What are the common causes of biatrial enlargement?

Causes of Biatrial Enlargement

Biatrial enlargement most commonly results from dilated cardiomyopathy, chronic valvular heart disease (especially combined mitral and tricuspid regurgitation), atrial fibrillation, and restrictive cardiomyopathy. 1

Primary Cardiac Causes

Dilated Cardiomyopathy

• Dilated cardiomyopathy is characterized by biventricular and biatrial enlargement with elevated left- and right-sided filling pressures, representing the most common structural cause of biatrial dilation. 1
• The DCM phenotype produces annular dilatation of both mitral and tricuspid valves, leading to atrioventricular valve regurgitation that perpetuates biatrial enlargement. 1
• Primary etiologies include idiopathic DCM linked to genetic mutations in cytoskeletal, sarcolemmal, sarcomeric, and nuclear envelope proteins. 1
• Secondary causes include ischemic cardiomyopathy, long-standing hypertension, viral myocarditis, Chagas disease, anthracycline chemotherapy, sustained tachycardia, autoimmune disorders, endocrine disorders (hypothyroidism, diabetes), excessive alcohol consumption, nutritional deficiencies, and peripartum cardiomyopathy. 1

Chronic Valvular Heart Disease

• Combined mitral and tricuspid regurgitation produces volume overload leading to progressive biatrial enlargement. 1
• Mixed mitral disease with predominant mitral regurgitation causes LV remodeling in addition to left atrial enlargement, while coexistent tricuspid regurgitation drives right atrial dilation. 1
• Progressive secondary mitral regurgitation leads to higher LV end-diastolic pressure, LA pressure, and pulmonary arterial pressure, resulting in worsening RV function and tricuspid regurgitation—a cascade that produces biatrial enlargement. 1
• Biatrial enlargement combined with atrial fibrillation is associated with progressive secondary tricuspid regurgitation and predicts higher long-term mortality in heart failure patients. 2

Atrial Fibrillation

• Atrial fibrillation itself causes progressive biatrial enlargement as a direct consequence of the arrhythmia, independent of underlying structural heart disease. 3
• In patients with initially normal atrial sizes and no significant structural cardiac abnormalities, atrial fibrillation produces significant increases in both left atrial volume (from 45.2 to 64.1 cm³) and right atrial volume (from 49.2 to 66.2 cm³) over an average of 20.6 months. 3
• The relative extent of left and right atrial volume increase does not differ, indicating that atrial fibrillation affects both atria equally. 3
• Advanced interatrial block (P-wave ≥120 ms with biphasic morphology in inferior leads) produces fibrotic atrial cardiomyopathy and is frequently associated with atrial fibrillation and other atrial arrhythmias (Bayés syndrome), leading to atrial remodeling, mechanical dyssynchrony, and enlargement. 4

Restrictive Cardiomyopathy

• Restrictive cardiomyopathy produces massive biatrial enlargement with normal ventricular cavity size and preserved ejection fraction, representing a distinct phenotype. 5
• This pattern results from impaired ventricular distensibility causing elevated atrial pressures despite normal ventricular pump function. 5

Congenital Heart Disease

• Single ventricle physiology and tricuspid atresia commonly present with biatrial enlargement due to abnormal hemodynamics and chronic volume/pressure overload. 1
• Right or left atrial enlargement is common in single ventricle patients, with the pattern depending on the morphology of the underlying ventricle and associated lesions. 1
• Patients with congenital heart defects who have not undergone definitive repair typically demonstrate cyanosis, increased precordial activity, and evidence of biatrial enlargement on ECG and imaging. 1

Pressure Overload States

Left Atrial Enlargement Leading to Biatrial Involvement

• Left atrial enlargement from any cause (valvular disease, left ventricular dysfunction, diastolic dysfunction, left ventricular hypertrophy, hypertension) can progress to involve the right atrium through elevated pulmonary pressures and secondary tricuspid regurgitation. 4
• Prolonged elevation of atrial pressure from diastolic dysfunction, left ventricular hypertrophy, or valvular heart disease produces atrial remodeling that may ultimately lead to mechanical dyssynchrony and biatrial enlargement. 4

Massive Left Atrial Enlargement with Secondary Effects

• Massive LA enlargement may result in flattening of the anterior mitral leaflet along the mitral annular plane, with bending of the posterior mitral leaflet toward the LV cavity, perpetuating mitral regurgitation and eventually affecting right-sided structures. 1

Physiological Adaptation

• Intensive endurance training in elite female athletes produces biatrial morphological and functional changes with increased left atrial volume index (24.0 to 26.7 mL/m²) and right atrial volume index (15.66 to 20.47 mL/m²) after 16 weeks. 6
• This biatrial enlargement occurs in a volume overload model with normal filling pressures and low atrial stiffness, representing physiological adaptation rather than pathology. 6
• These findings must be distinguished from cardiomyopathies in the differential diagnosis of biatrial enlargement. 6

Key Clinical Pitfalls

• Do not assume biatrial enlargement always indicates biventricular disease—restrictive cardiomyopathy can produce massive biatrial enlargement with normal ventricular size and function. 5
• Atrial fibrillation should be recognized as both a cause and consequence of biatrial enlargement, creating a vicious cycle that requires aggressive rhythm management to prevent progressive atrial remodeling. 3
• In athletes, biatrial enlargement with normal filling pressures represents physiological adaptation and should not trigger unnecessary restriction from competition or invasive evaluation. 6
• Progressive secondary tricuspid regurgitation in heart failure patients is strongly associated with biatrial enlargement and atrial fibrillation, identifying a high-risk phenotype that may benefit from closer surveillance and consideration of transcatheter repair. 2