The Use of Empagliflozin in Patients With Hypertrophic Cardiomyopathy

Description of the study: Hypertrophic cardiomyopathy (HCM) is the most common genetic disease of the myocardium. Conventionally, the incidence of this disease was estimated at 1: 500 people, but it is probably higher and amounts to about 1: 200 cases. In Poland, this gives 76,000 to 190,000 people. HCM is asymptomatic in some people. In others, it is associated with progressive left ventricular diastolic dysfunction due to myocardial hypertrophy and fibrosis, eventually leading to systolic dysfunction and progressive heart failure. Both heart failure with preserved left ventricular ejection fraction (LVEF) and reduced LVEF are inevitably associated with impaired physical function, often affecting young, professionally and socially active individuals. An additional significant problem in patients with HCM is arrhythmias leading to an increased risk of sudden death.

At present, for patients with HCM, there is no treatment available, which could inhibit the progression of the disease. The methods of treatment proposed so far, affecting the various pathogenic mechanisms of hypertrophic cardiomyopathy, have proved to be ineffective.

Empagliflozin is a reversible, potent and selective competitive inhibitor of sodium-glucose co-transporter-2 (SGLT2). It is the main transporter responsible for the reabsorption of glucose from the glomerular filtrate into the bloodstream. Its inhibition in people with type 2 diabetes leads to an increase in urinary glucose excretion and a decrease in its concentration in the blood. In the study in patients with type 2 diabetes and high cardiovascular risk, the use of empagliflozin was associated with a significant decrease in mortality and the number of hospitalizations due to heart failure. The mechanisms responsible for beneficial effects of empagliflozin are not fully understood. It is underlined that effects leading to a reduction of oxidative stress, improvement of diastolic function, inhibition of myocardial fibrosis and, what is important, improvement of myocardial energy status and reduction of cardiomyocyte calcium overload, increase of sarcoplasmic reticulum Ca2+ ATPase 2 (SERCA2) activity, which are important pathophysiological mechanisms of HCM, leading to progressive myocardial hypertrophy and the development of heart failure.