What causes atrial bigeminy?

Causes of Atrial Bigeminy

Atrial bigeminy results from ectopic atrial foci that fire prematurely after each sinus beat, most commonly originating from the pulmonary veins or atrial tissue with abnormal automaticity, triggered activity, or micro-reentry circuits.

Primary Mechanisms

Ectopic Focal Activity

• Pulmonary vein myocardial sleeves are the most common source of ectopic atrial activity, with unique anatomic and electrophysiological features including disparate fiber orientation and abbreviated action potentials that promote abnormal automaticity 1.
• Ectopic foci can arise from other atrial locations including the mitral annulus, right atrial septum, and coronary sinus ostium, where local tissue heterogeneity creates conditions for premature firing 2, 3.
• These rapidly firing foci demonstrate abnormal automaticity with shortened coupling intervals, creating the characteristic pattern where each sinus beat is followed by a premature atrial contraction 4.

Micro-Reentry Mechanisms

• Detailed ultrahigh-resolution mapping has revealed that some atrial bigeminy patterns result from micro-reentry circuits rather than pure focal mechanisms, particularly around the mitral annulus where continuous low-amplitude potentials connect successive beats 3.
• Structural abnormalities including fibrosis, inflammation, and heterogeneous conduction create the substrate for reentrant circuits even in patients without overt structural heart disease 1.

Underlying Cardiac Conditions

Structural Heart Disease

• Valvular heart disease (especially mitral valve disease), hypertension with left ventricular hypertrophy, coronary artery disease, and heart failure are the most common structural causes 1.
• Cardiomyopathies including hypertrophic cardiomyopathy, dilated cardiomyopathy, and restrictive cardiomyopathies (amyloidosis, hemochromatosis) alter atrial architecture and promote ectopic activity 1.
• Congenital heart disease, particularly atrial septal defects in adults, creates abnormal atrial hemodynamics and stretch that trigger premature beats 1.

Atrial Remodeling and Fibrosis

• Atrial fibrosis from chronic pressure or volume overload creates heterogeneous conduction that facilitates both focal ectopy and micro-reentry 1.
• Even in paroxysmal cases without recognized structural disease, atrial biopsies reveal inflammatory infiltrates consistent with myocarditis and fibrosis 1.
• Aging causes progressive cardiomyocyte loss (0.5-1.0% per year) with fibrous tissue replacement, creating an arrhythmogenic substrate 1.

Reversible and Acute Causes

Metabolic and Systemic Triggers

• Hyperthyroidism is a critical reversible cause that must be excluded, as thyroid hormone excess increases atrial automaticity and successful treatment eliminates the arrhythmia 1.
• Electrolyte disturbances, particularly hypokalemia and hypomagnesemia, alter atrial cellular electrophysiology and lower the threshold for ectopic firing 1.
• Acute alcohol intake ("holiday heart syndrome") triggers atrial ectopy through direct toxic effects and autonomic modulation 1.

Acute Cardiac Events

• Myocardial infarction, pericarditis, myocarditis, and pulmonary embolism create acute inflammatory and ischemic conditions that promote atrial ectopy 1.
• Cardiac surgery, particularly thoracic procedures, commonly triggers postoperative atrial arrhythmias through direct atrial trauma, inflammation, and autonomic imbalance 1.

Drug-Induced Causes

• An increasing number of cardiovascular, non-cardiovascular, and anticancer drugs can cause or exacerbate atrial bigeminy, though this is often overlooked in clinical practice 1.
• Drug-induced mechanisms include alterations in atrial action potential duration, effective refractory period, and intracellular calcium handling 1.
• Polypharmacy in elderly patients with multimorbidity creates particular risk for drug-induced atrial arrhythmias 1.

Autonomic and Functional Factors

Autonomic Influences

• Both vagal predominance and sympathetic predominance can trigger atrial bigeminy, with the balance between autonomic influences being critical 1.
• Some patients demonstrate vagal predominance in the minutes preceding onset (particularly those with structurally normal hearts), while others show sympathetic predominance 1.
• Athletes with elevated vagal tone represent a specific population prone to atrial ectopy 1.

Additional Risk Factors

• Obesity increases risk through left atrial dilation, with a graded increase in atrial size as body mass index rises 1.
• Sleep apnea syndrome is commonly associated with atrial arrhythmias through mechanisms involving hypoxia, autonomic dysfunction, and atrial pressure changes 1.
• Chronic kidney disease contributes through maladaptive changes in atrial tissue and electrolyte disturbances 1.

Calcium Handling Abnormalities

• Abnormal intracellular calcium homeostasis with sarcoplasmic reticulum calcium leak promotes triggered activity and spontaneous depolarizations 1.
• High atrial rates elevate diastolic calcium and alter ion channels controlling calcium reuptake and release, creating conditions for ectopic firing 1.
• These calcium-handling abnormalities persist after restoration of normal rhythm, increasing susceptibility to recurrent ectopy 1.

Genetic and Familial Factors

• Familial atrial arrhythmias occur more commonly than previously recognized, with specific chromosomal loci linked to susceptibility 1.
• Ion channel dysfunction from genetic mutations (channelopathies) can manifest as atrial bigeminy, particularly in younger patients without structural disease 1.
• The likelihood of developing atrial arrhythmias increases among offspring of parents with atrial fibrillation, suggesting inherited susceptibility 1.

Critical Clinical Pitfall

Do not dismiss atrial bigeminy as benign without excluding structural heart disease, reversible causes (especially hyperthyroidism), and drug-induced etiologies 1, 4. In patients presenting with blocked atrial bigeminy causing symptomatic bradycardia, the underlying mechanism is the premature atrial contractions resetting the sinoatrial node and prolonging RR intervals, which can be mistaken for primary conduction system disease 5, 6.