Clinical Features and Prognosis of Type 2 Myocardial Infarction in Acutely Decompensated Diabetic Patients.

BACKGROUND: After the introduction of the universal definition of myocardial infarction, the incidence and diagnosis of type 2 myocardial infarction have risen dramatically, yet there are no clear guidelines on clinical management. Diabetic patients are at high risk for developing type 2 myocardial infarction when admitted in a decompensated state, and they are also at high risk for future cardiovascular events. METHODS: We performed a retrospective analysis of 1058 patients admitted with diabetic ketoacidosis or hyperosmolar hyperglycemic state between 2011 and 2016. Patients were included if they had cardiac troponin I measured within 24 hours of admission, were older than 18 years of age, and had no evidence of acute coronary syndrome on admission. Baseline characteristics, admission laboratory test results, major adverse cardiovascular events, cardiac stress testing, and coronary angiography data up to 1 year after admission were reviewed. Patients were categorized into 2 groups: those with and those without type 2 myocardial infarction. The study had 2 endpoints: mortality and major adverse cardiac events (MACE) at 1 year and an abnormal result on stress test or coronary angiography at 1 year. RESULTS: Of the 845 patients who met the inclusion criteria, 133 patients (15%) had type 2 myocardial infarction on admission. Patients with type 2 myocardial infarction were at a significantly higher risk for mortality and MACE at 1 year than those without. Patients with type 2 myocardial infarction were also at higher risk for developing an abnormal result on stress test or coronary angiography within 1 year of admission as compared with those without type 2 myocardial infarction (40% vs 24%; odds ratio 2; P = .0699). CONCLUSION: Acutely decompensated diabetic patients with type 2 myocardial infarction are at increased risk for death and MACE. These patients may also be at risk for undiagnosed coronary artery disease.

Tcf19 is a novel islet factor necessary for proliferation and survival in the INS-1 ß-cell line.

Recently, a novel type 1 diabetes association locus was identified at human chromosome 6p31.3, and transcription factor 19 (TCF19) is a likely causal gene. Little is known about Tcf19, and we now show that it plays a role in both proliferation and apoptosis in insulinoma cells. Tcf19 is expressed in mouse and human islets, with increasing mRNA expression in nondiabetic obesity. The expression of Tcf19 is correlated with ß-cell mass expansion, suggesting that it may be a transcriptional regulator of ß-cell mass. Increasing proliferation and decreasing apoptotic cell death are two strategies to increase pancreatic ß-cell mass and prevent or delay diabetes. siRNA-mediated knockdown of Tcf19 in the INS-1 insulinoma cell line, a ß-cell model, results in a decrease in proliferation and an increase in apoptosis. There was a significant reduction in the expression of numerous cell cycle genes from the late G1 phase through the M phase, and cells were arrested at the G1/S checkpoint. We also observed increased apoptosis and susceptibility to endoplasmic reticulum (ER) stress after Tcf19 knockdown. There was a reduction in expression of genes important for the maintenance of ER homeostasis (Bip, p58(IPK), Edem1, and calreticulin) and an increase in proapoptotic genes (Bim, Bid, Nix, Gadd34, and Pdia2). Therefore, Tcf19 is necessary for both proliferation and survival and is a novel regulator of these pathways.