Objectives: Ourstudy was undertaken to analyze the impact of subtle noncompaction of the left ventricle on regional left ventricular function in patients with hypertrophic cardiomyopathy.
Methods: Speckle-tracking imaging and contrast echocardiography were performed in 40 patients with hypertrophic cardiomyopathy. Subtle noncompaction of the left ventricle was defined as myocardium with more than 3 trabeculations in a single imaging plane with a noncompaction to compaction ratio of greater than 0.4 and less than 2.0.
Results: Among 647 segments, noncompaction was present in 46 segments (7%) in the left ventricular apex in 18 patients (45%) on the standard 2-dimensional echocardiograms and in 181 segments (27%) in 32 patients (80%) on the contrast-enhanced images. The mean number of segments affected by noncompaction ± SD was 6 ± 2. The mean noncompacted thickness was 5.6 ± 0.2 mm, and the ratio of the noncompacted to compacted layers was 1.1 ± 0.4 on the contrast-enhanced images. The global peak systolic longitudinal strain in patients with hypertrophic cardiomyopathy with noncompaction (-12.8% ± 2.8%) had a significantly lower absolute value than that in patients with hypertrophic cardiomyopathy without noncompaction (-17.4% ± 1.5%; P < .05) and healthy control participants (-20.6% ± 1.3%; P < .05). The number of segments with noncompaction and the interventricular septal thickness were both independent predictors of the global peak systolic longitudinal strain.
Conclusions: Contrast echocardiography is superior to standard 2-dimensional echocardiography for detecting subtle noncompaction in patients with hypertrophic cardiomyopathy. We found that the global peak systolic longitudinal strain in patients with hypertrophic cardiomyopathy with noncompaction had a significantly lower absolute value than that in patients without noncompaction and healthy controls, indicating that the total number of segments affected by coexistent subtle noncompaction in patients with hypertrophic cardiomyopathy was an independent predictor of left ventricular systolic dysfunction.