CONGRESS ABSTRACT

CASE REPORT A 55-year-old man with no prior cardiac or family history was admitted for a first episode of heart failure. The echocardiogram revealed moderate left ventricular dilation, eccentric remodeling, and severe systolic dysfunction (LVEF 28%), along with mild right ventricular dysfunction and no significant valvular disease. The EKG showed sinus tachycardia, and diffuse T wave inversion. Coronary angiography demostrated non-critical stenosis in the anterior descending artery. Due to hemodynamic instability, the patient was treated with Levosimendan and optimized heart failure therapy, leading to clinical improvement. Tests for autoimmune, infectious, and thrombophilic diseases were negative. However, a follow-up echocardiogram 5 days later revealed persistent biventricular dysfunction and a large, mobile apical thrombus (42×27 mm) with a small stalk. The patient underwent urgent apical thrombectomy. Histopathology of intraoperative biopsy revealed severe mycotic degeneration and extensive interstitial and especially subendocardial fibrosis, suggestive of cardiomyopathy.   DISCUSSION In 20% of cases, left ventricular thrombosis it related to non-ischemic cardiomyopathy, with 8% linked to dilated cardiomyopathy. While Virchow's triad outlines thrombosis risk factors, few studies have explored those specific to NICM. In our patient, we hypothesize that endomyocardial dysfunction or injury, evidenced by extensive endocardial fibrosis, and blood stasis due to severe left ventricular dysfunction and dilation, contributed to the thrombus formation. The absence of significant functional mitral regurgitation, which typically prevents thrombus formation by enhancing blood flow, is notable.  A recent study proposed a risk stratification model incorporating laboratory markers such as D-dimer, WBC count, hs-CRP, hematocrit, and NT-proBNP, as indicators of myocardial inflammation and damage. This model estimated a 10% risk of thrombus development in our patient. The study highlighted the interdependence of thrombosis and inflammation, particularly in the context of immunothrombosis, found in this study to be independently associated with thrombotic formation. Nonetheless, cardiovascular intimal injury remains the primary cause of thrombosis, and these factors may be just hallmarks of such injury.