Background: Hypertrophic cardiomyopathy (HCM) is caused by gene mutations encoding proteins of the cardiac sarcomere. Untreated HCM leads to heart failure, stroke and is the most frequent cause of sudden cardiac death in young adults. Epicardial adipose tissue (EAT) is a visceral fat depot that surrounds the heart and the coronary arteries. It is associated with subclinical atherosclerosis as well as incidence of CAD manifestation. Moreover, in patients with HCM, EAT correlates with severity of hypertrophy. In addition, from a clinical observation, the impression occurs that EAT is increased in patients with HCM compared to patients without hypertrophy. However, no existing data is comparing EAT distribution in patients with and without HCM.

Aim: We aimed to evaluate the distribution of EAT thickness in patients with HCM as compared to patients without HCM. Subgroup analysis will evaluate EAT thickness patients with obstructive CAD both in the HCM and non-HCM group.

Methods: The present analysis is based on a retrospective evaluation of EAT thickness of patients with diagnosis of HCM, presenting to the West German Heart and Vascular Center with diagnosis of HCM between 2004 and 2019. In addition to cases with HCM, age, sex and BMI matched controls (2:1) were included. EAT thickness was measured in 2-dimensional transthoracic echocardiography. In subgroup analysis we evaluated EAT thickness in patients with and without coronary artery disease (CAD). CAD was defined as prior coronary revascularization therapy.  

Results: Overall 86 patients with HCM (age 61.2±17.8, 51.2% male) and 172 age, sex, and BMI-group matched controls without HCM (age 61.15±17.8, 51.2% male) were included in our analysis. Patients with HCM had significantly more EAT as compared to patients without HCM (9.34 ± 2.95 mm vs. 5.26 ± 2.54 mm, p <0.0001). We detected no significant difference in frequency of CAD in patients with HCM (38.4%) compared to patients without HCM (27.33%, p = 0.09). In univariate regression analysis, increase in EAT by 1 standard deviation was associated with the presence of CAD (OR 1.24 95% CI 1.13-1.35, p < 0.0001). In subgroup analysis, EAT was significantly associated with presence of CAD in patients without HCM (1.432 [1.226-1.673] p < 0.0001) but not in patients with HCM (1.15 [0.984-1.344] p 0.078).

Conclusion: Patients with the diagnosis of HCM have significantly more EAT as compared to patients without HCM. However, the well-established association of EAT with CAD is less pronounced in HCM, suggesting that genetic mutations in HCM may also cause alterations in the amount and composition of epicardial adipose tissue.