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Background Stroke is a serious complication of hypertensive disorders of pregnancy (HDP), with potentially severe and long-term sequelae. However, the temporal trends, predictors, and outcomes of stroke in women with HDP at delivery remain unknown. Methods and Results All HDP delivery hospitalizations with or without stroke event (ischemic, hemorrhagic, or unspecified) between 2004 and 2014 in the United States National Inpatient Sample were analyzed to examine incidence, predictors, and prognostic impact of stroke. Of 4 240 284 HDP delivery hospitalizations, 3391 (0.08%) women had stroke. While the prevalence of HDP increased over time, incident stroke rates decreased from 10 to 6 per 10 000 HDP delivery hospitalizations between 2004 and 2014. Women with stroke were increasingly multimorbid, with some risk factors being more strongly associated with ischemic strokes, including congenital heart disease, peripheral vascular disease, dyslipidemia, and sickle cell disease. Delivery complications were also associated with stroke, including cesarean section (odds ratio [OR], 1.58; 95% CI, 1.33-1.86), postpartum hemorrhage (OR, 1.91; 95% CI, 1.33-1.86), and maternal mortality (OR, 99.78; 95% CI, 59.15-168.31), independently of potential confounders. Women with stroke had longer hospital stays (median, 6 versus 3 days), higher hospital charges (median, $14 655 versus $4762), and a higher proportion of nonroutine discharge locations (38% versus 4%). Conclusions The incidence of stroke in women with HDP has declined over time. While a relatively rare event, identification of women at highest risk of ischemic or hemorrhagic stroke on admission for delivery is important to reduce long-term sequelae.Background Heart failure with preserved ejection fraction (HFpEF) constitutes half of hospitalized heart failure cases and is commonly associated with obesity. The role of natriuretic peptide levels in hospitalized obese patients with HFpEF, however, is not well defined. We sought to evaluate change in NT-proBNP (N-terminal pro-B-type natriuretic peptide) levels by obesity category and related clinical outcomes in patients with HFpEF hospitalized for acute heart failure. Methods and Results A total of 89 patients with HFpEF hospitalized with acute decompensated heart failure were stratified into 3 obesity categories nonobese (body mass index [BMI] less then 30.0 kg/m2, 19%), obese (BMI 30.0-39.9 kg/m2, 29%), and severely obese (BMI ≥40.0 kg/m2, 52%), and compared for percent change in NT-proBNP during hospitalization and clinical outcomes. Inhibitor Library Clinical characteristics were compared between patients with normal NT-proBNP (≤125 pg/mL) and elevated NT-proBNP. Admission NT-proBNP was inversely related to BMI category (nonobese, 2607 pg/mL [interquartile range, IQR 2112-5703]; obese, 1725 pg/mL [IQR 889-3900]; and severely obese, 770.5 pg/mL [IQR 128-1268]; P less then 0.01). Severely obese patients had the largest percent change in NT-proBNP with diuresis (-64.8% [95% CI, -85.4 to -38.9] versus obese -40.4% [95% CI, -74.3 to -12.0] versus nonobese -46.9% [95% CI, -57.8 to -37.4]; P=0.03). Nonobese and obese patients had significantly worse 1-year survival compared with severely obese patients (63% versus 76% versus 95%, respectively; P less then 0.01). Patients with normal NT-proBNP (13%) were younger, with higher BMI, less atrial fibrillation, and less structural heart disease than those with elevated NT-proBNP. Conclusions In hospitalized patients with HFpEF, NT-proBNP was inversely related to BMI with the largest decrease in NT-proBNP seen in the highest obesity category. These findings have implications for the role of NT-proBNP in the diagnosis and assessment of treatment response in obese patients with HFpEF.Background Perturbations in myocardial substrate utilization have been proposed to contribute to the pathogenesis of cardiac dysfunction in diabetic subjects. The failing heart in nondiabetics tends to decrease reliance on fatty acid and glucose oxidation, and increases reliance on ketone body oxidation. In contrast, little is known regarding the mechanisms mediating this shift among all 3 substrates in diabetes mellitus. Therefore, we tested the hypothesis that changes in myocardial glucose utilization directly influence ketone body catabolism. Methods and Results We examined ventricular-cardiac tissue from the following murine models (1) streptozotocin-induced type 1 diabetes mellitus; (2) high-fat-diet-induced glucose intolerance; and transgenic inducible cardiac-restricted expression of (3) glucose transporter 4 (transgenic inducible cardiac restricted expression of glucose transporter 4); or (4) dominant negative O-GlcNAcase. Elevated blood glucose (type 1 diabetes mellitus and high-fat diet mice) was astolytic capacity through multiple mechanisms and identifies a potential crosstalk between glucose and ketone body metabolism in the diabetic myocardium.Sudden out-of-hospital cardiac arrest is the third leading cause of death in industrialized nations. Many of these lives could be saved if bystander cardiopulmonary resuscitation rates were better. "All citizens of the world can save a life-CHECK-CALL-COMPRESS." With these words, the International Liaison Committee on Resuscitation launched the 2019 global "World Restart a Heart" initiative to increase public awareness and improve the rates of bystander cardiopulmonary resuscitation and overall survival for millions of victims of cardiac arrest globally. All participating organizations were asked to train and to report the numbers of people trained and reached. Overall, social media impact and awareness reached up to 206 million people, and >5.4 million people were trained in cardiopulmonary resuscitation worldwide in 2019. Tool kits and information packs were circulated to 194 countries worldwide. Our simple and unified global message, "CHECK-CALL-COMPRESS," will save hundreds of thousands of lives worldwide and will further enable many policy makers around the world to take immediate and sustainable action in this most important healthcare issue and initiative.Background Disparities in premature cardiac death (PCD) might stagnate the progress toward the reduction of PCD in the United States and worldwide. We estimated disparities across US counties in PCD rates and investigated county-level factors related to the disparities. Methods and Results We used US mortality data for cause-of-death and demographic data from death certificates and county-level characteristics data from multiple databases. PCD was defined as any death that occurred at an age between 35 and 74 years with an underlying cause of death caused by cardiac disease based on International Classification of Diseases, Tenth Revision (ICD-10), codes. Of the 1 598 173 PCDs that occurred during 1999-2017, 60.9% were out of hospital. Although the PCD rates declined from 1999-2017, the proportion of out-of-hospital PCDs among all cardiac deaths increased from 58.3% to 61.5%. The geographic disparities in PCD rates across counties widened from 1999 (Theil index=0.10) to 2017 (Theil index=0.23), and within-state differences accounted for the majority of disparities (57.

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