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Proarrhythmia is defined as the aggravation of an existing arrhythmia or the development of a new arrhythmia secondary to antiarrhythmic drug. Proarrhythmic events include drug-induced bradyarrhythmias, atrial and ventricular proarrhythmias. New onset sustained or incessant ventricular tachycardia and torsade de pointes can be life threatening. This article reviews the incidence, aggravating factors, and treatment of proarrhythmia.

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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.

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Amiodarone is an antiarrhythmic agent commonly used in the treatment of supraventricular and ventricular tachyarrhythmias. This article reviews the results and clinical implications of primary and secondary prevention trials in which amiodarone was used in one of the treatment arms. Key post-myocardial infarction primary prevention trials include the European Myocardial Infarct Amiodarone Trial (EMIAT) and the Canadian Amiodarone Myocardial Infarction Trial (CAMIAT), both of which demonstrated that amiodarone reduced arrhythmic but not overall mortality. In congestive heart failure patients, amiodarone was studied as a primary prevention strategy in two pivotal trials: Grupo de Estudio de la Sobrevida en la Insuficiencia Cardiac en Argentina (GESICA) and Amiodarone in Patients With Congestive Heart Failure and Asymptomatic Ventricular Arrhythmia (CHF-STAT). Amiodarone was associated with a neutral overall survival and a trend toward improved survival in nonischemic cardiomyopathy patients in CHF/STAT and improved survival in GESICA. In post-myocardial infarction patients with nonsustained ventricular tachycardia and a depressed ejection fraction, the Multicenter Automatic Defibrillator Implantation Trial (MADIT) demonstrated that implantable cardioverter-defibrillators (ICD) statistically improved survival compared to the antiarrhythmic drug arm, most of whose patients were taking amiodarone. In patients with histories of sustained ventricular tachycardia or ventricular fibrillation, the Cardiac Arrest Study in Seattle: Conventional Versus Amiodarone Drug Evaluation (CASCADE) trial demonstrated that empiric amiodarone lowered arrhythmic recurrence rates compared to other drugs guided by serial Holter or electrophysiologic studies. However, arrhythmic death rates were high in both treatment arms of the study. Several secondary prevention trials, including the Antiarrhythmics Versus Implantable Defibrillators Study (AVID), the Canadian Implantable Defibrillator Study (CIDS), and the Cardiac Arrest Study Hamburg (CASH), have demonstrated the superiority of ICD therapy compared to empiric amiodarone in improving overall survival. Based on the above findings, amiodarone is safe to use in post-myocardial infarction and congestive heart failure patients that need antiarrhythmic therapy. Although amiodarone is effective in treating malignant arrhythmias, high-risk patients should be considered for an ICD as frontline therapy.

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Amiodarone is an antiarrhythmic agent commonly used in the treatment of supraventricular and ventricular tachyarrhythmias. This paper reviews clinical trials in which amiodarone was used in one of the treatment arms. Key post-myocardial infarction trials include EMIAT and CAMIAT, both of which demonstrated that amiodarone reduced arrhythmic but not overall mortality. In patients with congestive heart failure (CHF), amiodarone was associated with a neutral survival in CHF/STAT and improvement in survival in GESICA. In patients with nonsustained ventricular tachycardia, the MADIT trial demonstrated that therapy with an implantable cardioverter-defibrillator (ICD) improved survival compared with the antiarrhythmic drug arm in such patients, most of whom were taking amiodarone. In sustained VT/VF patients, the CASCADE trial demonstrated that empiric amiodarone lowered arrhythmic recurrence rates compared with other drugs guided by serial Holter or electrophysiologic studies. Several trials including AVID, CIDS, and CASH have demonstrated the superiority of ICD therapy compared with empiric amiodarone in improving overall survival. Clinical implications of these trials are discussed.

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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.

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Multiple trials using antiarrhythmic drugs, pharmacologic therapy, and implantable cardioverter defibrillators have been performed in an attempt to improve survival in patients: (1) postmyocardial infarction; (2) with congestive heart failure, with and without nonsustained ventricular tachycardia; and (3) with sustained ventricular tachycardia and those who have survived an out-of-hospital cardiac arrest. This article reviews some of the key findings and limitations of completed and ongoing trials. We also make recommendations for the current treatment of such patients based on the results of these trials.

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Atrial fibrillation is the most common arrhythmia in patients visiting a primary care practice. Although many patients with atrial fibrillation experience relief of symptoms with control of the heart rate, some patients require restoration of sinus rhythm. External direct current (DC) cardioversion is the most effective means of converting atrial fibrillation to sinus rhythm. Pharmacologic cardioversion, although less effective, offers an alternative to DC cardioversion. Several advances have been made in antiarrhythmic medications, including the development of ibutilide, a class III antiarrhythmic drug indicated for acute cardioversion of atrial fibrillation. Other methods of pharmacologic and nonpharmacologic cardioversion remain under development. Until the results of several large-scale randomized clinical trials are available, the decision to choose cardioversion or maintenance of sinus rhythm must be individualized, based on relief of symptoms and reduction of the morbidity and mortality associated with atrial fibrillation.

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Ectopic ventricular foci were simulated at selected endocardial sites in 15 closed-chest canines using ventricular pacing. During this pacing, a noninvasive x-ray backscatter imaging technique was used to measure epicardial LV displacements at 5-ms intervals during the cardiac cycle. These displacement measurements were used to calculate epicardial surface velocities in each study and were presented as a time sequence of color coded velocity maps. Characteristic patterns in the timing and spatial propagation of LV surface velocities were noted for each pacing site, particularly during the expansion of the LV during isovolumic contraction and the inward motion of the LV during ejection. Average surface velocity maps for the 15 canines were computed for each pacing site. These average maps were used as standards for comparison with individual pacing studies to determine the probable site of pacing. Comparisons were made using a computer algorithm, based upon auto- and cross-correlation techniques in the time domain. This algorithm correctly identified pacing sites with sensitivities of RA 74%, LV 76%, RV 79%, and RVOT 77% and specificities of RA 98%, LV 96%, RV 90%, and RVOT 93%. The results show that this noninvasive mapping procedure has potential for identifying the location of an ectopic ventricular focus.

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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.

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Changes in epicardial LV velocity patterns during isovolumic contraction and ejection as induced by ventricular pacing were studied in 15 canines. A noninvasive imaging technique that provided high temporal resolution was used to study the timing of an outward expansion of the LV during isovolumic contraction and the propagation pattern of an inward LV velocity wavefront during ejection. With this technique, surface displacements were measured (+/- 0.1 mm SD) at 50-70 locations on the LV free wall at 5-msec intervals. Velocities were calculated by differentiating the surface displacement waveforms and an interpolation procedure was used to provide detailed color coded velocity maps of the LV surface. LV surface velocities were determined from data obtained during closed-chest endocardial pacing from each of four sites: right atrium, right ventricular apex, left ventricular apex, and right ventricular outflow tract. These surface velocities showed a distinct spatial and temporal pattern for each pacing site. The results show that this noninvasive mapping procedure has potential for determining the location of an ectopic ventricular focus.

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BACKGROUND: Autonomic modulation, especially increased sympathetic activity may play a role in the genesis of ventricular arrhythmias. The purpose of this study was to determine whether beta-sympathetic stimulation with isoproterenol would alter sustained ventricular tachycardia (VT) circuits similarly during the drug-free and antiarrhythmic drug-treated states. METHODS AND RESULTS: Twenty-five patients with repeatedly inducible, hemodynamically stable, sustained VT were evaluated by programmed ventricular stimulation. In the antiarrhythmic drug-free state, isoproterenol (0.03 microgram/kg per minute) shortened the following intervals (in milliseconds; mean +/- SEM; 25 patients; paired t test): sinus cycle length (792 +/- 37 to 568 +/- 18; (p < 0.001), ventricular paced QT interval (386 +/- 8 to 348 +/- 6; p < 0.001), ventricular paced QRS duration (185 +/- 4 to 182 +/- 4; p = 0.014), ventricular effective (238 +/- 5 to 208 +/- 4; p < 0.001) and functional (261 +/- 6 to 227 +/- 5; p < 0.001) refractory periods, and the VT cycle length (VTCL) (311 +/- 9 to 291 +/- 9; p < 0.001). Isoproterenol (0.03 microgram/kg per minute) was administered during 31 antiarrhythmic drug trials (procainamide, n = 18; quinidine, n = 13) in 22 patients. Isoproterenol shortened the sinus cycle length, QT interval during ventricular pacing, and ventricular effective and functional refractory periods before and during procainamide and quinidine therapy (ANOVA; isoproterenol effect, p < or = 0.0002 for all). The amount of decrease in these intervals with isoproterenol was the same before and during procainamide and quinidine therapy (ANOVA interaction, p = NS for all). The QRS duration during ventricular pacing and VTCL were also shortened by isoproterenol before and during procainamide (baseline, n = 17; QRS, 182 +/- 4 to 178 +/- 4 msec; VTCL, n = 18, 314 +/- 11 to 291 +/- 11 msec; during procainamide, QRS, 218 +/- 7 to 197 +/- 6 msec; VTCL, 422 +/- 15 to 359 +/- 11 msec) and quinidine (baseline, n = 13; QRS, 190 +/- 6 to 185 +/- 5 msec; VTCL, n = 12, 298 +/- 10 to 280 +/- 9 msec; during quinidine, QRS, 223 +/- 9 to 208 +/- 8 msec; VTCL, 415 +/- 14 to 355 +/- 10 msec) (isoproterenol effect p < or = 0.0003 for all). However, the amount of decrease in QRS duration and VTCL with isoproterenol was greater during procainamide and quinidine than in the drug-free state (ANOVA interaction, p < or = 0.02 for all). These changes continued to be significant when normalized for the initial QRS duration and VTCL (p < or = 0.03 for all). CONCLUSIONS: Isoproterenol affects presumed reentrant sustained VT circuits less in the absence of antiarrhythmic drugs but markedly attenuates the antiarrhythmic drug-induced slowing of sustained VT. To the extent that the change in QRS duration reflects a change in conduction within the VT circuit, these data imply that the attenuation of drug-induced slowing of VT by isoproterenol is due to a greater change in conduction rather than refractoriness.

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Paroxysmal supraventricular tachycardia (PSVT) can be reproducibly induced and terminated by critically timed atrial or ventricular depolarizations. In this study, noninvasive transcutaneous (external) cardiac pacing (NTCP) was compared to endocardial ventricular pacing for the termination and induction of PSVT. In 24 patients, either atrioventricular (AV) nodal reentrant tachycardia or AV reciprocating tachycardia was reproducibly terminated with either critically timed ventricular depolarizations or overdrive ventricular pacing from an endocardial right ventricular site. There were 32 trials of NTCP attempts to interrupt PSVT in the 24 patients. External pacing was successful at terminating PSVT in 23 patients and in 30 of 32 (94%) trials. In 20 patients, there were 26 trials of external pacing attempts to induce PSVT. External pacing initiated PSVT in 21 of 26 trials (81%). The pacing sequences used to induce and terminate PSVT with external pacing were copied from the endocardial sequences. The external pacing threshold averaged 77 +/- 22 mA but the current needed to terminate PSVT was about 1.5 greater than threshold at 117 +/- 27 mA. Serial external pacing studies were performed in seven patients. The thresholds for external pacing were similar from trial to trial as were the mode of termination and induction between the endocardial and external methods. External pacing can terminate most AV reciprocating tachycardias and many AV nodal reentrant tachycardias. It appears promising as a means of inducing PSVT. However, the high stimulation amplitudes needed will prohibit wide acceptance of external pacing for induction and termination of PSVT.

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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.

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It is nearly 40 years since the first reports of noninvasive external pacing for Stokes-Adams syncope. Despite the ease and safety, this method of pacing has yet to flourish despite a recent interest by several authors. At present, external pacing seems best suited for temporary pacing situations that arise as an emergency or for purely prophylactic indications. External pacing is the preferred method of pacing recommended in the advanced cardiac life support guidelines. However, most emergency room and prehospital cardiac arrest trials have not shown any significant benefit from early application of external pacing. The indications have been broadened to include symptomatic bradycardia and termination of some ventricular tachycardias. It may be useful for the termination of AV reciprocating tachycardia and AV nodal reentrant tachycardia. There is a vision that external pacing may be used for serial electrophysiological testing of antiarrhythmic agents. However, there is little data in this regard. More importantly, the external pacing thresholds must be reduced further to allow for sophisticated pacing protocols to be implemented. For practical purposes, external pacing does not capture the atrium. Since the left atrium is easily captured by esophageal pacing, it is likely that noninvasive external pacing will be combined with transesophageal pacing to perform noninvasive electrophysiological testing. The future for external pacing remains in limbo because of the discomfort associated with skeletal muscle contraction. If technical advances can reduce or eliminate this problem, then external pacing may find broader application for bradycardia and tachycardia.

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The strength-interval relationship obtained by external pacing (EXP) was compared to curves obtained by endocardial pacing from a right ventricular site. There were 17 patients, age 45 +/- 17 years. Effective and functional ventricular refractory periods (ERP, FRP) were determined during a ventricular drive train of 8 stimuli at a cycle length 500 msec. Endocardial pacing threshold current averaged 0.5 +/- 0.3 mA (range 0.2-1.0 mA) and EXP threshold current averaged 64 +/- 14 mA (range 40-80 mA). At twice threshold, endocardial ventricular ERP was 235 +/- 32 msec and FRP was 262 +/- 29 msec. At 10 mA above threshold, EXP ventricular ERP was 276 +/- 29 msec and was significantly longer than endocardial ERP at twice threshold (P less than 0.001). EXP ventricular FRP shortened to 237 +/- 39 msec at twice threshold and was similar to endocardial ERP (P = 0.55). EXP ventricular FRP was significantly longer than endocardial ERP (280 +/- 29 vs 262 +/- 29 msec, P less than 0.001) at twice threshold. EXP strength-interval curves were similar to endocardial curves in 14 of 17 (82%) patients. We conclude, that at twice threshold, similar coupling intervals can be obtained with both endocardial and EXP. Therefore, EXP can provide critically coupled extrastimuli for programmed ventricular stimulation.

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Amiodarone, an antiarrhythmic drug with predominantly class III effects, has demonstrated serious adverse drug reactions and interactions. The Departments of Pharmacy and Cardiology retrospectively evaluated the monitoring parameters at this institution. Criteria based on current literature were developed. Twenty-six patients were administered amiodarone, qualifying for entry into the audit. Of these patients, seven were excluded because their medical records were unavailable or incomplete. The 19 eligible patients were hospitalized during initiation of therapy and followed in the Outpatient Cardiology Clinic. The collected data extracted from the medical charts were compared with the following elements of the criteria selected: baseline evaluation prior to the start of therapy; monitoring for signs of pulmonary, hepatic, thyroid, cardiac, ophthalmologic, neurologic, and dermatologic toxicity; and evaluation of potential drug interactions with digoxin and warfarin-type anticoagulants. The percentage of criteria elements appropriately monitored on each patient ranged from 82 to 100 percent, with an average of 91 percent. The most frequently overlooked parameters were warning the patient of a possible photosensitivity reaction, decreasing the digoxin dose if the patient was concurrently taking amiodarone, and performing a slit-lamp examination every six months. Frequent examination of the patient's total organ system and laboratory tests, in addition to patient education, are essential to safe monitoring of amiodarone therapy.

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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.

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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.

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