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. AF creates left-sided thrombi that cause arterial emboli (strokes), not right-sided thrombi that would cause PE 1, 2.
Understanding the Distinct Pathophysiology
The critical distinction lies in cardiac anatomy and blood flow direction:
AF causes stroke through LEFT-sided pathology: Atrial fibrillation creates stasis in the left atrium and left atrial appendage, forming thrombi that embolize through the left ventricle into the systemic arterial circulation, causing stroke and other arterial emboli 1, 2.
PE requires RIGHT-sided pathology: Pulmonary embolism requires thrombi from the venous system or right heart chambers that embolize through the right ventricle into the pulmonary arterial circulation 2.
These are anatomically separate pathways: The left and right sides of the heart do not directly communicate in normal cardiac anatomy, making it mechanically impossible for left atrial thrombi to cause pulmonary embolism 1, 2.
The Relationship Between AF and PE
PE can trigger AF, but AF does not cause PE:
Pulmonary embolism is listed as an acute precipitant that can cause new-onset atrial fibrillation, along with surgery, myocardial infarction, and other acute medical conditions 3, 2.
When AF and PE coexist, the PE typically came first or they share common risk factors (age, obesity, heart failure, inflammatory states) rather than AF causing the PE 4.
Clinical Implications for Risk Assessment
Use different risk stratification tools for each condition:
For stroke prevention in AF: Use CHA₂DS₂-VASc scoring (congestive heart failure, hypertension, age ≥75 years [doubled], diabetes, prior stroke/TIA/thromboembolism [doubled], vascular disease, age 65-74 years, female sex) and prescribe anticoagulation when score is ≥2 in men or ≥3 in women 3, 1.
For PE prevention: Base decisions on traditional VTE risk factors including immobility, active malignancy, recent surgery, thrombophilia, and prior VTE—not on the presence of AF 1, 2.
Evidence Regarding Observed Associations
While some observational studies show statistical associations between AF and PE, this does not indicate causation:
One Swedish registry study found that after adjustment for age and comorbidities, AF without anticoagulation was not associated with increased PE risk (HR 1.03,95% CI 0.94-1.13), demonstrating that the higher crude PE rates in AF patients are fully explained by shared risk factors like advanced age 5.
Studies showing elevated PE rates in the first 30 days after AF diagnosis (HR 6.64-7.56) 6 likely reflect acute illness states that trigger both conditions simultaneously, or detection bias from increased medical surveillance, rather than AF directly causing PE 4.
Anticoagulation Considerations
When a patient has both AF and PE, anticoagulation decisions should address both conditions:
Direct oral anticoagulants (DOACs) including apixaban, rivaroxaban, dabigatran, and edoxaban are FDA-approved for both stroke prevention in nonvalvular AF and treatment/prevention of VTE 7, 8.
The presence of AF with appropriate CHA₂DS₂-VASc score (≥2 in men, ≥3 in women) mandates long-term anticoagulation for stroke prevention 3.
If PE occurs in a patient already anticoagulated for AF, investigate traditional VTE risk factors (malignancy, immobility, thrombophilia) rather than attributing the PE to inadequate AF management 1, 2.
Common Clinical Pitfall
Do not assume that anticoagulation for AF provides adequate PE prevention in high-risk VTE scenarios: While anticoagulation for AF will incidentally provide some VTE protection, patients with strong VTE risk factors (active cancer, recent major surgery, known thrombophilia) may require VTE-specific risk assessment and potentially different anticoagulation intensity or duration than AF alone would dictate 1, 2.