We report the case of a 22-year-old female with a history of David procedure and mechanical valve replacement (ATS 22 mm) due to bicuspid aortic valve and severe AR with ascending aorta aneurysm in 2015.
Regular annual clinical follow-up (EKG and ultrasound) was always normal.
Since 2022 the patient suffered from episodes of dyspnea, chest pain and sadness diagnosed as Panic Disorder.
Home-therapy: Warfarin, estroprogestinic pill.
At the latest outpatient visit she was asymptomatic and in good overall condition, but her EKG showed novel alterations (T wave inversion in antero-lateral leads and QT prolongation).
She was then sent to the ED.
LAB: troponin levels were normal (6.8 ng/ml) with an elevated Nt-proBNP (425 ng/ml) and a low INR (1.53). Questioned about recent events she reported a road trauma which occurred two weeks prior. She was then admitted to Cardiology clinic.
Ultrasound: apical akinesia with reduced wall thickness, EF 48%, E/E ‘ 10, and normal right ventricular function. The aortic valve prosthesis was functional without pathological regurgitation, and other echocardiographic parameters were within normal limits.
EKG and ultrasound abnormalities along with a recent history of trauma supported Takotsubo Syndrome diagnosis (InterTAK score = 79.8% – 67pt), even though troponin levels were normal. Throughout hospitalization there were no changes in the EKG or pathological increases in troponin, and the patient remained asymptomatic. The patient was treated with LMWH to achieve adequate INR levels and initiated on B-blocker, ACEi, and SGLT2i for HFmrEF.
Cardiac MRI revealed apical segment akinesia with dilation and reduced wall thickness (EDV 97 ml/m²), EF 41%, transmural ischemic LGE in the apical region and a ventricular thrombus (16×4 mm). The patient underwent coronary angiography which showed normal epicardial coronary arteries.
Upon careful history-taking, the patient admitted irregular intake of VKA in the previous months. Given this information, the MRI and angiographic findings the diagnosis of unrecognized prior acute coronary syndrome, likely due to coronary thromboembolism in a patient with PHV and suboptimal compliance with VKA, was established. The patient was discharged home upon achieving a persistently therapeutic INR, with instructions to discontinue contraceptive therapy.
Conclusion: coronary thromboembolism is a rare complication of PHV with inadequate anticoagulation leading, in this case, to an unrecognized MI.
