European journal of preventive cardiology最新文献

Aims: Inflammatory lipoprotein(a) [Lp(a)] and oxidized phospholipids (OxPLs) on lipoproteins convey residual cardiovascular disease risk. The LoDoCo2 (low-dose colchicine 2) trial showed that colchicine reduced the risk for cardiovascular events occurring on standard therapies in patients with chronic coronary disease (CCS). We explored the effects of colchicine on Lp(a) and oxidized lipoprotein associated risk in a LoDoCo2 biomarker subpopulation.

Methods: Lp(a), OxPLs on apolipoprotein(a) [OxPL-apo(a)] and apolipoprotein B (OxPL-apoB) levels were determined in the biomarker population of the LoDoCo2 trial (n = 1777). Cox regression analysis was used to compare the risk for the primary endpoint, consisting of myocardial infarction, ischemic stroke, or ischemia-driven revascularization by biomarker levels. Interactions between treatment, Lp(a) and OxPL levels were evaluated.

Results: Lp(a), OxPL-apo(a) and OxPL-apoB levels were similar between the colchicine and placebo groups. Consistent risk reduction by colchicine was observed in those with Lp(a) <125 nmol/L and ≥125 nmol/L, and the highest OxPL-apo(a) tertile compared to the lowest (Pinteraction=0.92 and 0.66). The absolute risk reduction for those with Lp(a) ≥125 nmol/L appeared higher compared to those with Lp(a) <125 nmol/L (4.4% vs 2.4%). A treatment interaction for colchicine was found in those with the highest OxPL-apoB tertile vs the lowest (Pinteraction=0.04).

Conclusion: In patients with CCS, colchicine reduces cardiovascular disease risk in those with and without elevated Lp(a) but absolute benefits appeared higher in those with Lp(a) ≥125 nmol/L. Patients with higher levels of OxPL-apoB experienced greater benefit of colchicine, suggesting colchicine may be more effective in subjects with heightened oxidation-driven inflammation.

Background: This study aims to explore whether conventional and emerging biomarkers could improve risk discrimination and calibration in secondary prevention of recurrent atherosclerotic cardiovascular disease (ASCVD), based on a model using predictors from SMART2.

Methods: In a cohort of 20,658 UK Biobank participants with medical history of ASCVD, we analysed any improvement in C indices and net reclassification index (NRI) for future ASCVD events, following addition of LP-a, ApoB, cystatin C, HbA1c, GGT, AST, ALT, and ALP, to a model with predictors used in SMART2 for the outcome of recurrent major cardiovascular event. We also examined any improvement in C indices and NRIs replacing creatinine based estimated glomerular filtration rate (eGFR) with cystatin C based estimates. Calibration plots between different models were also compared.

Results: Compared with the baseline model (C index=0.663), modest increment in C indices were observed when adding HbA1c (ΔC=0.0064, p<0.001), cystatin C (ΔC=0.0037, p<0.001), GGT (ΔC=0.0023, p<0.001), AST (ΔC= 0.0007, p<0.005) or ALP (ΔC=0.0010, p<0.001) or replacing eGFRCr with eGFRCysC (ΔC=0.0036, p<0.001) or eGFRCr-CysC (ΔC=0.00336, p<0.001). Similarly, the strongest improvements in NRI were observed with the addition of HbA1c (NRI=0.014), or cystatin C (NRI= 0.006) or replacing eGFRCr with eGFRCr-CysC (NRI=0.001) or eGFRCysC (NRI=0.002). There was no evidence that adding biomarkers modify calibration.

Conclusions: Adding several biomarkers, most notably cystatin C and HbA1c, but not LP-a, in a model using SMART2 predictors modestly improved discrimination.

Aims: The cause-specific mortality implications of social determinants of health (SDOH) in cancer survivors were unclear. This study aimed to explore associations between SDOH and cardiovascular and cancer mortality in cancer survivors.

Methods and results: Data from 2013 to 2017 National Health Interview Survey were used for this prospective cohort study. Social determinants of health were quantified using a 38 point, 6 domain score, with higher points indicating worse deprivation. Associations between SDOH and outcomes (primary: cardiovascular mortality; secondary: cancer and all-cause mortality) were assessed using cause-specific multivariable Cox regression, with cancer survivors and individuals without cancer modelled separately. Post hoc analyses were performed among cancer survivors to explore associations between each domain of SDOH and the risks of outcomes. Altogether, 37 882 individuals were analysed (4179 cancer survivors and 33 703 individuals without cancer). Among cancer survivors, worse SDOH was associated with higher cardiovascular [adjusted hazard ratio (aHR) 1.31 (1.02-1.68)], cancer [aHR 1.20 (1.01-1.42)], and all-cause mortality [aHR 1.16 (1.02-1.31)] when adjusted for demographics, comorbidities, and risk factors. Among individuals without cancer, SDOH was associated with cardiovascular mortality and all-cause when only adjusted for demographics, but not when further adjusted for comorbidities and risk factors; no associations between SDOH and cancer mortality were found. Among cancer survivors, psychological distress, economic stability, neighbourhood, physical environment and social cohesion, and food insecurity were varyingly associated with the outcomes.

Conclusion: Social determinants of health were independently associated with all-cause, cardiovascular, and cancer mortality among cancer survivors but not among individuals without cancer. Different domains of SDOH may have different prognostic importance.

The HF syndrome is characterized by an autonomic unbalance with sympathetic hyperactivity which contributes to increased myocardial oxygen demand, oxidative stress, peripheral vasoconstriction, afterload mismatch with a progressive desensitization and down-regulation of cardiac β1-receptors. These changes, together with a few other structural and peripheral changes, lead to chronotropic incompetence (CI), such as the inability to increase heart rate (HR) consistently with activity or demand. CI, regardless of the method and cut-off adopted to define it, is associated with reduced exercise capacity and a worse prognosis. Furthermore, different pharmacological classes might interfere with the physiologic exercise-induced HR response, thus generating some confusion. In particular, the β-blockers, albeit lowering peak HR, are known to improve prognosis and left ventricular inotropic reserve so that their withdrawal should be avoided at least in HF with reduced and mildly reduced ejection fraction. Similarly, a still debated strategy to counterbalance a blunted exercise-induced HR response, is represented by rate-adapting pacing. The present review, besides supplying an overview on possible CI definitions, discusses the clinical impact of CI and potential pharmacological and non-pharmacological therapeutic strategies.

Aims: The benefit of long-term beta-blocker therapy after acute coronary syndromes (ACS) without heart failure in the reperfusion era is uncertain. Two recent randomized trials found conflicting results. The present study assessed the safety of beta-blocker discontinuation within 12 months following ACS with LVEF ≥40%.

Methods: In a multicentre prospective real-world cohort (N=3,762) of patients hospitalized for ACS, patients with LVEF ≥40% and beta-blockers at discharge were included. Patients who continued beta-blockers at one year were compared with those who discontinued beta-blockers within 12 months post-ACS using target trial emulation and inverse probability weighting over an additional four-year follow-up. The primary endpoint was major adverse cardiovascular events (MACE), a composite of four-year cardiovascular death, myocardial infarction, stroke, transient ischemic attack, unplanned coronary revascularization, or unstable angina hospitalization.

Results: Of 2,077 patients, 1,758 (85%) continued beta-blockers and 319 (15%) had discontinued beta-blockers at one year. The risk of primary endpoint was similar in both groups (14.1% versus 14.3% with beta-blocker discontinuation versus continuation; adjusted hazard ratio [aHR]=0.98; 95% confidence interval, 0.72-1.34, P=0.91). Subgroup analysis suggested a higher risk of primary endpoint with beta-blocker discontinuation after STEMI (aHR=1.46 [0.99-2.16]) compared to NSTEMI (aHR=0.70 [0.40-1.22], Pinteraction=0.033), whereas there was no interaction with LVEF (Pinteraction=0.68).

Conclusions: Beta-blocker discontinuation within 12 months following ACS with LVEF ≥40% was not associated with an increased risk of MACE compared to long-term beta-blocker therapy. Subgroup analysis suggested potential risk in STEMI patients. Discontinuing beta-blockers 12 months after ACS appears safe in patients with LVEF ≥40%, particularly after NSTEMI.