Hypertrophic cardiomyopathy (HCM) is the most common genetic heart disorder with left ventricular (LV) wall hypertrophy which is not caused by abnormal loading conditions [1]. The clinical course of HCM is complicated with diastolic dysfunction, arrhythmic disorders, sudden cardiac death (SCD), and stroke. At the late stage of HCM patients present with systolic heart failure (HF), probably caused by myocardial fibrosis. Recently the risk
factors of SCD were extensively studied in patients with HCM and a great progress has been done in this field. We have newly proposed risk factors including late gadolinium enhancement (LGE) percentage by magnetic resonance imaging (MRI), apical aneurysm, and high-risk genetic mutations. The mortality from SCD in HCM decreased thanks to the improved risk assessment and increased number of implanted cardioverters defibrillators
(ICD). However, the problem of HF in HCM patients is not resolved. Progress is achieved in patients with LVOT obstruction due to the surgical septal reduction together with procedures on mitral valve apparatus. Of note, a decrease in LVOT gradient does not exactly mean prevention of myocardial fibrosis. In some patients with nonobstructive form of HCM, we can see a large amount of intramyocardial fibrosis which increases heart muscle
stiffness and leads to diastolic and finally systolic HF [2]. An early detection of subclinical myocardial impairment is needed to predict which patients are more prone to transition to overt HF. In this context, it is essential to assess the role of the comorbidity such as diabetes mellitus (DM) increasingly reported in HCM and to evaluate its effect on myocardial mechanics. To address the question, Badran et al. presented in the recent issue of Echocardiography [3] a report on the impact of DM on prognosis and myocardial function in patients with HCM.