Atrial Fibrillation

Pathobiology and Classification of Atrial Fibrillation

AF can be classified based on etiology, depending on whether it is present in patients without structural heart disease or occurs in association with other conditions. AF is defined as paroxysmal if it is self-terminating within 7 days, persistent if it is continuous greater than 7 days or permanent if it is chronic and accepted by the patient and physician. In case of permanent AF, rhythm control strategy is not a management option.

The pathogenesis of AF involves progressive structural changes in the atria, including atrial fibrosis, hypocontractility, fatty infiltration, inflammation, ischemia, vascular remodeling, ion channel dysfunction, and Ca ²⁺ instability.

Although there is an overlap, pulmonary vein triggers seem to play a dominant role in younger patients with relatively normal hearts and short episodes of AF, and an abnormal atrial tissue substrate may play a more important role in patients with structural heart disease and persistent/permanent AF. After a period of continuous AF, electrical remodeling occurs, further facilitating the continuance of AF (“AF begets AF”). These changes are initially reversible if sinus rhythm is restored but may become permanent and related to structural changes if AF continues (left atrial dilatation, cardiac fibrosis, and impairment of systolic/diastolic function). Of note is that AF, especially if early-onset, may have a genetic component, independent of cardiovascular comorbidities.

Symptoms

Patients with AF experience worse quality of life than healthy controls. AF is associated with symptoms including lethargy, dyspnea, palpitations, chest tightness, sleeping disorders, and psychosocial distress. However, these symptoms may reflect other concomitant diseases. The arrhythmia may be symptomatic or asymptomatic (“silent AF”), and AF patients may have both symptomatic and asymptomatic episodes. Importantly, silent AF is common, with severe consequences, such as stroke and/or death.

The modified European Heart Rhythm Association (EHRA) symptom scale has been proposed to assess symptom severity in patients with AF ( Table 147.1 ).

Stroke and Thromboembolism

Patients with AF have an elevated risk of stroke (a four- to five-fold increase), but this risk is not homogeneous and is dependent upon stroke risk factors (see Chapter 143 ). Ischemic strokes associated with AF usually result from cardioembolism to a large cerebral artery, and, therefore, AF-related strokes tend to be larger and more often fatal or result in greater disability, worse functional outcomes, and greater mortality compared with strokes from other causes. The arrhythmia is also associated with greater cognitive decline and increased risk of vascular dementia. Cognitive disturbances may occur in the absence of a clinically overt stroke because of multiple asymptomatic cerebral emboli.

In patients with AF, thrombi commonly form within the LAA due to stagnant flow and decreased emptying of this blind-ended structure. Most atrial thrombi in nonvalvular AF (approximately 90%) are formed within the LAA, which explains why, on the background of anticoagulant therapy, surgical occlusion of the LAA at the time of cardiac surgery reduced the risk of stroke by 33% compared with no occlusion. Thrombus formation in AF is consistent with the fulfilment of the Virchow triad of thrombogenesis, including intra-atrial stasis, endothelial dysfunction, and a prothrombotic or hypercoagulable state, due to elevated levels of D-dimer, P-selectin, and von Willebrand factor.

Heart Failure, Other Consequences and Death

Heart failure and AF coexist in many patients, and they can cause and exacerbate each other. Rapid ventricular rate in AF may precipitate signs and symptoms of acute heart failure in patients with an underlying heart failure with preserved LVEF. Poorly controlled ventricular rate in AF may also result in development of heart failure with reduced LVEF in individuals with previously normal left ventricular function (so-called tachycardiomyopathy), with or without clinically overt symptoms and signs of heart failure. Patients with AF and heart failure (with either preserved or reduced LVEF) have worse symptoms, poorer prognosis, and increased mortality compared with individuals with AF without heart failure. Regardless of the development of heart failure, AF is associated with a two-fold increased risk of all-cause mortality in women and a 1.5-fold increase in men.