Atrial Fibrillation

28 Atrial Fibrillation



Atrial fibrillation (AF), a supraventricular tachyarrhythmia characterized by uncoordinated atrial activation, is the most common sustained cardiac rhythm abnormality. The increase in the prevalence of AF is probably due to a combination of factors, including the aging of the population, a rising prevalence of chronic heart disease, and more frequent diagnosis by way of enhanced monitoring devices.


AF increases in prevalence with age, with rates of 5% to 10% reported in those older than 80 years. It is more common in men and less common among African Americans. Often AF is associated with structural heart disease, although a significant proportion of patients have no detectable heart disease.




Etiology and Pathogenesis


Histologically, the atria in patients with AF are frequently found to demonstrate patchy atrial fibrosis. Potential triggers of fibrosis may include inflammation or atrial stretch in response to heart disease such as valvular disease, hypertension, or heart failure. However, just as atrial stretch may lead to AF, AF itself worsens atrial stretch as a result of poor atrial contractility.


The onset and maintenance of AF require an initiating event in the setting of an anatomic substrate. Currently existing data support two schools of thought regarding the genesis of atrial fibrillation: (1) the automatic-focus hypothesis and (2) the multiple-wavelet hypothesis. The focal origin of AF gained credibility when it was found that often a focal source could be identified and that ablation of this source could abolish AF. It was established that cardiac muscle with preserved electrical properties extends into the pulmonary veins of the left atrium. Most often the pulmonary veins were the source of automatic foci that, when they propagate rapidly through an appropriate anatomic substrate, could lead to AF. The multiple-wavelet hypothesis proposes that fractionation of the electrical wavefronts in the atria leads to daughter wavelets of electrical activity. A large atrial mass in addition to other factors increases the number of wavelets, thereby leading to sustained AF. It is likely that these mechanisms are not mutually exclusive and may coexist in the same patient to a varying degree along a spectrum of disease.


AF acutely has adverse hemodynamic consequences as a result of loss of synchronous atrial mechanical activity, irregularity of ventricular response, rapid heart rate, and impaired coronary arterial blood flow (Fig. 28-2). Loss of atrial contraction may most markedly affect cardiac output in those with impaired diastolic filling who are most dependent on atrial function, such as those with left ventricular hypertrophy (LVH) or hypertension.



Persistently elevated ventricular rates can produce tachycardia-induced cardiomyopathy. Importantly, control of the ventricular rate may reverse the cardiomyopathic process.


AF is associated with a significantly increased risk of thromboembolic stroke (see Fig. 28-2). Reduced blood flow velocity in the left atrial appendage due to loss of organized mechanical contraction leads to stasis and thrombus formation. Thrombus formation generally requires continuation of AF for approximately 48 hours. However, even after cardioversion, atrial stunning (and minimally effective mechanical function of the atria) may be present for as long as 3 to 4 weeks, depending on the duration of AF.



Clinical Presentation and Diagnostic Approach


AF may be related to multiple causes (Box 28-1), including acute causes such as binge alcohol intake, surgery, myocardial infarction, pericarditis, pulmonary disease, or hyperthyroidism (see Fig. 28-1). Most often, treatment of these conditions will lead to resolution of the AF. AF has been associated with obesity and obstructive sleep apnea. Multiple cardiovascular conditions are associated with AF, including valvular heart disease, heart failure, coronary artery disease, hypertension (particularly with LVH), hypertrophic cardiomyopathy, restrictive cardiomyopathy, congenital heart disease, and pericardial disease. In these conditions, treatment of the underlying cause does not usually abolish the AF. Familial AF has been increasingly recognized and is probably a result of genetic abnormalities leading to abnormal function of cardiac ion channels. Finally, approximately 30% to 45% of cases of paroxysmal AF and 20% to 25% of persistent AF occurs in patients without underlying predisposing conditions and is classified as lone AF.


Jun 12, 2016 | Posted by in CARDIOLOGY | Comments Off on Atrial Fibrillation

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