RESUMEN
Metabolic syndrome is a pre-diabetic state characterized by several biochemical and physiological alterations, including insulin resistance, visceral fat accumulation, and dyslipidemias, which increase the risk for developing cardiovascular disease. Metabolic syndrome is associated with augmented sympathetic tone, which could account for the etiology of pre-diabetic cardiomyopathy. This review summarizes the current knowledge of the pathophysiological consequences of enhanced and sustained ß-adrenergic response in pre-diabetes, focusing on cardiac dysfunction reported in diet-induced experimental models of pre-diabetic cardiomyopathy. The research reviewed indicates that both protein kinase A and Ca2+/calmodulin-dependent protein kinase II play important roles in functional responses mediated by ß1-adrenoceptors; therefore, alterations in the expression or function of these kinases can be deleterious. This review also outlines recent information on the role of protein kinase A and Ca2+/calmodulin-dependent protein kinase II in abnormal Ca2+ handling by cardiomyocytes from diet-induced models of pre-diabetic cardiomyopathy.
RESUMEN
Heart rate variability (HRV) is highly influenced by the Autonomic Nervous System (ANS). Several illnesses have been associated with changes in the ANS, thus altering the pattern of HRV. However, the variability of the heart rhythm is originated within the Sinus Atrial Node (SAN) which has its own variability. Still, although both oscillators produce HRV, the influence of the SAN on HRV has not yet been exhaustively studied. On the other hand, the complications of diabetes mellitus (DM), for instance, nephropathy, retinopathy, and neuropathy, increase cardiovascular morbidity and mortality. Traditionally, these complications are diagnosed only when the patient is already suffering from the negative symptoms these complications implicate. Consequently, it is of paramount importance to develop new techniques for early diagnosis prior to any deterioration on healthy patients. HRV has been proved to be a valuable, noninvasive clinical evidence for evaluating diseases and even for describing aging and behavior. In this study, several ECGs were recorded and their RR and PP intervals were analyzed to detect the interpotential interval (ii) of the SAN. Additionally, HRV reduction was quantified to identify alterations in the nervous system within the nodal tissue via measuring the SD1/SD2 ratio in a Poincaré plot. With 15 years of DM development, the data showed an age-dependent increase in HRV due to the axon retraction of ANS neurons from its effectors. In addition, these alterations modify the heart rhythm-producing fatal arrhythmias. Therefore, it is possible to avoid the consequences of DM identifying alterations in SAN previous to its symptomatic appearance. This could be used as an early diagnosis indicator.
