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Treatment of heart failure with reduced ejection fraction (EF) may improve patient-reported health outcomes.

The purpose of this study was to determine timing and magnitude of change in Kansas City Cardiomyopathy Questionnaire (KCCQ)-23 scores following initiation of sacubitril/valsartan and interaction with change in amino-terminal pro-B-type natriuretic peptide (NT-proBNP) concentrations.

From a single-arm, open-label study of patients initiated on sacubitril/valsartan, KCCQ-23 scores and NT-proBNP were obtained at baseline and follow-up through 12months. Cross-sectional and longitudinal analyses evaluated magnitude and rate of change in KCCQ-23 scores and associations with NT-proBNP. selleckchem Patient-level data from the randomized EVALUATE-HF study were used as historic controls.

The analysis cohort (n=678, age 64.7 years, 71.5% men, EF 28.9%) had a baseline KCCQ-23 overall score (OS) of 65.6. Following sacubitril/valsartan initiation, the majority (n=412; 60.8%) of participants experienced a rise in KCCQ-2T-proBNP. (Effects of Sacubitril/Valsartan Therapy on Biomarkers, Myocardial Remodeling and Outcomes [PROVE-HF]; NCT02887183).

This study investigated whether patients with chronic heart failure (HF) can be stratified according to the combination of soluble neprilysin and corin concentrations and whether this is related to clinical outcome.

Natriuretic peptide processing by the enzymes corin and neprilysin plays a pivotal role in conversion of pro-natriuretic peptides to active natriuretic peptides, as well as their degradation, respectively.

A prospective cohort of patients with chronic HF (n=1,009) was stratified into 4 equal groups based on high or low neprilysin/corin concentration relative to the median 1) low neprilysin/low corin; 2) low neprilysin/high corin; 3) high neprilysin/low corin; and 4) high neprilysin/high corin. Cox regression survival analysis was performed for the composite primary endpoint of cardiovascular death and HF hospitalization.

Median neprilysin and corin concentrations were not correlated (rho-0.04; p=0.21). Although in univariate analysis there was no association with outcome, after correction h HF in a step toward individualized HF patient management.

The authors aimed to quantify the extent to which the effect of antihypertensive drugs on incident heart failure (HF) is mediated by their effect on kidney function.

The authors hypothesized that the dynamic change in kidney function is the mechanism behind differences in the rate of incident HF in ALLHAT (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial) participants randomized to lisinopril and chlorthalidone, in comparison with those randomized to amlodipine and doxazosin.

Causal mediation analysis of ALLHAT data (1994 to 2002) included participants with available baseline and 24- to 48-month estimated glomerular filtration rate (eGFR) (N=27,918; mean age 66 ± 7.4 years; 32.4% Black, 56.3% men). Change in eGFR was the mediator. Incident symptomatic HF was the primary outcome. Hospitalized/fatal HF was the secondary outcome. Linear regression (for mediator) and logistic regression (for outcome) analyses were adjusted for demographics, cardiovascular disease, and risk factors.

There were 1,769 incident HF events, including 1,359 hospitalized/fatal HF events. In fully adjusted causal mediation analysis, the relative change in eGFR mediated 18% of the effect of chlorthalidone, and 33% of lisinopril on incident symptomatic HF, and 25% of the effect of chlorthalidone, and 41% of lisinopril on hospitalized/fatal HF. In participants with diabetes, the relative change in eGFR mediated nearly 50% of the effect of lisinopril on incident symptomatic HF, whereas in diabetes-free participants, only 17%.

On the risk difference scale, change in eGFR accounts for up to 50% of the mechanism by which antihypertensive medications affect HF. (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial[ALLHAT]; NCT00000542).

On the risk difference scale, change in eGFR accounts for up to 50% of the mechanism by which antihypertensive medications affect HF. (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial [ALLHAT]; NCT00000542).The US Food and Drug Administration issued a black box warning in 2012 regarding the association of statin use with cognitive impairment. This may deter patients and practitioners from using statins for guideline-directed indications. Large studies have not shown an increase in cognitive impairment with statin use. MEDLINE, EMBASE, and Cochrane databases were searched up to October 2019. We present an up-to-date systematic review of randomized controlled trials (RCTs) and prospective observational studies examining the association between statin use and cognitive status in a population aged ≥60 years. Twenty-four studies with 1,404,459 participants were included in the review. Twenty-one were prospective observational studies, and 3 were RCTs. All 3 RCTs, which ranged from 3.2 to 5.6 years of follow-up, showed no significant association between statin use and adverse cognitive effects (odds ratio [OR] 1.03 [0.82-1.30]) and (OR 1.0 [0.61-1.65]). The mean difference in the Mini-Mental State Examination was insignificant (0.06 [-0.04 to 0.16]) in the third RCT. The follow-up for observational studies ranged from 3 to 15 years. Ten observational studies showed reduced incidence of dementia. Seven showed no association with incident dementia. Three studies showed decline in cognition was similar, whereas one showed slower decline with statin use. There was no evidence of adverse cognitive effects, including incidence of dementia, deterioration in global cognition, or specific cognitive domains associated with statin use in individuals aged ≥60 years. Future studies should examine this association in studies with longer follow-up periods.

Hyperlipoproteinemia Type III (HLP3), also known as dysbetalipoproteinemia, is defined by cholesterol and triglyceride (TG) enriched remnant lipoprotein particles (RLP). The gold standard for diagnosis requires demonstration of high remnant lipoprotein particle cholesterol (RLP-C) by serum ultracentrifugation (UC), which is not readily available in daily practice. The apoB algorithm can identify HLP3 using total cholesterol (TC), plasma triglyceride (TG), and apoB. However, the optimal TG cutoff is unknown.

We analyzed apoB algorithm defined HLP3 at different TG levels to optimize the TG cutoff for the algorithm.

128,485 UC lipid profiles in the Very Large Database of Lipids (VLDbL) were analyzed. RLP-C was assessed at TG≥133mg/dL, ≥175mg/dL, ≥200mg/dL, and ≥ 250mg/dL. Sensitivity (Sn), specificity (Sp), positive predictive value (PPV), negative predictive value (NPV), and prevalence adjusted and bias-adjusted kappa (PABAK) were calculated against UC Criterion (VLDL-C/TG≥0.25) for HLP3.

The median age (IQR) was 57years (46-68).