What question did this study set out to answer?

To illustrate how chronic volume overload from a congenital atrial septal defect can lead to severe hemodynamic changes, unmasked by an acute embolic event.

May 20, 2026

B64-15 Unmasking Eisenmenger Physiology After a Large Embolic Stroke in a Patient With Sinus Venosus Asd and Pfo

Key Points

To illustrate how chronic volume overload from a congenital atrial septal defect can lead to severe hemodynamic changes, unmasked by an acute embolic event.
Case presentation of a 60-year-old male with atrial fibrillation, cirrhosis, and chronic lung disease.
Transthoracic echocardiography and brain imaging were performed to assess cardiac and cerebral conditions.
Multidisciplinary evaluation to consider treatment options for identified conditions.
Severe pulmonary hypertension characterized by right atrial and ventricular dilation, and systolic pressure >70 mmHg.
Documented large left MCA and PCA strokes with significant encephalopathy.
Patient transitioned to comfort-focused management due to severe comorbidities and ineligibility for surgical interventions.

Abstract

Abstract We describe a 60-year-old male with atrial fibrillation, cirrhosis, chronic lung disease, and an unrecognized congenital atrial septal defect (sinus venosus type) with patent foramen ovale (PFO), who developed severe pulmonary hypertension and a massive left middle cerebral artery (MCA) and posterior cerebral artery (PCA) stroke. This case highlights how chronic right-sided volume overload from an undiagnosed shunt can obscure evolving Eisenmenger physiology until an acute embolic event unmasks profound hemodynamic instability. Case Presentation 60-year-old man with atrial fibrillation on apixaban, cirrhosis, COPD, and prior ischemic stroke presented with aphasia. Brain imaging revealed a left MCA infarct and chronic occlusion of the right MCA posterior division, precluding reperfusion therapy. Anticoagulation was withheld due to hemorrhagic risk. During hospitalization, he experienced cardiac arrest with return of spontaneous circulation after 14 minutes, necessitating ICU transfer. Transthoracic echocardiography showed normal left ventricular function but severe right atrial and ventricular dilation, severe tricuspid regurgitation, and estimated right ventricular systolic pressure 70 mmHg. Agitated saline contrast demonstrated early right-to-left shunting consistent with sinus venosus ASD and possible anomalous pulmonary venous return with a PFO. The Qp/Qs ratio of 1.38 indicated a small left-to-right shunt, below the threshold for surgical closure. Subsequently, he developed QT prolongation and polymorphic ventricular tachycardia requiring antiarrhythmic therapy. Neurologic reassessment confirmed large left MCA and PCA infarctions with severe encephalopathy. Given his comorbidities—cirrhosis, COPD, and severe pulmonary hypertension—surgical or percutaneous closure was contraindicated. Discussion and Outcome This case illustrates how chronic right-sided overload and pulmonary vascular remodeling from sinus venosus ASD and PFO may progress silently until a paradoxical embolic stroke exposes advanced Eisenmenger physiology. The relatively low Qp/Qs ratio belied severe pulmonary vascular resistance, producing bidirectional shunting and systemic embolization risk. Multidisciplinary evaluation determined he was ineligible for shunt repair or vasodilator therapy. Care transitioned to comfort-focused management. Conclusion Sinus venosus ASD with PFO may remain undetected until adulthood, when irreversible pulmonary hypertension and paradoxical embolism reveal late Eisenmenger physiology. Recognition of subtle hemodynamic clues and early screening for congenital defects in adults with unexplained right-sided dilation or pulmonary hypertension is essential for timely intervention and prognostic counseling. This abstract is funded by: None

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