Anorexia Heart Problems: Lifelong Risks and Cardiac Changes

Anorexia nervosa affects multiple organ systems, but its impact on the heart is particularly concerning. Malnutrition forces the body to conserve energy in ways that weaken cardiac function, sometimes leading to long-term or even permanent complications. Even after recovery, some individuals continue to experience cardiovascular issues due to lasting structural and functional changes.

Understanding how anorexia affects the heart is crucial for both prevention and treatment.

Structural Changes In The Heart

Prolonged malnutrition leads to significant remodeling of the heart due to severe caloric restriction and muscle wasting. The myocardium, like any other muscle, requires adequate energy and protein to maintain its mass and function. When the body enters a prolonged state of energy deficiency, it begins breaking down muscle tissue, including the heart. Echocardiographic studies have consistently shown a reduction in left ventricular mass, with some research indicating decreases of up to 30% in severe cases (Möbius-Winkler et al., 2012). This atrophy weakens the heart’s ability to contract effectively, compromising cardiovascular performance.

Beyond muscle loss, the heart’s chambers also change. The left ventricle, responsible for pumping oxygenated blood, often becomes smaller due to myocardial tissue loss, reducing stroke volume. Pericardial effusion—fluid accumulation around the heart—has been observed in some individuals, likely due to protein deficiencies affecting vascular permeability (Mont et al., 2003). While often asymptomatic, severe cases can contribute to hemodynamic instability.

Structural deterioration also occurs at the cellular level. Prolonged starvation leads to increased fibrosis, where normal cardiac muscle is replaced with stiff, non-contractile connective tissue (Katzman et al., 2016). This remodeling impairs the heart’s elasticity, making it less efficient at filling and ejecting blood, potentially leading to diastolic dysfunction, where the heart struggles to relax and fill properly between beats.

Cardiac Output And Circulation

The loss of cardiac muscle mass and structural changes directly impact cardiac output, the volume of blood ejected per minute. This parameter depends on stroke volume—the amount of blood pumped per beat—and heart rate. Individuals with anorexia often exhibit significantly reduced stroke volume due to myocardial atrophy and chamber shrinkage. Studies have shown that in severe cases, cardiac output can drop by as much as 40%, leading to systemic hypoperfusion and diminished oxygen delivery to tissues (Katzman et al., 2016).

Compounding this issue, the autonomic nervous system adapts to prolonged caloric deprivation. The parasympathetic nervous system, which slows heart rate to conserve energy, becomes dominant, often resulting in bradycardia. While a slow heart rate is normal in well-conditioned athletes, in malnutrition, it reflects an energy-conserving mechanism rather than cardiovascular efficiency. Decreased cardiac output can lead to dizziness, fatigue, and cold extremities due to inadequate circulation.

Circulatory changes extend beyond cardiac function. Blood viscosity and vascular tone are altered, contributing to impaired perfusion. Chronic malnutrition reduces plasma volume due to dehydration and decreased protein levels affecting oncotic pressure. This places additional strain on the heart, which must work harder despite its weakened state. Doppler ultrasound studies have documented decreased peripheral blood flow, particularly in the extremities, leading to acrocyanosis—a bluish discoloration of the hands and feet (Mont et al., 2003).

Heart Rhythm Disturbances

Electrical activity in the heart is regulated by specialized cells, but anorexia disrupts this balance, increasing the likelihood of arrhythmias. The depletion of key electrolytes such as potassium, magnesium, and calcium—often due to inadequate intake or purging—alters the heart’s ability to generate and propagate electrical impulses. Hypokalemia is strongly associated with prolonged QT intervals on an electrocardiogram (ECG), heightening the risk of torsades de pointes, a dangerous ventricular tachycardia that can lead to sudden cardiac death. Magnesium deficiency worsens this risk by impairing electrical conduction stability.

Bradycardia is another common rhythm disturbance, often presenting as a resting heart rate below 50 beats per minute. While partly an adaptive response, severe cases can result in inadequate circulation. Profound bradycardia may cause syncope (fainting) due to decreased cerebral perfusion. In extreme cases, sinus node dysfunction can develop, leading to pauses in cardiac activity that may require pacemaker implantation. Clinicians have documented heart rates as low as 30 beats per minute, raising concerns about asystole, or complete cessation of electrical activity.

Structural changes in the myocardium also contribute to arrhythmias. Fibrotic remodeling disrupts electrical signal conduction, creating areas of slowed conduction that predispose the heart to reentrant arrhythmias. Post-mortem examinations of individuals with severe anorexia have revealed myocardial scarring despite the absence of traditional risk factors for fibrosis, such as hypertension or ischemic heart disease. These microscopic disruptions make arrhythmias more persistent and resistant to treatment, even after nutritional rehabilitation.

Blood Pressure Alterations

Blood pressure regulation is significantly affected by anorexia, with hypotension being one of the most common cardiovascular abnormalities. Severe caloric restriction, dehydration, and reduced circulating blood volume strain the body’s ability to maintain vascular tone. Many individuals exhibit systolic blood pressures below 90 mmHg, leading to dizziness, fatigue, and fainting due to insufficient cerebral perfusion. The body attempts to compensate through vasoconstriction, but with limited energy reserves and impaired autonomic function, these mechanisms often fail.

The autonomic nervous system, critical for blood pressure regulation, undergoes significant changes in response to chronic malnutrition. The sympathetic nervous system, responsible for maintaining vascular resistance and cardiac output, becomes suppressed, contributing to persistent low blood pressure. Orthostatic hypotension, where blood pressure drops sharply upon standing, is particularly common. This occurs because the body struggles to adjust vascular resistance quickly enough to counteract gravitational shifts in blood distribution, leading to lightheadedness or loss of consciousness. Clinicians often use orthostatic blood pressure measurements to assess cardiovascular instability in individuals with eating disorders.

Long-Term Cardiac Concerns

Even after weight restoration and recovery, many individuals experience lingering cardiovascular effects due to the structural and functional changes induced by prolonged malnutrition. The severity and duration of the illness, as well as the timing of intervention, influence the extent of these complications. Some abnormalities, such as reduced heart mass and bradycardia, may improve with proper nutrition, but others, particularly fibrosis or chronic autonomic dysfunction, can persist for years. This raises concerns about an increased risk of cardiovascular disease later in life, even for those who have fully recovered.

Diastolic dysfunction, where the heart struggles to relax and fill efficiently, has been observed in recovered individuals, particularly those with severe myocardial atrophy. This impairment can reduce exercise tolerance and contribute to persistent fatigue or shortness of breath. Additionally, autonomic nervous system imbalances, including exaggerated parasympathetic dominance, can result in lasting abnormalities in heart rate variability, linked to an increased risk of arrhythmias and sudden cardiac events. Some studies suggest former anorexia patients have a higher prevalence of endothelial dysfunction, affecting blood vessel dilation. Over time, this may contribute to an elevated risk of hypertension and atherosclerosis, conditions typically associated with metabolic syndrome but now recognized as potential concerns in individuals with a history of severe malnutrition.