![]() ![]() Several mechanisms have been postulated to explain bradycardia: increased parasympathetic tone, decreased intracardiac glycogen stores, and myocardial atrophy with resultant structural changes, including fibrosis, on gadolinium-enhanced magnetic resonance imaging.ĭespite functional and structural myocardial changes, bradycardia may principally reflect reduced metabolic demand and cardiac output as a compensatory response to starvation. In a prior inpatient case series the mean heart rate was 44 bpm, with 69% of patients less than 50 bpm. The degree of bradycardia can be extreme, with junctional escape rhythms as low as 20 beats per minute (bpm) and may be an indication for hospitalization. ![]() Guidelines on the evaluation and management of patients with bradycardia enumerate many potentially reversible causes of sinus node dysfunction, but do not mention severe AN, nor do they proscribe PPM among eating disorder populations. However, symptoms may not reflect bradycardia per se, but rather extreme malnutrition, deconditioning, and hypovolemia associated with restricted caloric intake and purging. While most patients are asymptomatic, a significant minority present with presyncope, lightheadedness, fatigue, and exercise intolerance that could be construed as concordant with current guidelines for permanent pacemaker (PPM) implantation. Though generally reversible, marked bradycardia may be worrisome to clinicians with limited experience treating eating disorders. Bradycardia is common among patients with severe anorexia nervosa (AN). ![]()
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