Atrial fibrillation: Clinical presentation and evaluation

Symptomatic atrial fibrillation

Atrial fibrillation (AF) can be symptomatic or asymptomatic, even in the same patient. Symptoms associated with AF vary, depending on the ventricular rate, the underlying functional status, the duration of AF, the presence and severity of structural heart disease, and the individual patient’s perception. Of note, women with AF are more likely to report more clinical symptoms and poorer quality of life.

The hemodynamic consequences of AF are related to loss of coordinated atrial contraction, rapid ventricular rate, and irregularity of ventricular rhythm (independent of rate), as well as long-term consequences such as atrial and ventricular cardiomyopathy. Loss of effective atrial contraction can potentially reduce cardiac output by 15% to 25%. These consequences are magnified in the presence of impaired diastolic ventricular filling, hypertension, mitral stenosis, left ventricular (LV) hypertrophy, and restrictive cardiomyopathy. Irregularity of the cardiac cycle, especially when accompanied by short coupling intervals, and rapid heart rates in AF can lead to reduction in diastolic filling, stroke volume, and cardiac output.

Most patients with AF complain of palpitations, dyspnea, generalized fatigue, activity intolerance, chest discomfort, and dizziness. However, significant interindividual and intraindividual variability exists. The first presentation of asymptomatic AF can be catastrophic, an embolic complication or acute decompensation of heart failure.

Although palpitation, or awareness of the irregularity of the heartbeat, is prominent in more than half of patients with AF (more common in those with paroxysmal AF), its correlation with documented arrhythmia is unimpressive.

Chest pain can be related to demand ischemia secondary to reduced cardiac output during AF in patients with coronary artery disease; however, chest pain can occur in AF patients despite the absence of coronary artery disease, potentially related to impaired microvascular flow. Furthermore, AF with a chronically rapid heart rate (more than 120–130 beats/min) can lead to tachycardia-mediated cardiomyopathy and heart failure.

Syncope is an uncommon complication of AF that can occur on termination of the arrhythmia in patients with sinus node dysfunction or because of rapid ventricular rates (especially at the onset of an episode) in patients with hypertrophic cardiomyopathy, aortic stenosis, or ventricular preexcitation over a bypass tract (BT).

AF is associated with two to three times higher risk of cognitive decline and all forms of dementia, including Alzheimer’s disease, senile dementia, and vascular dementia. Potential mechanisms of dementia in AF patients include embolic or hemorrhagic strokes, cerebral microinfarctions and microhemorrhages, AF-related cerebral hypoperfusion, systemic atherosclerotic vascular disease, oxidative stress, inflammatory and autoimmune mechanisms, and genetic predisposition. Early and effective use of anticoagulation and strategies to improve brain perfusion through rhythm control approaches can potentially reduce the risk of dementia.

In some patients, paroxysmal AF can be classified as either vagal or adrenergic, depending on the types of triggers and the temporal distribution of the arrhythmic episodes. Vagal AF typically occurs in young male patients without structural heart disease and characteristically develops during sleep or postprandial. In contrast, patients with adrenergic AF are usually older, often with evidence of underlying heart disease, and AF episodes usually occur during the day and are associated with physical or emotional stress. In patients with paroxysmal AF, the prevalence of vagal AF probably ranges between 6% and 25%, whereas that of adrenergic AF ranges between 7% and 16%. Pure adrenergic and vagotonic forms of paroxysmal AF are uncommon. Approximately 12% of patients with paroxysmal AF exhibit features of mixed vagal and adrenergic patterns.

Not infrequently, symptomatic AF patients report specific triggers for AF episodes. Alcohol consumption, caffeine, and exercise are the most frequently reported triggers of AF.

It is important to note that many patients with AF do not complain of palpitations and present primarily with occult cardiac symptoms, such as fatigue and effort intolerance. Such complaints should not be dismissed as “unrelated,” and those patients should not be labeled “asymptomatic.” On the other hand, many patients with persistent or permanent AF have one or more comorbid conditions (such as sleep apnea, heart failure, pulmonary disease) that can considerably contribute to specific complaints and to overall quality of life. Therefore, it is imperative to establish a correlation between any symptoms and AF, as well as ventricular response rates. The effect of regulation of ventricular rate during persistent AF or conversion to normal sinus rhythm (NSR) on a patient’s symptoms and quality of life can help assess the relative contribution of AF to the patient’s complaints. This is particularly important when the impact of AF on patient’s symptoms and quality of life is being considered the indication for therapeutic interventions (such as ablation).

Atrial fibrillation symptom scales

Several symptom scales have been developed to describe symptom severity and assess the functional consequences of symptoms in AF patients (analogous to the New York Heart Association [NYHA] congestive heart failure functional class and the CCS angina severity class). These scales can provide objective assessment of the patient’s subjective state, help guide symptom-orientated treatment decisions, and facilitate longitudinal patient profiling. This is imperative, since studies have demonstrated that evaluation at a single “point estimate” by physicians and patients can be susceptible to substantial discrepancy in both underestimation and overestimation of the severity of both physical and mental symptoms and quality of life in patients with AF. The most widely used symptom scores include the Canadian Cardiovascular Society Severity in Atrial Fibrillation (CCS-SAF) scale ( Table 17.1 ) and the modified European Heart Rhythm Association (EHRA) symptom scale ( Table 17.2 ).

Systemic thromboembolism

AF-related thromboembolism usually manifests as ischemic strokes, which are the most debilitating complication of AF and are responsible for 80% of embolism-related deaths in AF patients. Up to 125,000 strokes annually in the United States, 36% of all strokes in patients older than 80 years are attributed to AF. Cardioembolic strokes caused by AF are large and are associated with higher risk of morbidity and mortality as compared with non-AF-associated strokes.

Thromboembolism can also involve peripheral and visceral arteries. AF-related thromboembolism is responsible for up to 55% of acute splenic thromboembolic infarctions, 40% to 70% of acute renal thromboembolic infarctions, and 50% of acute mesenteric arterial embolism. Additionally, AF is diagnosed in 6% to 95% of patients with acute limb ischemia.

Atrial fibrillation-mediated cardiomyopathy

AF is strongly associated with heart failure. Heart failure can be observed in 33% of paroxysmal, 44% of persistent, and 56% of permanent AF patients. Patients with concomitant heart failure and AF exhibit a grim prognosis, with a 1-year mortality of approximately 10% and worsening of heart failure in almost 25%. AF and heart failure share underlying risk factors but also are independent risk factors for one another. Heart failure is a potent risk factor for incident AF, with a sixfold increase in the risk of developing AF, while AF is associated with a threefold increased risk of incident heart failure.

AF-mediated cardiomyopathy describes AF either as the sole cause for ventricular dysfunction or exacerbating ventricular dysfunction in patients with existing preexisting cardiomyopathy or heart failure. AF-mediated cardiomyopathy can be at least partially reversed with the restoration of NSR.

The prevalence of AF-mediated cardiomyopathy remains uncertain and likely is underestimated. The diagnosis of AF-mediated cardiomyopathy requires a high index of suspicion and often is made when the onset of an otherwise unexplained heart failure or rapid decline of preexisting heart failure or cardiomyopathy is temporally associated with the onset or increased burden of AF. Additionally, partial or complete improvement of heart failure or cardiomyopathy after successful rhythm or rate control, especially when rapid decline in ventricular function and heart failure symptoms develop with AF recurrence, are consistent with the diagnosis of AF-mediated cardiomyopathy. This diagnosis is further supported by demonstrating the severity of ventricular dysfunction typically is disproportional to the size of late-gadolinium enhancement on cardiac magnetic resonance or the severity of known structural heart disease. Also, acute decline of brain natriuretic peptide and N-terminal pro-B-type natriuretic peptide after termination of AF supports the diagnosis of AF-mediated cardiomyopathy.

The prevalence of AF-mediated cardiomyopathy remains uncertain and is likely underestimated, though it is important to consider whenever AF and heat failure coexist, since such diagnosis would support an aggressive approach for management of AF, preferably with rhythm control strategies.

AF-mediated cardiomyopathy is mediated by changes in cellular and neurohumoral factors, as well as extracellular remodeling, and is more likely in the presence of underlying structural heart disease. The atria serve as a volume reservoir to regulate ventricular filling and a booster pump in late diastole. The loss of atrial contraction during AF impairs ventricular filling and can worsen diastolic function. Chronic elevations in ventricular filling pressures can lead to ventricular remodeling with chamber dilatation that predisposes to worsening of both AF and heart failure. Also, the irregular ventricular rhythm may contribute to ventricular dysfunction.

While rapid ventricular rates during AF can contribute to the development of LV dysfunction, AF-mediated cardiomyopathy can manifest in patients with adequate rate control. In this setting, restoration and maintenance of sinus rhythm have been shown to result in improved LVEF. Also, higher AF burden is likely a precipitator of AF-mediated cardiomyopathy; however, whether a threshold of AF burden exists that warrants clinical intervention remains unknown.

Of note, patients with persistent AF who have normal LV systolic function at initial evaluation may yet develop AF-related cardiomyopathy, for unclear reasons. Attention to changes in symptoms and periodic reassessment of ventricular function are thus important aspects of management. Encouraging patients to begin a regular, repetitive exercise routine can help in this assessment, as this allows decreases in functional capacity to be more readily perceived than when patients are more sedentary.

Additionally, AF can result in functional mitral regurgitation to varying degrees; restoration and maintenance of NSR can correct some or all of the regurgitation, if related to the rhythm and not structural valve abnormalities.

Silent atrial fibrillation

Asymptomatic (subclinical or silent) AF occurs frequently; approximately one-third of patients with AF and up to 65% of AF episodes have been shown to be asymptomatic. Furthermore, a poor correlation between symptoms and AF has been demonstrated, and perception of AF patients of their prevailing rhythm is often inaccurate. Continuous monitoring with a pacemaker with dedicated functions for AF detection showed that as many as 40% of patients experienced AF-like symptoms in the absence of AF, whereas 38% of patients with a history of AF had episodes of AF lasting more than 48 hours noted at the time of interrogation even though these patients were asymptomatic. Therefore, the lack of symptoms should not be equated with the absence of AF, even in patients previously presented with symptomatic episodes of AF.

In individuals with no prior history of AF, silent AF can be noticed incidentally on routine physical examination or preoperative assessment, during active electrocardiographic screening in at-risk populations (e.g., patients with ischemic strokes), or in patients with cardiac implantable electronic devices (CIEDs; pacemakers, defibrillators, loop recorders). Furthermore, AF can be detected by new technologies, such as smartphone cases with ECG electrodes, smartwatches, and blood pressure machines with AF detection algorithms. Occasionally, AF is discovered only after a complication attributable to AF (e.g., stroke or congestive heart failure). Up to 30% of patients presenting with cryptogenic strokes are found to have AF that was not previously recognized.

Asymptomatic AF, especially when paroxysmal, is often missed. It is estimated that 10% to 27% of all patients with AF remain undiagnosed due to the lack of symptoms. In the United States, the prevalence of undiagnosed AF is about 1% to 2% in the general population. Importantly, clinically silent AF is similar to symptomatic AF in terms of overall risks of death, cardiovascular death, or thromboembolic events.