Plasma levels of NT-pro-BNP in patients with atrial fibrillation before and after electrical cardioversion

Summary Objective Plasma levels of brain natriuretic peptide (BNP) have been examined in studies on patients with persistent atrial fibrillation, both before and after electrical cardioversion. Studied patients often showed a comorbidity with congestive heart failure, which complicates interpretation of measured BNP values as a natriuretic peptide. The aim of this study was to examine plasma levels of N-terminal fragment pro-brain natriuretic peptide (NT-pro-BNP), which is the more stable but inactive cleavage product of pro-BNP in patients with atrial fibrillation, but normal left ventricular ejection fraction, before and after electrical cardioversion. Patients and methods NT-pro-BNP plasma levels of 34 consecutive patients were measured before, shortly after and 11 days after electrical cardioversion. All patients showed a normal ejection fraction after echocardiographic or laevocardiographic criteria. Results At baseline, all patients showed elevated NT-pro-BNP compared to a healthy control group (1086 vs. 66.9 pg/ml, p<0.001). After a mean follow-up time of 11 days in patients with persistent restored sinusrhythm, NT-pro-BNP decreased from 1071 pg/ml at baseline to 300 pg/ml (p<0.001). In contrast, patients with recurrence of atrial fibrillation showed increased levels from 1570.5 pg/ml at baseline to 1991 pg/ml (p=0.13; n.s.). Recurrence of atrial fibrillation was independent from height of NT-pro-BNP levels at baseline (p=0.23). Conclusions Atrial fibrillation in patients with a normal left ventricular ejection fraction is associated with elevated NT-pro-BNP plasma levels, which decrease when a persistent sinus-rhythm can be restored by electrical cardioversion. On the other hand, NT-pro-BNP seems to increase (n.s.) when recurrence of atrial fibrillation occurs. Finally, NT-pro-BNP is no valid predictor for long-term success of sinus-rhythm restoration by electrical cardioversion.      

Thromboembolism in heart failure: who should be treated?

The risk of thromboembolic complications in patients with heart failure and/or chronic left-ventricular systolic dysfunction is increased. Nevertheless, anticoagulant therapy in these patients is still a subject of debate. Atrial fibrillation is the only prospectively evaluated, proven thromboembolic risk factor and patients with atrial fibrillation benefit from long term anticoagulant therapy. The significance of other proposed thromboembolic risk factors in heart failure and/or chronic left-ventricular dysfunction such as gender, cause of myocardial disease, severity of heart failure, left-ventricular ejection fraction, left-ventricular thrombus, left ventricular aneurysm and history of previous thromboembolic event is less clear. This article summarizes key studies, assesses the incidence of thromboembolism, evaluates risk factors and proposes guidelines for anticoagulation of patients with heart failure and/or left ventricular systolic dysfunction.     

Brain natriuretic peptide predicts successful cardioversion in patients with atrial fibrillation and maintenance of sinus rhythm

BACKGROUND: Brain natriuretic peptide (BNP) is released from the heart by hemodynamically induced muscle stretch. Patients with atrial fibrillation have higher levels of BNP than those in sinus rhythm. OBJECTIVE: To assess the usefulness of BNP as a predictor of successful cardioversion in patients with persistent atrial fibrillation and subsequent maintenance of sinus rhythm. SUBJECTS AND METHODS: Twenty patients undergoing cardioversion for persistent atrial fibrillation were enrolled. BNP levels were measured before electric cardioversion, and 30 min and two weeks after cardioversion. Baseline echocardiograms and 12-lead electrocardiograms were obtained from all patients. Patients with valvular disease, previous mitral valve surgery or significant left ventricular dysfunction were excluded. RESULTS: The mean BNP level and the mean heart rate were significantly higher before cardioversion than 30 min after (197+/-132 pg/mL versus 164+/-143 pg/mL, P=0.02, and 77+/-17 beats/min versus 57+/-12 beats/min, P=0.0007, respectively). Patients who reverted back to atrial fibrillation after two weeks had a baseline BNP of 293+/-106 pg/mL, while those who remained in sinus rhythm for two weeks had a lower baseline BNP of 163+/-122 pg/mL (P=0.02). CONCLUSION: In patients with persistent atrial fibrillation, BNP levels are associated with successful cardioversion and maintenance of sinus rhythm two weeks after cardioversion.     

Impact of acute left ventricular apical thrombus on cardioversion for atrial fibrillation

Among patients undergoing cardioversion for atrial fibrillation, the presence of left ventricular thrombus is a relatively uncommon and challenging clinical dilemma. While left atrial appendage thrombus is a contraindication to cardioversion, there is paucity of data regarding the safety of cardioversion in with the presence of left ventricular apical thrombus. Also, thrombus characteristics such as protrusion and mobility on echocardiography are known risk factors for systemic embolism. In this article, we present a case highlighting the management of atrial fibrillation in the setting of left ventricular dysfunction, acute heart failure, and echocardiographic evidence of acute left ventricular apical thrombus.     

Prevention of and medical therapy for atrial arrhythmias in heart failure

A large proportion of heart failure patients suffer from atrial arrhythmias, prime amongst them being atrial fibrillation (AF). Ventricular dysfunction and the syndrome of heart failure can also be a concomitant pathology in up to 50% of patients with AF. However this association is more than just due to shared risk factors, research from animal and human studies suggest a causal relationship between AF and heart failure. There are numerous reports of tachycardia-induced heart failure where uncontrolled ventricular rate in AF results in heart failure, which is reversible with cardioversion to sinus rhythm or ventricular rate control. However the relationship extends beyond tachycardia-induced cardiomyopathy. Optimal treatment of AF may delay progressive ventricular dysfunction and the onset of heart failure whilst improved management of heart failure can prevent AF or improve ventricular rate control. Prevention and treatment of atrial arrhythmias, and in particular atrial fibrillation, is therefore an important aspect of the management of patients with heart failure.This review describes the incidence and possible predictors of AF and other atrial arrhythmias in patients with heart failure and discusses the feasibility of primary prevention. The evidence for the management of atrial fibrillation in heart failure is systematically reviewed and the strategies of rate versus rhythm control discussed in light of the prevailing evidence.     

Reversible thyrotoxic cardiomyopathy--report of three cases

Three patients with thyrotoxicosis, atrial tachyarrhythmia and congestive heart failure despite successful treatment of hyperthyroidism revealed atrial fibrillation/flagellation and left ventricular systolic dysfunction. Congestive heart failure resolved and left ventricular systolic function normalized only after successful cardioversion to sinus rhythm. In some patients treated for hyperthyroidism, achievement of euthyroid state is not by itself sufficient to reverse left ventricular failure. Improvement after successful reversion of atrial tachyarrhythmia suggest its essential role in pathogenesis of thyrotoxic cardiomyopathy.     

Functional capacity before and after cardioversion of atrial fibrillation: a controlled study.

OBJECTIVE--To evaluate the effect of cardioversion on peak oxygen consumption (peak VO2) in patients with long-standing atrial fibrillation, to assess the importance of underlying heart disease with respect to the response to exercise, and to relate functional capacity to long-term arrhythmia outcome. DESIGN--Prospective controlled clinical trial. SETTING--Tertiary referral centre. PATIENTS--63 consecutive patients with chronic atrial fibrillation accepted for treatment with electrical cardioversion. Before cardioversion all patients were treated with digoxin, verapamil, or a combination of both to attain a resting heart rate < or = 100 beats per minute. INTERVENTIONS--Electrical cardioversion. MAIN OUTCOME MEASURES--Peak VO2 measured before and 1 month after electrical cardioversion to compare patients who were in sinus rhythm and those in atrial fibrillation at these times. Maintenance of sinus rhythm for a mean follow up of 19 (7) months. RESULTS--Mean (1SD) peak VO2 in patients in sinus rhythm after 1 month (n = 37) increased from 21.4 (5.8) to 23.7 (6.4) ml/min/kg (+11%, P < 0.05), whereas in patients with a recurrence of atrial fibrillation 1 month after cardioversion (n = 26) peak VO2 was unchanged. In patients who were in sinus rhythm both those with and without underlying heart disease improved, and improvement was not related to functional capacity or left ventricular function before cardioversion. Baseline peak VO2 was not a predictive factor for long-term arrhythmia outcome. CONCLUSION--Restoration of sinus rhythm improved peak VO2 in patients with atrial fibrillation, irrespective of the presence of underlying heart disease. Peak VO2 was not a predictive factor for long-term arrhythmia outcome after cardioversion of atrial fibrillation. These findings suggest that cardioversion is the best method of improving functional capacity in patients with atrial fibrillation, whether or not they have underlying heart disease and whatever their functional state.     

Atrial natriuretic peptide response to cardioversion of atrial flutter and fibrillation and role of associated heart failure.

Plasma atrial natriuretic peptide (ANP) concentrations were measured before and 1 hour after cardioversion in 40 patients (27 with atrial flutter and 13 with atrial fibrillation) admitted for elective cardioversion. Fourteen (11 with atrial flutter and 3 with atrial fibrillation) had clinical evidence of congestive heart failure (CHF). Conversion to sinus rhythm was successful in 39 patients. The mean ANP concentration in the entire group decreased after cardioversion from 38 +/- 4 to 17 +/- 2 pmol/liter (p less than 0.001). In the subgroup with CHF, the ANP level, which was not significantly higher than that in the group without CHF, decreased from 47 +/- 8 to 19 +/- 3 pmol/liter (p less than 0.01). Neither mode of cardioversion (spontaneous 1, pharmacologic 2 and direct-current countershock 36) nor associated CHF influenced ANP response to cardioversion. One patient with atrial flutter and "failed cardioversion" had unchanged ANP level. The decrease after cardioversion in ANP concentration correlated with its control level (r = 0.88, p less than 0.001) but not with the decrease in heart rate. The ANP level in patients with atrial fibrillation was 45 +/- 9 vs 38 +/- 5 pmol/liter in those with atrial flutter (difference not significant). Arrhythmia duration, left atrial size, and ventricular rate or arterial blood pressure did not correlate with ANP concentration in any subgroup. It is concluded that (1) the ANP level is elevated comparably in patients with both atrial flutter and fibrillation regardless of the presence or absence of CHF; and (2) the level decreases, independent of the mode of cardioversion or presence of CHF, promptly after successful cardioversion.     

B-type natriuretic peptide levels: diagnostic and therapeutic potential

A blood test that would aid in the diagnosis and management of patients with congestive heart failure would have a favorable impact on the staggering costs of the disease. B-type naturetic peptide (BNP) is synthesized in the cardiac ventricles and its release is directly proportional to ventricular volume expansion and pressure overload. Levels of BNP correlate with left ventricular pressure, amount of dyspnea, and the state of neurohumoral modulation. BNP also correlates closely with New York Heart Association classification. A cut point of 100 pg/mL appears to discriminate patients with congestive heart failure from those without congestive heart failure. Measurement of BNP may also be an excellent screening tool for LV dysfunction. Key Words: Natriuretic peptides; neurohormonal; left-ventricular pressure;     

Atrial fibrillation and heart failure comorbidity

Atrial fibrillation and heart failure have in common that they mainly occur in older patients and the patients have similar underlying heart diseases. The prevalence of atrial fibrillation in heart failure patients varies from 10% to 30%. There are conflicting data whether the presence of atrial fibrillation is an independent predictor for an increased mortality in heart failure. Optimal medical heart failure therapy can improve outcome and may influence the relationship between atrial fibrillation and survival. Keystones for the management of atrial fibrillation in heart failure patients are the optimal treatment of heart failure, the use of oral anticoagulation, the case-adjusted decision of rhythm or rate control, and the primary prevention of sudden cardiac death. Heart failure patients with atrial fibrillation should receive long-term oral anticoagulation. The two options to treat atrial fibrillation are rhythm control and rate control. Given the findings of randomised trials, rhythm control of atrial fibrillation with the aim to improve survival is not justified in heart failure patients because of uncertainty about the role of atrial fibrillation as a predictor of worse outcomes and the safety of antiarrhythmic drugs. Rhythm control can be attempted, if rate control is chosen and symptoms persist. The indications for rhythm control are to control symptoms, including a deterioration of heart failure related to a loss of atrial contraction. Amiodarone seems to be the drug of choice to maintain sinus rhythm in patients with paroxysmal atrial fibrillation as well as in patients who returned to sinus rhythm after cardioversion. New non pharmacologic approaches for rhythm control such as catheter-based techniques seem to be highly effective. Rate control to prevent rapid atrial fibrillation is an acceptable approach in otherwise asymptomatic heart failure patients. Slowing of the ventricular rate often leads to a moderate improvement in left ventricular function in many patients. Standard therapy for rate control in heart failure patients consists of partial atrioventricular (AV) node blockade with digoxin and a beta-blocker. Amiodarone is also highly effective to reduce ventricular rate in patients with atrial fibrillation. When rate control remains refractory to medical therapy, rate control is achieved with AV node ablation and subsequent pacemaker implantation. Non pharmacological treatments for the primary prevention of sudden cardiac death are the implantation of a defibrillator.     

Heterogeneity and time course of improvement in cardiac function after cardioversion of chronic atrial fibrillation: assessment of serial echocardiographic indices.

OBJECTIVE--To assess the clinical characteristics of patients in whom cardiac function improved after cardioversion of atrial fibrillation and the time course of the improvement. DESIGN--A prospective serial study of echocardiograms recorded before cardioversion and one day, seven days, one month, and three months after cardioversion. SETTING--Echocardiography laboratory of a university hospital. PATIENTS--23 patients with chronic atrial fibrillation in whom cardioversion was successful. MAIN OUTCOME MEASURES--M mode indices of the left ventricular wall motion and pulsed Doppler indices of the left ventricular inflow. RESULTS--Three months after cardioversion percentage fractional shortening had increased by more than 5% in 14 patients (improved group) and by less than 5% in nine patients (non-improved group). Those in whom cardiac function improved had significantly higher heart rates and a greater reduction in ventricular filling during atrial fibrillation and a more prominent atrial filling wave three months after cardioversion than those patients in the non-improved group. Over the three months of follow up the mean (1SD) percentage fractional shortening increased from 22 (3)% to 30 (4)% in the improved group and in this group heart rate fell one day after cardioversion. A month after cardioversion the percentage fractional shortening had increased to 35 (5)% and the atrial systolic contribution to left ventricular filling increased from 30 (9)% on day 1 to 47 (12)%. CONCLUSIONS--Cardioversion improved cardiac function in patients with tachycardia and reduced ventricular filling during atrial fibrillation. Because both an immediate reduction of heart rate and a delayed recovery of atrial booster pump function played an important part in the improvement of cardiac function the long-term effects of cardioversion should be assessed at least a month after cardioversion.     

Atrial natriuretic factor during atrial fibrillation and supraventricular tachycardia

Plasma immunoreactive atrial natriuretic factor was measured in 10 patients with chronic atrial fibrillation before and after cardioversion to sinus rhythm, and in 14 patients during electrophysiologic evaluation of paroxysmal supraventricular tachycardia. The mean plasma concentration of atrial natriuretic factor in atrial fibrillation was 138 +/- 48 pg/ml and decreased to 116 +/- 45 pg/ml 1 hour after cardioversion to sinus rhythm (p less than 0.005). The mean plasma concentration of atrial natriuretic factor increased from 117 +/- 53 pg/ml in sinus rhythm to 251 +/- 137 pg/ml during laboratory-induced supraventricular tachycardia (p less than 0.005). Right atrial pressures were recorded in 12 patients; the baseline atrial pressure was 4.3 +/- 1.9 mm Hg and increased to 7.4 +/- 3.6 mm Hg during supraventricular tachycardia (p less than 0.005). A modest but significant linear relation was noted between the changes in plasma atrial natriuretic factor and right atrial pressure measurements during induced supraventricular tachycardia (r = 0.60, p less than 0.05). In conclusion, changes in atrial rhythm and pressure may be an important factor modulating the release of atrial natriuretic factor in the circulation and raised levels of this hormone may be a contributing factor for the polyuria and the hypotension associated with paroxysmal supraventricular tachyarrhythmias.     

Heart failure and atrial fibrillation: current concepts and controversies.

Heart failure and atrial fibrillation are very common, particularly in the elderly. Owing to common risk factors both disorders are often present in the same patient. In addition, there is increasing evidence of a complex, reciprocal relation between heart failure and atrial fibrillation. Thus heart failure may cause atrial fibrillation, with electromechanical feedback and neurohumoral activation playing an important mediating role. In addition, atrial fibrillation may promote heart failure; in particular, when there is an uncontrolled ventricular rate, tachycardiomyopathy may develop and thereby heart failure. Eventually, a vicious circle between heart failure and atrial fibrillation may form, in which neurohumoral activation and subtle derangement of rate control are involved. Treatment should aim at unloading of the heart, adequate control of ventricular rate, and correction of neurohumoral activation. Angiotensin converting enzyme inhibitors may help to achieve these goals. Treatment should also include an attempt to restore sinus rhythm through electrical cardioversion, though appropriate timing of cardioversion is difficult. His bundle ablation may be used to achieve adequate rate control in drug refractory cases.     

Atrial fibrillation in heart failure

BACKGROUND: Atrial fibrillation is a common arrhythmia in patients with congestive heart failure caused by left ventricular dysfunction and is associated with significant morbidity and possibly increased mortality rates. It occurs with increasing frequency as the severity of heart failure increases. TREATMENT: As therapeutic options, two basic strategies are available: rhythm control with or without pharmacological manipulation to increase the chance of successful cardioversion and to maintain sinus rhythm, and rate control with anticoagulation. So far, a clear benefit of one of these two strategies over the other has not been demonstrated for patients with atrial fibrillation generally, nor have there been convincing data for the subgroup of heart failure patients. Traditionally, digoxin has been used in patients with heart failure and atrial fibrillation; however, it has no proven potential to restore sinus rhythm and is slow and not very effective in rate control requiring the addition of another rate-limiting agent, preferably a beta-blocker or calcium antagonist. Amiodarone has been evaluated in numerous clinical trials in patients with heart failure and appears to be safe and effective in terms of conversion to sinus rhythm, maintenance of sinus rhythm as well as control of ventricular rate. Dofetilide may be another option in patients with atrial fibrillation and heart failure, although a direct comparison with amiodarone is lacking. The problem with all antiarrhythmic drugs specifically in patients with heart failure is their toxicity. Because of their proarrhythmic effects, Class I antiarrhythmics are contraindicated in patients with heart failure. Torsades de pointes is the most serious adverse effect of sotalol and dofetilide. Amiodaron has less proarrhythmic risk but has numerous non-cardiac toxicities that require frequent monitoring. CONCLUSION: Overall, due to a low efficacy rate and high proarrhythmic risks, an ideal antiarrhythmic agent for patients with atrial fibrillation and heart failure does not exist, and drug selection should be highly individualized. In patients with chronic atrial fibrillation and heart failure, anticoagulation with warfarin for prevention of thromboembolic events is mandatory.     

Atrial fibrillation

The prevalence and incidence of atrial fibrillation increase with age. Atrial fibrillation is associated with a higher incidence of coronary events, stroke, and mortality than sinus rhythm. A fast ventricular rate associated with atrial fibrillation may cause tachycardia-related cardiomyopathy. Management of atrial fibrillation includes treatment of underlying causes and precipitating factors. Immediate direct-current cardioversion should be performed in persons with atrial fibrillation associated with acute myocardial infarction, chest pain due to myocardial ischemia, hypotension, severe heart failure, or syncope. Intravenous beta-blockers, verapamil, or diltiazem may be used to immediately slow a fast ventricular rate associated with atrial fibrillation. An oral beta-blocker, verapamil, or diltiazem should be given to persons with atrial fibrillation if a rapid ventricular rate occurs a rest or during exercise despite digoxin. Amiodarone may be used in selected persons with symptomatic life-threatening atrial fibrillation refractory to other drug therapy. Nondrug therapies should be performed in persons with symptomatic atrial fibrillation in whom a rapid ventricular rate cannot be slowed by drug therapy. Paroxysmal atrial fibrillation associated with the tachycardia-bradycardia syndrome should be managed with a permanent pacemaker in combination with drugs. A permanent pacemaker should be implanted in persons with atrial fibrillation in whom symptoms such as dizziness or syncope associated with non-drug-induced ventricular pauses longer than 3 seconds develop. Elective direct-current cardioversion has a higher success rate and a lower incidence of cardiac adverse effects than medical cardioversion in converting atrial fibrillation to sinus rhythm. Unless transesophageal echocardiography shows no thrombus in the left atrial appendage before cardioversion, oral warfarin should be given for 3 weeks before elective direct-current or drug cardioversion of atrial fibrillation and continued for at least 4 weeks after maintenance of sinus rhythm. Many cardiologists prefer the treatment strategy of ventricular rate control plus warfarin rather than to maintain sinus rhythm with antiarrhythmic drugs, especially in older patients. Digoxin should not be used in persons with paroxysmal atrial fibrillation. Patients with chronic or paroxysmal atrial fibrillation who are at high risk for stroke should be treated with long-term warfarin to achieve an International Normalized Ratio (INR) of 2.0 to 3.0. Persons with atrial fibrillation who are at low risk for stroke or who have contraindications to warfarin should receive 325 mg aspirin daily.     

Steady-state B-type natriuretic peptide levels in patients with atrial fibrillation of various clinical backgrounds

B-type natriuretic peptide level is increased in patients with atrial fibrillation. The aim of the present study was to present the distribution of steady-state B-type natriuretic peptide levels of various clinical backgrounds and to elucidate the usefulness of measuring them in patients with atrial fibrillation. B-type natriuretic peptide was measured in stable conditions in patients with atrial fibrillation (74?±?10?y/o, n?=?473). The average B-type natriuretic peptide level was 161?±?202 (median 101)?pg/ml. Multiple regression analysis showed that age, left ventricular ejection fraction, left atrial diameter, structural heart disease, chronic atrial fibrillation, and heart failure symptoms were independently associated with elevated B-type natriuretic peptide levels. However, in chronic atrial fibrillation patients without structural heart disease, B-type natriuretic peptide levels did not differ between those with and without heart failure symptoms. Notably, B-type natriuretic peptide levels were high (??150?pg/ml) in 41% of asymptomatic chronic atrial fibrillation without structural heart disease. Steady-state B-type natriuretic peptide levels of various clinical backgrounds were presented. Contributions of BNP elevation by clinical variables were somewhat different in different population. B-type natriuretic peptide was elevated in substantial percentage of asymptomatic chronic atrial fibrillation even without structural heart disease.     

Transesophageal echocardiography before and during direct current cardioversion of atrial fibrillation: Evidence for “atrial stunning” as a mechanism of thromboembolic complications

Objectives. The purpose of this study was to evaluate the usefulness of transesophageal echocardiography before electrical cardioversion in patients with atrial fibrillation and to determine the mechanism of thromboembolism after cardioversion.Background. Thromboembolic complications after electrical cardioversion of atrial fibrillation have been attributed to the dislodgment of preexistent left atrial thrombus during the resumption of atrial contraction. Transesophageal echocardiography has been proposed as a method of screening patients for left atrial thrombus before cardioversion.Methods. Seventy transesophageal echocardiographic studies were performed in 66 patients, predominantly with nonvalvular atrial fibrillation, before direct current cardioversion. In addition, transesophageal echocardiography was performed during the cardioversion procedure in 15 patients and immediately after in 1 patient.Results. Left atrial thrombus was detected in one patient (1.4%), and cardioversion was canceled. Thromboembolic complications occurred in 4 patients, none of whom had evidence of left atrial thrombus before cardioversion. Within 10 s of successful cardioversion, left atrial spontaneous echo contrast appeared in five patients, increased in one patient and was unchanged in nine patients. Patients with new or increased spontaneous echo contrast had more impaired atrial contraction and slower initial heart rates after cardioversion than those without. Left ventricular contraction was also impaired transiently by cardioversion.Conclusions. Transesophageal echocardiographic detection of left atrial thrombus before direct current cardioversion is important but infrequent in patients with predominantly nonvalvular atrial fibrillation. The occurrence of thromboembolic complica tions in the absence of demonstrable left atrial thrombus and the new development of spontaneous echo contrast in association with the transient atrial dysfunction (“stunning”) caused by cardioversion suggest that cardioversion may promote new thrombus formation, in which case all patients should receive full anticoagulant therapy at the time of cardioversion.     

Atrial fibrillation in patients with heart failure: pharmacologic options

Atrial fibrillation is a common arrhythmia in patients with heart failure. The presence of atrial fibrillation deteriorates cardiac function and increases the risk of thromboembolic events. The management of patients with atrial fibrillation in association with heart failure should consist of ventricular rate control, prevention of thromboembolic events, and conversion to normal sinus rhythm. Traditionally, digoxin has been widely used in patients with heart failure and atrial fibrillation; however, it does very little to restore sinus rhythm and requires the addition of another rate-limiting agent to control ventricular rate. The likelihood of successful cardioversion is dependent on the duration of heart failure and the degree of neurohormonal activation. The initiation of antiarrhythmic drug therapy in patients with heart failure should be guided by safety issues as well as consideration of potential benefits vs. risks associated with therapy. Amiodarone has been evaluated in numerous clinical trials and appears to be safe and effective when used in low dosage. Treatment with dofetilide is another option. Comparative studies with oral dofetilide vs. amiodarone are needed to evaluate their efficacy in restoration and maintenance of sinus rhythm in patients with heart failure. Such trials will clearly define the role of dofetilide in the treatment of atrial fibrillation. Routine prophylactic use of antiarrhythmic drug therapy for chronic atrial fibrillation in the setting of heart failure is not recommended due to a low efficacy rate and high proarrhythmic risk. Anticoagulation with warfarin and rate control remain the standard therapy. (c)2001 by CHF, Inc.     

Systematic review of the management of atrial fibrillation in patients with heart failure.

AIMS: To systematically review the management of atrial fibrillation (AF) in patients with heart failure. METHODS: Studies investigating the management of AF in patients with heart failure published between 1967 to 1998 were identified using MEDLINE, the Cochrane register and Embase databases. Reference lists from relevant papers and reviews were hand searched for further papers. RESULTS: Eight studies pertaining to acute and twenty-four pertaining to chronic AF were identified. For patients with acute AF ventricular rate control, anticoagulation and treatment of heart failure should be pursued simultaneously before cardioversion is attempted. Digoxin is relatively ineffective at controlling ventricular response and for cardioversion. Intravenous diltiazem is rapidly effective in controlling ventricular rate and limited evidence suggests it is safe. Amiodarone controls ventricular rate rapidly and increases the rate of cardioversion. There are insufficient data to conclude that immediate anti-coagulation, trans-oesophageal echocardiography to exclude atrial thrombi followed by immediate cardioversion is an appropriate strategy. Patients with chronic AF should be anti-coagulated unless contra-indications exist. It is not clear whether the preferred strategy should be cardioversion and maintenance of sinus rhythm with amiodarone or ventricular rate control of AF combined with anticoagulation to improve outcome including symptoms, morbidity and survival. Electrical cardioversion has a high initial success rate but there is also a high risk of early relapse. Amiodarone currently appears the most effective and safest therapy for maintaining sinus rhythm post-cardioversion. Digoxin is fairly ineffective at controlling ventricular rate during exercise. Addition of a beta-blocker reduces ventricular rate and improves symptoms. Whether digoxin is required in addition to beta-blockade for the control of AF in this setting is currently under investigation. If pharmacological therapy is ineffective or not tolerated then atrio-ventricular node ablation and permanent pacemaker implantation should be considered. CONCLUSION: There is a paucity of controlled clinical trial data for the management of AF among patients with heart failure. The interaction between AF and heart failure means that neither can be treated optimally without treating both. Presently treatment should be on a case by case basis.     

Angiotensin receptor blockers and cardiac rhythm disorders

Angiotension Receptor Blockers (ARB) are able to prevent the occurrence of atrial fibrillation (AF) through various mechanisms among them: neurhumoral antagonism and hemodynamic control. This occurs during arterial hypertension and chronic heart failure both diseases known to be associated with left atrial dysfunction. In the CHARM program, candesartan reduced by 20% the incidence of AF and thus also mortality and the incidence of hospitalisation for heart failure related to AF This beneficial effect is also observed with ACE inhibitors but is more important and potentated by ARB. In the Val-Heft study, valsartan on the top of standard treatment including ACE inhibitors, significantly lowered the cases of AF In hypertensive patients, ARB are more powerful than ACE inhibitors for the prevention of AF In the LIFE study, patients in the losartan arm had 33% less AF than patients from the other arm, despite treatment with atenolol and similar blood pressure reduction. Moreover ARB beside their specific effects are also able to increase efficiency of anti-arrhythmic agent; since after cardioversion patients treated with amiodarone plus irbesartan had a lower rate of recurrence of atrial fibrillation than patients treated with amiodarone alone. Finally ARB may reduce the risk of sudden death by ventricular arrhythmias in patients with diabetes mellitus.