NCMP-20. A RETROSPECTIVE SINGLE-CENTER EXPERIENCE WITH NONBACTERIAL THROMBOTIC ENDOCARDITIS AND STROKE - OUTCOMES, ANTICOAGULATION STRATEGIES, AND INCORPORATION OF NEXT-GENERATION SEQUENCING DAT

Abstract

Abstract BACKGROUND Acute ischemic stroke is a common neurologic complication of cancer and contributes to worse prognosis. Hypercoagulable state is an important stroke mechanism in cancer. Nonbacterial thrombotic endocarditis (NBTE) represents an extreme manifestation of such hypercoagulability. Evidence comparing LMHW to unfractionated heparin or direct oral anticoagulants (DOACs) for secondary stroke prevention is lacking in cancer patients. It is also unknown whether certain tumor mutations are associated with increased risk of NBTE. METHODS We reviewed clinical documents at MD Anderson Cancer Center using a RichSearch Natural Language Processing application to search for terms related to marantic endocarditis. Each patient was assessed for documentation of both valvular thickening or vegetations on echocardiogram, and negative blood cultures. Targeted next generation sequencing (NGS) information was interrogated using the PROACTIVE database. RESULTS 100 patient records were reviewed and of these 41 patients were determined to have likely NBTE based on the above criteria. 12 patients had recurrent strokes despite anticoagulation, two of whom had two recurrent strokes despite different anticoagulation strategies (4 strokes through therapeutic dose LMWH, 4 through rivaroxaban, 3 through apixaban, 1 through fondaparinux). The most common primary malignancies were non-small cell lung cancer (n=14) and pancreatic cancer (n=11). NGS data was available for 13 patients, and the most common mutations were KRAS (n=8), TP53 (n=7), EGFR (n=4), and BRAF (n=2) CONCLUSIONS NBTE is an important stroke mechanism in cancer, and the optimal secondary prevention strategy is unknown. These results confirm that NBTE is common in NSCLC and pancreatic cancer. These cancer types commonly harbor mutations such as KRAS, TP53 and EGFR, and work is ongoing to clarify how such mutations might contribute to hypercoagulability. Recurrent stroke is possible with all anticoagulation strategies. Further analysis of outcomes, serum biomarkers (ex. D-dimer), and comorbid medical diagnoses known to confer increased cardiovascular risk is underway.