Acta Medica Colombiana
Print version ISSN 0120-2448
GOMEZ LOPEZ, Efraín Alonso. Metabolic syndrome and heart failure. Acta Med Colomb [online]. 2005, vol.30, n.3, pp. 154-163. ISSN 0120-2448.
As a result of aging, increased numbers of obese people and its association with metabolic syndrome, and the reduction in physical activity overall, the global incidence and prevalence of diabetes mellitus is growing at a very fast pace. There are many biophysical and biochemical abnormalities in the failing heart. In diabetes, there are dramatic changes in energy metabolism that may contribute to a reduction of the contractile function both in heart failure following acute myocardial infarction as well as in diabetic cardiomyopathy. Diabetes also induces alterations in glucose metabolism, especially in myocardial glucose transport, glycolysis and glucose oxidation, which are all present in low levels in diabetic patients. Insulin resistance is an important risk factor for the development of cardiovascular disease, including hypertension, left-ventricular dysfunction and heart failure. Moreover, insulin resistance is a key component of metabolic syndrome and diabetes. There are myocyte adaptive and maladaptive processes in diabetic patients. In maladaptive processes there are three factors that play a relevant role: glycotoxicity, lipotoxicity and gluco-lipotoxicity. There are other factors associated with the development of heart failure such as diabetic cardiomyopathy, which requires early recognition and treatment. The general management guidelines for heart failure are used for the treatment of heart failure associated with metabolic syndrome, emphasizing those medications that provide a metabolic benefit to patients with metabolic syndrome or diabetes mellitus.
Keywords : síndrome metabólico; diabetes mellitus tipo 2; falla cardiaca; metabolismo cardiaco; adaptación miocárdica; desadaptacion miocárdica; metabolic syndrome; type-2 diabetes mellitus; heart failure; cardiac metabolism; myocardial adaptation and maladaptation.