Comparison of the pathways of care and life courses between first-time ST-elevation myocardial infarction (STEMI) and STEMI with prior MI: findings from the OSCAR registry.

OBJECTIVES: We hypothesised that patients having experienced one coronary event in their life were susceptible to present differences in their pathways of care and within 1 year of their life courses. We aimed to compare pathways between first-time ST-elevation myocardial infarction (STEMI) and STEMI with prior myocardial infarction (MI). DESIGN: A retrospective observational study based on the Observatoire des Syndromes Coronariens Aigus du réseau RESCUe (OSCAR) registry collecting all suspected STEMI from 10 percutaneous coronary intervention centres in France. SETTING: All patients with STEMI from 2013 to 2017 were included (N=6306 with 5423 first-time STEMI and 883 STEMI with prior MI). We provided a matching analysis by propensity score based on cardiovascular risk factors. PARTICIPANTS: We defined first-time STEMI as STEMI occurring at the inclusion date, and STEMI with prior MI as STEMI with a history of MI prior to the inclusion date. RESULTS: Patients with first-time STEMI and patients with STEMI with prior MI were equally treated during hospitalisation and at discharge. At 12 months, patients with first-time STEMI had a lower adherence to BASIC treatment (ie, beta-blocker, antiplatelet therapy, statin and converting enzyme inhibitor) (48.11% vs 58.58%, p=0.0167), more frequently completed the cardiac rehabilitation programme (44.33% vs 31.72%, p=0.0029), more frequently changed their lifestyle behaviours; more frequently practiced daily physical activity (48.11% vs 35.82%, p=0.0043) and more frequently stopped smoking at admission (69.39% vs 55.00%, p=0.0524). The estimated mortality was higher for patients with STEMI with prior MI at 1 month (p=0.0100), 6 months (p=0.0500) and 1 year (p=0.0600). CONCLUSIONS: We provided an exhaustive overview of the real-life clinical practice conditions of STEMI management. The patients with STEMI with prior MI presented an optimised use of prehospital resources, which was probably due to their previous experience, and showed a better adherence to drug therapy compared with patients with first-time STEMI. TRIAL REGISTRATION NUMBER: Commission Nationale de l'Informatique et des Libertés (number 2 013 090 v0).

Role of hypoxia-induced anorexia and right ventricular hypertrophy on lactate transport and MCT expression in rat muscle.

To dissect the independent effects of altitude-induced hypoxemia and anorexia on the capacity for cardiac lactate metabolism, we examined the effects of 21 days of chronic hypobaric hypoxia (CHH) and its associated decrease in food intake and right ventricle (RV) hypertrophy on the monocarboxylate transporter 1 and 4 (MCT) expression, the rate of lactate uptake into sarcolemmal vesicles, and the activity of lactate dehydrogenase isoforms in rat muscles. In comparison with control rats (C), 1 mmol/L lactate transport measured on skeletal muscle sarcolemmal vesicles increased by 33% and 58% in hypoxic (CHH, barometric pressure = 495 hPa) and rats pair-fed an equivalent quantity of food to that consumed by hypoxic animals, respectively. The increased lactate transport was higher in PF than in CHH animals ( P < .05). No associated change in the expression of MCT1 protein was observed in skeletal muscles, whereas MCT1 mRNA decreased in CHH rats, in comparison with C animals (42%, P < .05), partly related to caloric restriction (30%, P < .05). MCT4 mRNA and protein increased during acclimatization to hypoxia only in slow-oxidative muscles (68%, 72%, P < .05, respectively). The MCT4 protein content did not change in the plantaris muscle despite a decrease in transcript levels, related to hypoxia and caloric restriction. In both the left and right ventricles, the MCT1 protein content was unaffected by ambient hypoxia or restricted food consumption. These results suggest that MCT1 and MCT4 gene expression in fast-glycolytic muscles is mainly regulated by posttranscriptional mechanisms. Moreover, the results emphasize the role played by caloric restriction on the control of gene expression in response to chronic hypoxia and suggest that hypoxia-induced right ventricle hypertrophy failed to alter MCT proteins.

Effects of streptozotocin-induced diabetes on markers of skeletal muscle metabolism and monocarboxylate transporter 1 to monocarboxylate transporter 4 transporters.

Diabetes is known to alter both oxidative and glycolytic pathways in a fiber type-dependent manner. In various skeletal muscles of normal rats, monocarboxylate transporter 1 (MCT1) has been found to be highly correlated to lactate uptake, as well as to oxidative capacity, whereas the distribution and characteristics of MCT4 make it a good candidate for the extrusion of lactic acid from glycolytic muscle cells. Since a previous study found decreased sarcolemmal lactate uptake in streptozotocin (STZ)-diabetic rats, we investigated the presence of MCT1 in relation to enzymatic markers of both oxidative and glycolytic pathways, as well as MCT4 content, in STZ-diabetic rats. Soleus (SOL), red tibialis anterior (RTA), extensor digitorus longus (EDL), heart, and preparations of purified sarcolemmal vesicles (SV) from control and STZ-diabetic rats were harvested for MCT1 and MCT4 content, citrate synthase activity (CS), and lactate dehydrogenase (LDH) isozymes. Basal blood lactate concentration was increased by 38% in the diabetic rats (close to 1.91 mmol/L). However, no change was found in either MCT1 or MCT4 content in these rats. The diabetic rats presented fiber type-specific decrease in CS activity. We noted a redistribution in LDH isozymes in diabetic muscles with a general increase in type H-LDH. Regression analyses indicated (1) a strong relationship between LDH-4 and LDH-5 and (2) MCT1 was still correlated with CS activity in diabetic muscles. These results suggest that diabetes-induced hyperlactatemia is not associated with changes in MCT1 or MCT4 expression, but with alterations of oxidative and glycolytic enzymes.