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BackgroundHeart failure is a common and devastating complication of type 2 diabetes (T2D). Prompt recognition of heart failure may avert hospitalization, facilitate use of guideline-directed therapies, and impact choice of T2D medications. We sought to determine the rate and factors associated with heart failure documentation in T2D patients with evidence of volume overload requiring loop diuretics.MethodsDCR is an on-going, prospective US registry of outpatient T2D patients from > 5000 cardiology, endocrinology, and primary care clinicians (current analysis used data from 2013-2019). Among T2D patients receiving loop diuretics, we examined the rate of chart documentation of heart failure. We used a 3-level hierarchical logistic regression model (patients nested within physician within practice) to examine factors associated with heart failure diagnosis.ResultsAmong 1,322,640 adults with T2D, 225,125 (17.0%) were receiving a loop diuretic, of whom 91,969 (40.9%) had documentation of heart failure. Male sex, lower body mass index, atrial fibrillation, chronic kidney disease, and coronary artery disease were associated with greater odds of heart failure diagnosis. After accounting for patient factors, patients seen by cardiologists were the most likely to have HF documented followed by PCPs and then endocrinologists.ConclusionsAmong US outpatients with T2D, 17% of patients had evidence of volume overload-defined by loop diuretic prescription-of whom fewer than half had a clinical diagnosis of heart failure. While there may be non-heart failure indications for loop diuretics, our data suggest that a substantial proportion of T2D patients may have unrecognized heart failure and therefore could be missing opportunities for targeted therapies that could alter the clinical course of heart failure.

Aim: To compare adverse outcomes among COVID‐19 patients with pre‐existing type 2 diabetes (T2D) only, T2D and cardiovascular disease (CVD), or neither. Methods: This retrospective cohort study used administrative claims, laboratory and mortality data from the HealthCore Integrated Research Database. Patients with COVID‐19 were identified from 3 January 2020 to 31 May 2021 and stratified by the presence of T2D and CVD. Outcomes included hospitalization, intensive care unit (ICU) admission, mortality and complications following COVID‐19 infection. Propensity score matching and multivariable analyses were performed. Results: A total of 321 232 COVID‐19 patients were identified (21 651 T2D + CVD, 28 184 T2D only, and 271 397 neither) with a mean (SD) follow‐up of 5.4 (3.0) months. After matching, 6 967 patients were identified for each group, and residual baseline differences remained. Adjusted analyses showed that COVID‐19 patients with T2D + CVD were 59% more probable to be hospitalized, 74% more probable to be admitted to the ICU, and had a 26% higher mortality risk than those with neither. COVID‐19 patients with T2D only were 28% and 32% more probable to be admitted to the hospital and ICU than those with neither, respectively. Among all T2D + CVD patients, acute respiratory distress syndrome (31%) and acute kidney disease (24%) were observed. Conclusion: Our study highlights the incrementally poorer outcomes associated with pre‐existing T2D + CVD in COVID‐19 patients compared with those without T2D/CVD and suggests consideration of a more optimal management approach in these patients. [ABSTRACT FROM AUTHOR]

Elevated plasma lipoprotein(a) may be an additional risk factor for coronary heart disease in middle-aged men. This was demonstrated in the Framingham Offspring study, which has followed the children of the original Framingham population since 1971. At the fourth examination between 1987 and 1991, men whose lipoprotein(a) was elevated in the early 1970s were twice as likely to develop coronary heart disease. The risk was as strong as the risk of elevated cholesterol. However, smoking was the strongest risk factor for coronary heart disease in these men., Objective.--To establish whether elevated lipoprotein(a) [Lp(a)], detected as a sinking pre-[Beta]-lipoprotein band on electrophoresis of fresh plasma, is an independent risk factor for the development of premature coronary heart disease (CHD) in men. Design and Setting.--Prospective study of the Framingham offspring cohort. Participants.--A total of 2191 men aged 20 to 54 years old who were free of cardiovascular disease when they were examined between 1971 and 1975. Main Outcome Measures.--Incident CHD (myocardial infarction, coronary insufficiency, angina pectoris, or sudden cardiac death) occurring by age 55 years. Results.--After a median follow-up of 15.4 years, there were 129 CHD events. The relative risk (RR) estimates (with 95% confidence intervals [Cis]) for premature CHD derived from a proportional hazards model that included age, body mass index, and the dichotomized risk factor covariables elevated plasma Lp(a) level, total cholesterol level of 6.2 mmol/L (240 mg/dL) or more, high-density lipoprotein (HDL) level less than 0.9 mmol/L (35 mg/dL), smoking, glucose intolerance, and hypertension were as follows: elevated Lp(a) level, RR, 1.9 (95% Cl, 1.2-2.9), prevalence, 11.3%; total cholesterol level of 6.2 mmol/L or more, RR, 1.8 (95% Cl, 1.2-2.7), prevalence, 14.3%; HDL level of less than 0.9 mmol/L, RR, 1.8 (95% Cl, 1.2-2.6), prevalence, 19.2%; smoking, RR, 3.6 (95% Cl, 2.2-5.5), prevalence, 46.7%; glucose intolerance, RR, 2.7 (95% Cl, 1.4-5.3), prevalence, 2.6%; hypertension, RR, 1.2 (95% Cl, 0.8-1.8), prevalence, 26.3%. Conclusions.--Elevated plasma Lp(a) is an independent risk factor for the development of premature CHD in men, comparable in magnitude and prevalence (ie, attributable risk) to a total cholesterol level of 6.2 mmol/L (240 mg/dL) or more, or an HDL level less than 0.9 mmol/L (35 mg/dL). JAMA. 1996;276:544-548

The 1245.29 Trial recently showed that empaglifozin improved both blood pressure and glucose control in African American (AA) patients with type 2 diabetes (T2D) and hypertension. Using the Diabetes Collaborative Registry, a large‐scale US registry of outpatients with diabetes recruited from primary care, cardiology and endocrinology practices, we sought to understand the potential impact of these observations in routine clinical practice. Among 74 290 AA patients with T2D from 368 US clinics, 60.4% had hypertension, of whom 34.5% had systolic blood pressure ≥ 140 mm Hg (20.8% of the total AA T2D population). Only 1.7% of this eligible population had been prescribed a sodium‐glucose co‐transporter two inhibitor. The mean estimated 5‐year risk of cardiovascular death was 7.7%, which could be reduced to 6.2% when modelling the antihypertensive effect of empagliflozin across the eligible population (based on an 8‐mm Hg blood pressure reduction). These findings may represent a potential opportunity for better management of cardiovascular risk factors and improved outcomes in this vulnerable cohort. [ABSTRACT FROM AUTHOR]

Objective: Black/African American individuals have a higher prevalence of type 2 diabetes mellitus (T2DM), diabetes-related complications and hypertension, but they are often underrepresented in clinical trials. The sodium-glucose co-transporter 2 inhibitor, empagliflozin, was associated with significant improvements in glucose control (via hemoglobin [Hb] A1c) and reductions in blood pressure (BP; via office and ambulatory BP monitoring) in a primarily white population with T2DM and hypertension. The aim of this ongoing study is to assess the safety and efficacy of empagliflozin in terms of glucose- and BP-lowering in a self-identified black/African American population with T2DM and hypertension.Methods: This was a multicenter, randomized, double-blind, placebo-controlled, parallel-group, phase 3b study carried out at 85 centers in the USA. It was designed to assess the safety and efficacy of empagliflozin (10 or 25 mg/day) versus placebo in black/African American patients with uncontrolled T2DM and hypertension. Patients receiving stable glucose-lowering therapy prestudy continued at the same dose during the trial; BP-lowering medication was also held stable. The primary endpoint was the change from baseline in HbA1c at Week 24. Key secondary endpoints were change from baseline in: mean 24-hour ambulatory systolic BP (SBP) at Week 12, mean trough ambulatory SBP at Week 12, body weight at Week 24 and trough seated SBP at Week 12.Results: The study will report final data in 2018.Conclusions: Results of this study will add to our understanding of the efficacy and safety of empagliflozin in self-identified black/African American patients with T2DM and hypertension. (ClinicalTrials.gov identifier: NCT02182830.). [ABSTRACT FROM AUTHOR]

1. The absorption, biotransformation and excretion of empagliflozin, an SGLT2 inhibitor, were evaluated in eight healthy subjects following a single 50 mg oral dose of empagliflozin containing ∼100 µCi [14C]-empagliflozin. 2. Radioactivity was rapidly absorbed, with plasma levels peaking 1 h post-dose. Total exposure was lower in blood versus plasma, consistent with moderate (28.6-36.8%) red blood cell partitioning. Protein binding was 80.3-86.2%. 3. Most of the radioactive dose was recovered in urine (54.4%) and faeces (41.1%). Unchanged empagliflozin was the most abundant drug-related component in plasma, representing 75.5-77.4% of plasma radioactivity and 79.6% plasma radioactivity AUC0-12 h. Unchanged empagliflozin was the most abundant drug-related component in urine and faeces, representing 43.5% (23.7% of dose) and 82.9% (34.1% of dose) of radioactivity in urine and faeces, respectively. Six metabolites were identified in plasma: three glucuronide conjugates representing 4.7-7.1% of AUC0-12 h and three less abundant metabolites (<0.2-1.9% AUC0-12 h). The most abundant metabolites in urine were two glucuronide conjugates (7.8-13.2% of dose) and in faeces was a tetrahydrofuran ring-opened carboxylic acid metabolite (1.9% of dose). 4. To conclude, empagliflozin was rapidly absorbed and excreted primarily unchanged in urine and faeces. Unchanged parent was the major drug-related component in plasma. Metabolism was primarily via glucuronide conjugation. [ABSTRACT FROM AUTHOR]

The effects of atorvastatin (40 mg/day) versus placebo on fasting and postprandial plasma levels of high-sensitivity C-reactive protein (hs-CRP) and lipoprotein-associated phospholipase A2 (Lp-PLA2) were examined over 36 weeks in 84 patients who had coronary heart disease and low-density lipoprotein cholesterol levels >130 mg/dl and compared directly with the effects of fluvastatin, lovastatin, pravastatin, and simvastatin. Results were also compared with those obtained in age- and gender-matched control subjects (n = 84). Feeding increased median hs-CRP levels by 2% in patients (p = NS) and 22% in controls (p &#60;0.01) and increased mean Lp-PLA2 values by 9% in patients (p = NS) but decreased values by 21% in controls (p &#60;0.0001). Patients had 51% higher median hs-CRP values and 29% higher mean Lp-PLA2 values than did controls (p &#60;0.05 for hs-CRP and Lp-PLA2) in the fasting state; however, Lp-PLA2 values were 62% higher (p &#60;0.0001) in the fed state in patients compared with controls. Atorvastatin decreased median hs-CRP levels by 32% (p &#60;0.01) and mean Lp-PLA2 values by 26% in patients (p &#60;0.0001), with similar decreases in the fed state, and none of the other statins had any significant effect on these parameters. Change in Lp-PLA2 was significantly related to change in low-density lipoprotein cholesterol (p &#60;0.01), with no significant relations with change in hs-CRP. Our data indicate greater differences in patients with coronary heart disease compared with controls in Lp-PLA2 in the fed state than in the fasting state and that atorvastatin is more effective than fluvastatin, lovastatin, pravastatin, or simvastatin for decreasing not only low-density lipoprotein cholesterol but also hs-CRP and Lp-PLA2. [Copyright &y& Elsevier]

Examines the cause of coronary heart disease in the United States. Effect of increase level of low-density lipoprotein cholesterol; Percentage of adults with cholesterol levels over 200 mg/dl.; Diagnosis and treatment of lipid disorders.