The Impact of Coronary Artery Disease on Outcomes in Patients With Peripartum Cardiomyopathy.

Introduction The purpose of this study was to determine the prevalence of coronary artery disease (CAD) among patients admitted with peripartum cardiomyopathy (PPCM) as well as to analyze the independent association of CAD with in-hospital outcomes among PPCM patients. Methods Data were obtained from the National Inpatient Sample from January 2016 to December 2019. We assessed the independent association of CAD with outcomes in patients admitted with PPCM. Predictors of mortality in patients admitted with PPCM were also analyzed. Results There was a total of 4,730 patients with PPCM, 146 of whom had CAD (3.1%). Multivariate analysis demonstrated that CAD in patients with PPCM was independently associated with several outcomes, and, among them, ST-segment elevation myocardial infarction (STEMI) (adjusted odds ratio (aOR): 58.457, 95% CI: 5.403-632.504, p= 0.001) was positively associated with CAD. CAD was found to be protective against preeclampsia (aOR: 0.351, 95% CI: 0.126-0.979, p = 0.045). Predictors of in-hospital mortality for patients with PPCM include cardiogenic shock (aOR: 12.818, 95% CI: 7.332-22.411, p = 0.001), non-ST elevation myocardial infarction (NSTEMI) (OR: 3.429, 95% CI: 1.43-8.22, p = 0.006), chronic kidney disease (OR: 2.851, 95% CI: 1.495-5.435, p = 0.001), and atrial fibrillation (OR: 2.326, 95% CI: 1.145-4.723, p = 0.020). Conclusion In a large cohort of patients admitted with PPCM, we found the prevalence of CAD to be 3.1%. CAD was associated with several adverse outcomes, including STEMI, but protective against preeclampsia.

Glucose-sensing glucagon-like peptide-1 receptor neurons in the dorsomedial hypothalamus regulate glucose metabolism.

Glucagon-like peptide-1 (GLP-1) regulates energy homeostasis via activation of the GLP-1 receptors (GLP-1Rs) in the central nervous system. However, the mechanism by which the central GLP-1 signal controls blood glucose levels, especially in different nutrient states, remains unclear. Here, we defined a population of glucose-sensing GLP-1R neurons in the dorsomedial hypothalamic nucleus (DMH), by which endogenous GLP-1 decreases glucose levels via the cross-talk between the hypothalamus and pancreas. Specifically, we illustrated the sufficiency and necessity of DMHGLP-1R in glucose regulation. The activation of the DMHGLP-1R neurons is mediated by a cAMP-PKA-dependent inhibition of a delayed rectifier potassium current. We also dissected a descending control of DMHGLP-1R -dorsal motor nucleus of the vagus nerve (DMV)-pancreas activity that can regulate glucose levels by increasing insulin release. Thus, our results illustrate how central GLP-1 action in the DMH can induce a nutrient state-dependent reduction in blood glucose level.