of heart disease failed to distinguish a low risk group. Multivariate analysis identified absence of a pacemaker as the only significant predictor of arrhythmia complications (p = 0.022). CONCLUSIONS Because clinically significant complications can be detected with in-hospital monitoring in one of five patients starting sotalol therapy, hospital admission is warranted for initiation of sotalol. Patients without pacemakers are at higher risk for these complications.