Noncompaction Cardiomyopathy and Embolic Events: A Mini-Review

Abstract

Left ventricular noncompaction cardiomyopathy (LVNC) is characterized by prominent ventricular trabeculations and deep intertrabecular recesses. Patients with LVNC have an increased risk of embolic events. The presence of symptoms at the time of diagnosis can be a risk marker for stroke/embolic events. Left ventricular ejection fraction (LVEF), as measured by transthoracic echocardiography and left atrial diameter, has been found to be a significant predictor of systemic embolism in LVNC patients. Furthermore, CHADS2 (congestive heart failure, hypertension, age ≥75 years, diabetes mellitus and stroke or transient ischemic attack) and CHA2DS2-VASc (congestive heart failure, hypertension, age ≥75 years, diabetes, stroke, vascular disease, age 65–74 years and sex category [female]) scores were significantly higher in patients with stroke or embolism. Although the difference was not statistically significant, pediatric patients with LVNC combined with other congenital heart defects had more thromboembolic events compared to patients with isolated LVNC. On the other hand, stroke/transient ischemic attacks did not differ significantly between patients with isolated apical LVNC and mid-basal noncompaction. Furthermore, no differences in the prevalence of stroke between the quantiles of the maximal ratio of noncompacted to compacted myocardium have been revealed. Additionally, current data show no association between N-terminal pro-B-type natriuretic peptide levels and stroke/embolic events. Current evidence suggests anticoagulation treatment in LVNC patients with prior embolic events, atrial fibrillation, presence of left ventricular (LV) thrombus, and/or LV dysfunction. In patients with LVNC without a clear indication for anticoagulation, anticoagulant therapy may be considered in patients with CHADS2 score ≥2. More data are needed to identify patients at higher risk of embolic events who will be benefited from anticoagulation treatment.