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BACKGROUND Nighttime blood pressure (BP) has greater prognostic importance for cardiovascular disease (CVD) than daytime BP, but less is known about nighttime and daytime BP associations with measures of subclinical CVD. METHODS Among 897 Systolic Blood Pressure Intervention Trial Study (SPRINT) participants with 24-hour ambulatory BP monitoring obtained near the 27-month study visit, 849 (95%) had N-terminal pro-B-type natriuretic peptide (NT-proBNP) and high-sensitivity cardiac troponin T (hs-cTnT) measured at the 24-month study visit. Multivariable linear regression analyses were performed to evaluate the associations of nighttime and daytime BP with cardiac biomarker levels. RESULTS The mean age was 69 ± 12 years, 28% were African American, and mean nighttime and daytime SBP were 121 ± 16 mm Hg and 132 ± 14 mm Hg, respectively. In multivariable models, compared with the lowest tertile of nighttime systolic BP, the highest tertile was associated with 48% higher NT-proBNP levels (adjusted geometric mean ratio [GMR] = 1.48, 95% CI: 1.22, 1.79), and 19% higher hs-cTnT levels (adjusted GMR = 1.19, 95% CI: 1.07, 1.32). In contrast, the highest vs. lowest tertile of daytime systolic BP was not associated with NT-proBNP (adjusted GMR = 1.09, 95% CI: 0.88, 1.34), but was associated with 16% higher hs-cTnT levels (adjusted GMR = 1.16, 95% CI: 1.04, 1.30). Similar results were observed using diastolic BP. CONCLUSIONS In SPRINT, both higher nighttime and daytime BP were independently associated with higher hs-cTnT levels, but only higher nighttime BP was associated with higher NT-proBNP levels. [ABSTRACT FROM AUTHOR]

Aims Levels of growth differentiation factor 15 (GDF-15), a cytokine secreted in response to cellular stress and inflammation, have been associated with multiple types of cardiovascular (CV) events. However, its comparative prognostic performance across different presentations of atherosclerotic cardiovascular disease (ASCVD) remains unknown. Methods and results An individual patient meta-analysis was performed using data pooled from eight trials including 53 486 patients. Baseline GDF-15 concentration was analyzed as a continuous variable and using established cutpoints (<1200 ng/L, 1200–1800 ng/L, > 1800 ng/L) to evaluate its prognostic performance for CV death/hospitalization for heart failure (HHF), major adverse cardiovascular events (MACE), and their components using Cox models adjusted for clinical variables and established CV biomarkers. Analyses were further stratified on ASCVD status: acute coronary syndrome (ACS), stabilized after recent ACS, and stable ASCVD. Overall, higher GDF-15 concentration was significantly and independently associated with an increased rate of CV death/HHF and MACE (P < 0.001 for each). However, while GDF-15 showed a robust and consistent independent association with CV death and HHF across all presentations of ASCVD, its prognostic association with future myocardial infarction (MI) and stroke only remained significant in patients stabilized after recent ACS or with stable ASCVD [hazard ratio (HR): 1.24, 95% confidence interval (CI): 1.17–1.31 and HR: 1.16, 95% CI: 1.05–1.28 for MI and stroke, respectively] and not in ACS (HR: 0.98, 95% CI: 0.90–1.06 and HR: 0.87, 95% CI: 0.39–1.92, respectively). Conclusion Growth differentiation factor 15 consistently adds prognostic information for CV death and HHF across the spectrum of ASCVD. GDF-15 also adds prognostic information for MI and stroke beyond clinical risk factors and cardiac biomarkers but not in the setting of ACS. [ABSTRACT FROM AUTHOR]

Higher levels of hs-cTnT and of hs-cTnI with each of the three assays independently associated with all-cause and CVD mortality. Although not fully consistent across assay platforms, some of the hs-cTnI assays remained associated with all-cause and CVD mortality after adjusting for results of other hs-cTnI assays. Confirming prior studies,[9] hs-cTnT remained significantly associated with all-cause and CVD mortality after adjusting for hs-cTnI, and most hs-cTnI assays remained associated with outcomes after accounting for hs-cTnT. [Extracted from the article]

A study to evaluate relevant outcomes of patients from randomized controlled trials comparing early statin therapy with placebo or usual care at 1 and 4 months following acute coronary syndrome (ACS) is illustrated. Based on available evidence it is concluded that initiation of statin therapy within 14 days following onset of ACS does not reduce death, myocardial infarction, or stroke up to 4 months.

A study to determine whether concentrations of B-type natriuretic peptide (BNP) at study entry and at outpatient follow-up at 4 months and 12 months are associated with subsequent clinical outcomes is presented. Serial determinations of BNP levels during outpatient follow-up after acute coronary syndrome (ACS) predict the risk of death or new congestive heart failure (CHF).

The early initiation of an intensive statin regimen with delayed inititation of a less intensive regimen in patients with acute coronary syndrome (ACS) is compared. Results reveal that among patients with ACS, the early initiation of an aggressive simvastatin regimen indicated a favorable trend toward reduction of major cardiovascular events.

Unstable angina combined with non-ST-segment elevation myocardial infarction (UA/NSTEMI) acute coronary syndromes (ACS) is the most common manifestations of coronary heart disease that lead to death. More than twenty thousand patients were studied across the ACS spectrum, and it was found that enoxaparin is more effective than unfractionated heparin in preventing combined end point of death or myocardial infarction.

Tests were conducted to check the efficacy of the combination of enoxaparin and tirofiban in comparison with unfractionated heparin and tirofiban in patients with non-ST-elevation acute coronary syndromes (ACS). It was found that in patients receiving tirofiban and aspirin enoxaparin is a good alternative when compared to unfractionated heparin.

Background Measures of kidney tubule health are risk markers for acute kidney injury (AKI) in persons with chronic kidney disease (CKD) during hypertension treatment, but their associations with other adverse events (AEs) are unknown. Methods Among 2377 Systolic Blood Pressure Intervention Trial (SPRINT) participants with CKD, we measured at baseline eight urine biomarkers of kidney tubule health and two serum biomarkers of mineral metabolism pathways that act on the kidney tubules. Cox proportional hazards models were used to evaluate biomarker associations with risk of a composite of pre-specified serious AEs (hypotension, syncope, electrolyte abnormalities, AKI, bradycardia and injurious falls) and outpatient AEs (hyperkalemia and hypokalemia). Results At baseline, the mean age was 73 ± 9 years and mean estimated glomerular filtration rate (eGFR) was 46 ± 11 mL/min/1.73 m2. During a median follow-up of 3.8 years, 716 (30%) participants experienced the composite AE. Higher urine interleukin-18, kidney injury molecule-1, neutrophil gelatinase-associated lipocalin (NGAL) and monocyte chemoattractant protein-1 (MCP-1), lower urine uromodulin (UMOD) and higher serum fibroblast growth factor-23 were individually associated with higher risk of the composite AE outcome in multivariable-adjusted models including eGFR and albuminuria. When modeling biomarkers in combination, higher NGAL [hazard ratio (HR) = 1.08 per 2-fold higher biomarker level, 95% confidence interval (CI) 1.03–1.13], higher MCP-1 (HR = 1.11, 95% CI 1.03–1.19) and lower UMOD (HR = 0.91, 95% CI 0.85–0.97) were each associated with higher composite AE risk. Biomarker associations did not vary by intervention arm (P > 0.10 for all interactions). Conclusions Among persons with CKD, several kidney tubule biomarkers are associated with higher risk of AEs during hypertension treatment, independent of eGFR and albuminuria. [ABSTRACT FROM AUTHOR]

Objectives To investigate biotin interference on three cardiac troponin (cTn) assays and demonstrate a method to overcome biotin interference. Methods cTn levels were measured in (1) plasma from healthy volunteers on 10-mg daily biotin supplementation mixed with a plasma with known elevated troponin, (2) plasmas with known elevated cTn after mixing in reagent biotin to simulate supplementation, and (3) biotin-spiked plasma specimens pretreated with streptavidin-agarose beads. Results Daily biotin ingestion (10 mg) and studies simulating daily biotin use resulted in significant interference in the Gen5 cardiac troponin T (cTnT) assay; the contemporary Gen 4 cTnT and high-sensitivity cardiac troponin I (hs-cTnI) assays were unaffected. The biotin interference threshold was 31, 315, and more than 2,000 ng/mL for Gen5 cTnT, cTnT, and hs-cTnI assays, respectively. Streptavidin pretreatment blocked biotin interference in cTn assays. Conclusions Biotin interference is possible at plasma concentrations achievable by ingestion of over-the-counter supplements that may lead to delayed or missed diagnosis of myocardial injury with the Gen5 cTnT assay. [ABSTRACT FROM AUTHOR]