Left ventricular hypertrabeculation in patients with dilated cardiomyopathy was not associated with increased embolic risk (HR 1.5; 95% CI 0.75-3.00).
Cohort (n=1,160)
Yes
Does the presence of left ventricular hypertrabeculation increase the risk of embolic events, advanced heart failure, or major ventricular arrhythmias in patients with dilated cardiomyopathy?
Left ventricular hypertrabeculation in dilated cardiomyopathy is common but not associated with worse outcomes or increased embolic risk, suggesting it should not prompt prophylactic anticoagulation.
Hazard Ratio: 1.5 (95% CI 0.75–3)
BACKGROUND: Left ventricular (LV) hypertrabeculation, formerly termed LV noncompaction, is a heterogeneous myocardial entity linked to adverse cardiovascular outcomes. This study evaluated embolic risk in patients with dilated cardiomyopathy (DCM) according to the presence of hypertrabeculation and examined its prevalence and prognostic relevance across DCM genotypes. METHODS: Clinical data from 1160 patients with DCM evaluated by cardiac magnetic resonance imaging and genetic testing (n=997 86%) were collected from 22 international centers. End points included embolic events, advanced heart failure events, and major ventricular arrhythmias. RESULTS: LV hypertrabeculation was identified in 354 patients (30.5%) by fractal analysis and in 343 (29.7%) according to Petersen criteria, with good concordance. After a median follow-up of 5.1 years (interquartile range, 2.8–7.4), embolic events occurred in 37 patients (3.2%), advanced heart failure in 62 (5.3%), and major ventricular arrhythmias in 136 (11.7%). Hypertrabeculation was not associated with increased embolic risk (hazard ratio, 1.5 95% CI, 0.75–3.00), even among patients in sinus rhythm with LV ejection fraction ≤40% (hazard ratio, 1.89 95% CI, 0.7–5.5). In contrast, atrial fibrillation and reduced LV ejection fraction were associated with embolic events (both P <0.01). LV hypertrabeculation was not associated with an increased risk of major ventricular arrhythmias or advanced heart failure; genotype, LV ejection fraction, and late gadolinium enhancement emerged as the main predictors of adverse outcomes. The prevalence of LV hypertrabeculation varied across genotypes, with the highest prevalence observed in patients with sequence variants in motor sarcomeric genes (58%), TTN (38%), and genotype-negative status (33%), and the lowest prevalence observed among those with variants in cytoskeletal/Z-disk (7%) and nuclear envelope (5%) genes. Hypertrabeculation was not associated with adverse outcomes within any genotype. CONCLUSIONS: Although LV hypertrabeculation is common in DCM, it is not associated with worse outcomes and should not prompt differential clinical management. The embolic risk in patients with DCM and hypertrabeculation is low, including in those with reduced LV ejection fraction without atrial fibrillation, and does not support prophylactic anticoagulation in these patients.
“The presence of hypertrabeculation did not modify clinical risk in any of the genetic subgroups analyzed, confirming that it does not confer a worse prognosis.”
Ayestarán et al. (Mon,) conducted a cohort in Dilated cardiomyopathy (n=1,160). Left ventricular hypertrabeculation vs. Absence of left ventricular hypertrabeculation was evaluated on Embolic events (HR 1.5, 95% CI 0.75-3.00). Left ventricular hypertrabeculation in patients with dilated cardiomyopathy was not associated with increased embolic risk (HR 1.5; 95% CI 0.75-3.00).