Failing heart undergoes mechanical and electrical remodeling that promotes proarrhythmic changes at the cellular and organ level. All major arrhythmia mechanisms are promoted and facilitated by the typical progression of the myocardial injury from the time of the acute insult, through the compensated phase of recovery to the long-term myocardial dysfunction and progressive loss of the cellular integrity and organ function. The increased levels of the serum and tissue norepinephrine, beta-receptor down regulation and unopposed activation of the sympathetic autonomic nervous system with the associated loss of the vagal input promote enhanced normal and pathological automaticity of the atrial pacemaker cells. Similarly, intracellular calcium perturbations, increased catecholamines levels, ischemia and proarrhythmic effects of the medications and electrolyte disorders facilitate triggered activity. Reentry, both functional as well as based on the presence of a fixed anatomical obstacle is also more likely to occur in CHF. The substrate necessary for reentry is created by the diffuse or focal cardiac tissue fibrosis leading to the loss of the gap junction function and enhancement in the anisotropic conduction properties. While the cellular changes are potentially reversible if addressed early, the loss of electrical and mechanical function of the atrium is generally irreversible once extensive tissue necrosis and fibrosis has occurred [9, 10].

Atrial arrhythmias are usually classified on the basis of the anatomical structures involved in their initiation and propagation. Supraventricular tachycardias including atrioventricular node re-entrant tachycardia, atrioventricular re-entrant tachycardia and focal automatic atrial tachycardia are typically seen in younger patients without structural heart disease. Their prevalence is approximately 0.22 % in general population [11]. Diagnosis is usually established when a 12 lead electrocardiogram or a rhythm strip is recorded during the symptomatic episode of arrhythmia. There are only sporadically associated with the development of structural heart disease and carry overall benign prognosis. In rare cases of the rapid incessant arrhythmia, tachycardia-induced cardiomyopathy may develop. Cardiomyopathy is usually reversible once the tachycardia is controlled. Options of the therapy include rate control with atrioventricular node blocking agents (β-blockers, calcium channel blockers, digoxin), antiarrhythmic drugs (sotalol, amiodarone) or catheter ablation. Catheter ablation of all types of supraventricular tachycardia is very effective and carries a very low risk of the periprocedural complications. Thus, it is the therapy of choice for the majority of patients regardless of the status of the underlying cardiac disease. Moreover, in the cases of supraventricular tachycardia occurring in patients with the preexisting structural heart disease, CHF and tachycardia-induced cardiomyopathy catheter ablation should be used preferentially to maximize the likelihood of the arrhythmia cure and avoid the long-term risks and complications of drug therapy.

Conversely, micro and macro reentrant atrial tachycardias, atrial flutters and atrial fibrillation are the typical atrial arrhythmias associated with structural heart disease and CHF. Despite the occasional differences in the underlying basic arrhythmia mechanism, atrial rates and the anatomical substrates involved, they are all producing similar clinical symptoms and share the same long term impact on the atrial transport mechanics and overall cardiac performance. They also create similar increased risk of thromboembolic complications and respond to similar therapies. They will collectively be addressed as atrial fibrillation (AF) and as such will be the focus of this chapter. AF is often classified as first detected or recurrent as well as paroxysmal (when it terminates spontaneously), persistent (when it lasts more than 7 days or requires some form of cardioversion for termination) or permanent (when it no longer responds to any therapeutic intervention). These categories are not mutually exclusive as the dominant pattern of AF may change over time depending on the patient’s clinical status and the therapies used for arrhythmia control.

AF is the most common heart rhythm abnormality. It is uncommon in young healthy individuals but rapidly increases in prevalence after the age of 50 up to approximately 10 % of patients over the age of 80 years old. Men are affected earlier in life but women catch up rapidly when in their 70s and 80s with the slight overall higher prevalence in women. Lifetime risk of AF development in the Western countries is about 1 in 4. The AF association with structural heart disease is well established. The most common associated conditions are hypertensive heart disease, coronary artery disease, and congestive heart failure [2]. The AF epidemiology in the non-Caucasian populations is not well studied but the available data reveals risk factors pattern similar to Caucasian patients but overall lower AF age-adjusted incidence and prevalence.

Atrial fibrillation is diagnosed with a combination of clinical history, physical examination findings and electrocardiographic recordings. Patient’s usually report palpitations, sensation of irregular pulse, dizziness, fatigue, shortness of breath and decreased exercise capacity. On physical examination pulse and heart rate are irregularly irregular and excessive resting or exercional tachycardia or bradycardia may be present. Findings of associated decompensated heart failure including low peripheral pulses, cool extremities, peripheral or pulmonary congestion and S3 gallop often coexist. Recording of at least single lead electrocardiographic rhythm strip is necessary to confirm the diagnosis. AF may also be asymptomatic and the diagnosis is made solely on the basis of abnormal physical examination and/or electrocardiographic recordings. There is a wide spectrum of the ECG recording methods useful in AF diagnosis including “spot check” 12-lead ECG, ambulatory 24 h Holter monitors, extended use ECG loop recorders as well as implantable loop recorders. The accuracy of AF detection varies substantially between the methods but generally improves with the length of the monitoring and the patient compliance. The implantable loop recorders provide the best compliance and their overall accuracy for AF detection was reported at 98.5 % in the XPECT trial [12]. The ECG monitoring is also useful in the long term rate control assessment, monitoring the symptoms and evaluation of the efficacy of the therapy.

Once the diagnosis of AF is established, basic ancillary testing is recommended including blood tests (CBC, serum electrolytes, hepatic, renal and thyroid function tests) transthoracic echocardiography and in selected patients chest x-ray, transesophageal echocardiography, 6-min walk test, stress testing and electrophysiological study.

Many of these tests are also routinely used for evaluation of congestive heart failure status and if available may not need to be repeated [13].

Therapy of atrial arrhythmias in CHF is focused on preventing thromboembolic complications and controlling the arrhythmia associated symptoms. Successful restoration and maintenance of normal sinus rhythm should bring about the theoretical benefits of restoring the atriventricular synchrony, improvement in the atrial transport, reduction in the long-term thromboembolic risk and return of the normal chronotropic competency. However these potential advantages were thus far not demonstrated to provide survival benefit in the clinical trials comparing diverse rhythm controlling strategies to rate control only.

CHF is a prothrombotic state. The neurohormonal changes triggered by CHF lead to increased risk of intracardiac thrombus formation leading to systemic thromboembolism. In the WARCEF study, patients with CHF in normal sinus rhythm were treated with either oral aspirin or warfarin. The risk of the ischemic stroke in the anticoagulated patient was 2.5 % in warfarin group and 4.7 % in aspirin group, significantly exceeding the stroke risk in general population [14]. However, the association of CHF and stroke in patients with preexisting AF is not as robust although the data is largely from older trials with variable CHF definitions [15]. AF is known to substantially increase the risk of stroke and systemic embolization in all patients with the possible exception of young patients with no structural heart disease and no associated risk factors who have paroxysmal AF only. No single risk assessment scale is proven to predict the individual occurrence of stroke with a high accuracy. In clinical practice CHADS2 and CHA2DS2-VASc scores serve as a convenient while imperfect tool for a rapid stroke risk assessment. Other scales like HAS-BLED are helpful in assessing the risk of anticoagulation related complications [16]. Coincidentally, CHF patients often have additional stroke risk factors and generally should be considered for chronic anticoagulation with warfarin with the international normalized ratio (INR) target of 2.0 to 3.0. Currently approved and available oral anticoagulant alternatives to warfarin include direct thrombin inhibitor dabigatran and oral factor Xa inhibitors rivaroxiban and apixaban. The pivotal trials of the newer anticoagulants included a significant number of patients with clinical CHF and systolic LV dysfunction. In all these trials, the outcomes in the CHF subgroup were similar to the overall positive results of the general study population without excess risk of complications thus, the newer anticoagulants are considered safe and effective in CHF patients [17–19]. Given their decreased level of bleeding complications and excellent efficacy, novel oral anticoagulants are a valuable option for most of the patients with existing stroke risk factors including CHF population. Individuals who are intolerant to oral anticoagulants may be treated with aspirin or aspirin and clopidogrel combination. However, the antiplatelet therapy is less effective than warfarin while the risk of bleeding complications is as high as with the oral anticoagulants [20, 21]. The alternative strategies of the thromboembolic risk reduction in AF in a form of a percutaneous left atrial appendage occlusion device, percutaneous left atrial appendage ligation or surgical ligation may be considered in selected patient even if no outcomes data for their use in CHF patients is yet available.

Rate control and rhythm control strategies result in similar outcomes in both mildly symptomatic patients as well as patients with more advanced CHF. AFFIRM trial of rate versus rhythm control in mildly symptomatic AF patients included over 4000 patients. 23 % of patients had a history of mild CHF. No advantage of restoration of normal sinus rhythm over rate control was seen [22]. AF-CHF trial studied 1376 AF patients with more advanced CHF. Sinus rhythm restoration and maintenance primarily with amiodarone resulted in the same outcomes for mortality, stroke and CHF hospitalization as rate control only [23]. Interestingly, the ability to maintain normal sinus rhythm with the antiarrhythmic drug therapy is associated with improved prognosis both in patients with mild and advanced CHF. It is not clear whether this phenomenon represents a true causative effect or is simply a marker of a lower risk patient.