Can atrial fibrillation, especially in patients with a history of hypertension and other comorbidities, increase the risk of pulmonary embolism?

Can Atrial Fibrillation Cause Pulmonary Embolism?

Atrial fibrillation does not cause pulmonary embolism—the relationship is reversed: pulmonary embolism can trigger atrial fibrillation, and when AF and PE coexist, it reflects shared risk factors and comorbidities rather than a causal pathway from AF to PE. 1

The Directional Relationship Between AF and PE

AF Does Not Independently Cause PE

• After adjustment for age and comorbidities, atrial fibrillation without oral anticoagulation is not associated with increased risk for pulmonary embolism (HR 1.03, CI 0.94-1.13). 1

• The higher crude rate of PE observed in AF patients (2.91 vs 1.09 per 1000 person-years) is fully explained by differences in age (AF patients are >25 years older on average) and comorbidity burden, not by AF itself. 1

• The pathophysiology of thromboembolism in AF involves left atrial appendage stasis and embolization to the systemic circulation (causing stroke), not right-sided thrombus formation that would cause PE. 2

PE Can Trigger AF

• Pulmonary embolism is recognized as a reversible cause of atrial fibrillation, occurring through acute increases in pulmonary vascular resistance and right atrial pressure. 2

• The mechanism involves abrupt right ventricular strain, right atrial dilation, and increased wall stress that creates the substrate for AF initiation. 3, 4

• Among patients presenting with AF during acute PE, approximately 60% have newly diagnosed AF, suggesting PE as the precipitating event. 5

Clinical Implications in Patients with Hypertension and Comorbidities

Understanding the Coexistence

• When AF and PE occur together, this reflects:
  • Shared cardiovascular risk factors (hypertension, heart failure, advanced age, diabetes) that independently predispose to both conditions 2
  • PE as the acute trigger for new-onset AF in the setting of right heart strain 3
  • Coincidental occurrence in elderly patients with multiple comorbidities 1

Hypertension's Role

• Hypertension in AF patients is associated with left atrial appendage thrombus formation and stroke risk through left-sided mechanisms (reduced LAA flow velocity, spontaneous echo contrast). 2

• Hypertension does not create a pathway for right atrial thrombus formation that would lead to PE. 2

• The American College of Cardiology notes that hypertension is present in up to 88% of AF patients and contributes to left ventricular hypertrophy and left atrial remodeling—mechanisms relevant to stroke, not PE. 6

Prognostic Implications When AF and PE Coexist

Impact on PE Severity and Outcomes

• Patients with AF presenting with acute PE have higher rates of massive PE (OR 1.59,95% CI 1.4-1.81) and increased in-hospital mortality (adjusted OR 1.48,95% CI 1.27-1.71). 7

• AF patients with PE experience longer hospital stays (6.24 vs 4.79 days), higher rates of mechanical ventilation, cardiac arrest, and nonhome discharge. 7

• However, AF does not affect the prognostic performance of PE risk stratification tools—elevated cardiac biomarkers and higher risk class remain the independent predictors of adverse outcomes regardless of heart rhythm. 5

Critical Clinical Pitfall

• The presence of AF on admission in PE patients reflects greater comorbidity burden and more severe hemodynamic compromise, not an independent mortality risk from AF itself. 5

• Clinicians should use standard PE risk assessment models (NT-proBNP, troponin elevation, risk scores) irrespective of whether AF is present. 5

Diagnostic Considerations

When to Consider PE in AF Patients

• Consider PE as a reversible cause in patients presenting with new-onset AF, particularly when deep vein thrombosis cannot be confirmed and other typical AF triggers are absent. 2, 3

• Echocardiography provides valuable diagnostic information by identifying right ventricular strain, right atrial enlargement, and potential sources of embolic material. 3

• The ACC/AHA guidelines list pulmonary embolism among acute, temporary causes of AF where successful treatment of the underlying condition often eliminates the arrhythmia. 2

Avoiding Misattribution

• Do not attribute PE to AF in patients with chronic AF and hypertension—instead, investigate standard PE risk factors (immobility, malignancy, thrombophilia, recent surgery). 1

• The prothrombotic state in AF is mediated by left atrial stasis, endothelial dysfunction, and systemic hypercoagulability affecting the arterial circulation, not venous thromboembolism pathways. 2

Anticoagulation Management

Distinct Therapeutic Targets

• Anticoagulation in AF targets stroke prevention through left atrial appendage thrombus prevention, using risk stratification tools like CHA₂DS₂-VASc. 2

• Anticoagulation for PE targets venous thromboembolism and requires different duration and intensity considerations. 3

• When both conditions coexist, anticoagulation serves dual purposes, but the indication for anticoagulation should be clearly documented based on the primary pathology. 3