bluuebunny/crossref_metadata_2025_split huggingface dataset:
ODP154 Reduction of Cardiac Adipose Tissue Volume with Short-Term Empagliflozin in Patients with Type 2 Diabetes: Results from the SIMPLE Randomized Clinical Trial
Authors: Brandt-Jacobsen Niels , Jürgens Mikkel , Hasbak Phillip , Gæde Peter , Rossing Peter , Rasmussen Jon , Andersen Camillla Fuchs , Forman Julie , Faber Jens , Inzucchi Silvio , Gustafsson Finn , Schou Morten , Kistorp Caroline 
Published: November 2022

Abstract

Background
Sodium-glucose transporter 2 inhibitors (SGLT2-is) appear to have rapid clinical cardiovascular benefits in type 2 diabetes. Furthermore, SGLT2-is have known effects on fat metabolism. Cardiac adipose tissue (CAT) correlates with known markers of cardiovascular risk and left ventricular function. The effects of SGLT2-i treatment on CAT is largely unknown.

Objective
In this exploratory sub-study from the SIMPLE-trial, we investigated whether empagliflozin affects CAT volume in patients with type 2 diabetes.

Methods
Between April 4, 2017, and May 11, 2020, we randomized 90 patients with type 2 diabetes and established or high risk of cardiovascular disease to either 25 mg empagliflozin or placebo for 13 weeks. The primary focus of this sub-study was change in CAT evaluated by computer-tomography (CT). The analysis included 78 patients who had at least one CT scan. Furthermore, we investigated the effect of empagliflozin on left ventricular mass (LVM), end-diastolic volume (EDV) and end-systolic volume (ESV) evaluated by rest and stress 82Rubidium Positron Emission Tomography CT and changes in whole-body metabolism evaluated by fat mass distribution via dual x-ray absorptiometry and measurements of various parameters of glucose, ketone and lipid metabolism.

Results
Mean ±SD baseline CAT volume was 258.5 mL ±117.9. Empagliflozin reduced CAT after 13 weeks by 12.41 mL (95%CI [-23.83 to -0.99], P=0. 034) as compared with placebo. LVM (-5.16 g, 95%CI [-8.80 to -1.52], P=0. 006), EDV (-7.90 mL, 95%CI [-13.70 to -2.10], P=0. 008) and ESV (-5.46 mL 95%CI [-9.78 to -1.15], P=0. 014) decreased with empagliflozin when comparing groups at week 13. In addition, improvements were observed in whole body metabolic parameters: mean total body weight (-1.48 kg, 95%CI [-2.41 to -0.55], P=0. 002), total fat mass (-0.81 kg, 95%CI [-1.40 to -0.22], P=0. 008), fasting plasma (-1.82 mmol/L, 95%CI [-2.83 to -0.80], P=0. 001), HbA1c (NGSP: -0.76%, 95%CI [-1. 00 to -0.51], P&lt;0. 001; IFCC: -8.28 mmol/mol, 95%CI [-11. 01 to -5.54], P&lt;0. 001), beta-hydroxybutyrate (0. 07 mmol/L, 95%CI [0. 00 to 0.14], P=0. 044), and triglycerides (-16.1%, 95%CI [-27.3 to -3.2], P=0. 017), when comparing groups at week 13. We observed no significant correlation between changes in CAT and changes in LVM, EDV and ESV.

Conclusion
Treatment with empagliflozin provides an early reduction of CAT and improves myocardial structure and function which may explain some of this SGLT2-i's clinical cardiovascular benefits.
Presentation: No date and time listed
OR02-4 Prediabetes is a Risk Factor for Myocardial Infarction-A National Inpatient Sample Study
Authors: Jyotheeswara Pillai Keerthana , Luo Hongxiu , Raj Kavin , Xu Shuang , Thota Geethika 
Published: November 2022

Abstract

Introduction
Prediabetes is defined as Hba1c 5.7% - 6.4%, with an intermediate metabolic state and includes impaired glucose tolerance and impaired fasting glucose due to insulin resistance. While Type 2 Diabetes Mellitus is a well-established risk factor for cardiovascular disease, the possible link between Prediabetes and risk of Myocardial infarction (MI) has become a focus of interest in recent years. We wanted to evaluate if Prediabetes is independently associated with increased risk for MI.

Methods
We included adult patients admitted to teaching hospitals with a primary or secondary diagnosis of "acute myocardial infarction" from the National inpatient sample of 2016, 2017, and 2018. We created three separate multivariate logistic regression models with outcomes as MI, Percutaneous intervention (PCI), and CABG (Coronary artery bypass grafting).

Results
A total of 1,794,149 (95% CI 1,753,742-1,834,556) weighted hospitalizations with MI were included. Out of the 1.79 million patients with MI, 1% had Prediabetes. Prediabetes was greatly associated with increased odds for MI (OR 1.41, 95% CI 1.35-1.47, P=0.000). After adjusting for age, sex, race, family history of MI, dyslipidemia, hypertension, Diabetes, nicotine dependence, and obesity, Prediabetes was significantly associated with increased odds of MI (OR 1.25, 95% CI 1.20-1.31, P=0.000), increased odds of PCI (OR 1.45, 95% CI 1.37-1.53, P=0.000) and increased odds of CABG (OR 1.95, 95% CI 1.77-2.16, P=0.000).

Discussion
Our study shows that Prediabetes may be an independent risk factor for MI despite adjusting for the well-established risk factors. Coronary interventions such as PCI and CABG were highly associated with Prediabetes, suggesting macrovascular CAD. This growing evidence indicates the need to identify patients with Prediabetes and aggressively manage their cardiovascular risk factors to prevent MI. Although Prediabetes is commonly missed during coding and adds a limitation to this study, we would highlight that the association of Prediabetes with Myocardial Infarction, PCI, and CABG is a significant addition to the literature. Our study serves as a wake-up call for clinicians and patients to shift the focus to preventing Prediabetes and not just Diabetes. Our findings reinforce the importance of early recognition by screening and early intervention of Prediabetes by lifestyle changes and/or medications to decrease the risk of cardiovascular events.
Presentation: Saturday, June 11, 2022 12:15 p.m. - 12:30 p.m.
RF32 | PSUN45 Nicotine E-Cigarette Vapors Exposure Disturbs 11β-Hydroxysteroid Dehydrogenase Type 2 Expression in the Kidney May Contribute to E-Cigarette-Induced Blood Pressure Elevation in Mice
Authors: Liu Jenny , Wang Jian , Wang Ying , Shao Xuesi , Lutfy Kabirullah , Friedman Theodore , Jiang Meisheng , Liu Yanjun 
Published: November 2022

Abstract
Inhalation of electronic (e)-cigarettes containing nicotine may elevate blood pressure (BP), but the underlying mechanisms are poorly understood. 11β-HSD2 is crucial for BP regulation by inactivating glucocorticoids in the kidney. Little is known about the effect of e-cigarettes on 11β-HSD2 and their contribution to the process of BP elevation. To examine the possible effects of e-cigarette vapor exposures on renal 11β-HSD2 and BP, four groups of mice were exposed to aerosolized PBS, nicotine-free or nicotine-containing e-cigarettes, with concurrent exposure to either saline or the nicotine antagonist hexamethonium (Hex). Mouse renal M1 CCD cells were used to identify the effects of nicotine on 11β-HSD2 and its transcription factor C/EBPβ. Our results showed that mice exposed to e-cigarettes containing nicotine for 4 weeks markedly decreased the expression and activity of renal 11β-HSD2 and elevated the systolic BP in C57BL/6J mice. Reduction of 11β-HSD2 by nicotine inhalation was accompanied by reduction of renal C/EBPβ and responded to elevated plasma nicotine levels. In contrast, these effects were not observed in mice exposed to e-cigarettes vapor without nicotine compared to PBS controls. Treatment with Hex significantly decreased the elevated ratio of urinary corticosterone to 11-DHC along with stimulation of renal C/EBPβ and prevented the raised BP in mice exposed to e-cigarette vapor containing nicotine. Treating CCD M1 cells with vaporized e-cigarettes containing nicotine extract showed comparable effects with those of pure nicotine for suppression of C/EBPβ and 11β-HSD2, and these effects are blocked by Hex, indicating a mechanistic specificity. Our results indicate that the inhalation of nicotine e-cigarette vapors has potential adverse effects on renal health suggesting that disturbance of renal 11β-HSD2 may contribute to e-cigarette nicotine-induced BP elevation. These findings highlight the potential health risk of e-cigarettes.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m., Monday, June 13, 2022 1:00 p.m. - 1:05 p.m.
RF32 | PSUN46 Impact of Hyperparathyroidism on Atrial Fibrillation In-Hospital Outcomes: A Nationwide Perspective
Authors: Chauhan Aditya , Devarakonda Pradeep , Pujari Sai Harika , Gopalakrishnan Akshaya , Karki Monika , Dhulipala Vishal , Reddy Sarath , Warman Jacob , Singh Surbhi , Singh Sohrab , Vigandt Erika 
Published: November 2022

Abstract

Background
Hyperparathyroidism, associated with calcium abnormalities has an increased probability of developing arrhythmias. However, there are very few studies to demonstrate the significance of hyperparathyroidism on Atrial Fibrillation (A-fib).

Methods
This is a retrospective cohort study using the 2017-2018 National Inpatient Sample. Patients with a primary discharge diagnosis of A-fib were extracted with ICD10. Patients with hyperparathyroidism were extracted as a secondary diagnosis. Demographics, clinical complications were compared, and outcomes were assessed using linear and logistic regression models to adjust for confounders.

Results
A total of 649,179 patients (Age &gt;18) were identified with A-fib as the primary diagnosis, and amongst them, 6254 had hyperparathyroidism. Notably, the patients with Hyperparathyroidism and A-fib were more likely to be female and blacks (26.8 vs 8). In-hospital mortality was higher in A-fib patients with hyperparathyroidism (2%) compared to A-fib patients without hyperparathyroidism (0.84%), with a crude odds ratio of 2.4 and adjusted odds ratio of 2.65 (p&lt;0.001). Mean length of stay (LOS) was greater in hyperparathyroidism patients (4.5 vs 3.2 days), with an adjusted odds ratio of 1.26, (p&lt;0.001). Similarly, mean total charges were also significantly higher in hyperparathyroidism patients ($53792 vs $39128).

Conclusions
Among patients with atrial fibrillation, those who have hyperparathyroidism as comorbidity are associated with more in-hospital mortality, LOS, and total charges. Further studies are required to study the causation of this association.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m., Monday, June 13, 2022 12:54 p.m. - 12:59 p.m.
RF32 | PSUN50 Hypertriglyceridemia as an Independent Risk Factor on Outcomes of Admissions for SIADH
Authors: Kwei-Nsoro Robert , Awoyomi Moyosoluwa , Khoshbin Katayoun , Ojemolon Pius , Olafimihan Ayobami , Shaka Hafeez 
Published: November 2022

Abstract

Introduction
The syndrome of inappropriate secretion of anti-diuretic hormone (SIADH) is one of the most significant causes of potentially life-threatening hyponatremia. Hypertriglyceridemia (HTG), on the other hand, is one of the few disorders that spuriously reduce sodium levels and should be ruled out in the evaluation of patients with hyponatremia. Very scant literature exists on the coexistence of both conditions, and even less literature compares outcomes in patients with concomitant SIADH and HTG.

Method
We extracted data from the US Nationwide Inpatient Sample (NIS) for 2019. The NIS contains hospital discharge information estimating yearly US hospitalizations. We included hospitalizations with a principal discharge diagnostic code for SIADH using the ICD-10-CM code (E22.2). Hospitalizations of patients less than 18 years were excluded. We then sub-divided the cohort based on the presence/absence of a secondary diagnosis of HTG.
Outcomes compared include inpatient mortality rates, mean length of hospital stay (LOS), mean hospitalization cost (THC), and rates of comorbid septic shock, acute myocardial infarction (AMI), acute respiratory failure (ARF), acute renal failure (AKI), and acute pulmonary edema (PE) between the subgroups. An adjustment was made for age, sex, race, primary payer, median household income by zip code, Charlson Comorbidity Index (CCI), hospital location, bed-size, and teaching status using multivariate regression analysis. Statistical significance was set at a p-value &lt; 0.05.

Results
There were 39,110 hospitalizations involving patients with SIADH as the reason for the admission in 2019. Of these hospitalizations, 41.8% had comorbid HTG. A higher proportion of SIADH hospitalizations involved females, with no significant difference between both cohorts (61 vs 62.7%, p=0.119). Patients with HTG had a higher mean age (75.8±11.1 vs 70.4±14.4 years, p&lt;0.001), a higher proportion of CCI &gt;2, and a higher proportion of ethnic minorities compared to patients without HTG.
Hospitalizations for SIADH with comorbid HTG were associated with lower adjusted odds ratio (aOR) for mortality (0.7 vs 1.4% in patients with HTG, aOR: 0.42, p&lt;0.001), reduced LOS (4.9 vs 5 days, p=0.002), and reduced THC (10,263 vs 11,013 US$, p=0.005). There was no difference in the odds of comorbid septic shock, CVA, AMI, PE, ARF or AKI.

Conclusions
Interestingly, comorbid HTG lowered odds of mortality, LOS, and THC amongst patients hospitalized for SIADH. More studies should be carried out to investigate this rather paradoxical relationship with a view to defining a better understanding and devising more therapeutic strategies for both conditions.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m., Monday, June 13, 2022 12:48 p.m. - 12:53 p.m.
LBODP019 Vitamin D Levels In A Population With Type 2 Diabetes
Authors: Elias Natalia Olga , Martinez Adriana Campos , Dicugno Mariana , Souto Julieta , Curria Marina Ines 
Published: November 2022

Abstract

Background
Little is known about the impact of over-the-counter ketone supplementation, used by patients to promote weight loss, on ketosis and serum ketone values. Recent literature suggests that acute ingestion of exogenous ketones leads to increased blood beta-hydroxybutyrate and decreased blood glucose1.

Clinical Case
A 61-year-old man with a history of type 2 diabetes mellitus, atrial fibrillation, hypertension, and hyperlipidemia presented as a transfer to the neurocritical care ICU from an outside hospital for subarachnoid hemorrhage secondary to intracranial saccular aneurysm. His admission hemoglobin A1c was 9.9% (ref 4.4-5.6), blood glucose was 205 mg/dL (ref 70-99), beta-hydroxybutyrate was markedly elevated at 26.2 mg/dL (ref 0-3), and urinalysis showed 80mg/dL ketones (ref 0). Serum toxicology screen was notable for detectable acetone 8mg/dL (ref: none detected). His lactate was 2 mmol/L (ref 0.5-1.9), Cr 0.99mg/dL (0.67-1.17), and HCO3 22 mmol/L (ref 22-27). Arterial blood gas showed pH of 7.37 (ref 7.38-7.47), and an anion gap metabolic acidosis (AGMA) of 15 mmol/L (ref &lt;12). Given the patient's profound ketosis, hyperglycemia, and mild AGMA, the patient was started on an insulin drip for presumed diabetic ketoacidosis (DKA). After 4 hours, the patient's anion gap had decreased to 12mmcol/L. The following day, he was transitioned to basal/bolus insulin, and underwent embolization of his cerebral aneurysm. After further recovery, Endocrinology was consulted for insulin recommendations. The patient denied any prior history of DKA or use of any SGLT2-inhibitors, and denied decreased oral intake or vomiting prior to admission. He did report taking ketone supplements, "Keto Strong: Ketogenic Weight Management – Advanced Formulation," two tabs (700mg "proprietary keto blend") BID for 2-3 years with ingredients listed as: sodium beta-hydroxybutyrate, calcium beta-hydroxybutyrate, magnesium beta-hydroxybutyrate, medium chain triglyceride oil, L-arginine, alpha-ketoglutaric acid, and 7-keto-dehydroepiandrosterone. Given a lack of acidosis, mild hyperglycemia, and mild lactic acidosis without risk factors for euglycemic DKA, it was suspected his profound ketosis out of proportion to clinical picture was secondary to ketone supplementation with a misdiagnosis of DKA.

Conclusion
This is one of the first cases to report profound ketosis in a hospitalized patient likely secondary to exogenous ketone supplementation. Ketosis secondary to nutritional supplementation should be considered once more common etiologies are ruled out. Additional research is needed to determine the role of exogenous ketone use on metabolism and glycemic control. References: Falkenhain, Kaja et al. "Effects of Exogenous Ketone Supplementation on Blood Glucose: A Systematic Review and Meta-Analysis." Advances in nutrition (Bethesda, Md.), nmac036. 5 Apr. 2022
Presentation: No date and time listed
LBODP035 When Is Ketosis Just Ketosis?
Authors: Cannon Sophie M , Angell Trevor E 
Published: November 2022

Abstract

Background
Little is known about the impact of over-the-counter ketone supplementation, used by patients to promote weight loss, on ketosis and serum ketone values. Recent literature suggests that acute ingestion of exogenous ketones leads to increased blood beta-hydroxybutyrate and decreased blood glucose1.

Clinical Case
A 61-year-old man with a history of type 2 diabetes mellitus, atrial fibrillation, hypertension, and hyperlipidemia presented as a transfer to the neurocritical care ICU from an outside hospital for subarachnoid hemorrhage secondary to intracranial saccular aneurysm. His admission hemoglobin A1c was 9.9% (ref 4.4-5.6), blood glucose was 205 mg/dL (ref 70-99), beta-hydroxybutyrate was markedly elevated at 26.2 mg/dL (ref 0-3), and urinalysis showed 80mg/dL ketones (ref 0). Serum toxicology screen was notable for detectable acetone 8mg/dL (ref: none detected). His lactate was 2 mmol/L (ref 0.5-1.9), Cr 0.99mg/dL (0.67-1.17), and HCO3 22 mmol/L (ref 22-27). Arterial blood gas showed pH of 7.37 (ref 7.38-7.47), and an anion gap metabolic acidosis (AGMA) of 15 mmol/L (ref &lt;12). Given the patient's profound ketosis, hyperglycemia, and mild AGMA, the patient was started on an insulin drip for presumed diabetic ketoacidosis (DKA). After 4 hours, the patient's anion gap had decreased to 12mmcol/L. The following day, he was transitioned to basal/bolus insulin, and underwent embolization of his cerebral aneurysm. After further recovery, Endocrinology was consulted for insulin recommendations. The patient denied any prior history of DKA or use of any SGLT2-inhibitors, and denied decreased oral intake or vomiting prior to admission. He did report taking ketone supplements, "Keto Strong: Ketogenic Weight Management – Advanced Formulation," two tabs (700mg "proprietary keto blend") BID for 2-3 years with ingredients listed as: sodium beta-hydroxybutyrate, calcium beta-hydroxybutyrate, magnesium beta-hydroxybutyrate, medium chain triglyceride oil, L-arginine, alpha-ketoglutaric acid, and 7-keto-dehydroepiandrosterone. Given a lack of acidosis, mild hyperglycemia, and mild lactic acidosis without risk factors for euglycemic DKA, it was suspected his profound ketosis out of proportion to clinical picture was secondary to ketone supplementation with a misdiagnosis of DKA.

Conclusion
This is one of the first cases to report profound ketosis in a hospitalized patient likely secondary to exogenous ketone supplementation. Ketosis secondary to nutritional supplementation should be considered once more common etiologies are ruled out. Additional research is needed to determine the role of exogenous ketone use on metabolism and glycemic control. References: Falkenhain, Kaja et al. "Effects of Exogenous Ketone Supplementation on Blood Glucose: A Systematic Review and Meta-Analysis." Advances in nutrition (Bethesda, Md.), nmac036. 5 Apr. 2022
Presentation: No date and time listed
LBODP041 Effects Of Sodium-glucose Co-transporter 2 Inhibitors (sglt-2 Inhibitors) On Adipokines And Inflammatory Biomarkers In Type2 Diabetic Patients
Authors: Kumtree Phonphruet 
Published: November 2022

Abstract

Background
Type 2 diabetes mellitus is a chronic metabolic disease associated with high cardiovascular (CV) risk. SGLT-2 inhibitors reduce HbA1c and show favorable effects on body weight, blood pressure, lipid profile, arterial stiffness, and endothelial function. More importantly, SGLT-2 inhibitors have demonstrated impressive cardioprotective and renoprotective effects. The main mechanisms of cardioprotective effects have been attributed to improvement in cardiac cell metabolism, improvement in ventricular loading conditions, inhibition of the Na+/H+ exchanger in myocardial cells, alteration in adipokines and cytokines production. This exploratory research aimed to observe the effects of Canagliflozin, Dapagliflozin, and Empagliflozin on select inflammatory biomarkers, adiponectin, for instance.

Methods
Comparison of serum adiponectin between baseline with 16-week after SGLT-2 inhibitors therapy were assessed in type 2 diabetic participants. Changes of chosen metabolic and anthropometric variables were discussed.

Results
At 16-week after SGLT-2 inhibitors treatment, a striking increment in mean serum adiponectin by 1.25 mcg/mL (95% CI: 0. 02, 2.48) or 81% was revealed. Furthermore, they showed a reduction of mean BMI 1.12% (95% CI: -1.74%, -0.50%), systolic blood pressure 1 mmHg (95% CI: -1.85, -0.72), diastolic blood pressure 1 mmHg (95% CI: -1.65, -0.52), fasting plasma glucose 34 mg/dL (95% CI: -51.66, -17.10), and HbA1c 0.73% (95% CI: -1.25%, -0.21%). No between-group differences were expressed with the other biomarkers. Serious side effects such as ketoacidosis, hypoglycemic status, genitourinary tract infection, acute kidney injury, or long-term dialysis dependence were not appeared.

Conclusions
SGLT-2 inhibitors can improve changes in serum adiponectin which appreciatively benefit in cardiovascular outcomes among type 2 diabetes. Keywords: SGLT-2 inhibitors, adipokines, inflammatory biomarkers, type 2 diabetes mellitus, adiponectin, cardiovascular outcomes, cardioprotective, renoprotective
Presentation: No date and time listed