Eating disorders (EDs), such as Anorexia Nervosa (AN), Bulimia Nervosa (BN), and Binge Eating Disorder (BED), are complex psychiatric illnesses that exert profound effects on the entire body. The cardiovascular system is especially vulnerable to the physiological stress caused by disordered eating behaviors and malnutrition. Cardiac complications are frequently reported as the leading cause of death associated with Anorexia Nervosa. Understanding how these conditions affect the heart is paramount for both patients and medical professionals.
The Acute Danger: Electrolyte Imbalance and Arrhythmias
The most immediate and life-threatening cardiac risks associated with eating disorders stem from severe electrolyte imbalances. These disruptions are commonly caused by purging behaviors, including self-induced vomiting or the misuse of laxatives and diuretics, often seen in Bulimia Nervosa or the binge-purge subtype of Anorexia Nervosa. The rapid loss of fluids and stomach contents depletes the body of essential minerals required for proper heart function, particularly potassium, magnesium, and phosphate.
A deficit in potassium, known as hypokalemia, is a significant concern because this mineral regulates the heart’s electrical signaling. Low potassium levels interfere with the repolarization phase of the cardiac cycle, leading to an abnormal delay visible on an electrocardiogram (ECG) as a prolonged QT interval. A prolonged QT interval significantly increases the risk for a dangerous arrhythmia called Torsade de Pointes. This irregular rhythm can rapidly degenerate into ventricular fibrillation, preventing the heart from pumping blood effectively and resulting in sudden cardiac death (SCD).
Electrolyte abnormalities can also arise from dehydration and chronic fluid volume depletion, which further strains the cardiovascular system. The heart must work harder to circulate a reduced blood volume, potentially increasing the resting heart rate in an attempt to compensate. Furthermore, the misuse of substances like ipecac syrup to induce vomiting can directly damage the heart muscle, leading to a condition called cardiomyopathy.
Long-Term Effects: Cardiac Atrophy and Structural Damage
Beyond the immediate danger of chemical imbalances, sustained malnutrition primarily associated with Anorexia Nervosa causes physical, structural changes to the heart muscle itself. Prolonged starvation causes the body to break down muscle tissue, including the heart muscle, in a process known as cardiac atrophy. This wasting reduces the overall mass of the heart, diminishing the size of the heart chambers and weakening its ability to contract forcefully.
The heart attempts to adapt to this state of starvation by slowing down its overall activity to conserve energy. This adaptation results in bradycardia, a resting heart rate that is abnormally slow, often falling below 60 beats per minute. Low blood pressure, or hypotension, is also common due to the combined effects of reduced cardiac output and decreased blood volume.
The structural changes can also manifest as mitral valve prolapse, where the valve leaflets bulge into the left atrium during contraction. This condition can sometimes improve with weight gain.
In contrast to the wasting observed in Anorexia Nervosa, Binge Eating Disorder (BED) and associated weight gain lead to a different set of cardiac risks. These risks include hypertension (high blood pressure) and elevated cholesterol levels, which increase the likelihood of developing atherosclerotic heart disease over time.
Medical Intervention and Monitoring During Recovery
Recognizing and treating cardiac complications requires a specialized medical approach that begins with thorough assessment. Standard evaluations include an electrocardiogram (ECG or EKG) to check for electrical abnormalities like a prolonged QT interval or arrhythmias. An echocardiogram is often used to assess the heart’s physical structure, measuring the size of the chambers and the thickness of the muscle walls to check for atrophy or fluid accumulation (pericardial effusion).
The process of nutritional rehabilitation, while necessary for recovery, poses a specific cardiac danger known as Refeeding Syndrome. This syndrome occurs when a severely malnourished body is reintroduced to calories too quickly, triggering a rapid shift of electrolytes (phosphate, potassium, and magnesium) from the blood into the cells. This sudden drop in serum electrolyte concentrations can overwhelm the already weakened heart, potentially causing severe arrhythmias, acute heart failure, and sudden death.
Due to these severe risks, individuals starting recovery from severe malnutrition require specialized cardiac monitoring, often in an inpatient setting. The goal is to correct electrolyte imbalances gradually while initiating a carefully controlled caloric increase. Fortunately, many structural and functional changes to the heart, such as cardiac atrophy and bradycardia, are reversible with sustained weight restoration and treatment.