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Aim: Existing data on the association between blood pressure levels and adverse cardiovascular outcomes in patients with heart failure (HF) are inconsistent. The optimal blood pressure targets for patients with HF remain uncertain. This study sought to assess the associations between blood pressure (systolic [SBP] and diastolic blood pressure [DBP]) levels and adverse cardiovascular disease (CVD) outcomes in patients with HF. Methods and results: A systematic review and meta‐analysis were conducted using MEDLINE, Embase, the Cochrane Library, and Web of Science databases up to 5 May 2023. The outcomes of interest included adverse cardiovascular events and all‐cause mortality. Pooled relative risks (RRs) with corresponding 95% confidence intervals (CIs) were calculated. Forty‐three unique observational cohort studies, comprising 120 643 participants with HF, were included. The pooled RRs (95% CIs) for SBP thresholds of ≥140 mmHg versus <140 mmHg were 0.92 (0.83–1.01) for all‐cause mortality, 0.83 (0.67–1.04) for CVD death, and 0.98 (0.80–1.21) for HF hospitalization. The pooled RR (95% CI) for SBP thresholds of ≥160 mmHg versus <160 mmHg and all‐cause mortality was 0.67 (0.62–0.74). SBP levels below <130, <120, and <110 mmHg were each associated with an increased risk of various cardiovascular endpoints and all‐cause mortality. The pooled RR (95% CI) for DBP thresholds of ≥80 mmHg versus <80 mmHg and all‐cause mortality was 0.86 (0.67–1.10). A 10 mmHg increase in SBP or DBP was associated with a reduction in all‐cause mortality and other cardiovascular endpoints. Conclusions: The findings suggest that lower and normal baseline SBP levels (<130, <120, and <110 mmHg) may be associated with future risk of worse outcomes in patients with HF. Optimal baseline blood pressure levels for these patients may lie within the range of ≥140 mmHg for SBP. In the absence of observational studies with repeated blood pressure measurements or definitive trials evaluating optimal blood pressure targets, individualized blood pressure targets based on patients' unique circumstances are warranted in HF management. [ABSTRACT FROM AUTHOR]

Objectives. A general body of evidence suggests that low serum albumin might be associated with increased risk of adverse cardiometabolic outcomes, but findings are divergent. We aimed to quantify associations of serum albumin with the risk of type 2 diabetes (T2D), cardiovascular disease (CVD), all-cause mortality, and other adverse outcomes using a systematic review and meta-analyses of published observational cohort studies. Design. MEDLINE, Embase, Web of Science, and manual search of relevant bibliographies were systematically searched to January 2020. Relative risks (RRs) with 95% confidence intervals (CIs) comparing top versus bottom thirds of serum albumin levels were pooled. Results. Fifty-four articles based on 48 unique observational cohort studies comprising of 1,492,237 participants were eligible. Multivariable adjusted RRs (95% CIs) comparing the top vs bottom third of serum albumin levels were: 1.03 (0.86–1.22) for T2D; 0.60 (0.53–0.67) for CVD; 0.74 (0.66–0.84) for coronary heart disease (CHD); 0.57 (0.36–0.91) for CHD death; 0.76 (0.65–0.87) for myocardial infarction; 0.66 (0.55–0.77) for all-cause mortality; 0.71 (0.61–0.83) for venous thromboembolism; 0.65 (0.48–0.88) for cancer mortality; and 0.62 (0.46–0.84) for fracture. Heterogeneity between contributing studies of T2D was partly explained by sample sizes of studies (p for meta-regression =.035). Conclusions. Elevated levels of serum albumin are associated with reduced risk of vascular outcomes, all-cause mortality, certain cancers, and fracture. Inconsistent findings for T2D may be attributed to selective reporting by studies. Further research is needed to assess any potential causal relevance to these findings and the role of serum albumin concentrations in disease prevention. Systematic review registration: PROSPERO 2019: CRD42019125869 [ABSTRACT FROM AUTHOR]

Purpose: We aimed to assess the prospective association of serum albumin with venous thromboembolism (VTE) risk and evaluate if the association is independent of or modified by inflammation, as measured by high sensitivity C-reactive protein (hsCRP). Design: We analysed data of 2176 men aged 42-61 years free from VTE in the Kuopio Ischemic Heart Disease study, with serum albumin concentrations measured at baseline using Coulter’s bromocresol purple colorimetric assays. Hazard ratios (HRs) (95% confidence intervals [CI]) were calculated for VTE. Results: There were 109 validated cases of VTE recorded during a median follow-up of 24.9 years. The risk of VTE increased linearly below a serum albumin concentration of ∼48 g/l. In Cox regression analysis adjusted for established risk factors and other potential confounders, the HR (95% CI) for VTE per 1 standard deviation lower serum albumin was 1.23 (1.02-1.47). The association remained persistent on further adjustment for hsCRP 1.22 (1.01-1.46). Furthermore, the association was not modified by hsCRP and persisted on exclusion of men with elevated hsCRP levels. Conclusions: In middle-aged Caucasian men, low serum albumin is associated with an increased risk of VTE, consistent with a linear dose-response relationship. The association is independent of and not modified by inflammation. Key messages:   • Serum albumin may be associated with future risk of venous thromboembolism (VTE); however, the shape, nature, magnitude and consistency of the association is uncertain.   • In a population-based prospective cohort study, low serum albumin was associated with an increased risk of VTE in a linear dose-response manner and this association was independent of and not modified by inflammation.   • Serum albumin concentrations may play a role in the development of VTE. [ABSTRACT FROM AUTHOR]

Abstract Background Neutrophil gelatinase-associated lipocalin (NGAL), a novel biomarker of acute kidney injury, might play a role in the development of atherosclerotic cardiovascular disease (CVD). We aimed to assess the association of circulating NGAL with CVD risk. Materials and methods Plasma NGAL concentrations were measured at baseline in 5275 participants in the PREVEND prospective study. Hazard ratios (95% confidence intervals [CI]) for CVD were estimated. Results After a median follow-up of 8.3 years, 338 participants developed first CVD events. Plasma NGAL was weakly to moderately correlated with several CVD risk markers. There was a non-linear relationship between NGAL and CVD risk. In analyses adjusted for established risk factors, the hazard ratio (95% CI) for CVD in a comparison of the top quartile versus bottom quartiles 1–2 of NGAL values was 1.35 (1.05–1.75; P = 0.022), which was abrogated after additional adjustment for other potential confounders (mainly attributed to high sensitivity C-reactive protein) 1.20 (0.92–1.57; P = 0.176). The association was considerably attenuated following further adjustment for renal function 1.05 (0.79–1.40; P = 0.745). The association between NGAL and CVD risk did not vary importantly in relevant clinical subgroups. Conclusion Evidence suggests a non-linear association between NGAL and CVD risk, which is dependent on inflammation and renal function. Highlights • Increased NGAL is associated with an increased CVD risk in Caucasians. • The association is non-linear and is independent of cardiovascular risk factors. • The association is partly dependent on inflammation and renal function. [ABSTRACT FROM AUTHOR]

Background and aims We aimed to assess the association of circulating calprotectin, an inflammation-associated protein, with cardiovascular disease (CVD) risk and determine whether it improves risk prediction. Methods Plasma calprotectin measurements were made at baseline in 5290 participants in the PREVEND prospective study. Hazard ratios (95% confidence intervals [CI]) for CVD were calculated. Results After a median follow-up of 8.3 years, 339 first CVD events were recorded. Calprotectin concentration was correlated with several conventional risk factors as well as with high-sensitivity C-reactive protein (hsCRP) (r = 0.42). Calprotectin was log-linearly associated with CVD risk. The risk for CVD adjusted for conventional cardiovascular risk factors was 1.26 (95% CI, 1.13–1.41) per 1 standard deviation higher baseline log e calprotectin, and was 1.24 (95% CI, 1.11–1.39) following further adjustment for triglycerides, body mass index, and other potential confounders. The association remained present after further adjustment for hsCRP 1.15 (95% CI, 1.02–1.30). Comparing extreme quartiles of plasma calprotectin levels, the corresponding adjusted HRs for CVD were 1.96 (1.37–2.82), 1.89 (1.31–2.72), and 1.56 (1.07–2.29). The association of calprotectin with CVD risk did not vary importantly in several relevant clinical subgroups. Adding calprotectin to the Framingham CVD Risk Score was associated with a C-index change (0.0016; p =0.42) difference in −2 log likelihood ( p =0.038), IDI (0.0080; p  < 0.001), and NRI (4.03%; p =0.024). Conclusions There is a log-linear association of calprotectin concentration with risk of CVD, which may be partly dependent on hsCRP. Adding calprotectin to conventional risk factors improves CVD risk assessment using measures of reclassification and −2 log likelihood. [ABSTRACT FROM AUTHOR]