A recent study investigated the relationship between plasma free fatty acids (FFA) and HCM. In a study published online in BMC Cardiovascular Disorders, authors focused on the clinical importance of FFA metabolism in patients with HCM.

“There are more than 1,400 mutations in at least 11 of the genes producing cardiac sarcomere, which results in hypertrophic cardiomyopathy, a 2‰ percent prevalence of a typical genetic cardiovascular disease among the overall population,” the authors explained.

“Asymmetric left ventricular thickness, fibrosis, and reduced diastolic function are its hallmarks. Pathogenic variants of the sarcomere gene can cause high dynamic contraction, impaired relaxation, and increased cardiac energy consumption, which are all characteristics of hypertrophic cardiomyopathy and increase the risk of arrhythmia, heart failure, and even sudden death.”

The research was a single center retrospective observational study conducted at Beijing Anzhen Hospital from January 1, 2018, to December 31, 2022. The study included 420 patients with HCM and 1372 patients without HCM, with 391 matched controls without HCM via propensity score matching (PSM).

Key findings revealed significant correlations between FFA levels and several clinical parameters in patients with HCM. Specifically, FFA showed positive correlations with creatinine (r=0.115; P=0.023) and brain natriuretic peptide (BNP) (r=0.152; P=0.007), and negative correlations with estimated GFR (r=-0.130; P=0.010), left ventricular ejection fraction (LVEF) (r=-0.227; P<0.001), and left ventricular fractional shortening (r=-0.160; P=0.002). Notably, patients with HCM and atrial fibrillation and those in NYHA functional classes III or IV had higher FFA levels ( P=0.015 and P=0.022, respectively). Mul – tiple linear regression analysis identified BNP and LVEF as independent predictors of increased FFA (Standardized =0.139, P=0.013 and =-0.196, P<0.001, respectively).

The study supports previous research indicating that energy deficiency plays a crucial role in HCM pathophysiology. FFAs, a primary energy substrate for the heart, are reduced in patients with HCM, suggesting altered energy metabolism. These findings suggested that increased FFA levels in patients with advanced disease and atrial fibrillation may reflect compensatory mechanisms or disease severity. The findings emphasized the need for further research to explore the role of FFA and energy metabolism in HCM and its potential prognostic value. Overall, lower plasma FFA levels in patients with HCM, along with significant correlations with LVEF and BNP, highlight the importance of FFA metabolism in the disease’s pathogenesis. These insights could guide future efforts to address energy deficiency in HCM, potentially leading to improved patient outcomes.