Clinical Implications of Left Ventricular Apex Mechanics in Patients With Apical Hypertrophic Cardiomyopathy.

BACKGROUND

Apical hypertrophic cardiomyopathy (ApHCM) is a unique disease with pathologic hypertrophy mainly at the left ventricular (LV) apex. Although previous studies have indicated apical dysfunction in ApHCM, how apical mechanics change during disease progression has not been thoroughly examined. The aims of this study were to characterize the mechanics of the LV apex in patients with ApHCM at different disease stages and to explore the clinical significance of these alterations.

METHODS

One hundred four patients with ApHCM were divided into three subtypes on the basis of LV apical maximum wall thickness (AMWT) and extent of hypertrophy: relative type (isolated apical hypertrophy with AMWT < 15 mm), pure type (isolated apical hypertrophy with AMWT ≥ 15 mm), and mixed type (both apical and midventricular hypertrophy with AMWT ≥ 15 mm). Two-dimensional speckle-tracking echocardiography was used to analyze LV segmental strain, global strain, and twist. Comparisons of these parameters were performed among ApHCM subtypes and 30 healthy control subjects. Logistic regression and Cox proportional-hazards regression analyses were used to explore associations between myocardial mechanics and clinical indicators. A composite outcome of new-onset atrial fibrillation, heart failure hospitalization, myectomy, and all-cause mortality was assessed.

RESULTS

Even in relative ApHCM patients, apical longitudinal strain (LS), circumferential strain, and radial strain (RS) were significantly impaired compared with control subjects (LS: -14.6 ± 4.1% vs -20.0 ± 1.7% [P = .001]; circumferential strain: -19.6 ± 2.5% vs -25.6 ± 3.7% [P = .002]; RS: 26.6 ±7.4% vs 35.6 ± 11.1% [P = .026]), while apical rotation and LV twist remained unchanged. In patients with greater apical hypertrophy (mixed and pure patients), apical LS and RS were more abnormal. Moreover, apical rotation showed significant reductions compared with relative-type patients. After adjusting for clinical and myocardial mechanical parameters, apical rotation was independently associated with New York Heart Association functional class ≥ II (odds ratio, 0.81; 95% CI, 0.66-0.99; P = .036) and the composite outcome (hazard ratio, 0.82; 95% CI, 0.73-0.91; P = .001).

CONCLUSIONS

Relative ApHCM demonstrates apical dysfunction but sparing of apical rotation, which was abnormal in more extensive phenotypes. LV apex mechanics were closely related to clinical patterns, with apical rotation correlated with both New York Heart Association functional class ≥ II and clinical events.