The objective of the study was to assess the impact of DM2 at baseline on long-term mortality after acute myocardial infarction (MI) among different age groups. The data were taken from: “Register of Acute Myocardial Infarction.” A total of 862 patients were followed for five years after acute myocardial infarction. The primary endpoint was death from any cause. The patients were categorized into 2 groups based on their ages: group 1—comprised patients older than working age (n = 358) and group 2—comprised employable patients (n = 504). A total of 208 patients were diagnosed with both cardiovascular disease and DM2. Elderly patients with DM2 had worse prognosis and increased five-year mortality compared with patients of the same age group without DM2. Statistically significant differences in long-term outcomes were found in adult patients (p = 0.004) only in group with longer duration of diabetes, unlike the group with DM2 onset. In conclusion, Type 2 DM increased 5-year mortality rate of elderly patients with myocardial infarction. However, younger patients with both myocardial infarction and DM2 had more complications in the early post-MI period compared with patients of the same age group without DM2 but did not show any statistically significant differences in the long-term outcome.

The inotropic response of the myocardium to extrasystolic treatment was studied on isolated perfused papillary muscles from rats with postinfarction cardiosclerosis. The development of postinfarction cardiosclerosis was accompanied by a decrease in myocardial excitability. The amplitude of extrasystolic contractions in the remodeled myocardium far surpassed the control. However, the amplitude of postextrasystolic contraction did not surpass that in normal contraction-relaxation cycle. Our results suggest that the ability of the sarcoplasmic reticulum in cardiomyocytes to accumulate Ca2+ is impaired during postinfarction remodeling.

Coupling of the functional stability of rat myocardium and activity of lipid peroxidation processes in combined development of postinfarction remodeling and diabetes mellitus has been studied. The functional stability of myocardium was studied by means of the analysis of inotropic reaction on extrasystolic stimulus, the degree of left ventricular hypertrophy, and the size of scar zone. It was shown that in combined development of postinfarction cardiac remodeling of heart (PICR) with diabetes mellitus (DM) animal body weight decreased in less degree than in diabetic rats. Animals with combined pathology had no heart hypertrophy. The amplitude of extrasystolic contractions in rats with PICR combined with DM had no differences compared to the control group. In myocardium of rats with PICR combined with DM postextrasystolic potentiation was observed in contrast with the rats with PICR alone. The rats with combined pathology had the decreased value of TBA-active products. Thus, the results of study showed that induction of DM on the stage of the development of postinfarction remodeling increases adaptive ability of myocardium. It is manifested in inhibition of increase of LPO processes activity and maintaining of force-interval reactions of myocardium connected with calcium transport systems of sarcoplasmic reticulum of cardiomyocytes.

Background: Metabolic and structural changes in cardiomyocytes in diabetes mellitus lead to aggravation of contractile myocardial dysfunction in coronary heart disease (CHD). The contractility dysfunction of cardiomyocytes is determined by a change in the levels of sarcoplasmic reticulum (SR) Ca2+-ATPase and energetic supply of the cardiomyocytes. Aims: To study the features of functional remodeling of the heart muscle in coronary heart disease with and without type 2 diabetes mellitus (DM2) depend on the level of Ca2+-ATPase and the activity of enzymes involved in energy metabolism. Materials and methods: The work was performed on the heart biopsy of patients with CHD and patients with CHD combined with DM2. The inotropic reaction of myocardial strips on rest periods was assessed. The expression level of Ca2+-ATPase, the activity of enzymes succinate dehydrogenase (SDH) and lactate dehydrogenase (LDH) and the intensity of oxidative phosphorylation processes were determined. Results: The interval-force relationship in patients with CHD with and without DM2 had both negative and positive dynamics. The positive dynamics corresponds to the "high content" of the Ca2+-ATPase and the negative dynamics corresponds to the "low content" were found. At the combined pathology the positive inotropic dynamics is more pronounced and corresponds to a higher protein level. In the patients myocardium with CHD the activity of SDH and LDH was higher, while the oxygen uptake rate by mitochondria was higher in the myocardium with combined pathology. Conclusions: The potentiation of inotropic response of patient myocardium with CHD with and without DM2 corresponds to the "high level" of Ca2+-ATPase. In the combined pathology the inotropic capabilities of the myocardium are more expressed. In CHD the synthesis of ATP in cardiomyocytes is realized mainly due to glycolytic processes and Krebs cycle. In combined pathology the ATP synthesis is realized to a greater extent due to the oxidative phosphorylation.