Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide and constitute a substantial economic burden. Despite population aging, recent years have witnessed an increasing prevalence of conditions such as heart failure (HF), including among young adults. In this context, coronary artery disease (CAD) has also become an increasingly discussed issue. It has long been recognized that control of risk factors is crucial for prevention. Researchers stress the need to monitor these factors from the earliest stages of life, and detailed analyses indicate an influence of the prenatal period on the development of chronic diseases, including cardiovascular disorders. Transgenerational and intergenerational epigenetic mechanisms are also taken into account. This review aims to systematically evaluate the existing literature and summarize the mechanisms that may link these factors. We consider epigenetic, metabolic, immunological, and inflammatory influences. We describe examples of environmental exposures, such as air pollution, maternal diet, toxins, and infections, and analyze data derived from clinical studies. We discuss gaps in the literature and identify limitations, outlining directions for future research and emphasizing the need for CVD prevention initiated at the earliest stages of life.

Heart failure is a major public health issue and one of the leading causes of morbidity and mortality world-wide. Despite significant advances in heart failure treatment and improved patient prognosis, the effectiveness of standard therapies remains limited, prompting the search for new solutions. One of these are sodium-glucose co-transporter 2 inhibitors, initially introduced for the treatment of type 2 diabetes. They have demonstrated beneficial effects on the clinical course of heart failure, independent of the presence of carbohydrate metabolism disorders. Their mechanisms of action extend far beyond the hypoglycemic effect and involve multidimensional molecular processes. The most important include: modulation of cardiomyocyte energy metabolism, regulation of ionic homeostasis, effects on cardiac remodeling, and reduction of oxidative stress and inflammatory response. An increasing number of clinical studies confirm the role of these molecular effects in improving outcomes for HF patients. Understanding the complex mechanisms of sodium-glucose co-transporter 2 inhibitors provides new therapeutic opportunities and reinforces their position as a cornerstone of pharmacological heart failure management.