Anorexia Nervosa (AN) is a severe psychiatric disorder characterized by restrictive eating behaviors that lead to significantly low body weight. The physical consequences of AN are profound, with the cardiovascular system bearing the brunt of the damage caused by chronic malnutrition. Heart complications represent the most frequent cause of death in individuals with this disorder, making cardiac health management a primary concern. These cardiovascular issues largely attribute to the high mortality rate associated with AN, and can arise even in patients who do not appear severely underweight.
How Starvation Affects Cardiac Function
Chronic caloric restriction forces the body into a state of energy conservation, prioritizing survival over normal bodily functions. This adaptive response involves a reduction in the overall metabolic rate, causing the body to operate in a hypometabolic state. The heart, a muscle requiring constant energy, responds by slowing its activity to conserve fuel.
The autonomic nervous system plays a significant role in this slowdown, increasing the influence of the vagus nerve, which acts as the body’s natural brake on heart rate. This physiological change causes sinus bradycardia, where the resting heart rate drops considerably, sometimes falling below 40 beats per minute in severe cases. This decrease in heart rate is directly linked to the degree of weight loss and the duration of the disorder.
Beyond the mechanical slowdown, malnutrition destabilizes the heart’s electrical system through severe electrolyte imbalances. Key minerals like potassium, magnesium, and phosphate become depleted or improperly distributed as the body breaks down protein and fat for energy. Low levels of potassium (hypokalemia) and magnesium (hypomagnesemia) disrupt the precise electrical signals needed for a steady heart rhythm.
The depletion of phosphate (hypophosphatemia) also impacts heart function, as it is necessary for cellular energy production and muscle contraction. Without sufficient levels of these electrolytes, cardiac muscle cells cannot repolarize correctly, leading to electrical instability. This cellular disruption forms the underlying mechanism for dangerous cardiac complications.
Major Cardiovascular Complications
The prolonged lack of nutrients causes cardiac muscle atrophy, where the heart shrinks in size. This includes a reduction in both the thickness of the ventricular walls and the overall left ventricular mass. This reduction in mass is a direct consequence of the body consuming its own protein stores, including muscle tissue, for energy.
The structural wasting can lead to functional problems, such as mitral valve prolapse, where the valve leaflets become relatively too large for the shrunken chambers. A shrunken heart muscle is also less able to pump blood efficiently, resulting in low cardiac output and widespread low blood pressure (hypotension). The combination of bradycardia and hypotension often leads to symptoms like dizziness and fainting, especially when standing up.
Electrical instability due to electrolyte shifts often manifests as arrhythmias, or irregular heart rhythms. A particular concern is QT prolongation, an abnormality visible on an electrocardiogram (ECG) that represents a delay in the heart’s electrical recovery phase. This delay significantly increases the risk of a life-threatening arrhythmia called Torsades de Pointes, which can cause sudden cardiac death.
Another complication is pericardial effusion, the accumulation of fluid within the sac surrounding the heart. This condition is observed in up to 35% of patients with AN and is thought to be related to low thyroid hormone levels and low body mass index. While usually asymptomatic, a large effusion can restrict the heart’s ability to fill with blood, severely compromising its function.
Reversibility and Medical Management
The treatment of cardiac complications in AN requires medical monitoring alongside nutritional rehabilitation. Initial stabilization involves frequent checks of vital signs and telemetry monitoring to track the heart’s electrical activity. Electrolyte levels, specifically potassium, magnesium, and phosphate, are managed and maintained within a safe range to stabilize heart rhythm.
The introduction of nutrition must be carefully controlled due to the risk of Refeeding Syndrome, a potentially fatal metabolic shift. When a severely malnourished person begins eating, the sudden influx of carbohydrates triggers insulin release, which drives electrolytes like phosphate and potassium rapidly into the cells. This sudden depletion of electrolytes in the bloodstream strains the weakened heart, potentially causing acute heart failure or severe arrhythmias.
Medical teams must employ gradual refeeding protocols and closely monitor for signs of fluid retention and electrolyte imbalance, particularly during the first two weeks of nutritional support. Fortunately, many of the cardiac abnormalities caused by AN are reversible with sustained weight recovery and nutritional restoration. Studies show that cardiac dimensions, left ventricular mass, and heart rate often increase toward normal values after successful refeeding.
While structural and functional issues like bradycardia and muscle atrophy typically improve, some long-term effects may persist. In rare instances, chronic malnutrition may lead to microscopic scarring in the heart muscle, which could increase the risk for arrhythmias later in life. Consistent and complete recovery from AN remains the most effective strategy for reversing the damage to the heart.