Does Atrial Fibrillation Increase Risk of Pulmonary Embolism?
No, atrial fibrillation does not directly increase your risk of pulmonary embolism through the same mechanism that causes stroke. The thrombi formed in AF originate in the left atrium and embolize to the systemic arterial circulation (causing stroke), not to the pulmonary circulation 1, 2.
Understanding the Distinct Pathophysiology
AF creates left-sided, not right-sided thrombi:
- AF causes blood stasis in the left atrial appendage, leading to thrombus formation that embolizes through the left ventricle into systemic arteries, primarily causing stroke 1, 2
- Pulmonary embolism requires right-sided thrombi that travel through the right ventricle into the pulmonary arterial circulation—a completely different pathway 2
- The 2024 ESC guidelines explicitly state that AF is associated with "other thromboembolic events" which "typically include arterial thromboembolic events (preferred to the term systemic), although venous thromboembolism is also associated" 3
The Observed Association is Not Causal
When PE and AF coexist, it reflects shared risk factors and confounding, not direct causation:
- A large Swedish registry study (1.4 million residents) found that after adjusting for age and comorbidities, AF without anticoagulation was not associated with increased PE risk (HR 1.03,95% CI 0.94-1.13) 4
- The higher crude PE rates in AF patients (2.91 vs 1.09 per 1000 person-years) disappeared entirely after accounting for the fact that AF patients are >25 years older on average and have substantially more comorbidities 4
- Both conditions share common risk factors including advanced age, obesity, heart failure, and inflammatory states 5
When PE and AF Occur Together
PE can actually trigger AF as an acute precipitant:
- The 2024 ESC guidelines list pulmonary embolism as an acute temporary cause of AF, alongside surgery, myocarditis, and hyperthyroidism 3
- PE causes right ventricular pressure overload and inflammatory cytokine release, which can precipitate new-onset AF 5
- In the acute PE setting, incident AF within 2 days occurs in approximately 2.7% of patients and is associated with worse outcomes (OR 2.28 for 90-day mortality) 6
Clinical Decision-Making for Anticoagulation
Use separate risk stratification for stroke prevention versus VTE prevention:
- For stroke prevention in AF: Apply CHA₂DS₂-VASc scoring and prescribe anticoagulation when score ≥2 in men or ≥3 in women 3, 1
- For PE prevention: Base decisions on traditional VTE risk factors (immobility, malignancy, surgery, thrombophilia, prior VTE), not on AF diagnosis 1, 2
- The presence of AF alone does not justify extended anticoagulation for VTE prevention beyond what standard VTE risk factors would indicate 1
Important Caveats
Transient increased VTE risk immediately after AF diagnosis:
- A Swedish nationwide study showed markedly elevated VTE rates in the first 30 days after AF diagnosis (HR 6.64 in men, 7.56 in women) 7
- This early risk likely reflects acute illness, hospitalization, and immobility associated with the AF presentation rather than AF itself 7
- VTE risk normalized to population levels after 9 months in men (remained slightly elevated in women) as anticoagulation was initiated 7
The relationship is bidirectional but not through direct thromboembolism:
- While AF doesn't cause PE through embolization, patients with AF do have slightly elevated long-term VTE risk (HR 1.72 for PE beyond 6 months) due to shared risk factors and comorbidities 8
- This association does not justify different anticoagulation strategies—standard AF anticoagulation with DOACs or warfarin addresses stroke risk, and any VTE risk is managed based on VTE-specific factors 9, 10