Heart failure in type 2 diabetes: current perspectives on screening, diagnosis and management

Fig. 1. Pathophysiological mechanisms of cardiomyopathy in type 2 diabetes (CMiPD). Fatty acids (FAs) are preferentially metabolized to ATP, sustaining muscle contraction. During progression to severe stages of cardiomyopathy, both the increased FA metabolism and accumulated ceramide contribute to inflammation and fibrosis, leading to cardiac stiffness and reduced contractility

Fig. 2. Mechanism for interaction between the metabolism disturbances and the heart. Insulin interferes with the free fatty acids (FFAs) metabolism. Consequently, a high amount of FFAs is present in the bloodstream, which impairs the insulin-mediated glucose uptake leading to hyperglycemia and insulin resistance, and promotes hypertension via increased sodium reabsorption and chronic sympathetic activity. In addition, insulin itself promotes hypertension. Metabolic disturbances impart a high risk for type 2 diabetes and heart failure progression, apart from FFA-rich epicardial fat tissue (EFT) that also facilitates heart failure

Fig. 3. Heart-kidney interaction is mediated by the natriuretic peptide system counterbalanced by the RAAS and the SNS. In early heart failure, the natriuretic peptide action dominates, leading to suppression of the SNS manifested as vasorelaxation and to natriuresis and diuresis in the kidney, which all translate into a lowered blood pressure. In chronic heart failure, the effectiveness of natriuretic peptides is lost, and actions of the overactivated RAAS and SNS dominate leading to vasoconstriction and expression of renin and angiotensin, which both mediate an increased blood pressure