Upstream Treatments for Atrial Fibrillation

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Citation
US Cardiology, 2007;4(1):20-2

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Atrial fibrillation (AF) is the most frequently observed sustained cardiac arrhythmia encountered in clinical practice. Its incidence is increasing in the US.1 Numerous risk factors have been implicated in the development of AF, including non-modifiable risk factors such as age and gender, modifiable risk factors such as obesity—itself a risk factor for obstructive sleep apnea (OSA)—and smoking, and disease-specific risk factors such as hypertension (HTN), diabetes, heart failure (HF), coronary and valvular heart disease (particularly mitral regurgitation), and thyroid disease.2–5 The aim of this paper is to discuss the impact of the ‘upstream’ modulation of some these risk factors on the subsequent development of AF.

Obesity and Obstructive Sleep Apnea

The prevalence of obesity continues to rise at an alarming rate and represents a major public health concern in the US.6 Cardiovascular disease represents one of the major sequelae of this condition.7 Previous research has suggested that adiposity may adversely influence cardiac remodeling, thus raising the likelihood of AF as a possible consequence of obesity.8
The Framingham Heart Study examined the association between body mass index (BMI) and the risk of developing AF in a cohort of 5,282 patients.9 After 13.7 years of follow-up, 292 men and 234 women developed AF. After adjustment for age, a one-unit increase in BMI was associated with a 5% increase in the risk of AF for men and 4% for women. Of note, the relative risk of developing AF was 45 and 49% in obese (BMI ≥25) men and women, respectively. The higher risk of developing AF may be related to the left atrial (LA) enlargement seen in these patients. For example, the mean LA diameter was significantly greater in obese men (4.4cm) and women (4cm) compared with normal (BMI ≤25) men (3.8cm) and women (3.5cm).
Obesity is also the main patient risk factor for OSA, a condition that causes hypoxemia and nocturnal carbon dioxide retention and leads to sympathetic activation and surges in arterial pressure.10 Prospective data examining the effect of treatment of OSA on arrhythmias are currently limited. Kangala et al. evaluated the risk of recurrent AF following electrical cardioversion in patients with OSA.11 They identified 39 patients with OSA who underwent electrical cardioversion and then had at least 12 months of post-cardioversion follow-up.

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