Treatment of underlying atrial fibrillation: paced rhythm obscures recognition.

OBJECTIVES: The purpose of this study was to evaluate the rate of recognition of atrial fibrillation (AF), use of warfarin and prevalence of cerebrovascular accident (CVA) in paced versus unpaced patients during admission to a tertiary care teaching hospital. BACKGROUND: The presence of AF underlying a continuously paced rhythm may be under recognized and result in a lower rate of anticoagulation and higher incidence of CVA. METHODS: The identification of AF on 12 lead electrocardiogram (ECG) and telemetry, "optimal use" of anticoagulants that is, warfarin or aspirin, when warfarin is contraindicated and history of prior CVA was studied in three groups: 1) group A with continuously paced rhythm on ECG and telemetry (n = 30), 2) group B with intermittently paced rhythm on ECG and telemetry (n = 59), and 3) group C with persistent AF and no permanent pacemaker (n = 50). RESULTS: The identification and documentation of AF was significantly lower in the continuously paced group A (20%) versus the intermittently paced group B (44%). Both groups A and B were substantially lower than unpaced controls. "Optimal use" of anticoagulants was significantly lower in group A (40%) compared with groups B (78%) and C (72%) but was not different between groups B and C. The prevalence of prior CVA was not significantly different between the three groups. CONCLUSIONS: All ECGs in patients with paced rhythm should be examined closely for underlying AF to prevent under-recognition and under-treatment with anticoagulants.

Recurrent ventricular fibrillation in a marathon runner during exercise testing.

We report a case of a marathon runner who presented with chest tightness, ST-segment depression, and ventricular fibrillation following treadmill exercise testing. At cardiac catheterization, the patient was found to have an isolated lesion in the left anterior descending (LAD) artery that was hemodynamically insignificant by accepted angiographic and coronary flow reserve standards. Ventricular fibrillation was thought to be idiopathic, and an implantable cardioverter defibrillator was placed. Chest pain and ST-segment depression followed by ventricular fibrillation was reproduced during follow-up treadmill testing, prompting reconsideration of the original diagnostic hypothesis. A coronary stent was deployed in the LAD artery. The patient has been asymptomatic and arrhythmia free during follow-up treadmill testing and recreational running.

Acute complications of permanent pacemaker implantation: their financial implication and relation to volume and operator experience.

Complication rates after pacemaker implantation decline after increasing operator experiences (total cases), activity (cases per year), and facility with cephalic vein cutdown technique. The incremental cost of care is driven by hospital resource utilization and does not parallel medical severity.

Prophylactic oral amiodarone compared with placebo for prevention of atrial fibrillation after coronary artery bypass surgery.

BACKGROUND: Postoperative atrial fibrillation occurs in 20% to 40% of patients undergoing coronary artery bypass grafting (CABG) and contributes to delayed recovery, increased length of stay, and increased hospital cost. Measures at preventing postoperative atrial fibrillation have had mixed results. We report a double-blind trial comparing oral amiodarone with placebo for the prevention of atrial fibrillation after CABG. METHODS AND RESULTS: All patients undergoing CABG were considered eligible. Exclusion criteria included bradycardia (<50 beats/min), prior Atrial fibrillation, concurrent therapy with antiarrhythmic drugs, or concomitant valve surgery. Patients were given 2 g of amiodarone (73 patients) or placebo (70 patients) in divided doses 1 to 4 days before surgery and 400 mg daily for 7 days postoperatively. Atrial fibrillation occurred in 24.7% (18 of 43) of patients receiving amiodarone and 32. 8% (23 of 70) of patients receiving placebo (P =.30). Heart rate at onset of atrial fibrillation was 133.4 +/- 26.6 beats/min for amiodarone compared with 152.9 +/- 31.6 beats/min for placebo (P =. 04). Duration of atrial fibrillation was 10.2 +/- 8.1 hours for amiodarone compared with 16.2 +/- 27.5 hours for placebo (P =.67). Patients receiving both beta-blockade and amiodarone had a 16.7% incidence of atrial fibrillation compared with 31.9% in the remaining patients (P =.10). Atrial fibrillation was associated with an increased cost of $7011 compared with those who remained in sinus rhythm ($23,869 +/- $20,894 vs $16,857 +/- $5401 in sinus rhythm). Hospital cost of those taking amiodarone was $18,895 +/- $13,267 compared with $18,839 +/- $11,537.18 for placebo (P =.42). CONCLUSION: Postoperative CABG atrial fibrillation is associated with prolonged hospital stay and increased cost. Prophylactic oral amiodarone did not statistically alter the incidence or duration of atrial fibrillation after CABG, although favorable trends were noted. Hospital cost was not affected by therapy with amiodarone.

The value of the clinical history in the differentiation of syncope due to ventricular tachycardia, atrioventricular block, and neurocardiogenic syncope.

BACKGROUND: The present study was undertaken to identify and quantitate the symptoms associated with neurocardiogenic syncope, syncope due to ventricular tachycardia, and syncope resulting from atrioventricular block. PATIENTS AND METHODS: Eighty patients referred for evaluation of syncope in whom a diagnosis of neurocardiogenic syncope, atrioventricular block, or ventricular tachycardia was established were studied. Each patient was interviewed using a standard questionnaire. The clinical histories were then compared to identify which variables best differentiated the cause of syncope. RESULTS: The clinical histories of patients with syncope due to ventricular tachycardia and atrioventricular block were similar. Only age, the duration of prodromal symptoms, diaphoresis prior to syncope, and fatigue following syncope differed. In contrast, the clinical history in patients with neurocardiogenic syncope differed greatly from that obtained in patients with syncope due to atrioventricular block or ventricular tachycardia. Features of the clinical history that were predictive of syncope due to atrioventricular block or ventricular tachycardia were male sex, age > 54 years, < or = 2 episodes of syncope, and a duration of warning of < or = 5 seconds. Features of the clinical history predictive of syncope not due to ventricular tachycardia or atrioventricular block were palpitations, blurred vision, nausea, warmth, diaphoresis, or lightheadedness prior to syncope, and nausea, warmth, diaphoresis, or fatigue following syncope. CONCLUSIONS: The results of this study identify and compare the features of the clinical history obtained in patients with syncope due to ventricular tachycardia, atrioventricular block, and neurocardiogenic syncope and demonstrate that the clinical history is of value in distinguishing patients with these three causes of syncope.

Noncardiogenic pulmonary edema complicating massive verapamil overdose.

Noncardiogenic pulmonary edema has not been (to our knowledge) previously reported associated with a verapamil overdose. We describe a 27-year-old woman who developed this complication after an overdose of 15, 120-mg verapamil tablets (total of 1,800 mg). This report illustrates the possibility of serious pulmonary embarrassment in the course of a verapamil overdose and the need to avoid excessive crystalloid administration during the hypotensive period.

The effectiveness and safety of the simultaneous administration of quinidine and amiodarone in the conversion of chronic atrial fibrillation.

The effectiveness and safety of quinidine in the conversion of chronic atrial fibrillation after administration of amiodarone was assessed in 15 patients. A total quinidine dosage of 1097 +/- 408 mg was administered up the point of conversion or for a total of 48 hours. Nine of 15 patients (60%) converted to sinus rhythm. No clinical variable such as the duration of atrial fibrillation, left atrial size, left ventricular fractional shortening, amiodarone duration, or maintenance dose of amiodarone was able to discriminate between converters and nonconverters when patients were treated with the combination of amiodarone and quinidine. The mean QT interval with amiodarone was 414 +/- 44 msec and slightly increased to 434 +/- 40 msec (p = 0.01) when quinidine was added. The amiodarone-quinidine combination was well tolerated, and no side effects or proarrhythmias were recorded.

ICD implantation via thoracoscopy without the need for sternotomy or thoracotomy.

After development of the technique in mongrel dogs, implantable cardioverter defibrillator (ICD) patch and sensing lead implantation was attempted via thoracoscopy, without sternotomy or thoracotomy, in three patients. Two large titanium mesh defibrillator patches and two "screw-in" epicardial sensing leads were applied without difficulty in each of two patients. In a third patient, satisfactory placement of the defibrillator patches could not be achieved via thoracoscopy, necessitating thoracotomy. Defibrillation threshold (DFT), cardioversion energy requirement (CER), and rate and morphology signals in those patients with successful thoracoscopic implantation were comparable to those achieved by open technique. We conclude that ICD patch and sensing lead implantation via thoracoscopy is feasible.

Prolonged asystole during head-up tilt table testing after beta blockade.

Neurally mediated vasodepressor syncope is a common clinical problem. The diagnosis is generally associated with a benign prognosis, however, a less common "malignant" form has been identified. Head-up tilt table testing is helpful in the confirmation of the diagnosis of neurally mediated vasodepressor syncope and may be useful in the selection of therapy. One form of therapy commonly used is beta blockade. In this case report we describe a patient with neurally mediated vasodepressor syncope who developed asystole during head-up tilt table testing after treatment with a beta blocker.

Mexiletine. Long-term efficacy and side effects in patients with chronic drug-resistant potentially lethal ventricular arrhythmias.

The antiarrhythmic efficacy of mexiletine hydrochloride (Mexitil) was evaluated in 100 patients with potentially lethal and drug-resistant ventricular arrhythmia. The efficacy of arrhythmia suppression was assessed by Holter monitoring. The overall arrhythmia suppression of ventricular premature contractions of 70% and greater was low and seen in only 22% of patients, with an additional 16% responding to a combination of mexiletine and an additional antiarrhythmic drug. The suppression of high-grade forms, couplets of 90% and greater, and complete abolition of nonsustained runs of ventricular tachycardia was achieved in 22% of patients, with 9% responding to the addition of another antiarrhythmic agent. Ventricular premature contractions, couplets, and nonsustained ventricular tachycardia were suppressed in only 16% of the cohort. The drug was poorly tolerated, with intolerable side effects developing in 49% of patients receiving mexiletine alone and in 57% of patients receiving a combination of antiarrhythmic agents. Tolerable adverse effects were relatively common but transient and dose related.

Classification of antiarrhythmic drugs.

Although many classification schemes for antiarrhythmic drugs have been proposed, the system introduced by Vaughan Williams and later modified by Harrison has been widely accepted. This classification system is comprised of four categories. Class I agents block sodium channels. Class II agents are Beta blockers. Class III agents prolong the cardiac action potential. Class IV agents are calcium channel blockers. This classification scheme, based largely on clinical observation continues to be useful almost two decades after its introduction. The electrophysiologic bases, strengths and weaknesses of this system are discussed.

Long-term efficacy and toxicity of high- and low-dose amiodarone regimens.

Amiodarone is an effective antiarrhythmic drug for the control of potentially lethal and lethal ventricular arrhythmias (VA). In the United States, a high-dose regimen has been used at the expense of a high toxicity profile for the control of lethal VAs. Significant antiarrhythmic efficacy has also been established with low-dose regimens, which carry a low rate of intolerable side effects (5.4%) when compared with the high-dose regimen (16.7%). The high incidence of tolerable and intolerable adverse side effects is probably related to high amiodarone loading (31.92 g) and maintenance doses (520 mg/d). In contrast, the low-dose regimen uses much lower loading (7.2 g) and maintenance (280 mg/d) doses.

Potentially lethal ventricular arrhythmias: from mundane to esoteric.

Patients with potentially lethal ventricular arrhythmias (VAs) represent a heterogenous group with frequent and high grade ventricular arrhythmias (including couplets and runs of nonsustained ventricular tachycardia), structural heart disease and decreased left ventricular function. This is a group at intermediate risk of sudden death, with risks varying from 10% to 38%. The electrical and mechanical risks of patients with potentially lethal VA is discussed in relation to their ability of promoting sudden death. The studies reviewing the impact of antiarrhythmic treatment on survival of patients with potentially lethal VA is discussed.

Long-term efficacy, safety and survival of patients with potentially lethal ventricular arrhythmias treated with low-dose amiodarone.

The effect of low-dose amiodarone was prospectively evaluated in 110 patients with potentially lethal ventricular arrhythmias and structural heart disease. The patient population had frequent and high-grade ventricular premature complexes (VPCs) (greater than or equal to 39/h) (multifocal, couplets, nonsustained ventricular tachycardia) refractory to conventional antiarrhythmic drugs. All patients had structural heart disease (coronary artery disease in 61%) and also a decreased left ventricular ejection fraction (LVEF) (43 +/- 16%). Patients were treated with low-dose amiodarone (maintenance dose of 275 +/- 102 mg/day.) During follow-up over a period of 15 +/- 11.5 months, 24 patients died of cardiac cause and, of these, 13 died of sudden death. Ventricular arrhythmia suppression at 1, 2, 3, and 4 years was 69%, 80%, 78%, 92% for VPCs, respectively; 96%, 90%, 92%, and 98% for couplets, respectively, and 57%, 57%, 97%, and 91% for nonsustained VTs (NVTs), respectively. Intolerable, reversible side effects requiring withdrawal were encountered in 24 patients (22%) (neurologic 10%, gastrointestinal 6.5%, skin 3.7%, proarrhythmic 0.9%, and cardiac 0.9%). Except for keratopathy (less than or equal to grade II) seen in all patients, the tolerable side effects were transient with dose adjustment. The study population was divided into two groups according to LVEF: Group A (LVEF greater than or equal to 40%, mean 54.4 +/- 9.7) and Group B (LVEF less than 40% mean, 27.7 +/- 7.2). The patients were further classified into responders (suppression of at least 70% of VPCs, 90% of couplets, and 100% of NVTs) and nonresponders. The difference in survival between responders and nonresponders in groups A and B was not statistically significant. Cumulative survival at 1, 2, 3, and 4 years was 90%, 85%, 85%, and 85%, respectively. In conclusion, low-dose amiodarone treatment: 1) Is effective in controlling VPCs and its complex forms and maintains long-term arrhythmia suppression. 2) The side effect profile compares favorably with conventional antiarrhythmics; severe side effects associated with high dosages (pulmonary, hepatic, neurologic, etc.) were rare or absent. 3) Amiodarone improves survival of patients with potentially lethal ventricular arrhythmias.

The efficacy, electrophysiologic and electrocardiographic effects of intravenous pirmenol, a new class I antiarrhythmic agent, in patients with ventricular tachycardia: comparison with procainamide.

UNLABELLED: The electrophysiologic and electrocardiographic effects of intravenous pirmenol were compared with intravenous procainamide in 17 patients with symptomatic ventricular tachycardia. Pirmenol was found to prolong the PR interval, the QRS duration, the QTc interval, the HV interval, the atrial effective refractory period, and the ventricular effective refractory period. The sinus cycle length decreased following pirmenol administration. The sinus node recovery time, the PA interval, the AH interval, the Wenckebach cycle length, and the AV nodal ERP were unchanged. In patients whose ventricular tachycardias remained inducible on pirmenol, the cycle length was significantly prolonged compared to baseline. These changes were similar to those seen following the administration of procainamide. All 17 patients had sustained ventricular tachycardia inducible during programmed ventricular stimulation in the baseline state. In four patients the ventricular tachycardia was suppressed with both primenol and procainamide. In the remaining 13 patients ventricular tachycardia remained inducible on procainamide. Of these 13 patients, an additional two patients had their ventricular tachycardias rendered noninducible on pirmenol. IN CONCLUSION: (1) the electrophysiologic and electrocardiographic effects of pirmenol are similar to those of procainamide; (2) although ventricular tachycardia inducibility following procainamide was similar to that of pirmenol, an occasional patient with ventricular tachycardia inducible on procainamide had ventricular tachycardias suppressed on pirmenol.

Amiodarone in the management of refractory atrial fibrillation.

Thirty-eight patients were studied to evaluate amiodarone hydrochloride in the treatment of refractory atrial fibrillation. Among them were 25 with sustained atrial fibrillation and 13 with paroxysmal atrial fibrillation. All patients were symptomatic and refractory to therapeutic doses of at least two conventional drug trials, and patients with atrial fibrillation had relapsed from electroversion. Amiodarone hydrochloride was administered in doses of 5 mg/kg intravenously, then 600 to 800 mg/d for seven to ten days, followed by 200 to 400 mg/d. Holter recordings were obtained every one to three months. The effect of amiodarone on the ventricular rate during sustained atrial fibrillation was evaluated in 18 patients and decreased from 99/min (range, 72/min to 143/min) at baseline to 75/min (range, 60/min to 102/min) at follow-up before conversion. Conversion to normal sinus rhythm occurred in 19 patients (76%), including 11 with and eight without direct-current cardioversion. During long-term treatment, sinus rhythm was sustained on an average of 16 months (range, three to 27 months) in 20 patients (53%). This included 11 of 25 patients with sustained atrial fibrillation and nine of 13 patients with paroxysmal atrial fibrillation, with only four of these patients relapsing. Four patients (11%) developed intolerable side effects, but no serious toxic effects were encountered, perhaps because of the relatively low doses of amiodarone hydrochloride that were used (average, 232 +/- 80 mg/d). Amiodarone is a safe and effective alternative to standard therapy in patients with refractory sustained or paroxysmal atrial fibrillation.

Arrhythmia control and other factors related to sudden death in coronary disease patients at intermediate risk.

Thirty-three patients with coronary artery disease and frequent, complex ventricular arrhythmias (VA) were followed long-term to evaluate factors related to sudden death (SD). Patients with malignant VA (sustained ventricular tachycardia (VT), resuscitated SD, or acute myocardial infarction) were excluded. Baseline data included angiographic ejection fraction (EF), segmental wall motion, and Holter evidence of frequent (greater than 30/hr) and complex (repetitive) ventricular premature beats (VPBs). Control of VA was attempted with conventional or experimental agents and was defined as greater than or equal to 70% reduction in VPBs, greater than or equal to 90% reduction in couplets, and abolition of nonsustained VT on two consecutive Holter tapes. After 24 +/- 15 months of follow-up on the single most effective agent, 18 patients survived while 15 patients died suddenly. There was no difference between these groups with respect to age, sex, or baseline VA. Survivors had a higher EF (51% vs 34%, p less than 0.001), fewer dyskinetic segments (0.05 vs 1.0, p less than 0.01), and better VA control (83% vs 40%, p less than 0.01) than nonsurvivors. By analysis of variance, VA control was not independent of EF (F = 6.98, p less than 0.01). The 1-, 2-, and 3-year survival rates were 90%, 90%, and 82% for patients with EF greater than or equal to 40% and 22%, 11%, and 11%, for those with EF less than 40% and uncontrolled VA.(ABSTRACT TRUNCATED AT 250 WORDS)

Endless loop tachycardia started by an atrial premature complex in a patient with a dual chamber pacemaker.

In a patient with a dual chamber pacemaker that senses in both the atrium and ventricle (VDD, DDD), a ventricular depolarization temporally displaced from a P wave can cause retrograde atrial activation and initiate an endless loop pacemaker-mediated tachycardia. A case in which an endless loop tachycardia was initiated by an end-diastolic atrial premature complex is reviewed. Retrograde conduction occurred because of the change in the temporal relation of atrial sensing and atrioventricular (AV) node depolarization. The implanted pacemaker did not have the capability of atrial refractory programmability. Atrial refractory interval extension, which occurs in this model after a ventricular premature complex to protect against a retrograde P wave, was not invoked since the tachycardia was begun by an atrial rather than a ventricular premature complex. The tachycardia was controlled by shortening the programmable AV delay. The mechanism of tachycardia induction and its management are outlined. Atrial refractory programmability is required in all VDD or DDD pacemakers.