Abstract
Introduction: Left ventricular non-compaction (LVNC) is a rare genetic condition affecting 1 in 5000 people in which the myocardium of the left ventricle fails to adequately compact, forming deep recesses within the muscle wall. These recesses have been theorized to contribute to thrombus formation and embolic stroke, though the association has never been firmly established in the limited literature over the last 20 years. Hypothesis: We assessed the hypothesis that patients with LVNC, as well as those with hypertrabeculation not meeting LVNC criteria, would have increased rates of lifetime incidence of CVA, LV thrombus diagnosis, and distal arterial embolic events. Methods: We performed a retrospective control-matched cohort study assessing patients at Loyola University Medical Center diagnosed with LVNC, as well as those with hypertrabeculated left ventricles not meeting LVNC criteria, assembling the largest cohort of adult patients in the literature to date. We matched our study patients to controls based on age, HTN, DM, smoking status, history of atrial fibrillation, and history of DVT/PE. Results: Compared to matched controls, neither the LVNC group (n=98) nor the hypertrabeculation group (n=119) showed an increased risk of CVA, but both were associated with an increase in diagnosis of LV thrombus by TTE, TEE, or cMRI (p=0.045, p=0.003, respectively). Furthermore, in the LVNC group, each 10% increase in EF was found to reduce the risk of a composite endpoint of arterial thromboembolism (CVA, LV thrombus, distal arterial embolus) by 50%, while in the hypertrabeculation group, each 10% increase in EF reduced total arterial thromboembolism by 37%. Conclusions: These findings suggest that patients with hypertrabeculated left ventricles are either more likely to have LV thrombi that do not result in CVA events, or that due to the ventricle morphology, LV thrombi are being diagnosed when none are actually present. Furthermore, our study supports the existing literature that more severe systolic dysfunction increases risk for CVA and thromboembolic events, though that association seems largely multifactorial. Based on these results we cannot advocate for or against a particular anticoagulation strategy in patients with LVNC.
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