European journal of preventive cardiology最新文献

Aim: We aimed to 1) investigate associations between leisure time physical activity level cumulated over 20 years and multiple plasma proteins and 2) explore if proteins significantly associated with physical activity are also associated with risk of imminent myocardial infarction (MI), long-term MI and mortality.

Methods: In the cohort Uppsala Longitudinal Study of Adult Men (ULSAM), leisure time physical activity was self-reported at ages 50, 60, and 70. At age 70, 720 plasma proteins were analyzed in 782 participants with up to 19.3 years of follow-up for MI and 26.3 years follow-up for mortality. In the nested case-cohort study Markers of Imminent Myocardial Infarction (MIMI), plasma proteins were measured in disease-free individuals from six European cohorts. Cases (n=420) were those with acute MI within 6 months of a blood draw, with up to four cohort representatives per case (n=1,598).

Results: A higher level of leisure time physical activity level was inversely associated with 12 plasma proteins after adjusting for age, education, smoking and established cardiovascular risk factors (Bonferroni corrected p<0.000069). Of these 12 proteins, IL-6 was associated with increased incidence of imminent MI (HR 1.22 95%CI [1.09-1.37]), TNFRSF11A was associated with increased long-term MI incidence (HR 1.22 [1.01-1.48]) and 11 proteins were associated with increased mortality (HR 1.14-1.30 [1.01-1.42]).

Conclusions: These findings confirm and extend our understanding of how physical activity could assert its beneficial effect on cardiovascular health through proteins involved with modulating inflammatory, immune and metabolic pathways. Further research is needed to explore the causal mechanisms behind these associations.

Aims: Obesity increases the risk of heart failure (HF), partly due to hypervolaemia and excess epicardial adipose tissue (EAT).We aimed to investigate the effect of the sodium glucose co-transporter 2 inhibitor empagliflozin on estimated extracellular volume (eECV) and ventricular EAT mass in non-diabetic patients with overweight or obesity and risk of HF to evaluate the drug's potential for HF prevention.

Methods: In this randomised, double-blind, placebo-controlled trial, we recruited non-diabetic patients with body mass index (BMI) >28kg/m2 and risk of HF. Patients were randomised 1:1 to 180-days empagliflozin 10 mg or placebo. The primary endpoints were the baseline-adjusted mean differences in change of eECV and ventricular EAT mass in the intention-to-treat population with Bonferroni-adjustment for multiplicity.

Results: From September 2021 to July 2024, we randomised 191 patients (empagliflozin: 94, placebo: 97) with median age 68 years and median BMI 31·9 kg/m2. Analyses of eECV and EAT included 191 and 165 patients, respectively. Compared to placebo, empagliflozin significantly reduced eECV [empagliflozin, mean change (SD): -0·154 L (0·257); placebo, mean change: -0·029 L (0·261); estimated treatment difference (ETD): -0·123 L, 97.5% CI: -0·211 to -0·035, padj=0·004] but did not affect EAT mass [empagliflozin, mean change: -2·3 g (13·4); placebo, mean change: -3·7 g (15·8); ETD: 1·5 g, 97·5% CI: -3·8 to 6·7, padj=1.00].

Conclusion: In high-risk patients with overweight or obesity, treatment with empagliflozin resulted in a potentially favourable reduction in eECV compared to placebo. Meanwhile, the drug did not affect EAT mass.

Aims: Glucagon-like peptide-1 receptor agonists (GLP-1RA) reduce cardiovascular risk in patients with type 2 diabetes (T2D) and established atherosclerotic cardiovascular disease and are recommended in guidelines. We evaluated the real-world effectiveness of GLP-1RA therapy on cardiovascular outcomes in patients with T2D after myocardial infarction (MI) or ischemic stroke and examined trends and disparities.

Methods: Using nationwide Czech registry data (2015-2024), we identified patients with incident nonfatal MI or ischemic stroke and confirmed T2D. GLP-1RA users-initiating therapy within 12 months post-event-were propensity score-matched to non-users. The primary outcome was major adverse cardiovascular events (MACE: nonfatal MI, nonfatal stroke, cardiovascular death); secondary outcomes included individual components and all-cause mortality.

Results: GLP-1RA therapy was initiated in only ∼2% of MI and stroke survivors with T2D. Among 126,845 MI survivors, 28,206 had T2D; the matched cohort comprised 2,271 patients (401 GLP-1RA; median follow-up 35 months). GLP-1RA use was associated with lower risk of MACE (HR:0.7; 95%CI:0.52-0.93), all-cause (HR:0.61;95%CI:0.47-0.80) and cardiovascular death (HR:0.54, 95%CI:0.36-0.80). Among 177,115 stroke survivors, 73,750 had T2D; the matched cohort comprised 2,235 patients (385 GLP-1RA; median follow-up 27 months). GLP-1RA use was associated with lower risk of MACE (HR:0.71; 95%CI:0.54-0.94), all-cause (HR:0.59;95%CI:0.46-0.76) and cardiovascular death (HR:0.55; 95%CI:0.37-0.81).

Conclusions: GLP-1RA therapy after MI or stroke in T2D was associated with substantially lower risks of MACE, cardiovascular and all-cause death in real-world practice. Utilization remained low, particularly among women and older adults, underscoring the need for broader and more equitable implementation in secondary prevention.

Aim: Respiratory sarcopenia, characterised by reduced respiratory muscle mass and function, can impair ventilatory reserve and physical capacity, potentially worsening outcomes. However, its prevalence and prognostic significance in older patients with heart failure remain unclear. This study aimed to investigate the clinical significance of respiratory sarcopenia in this population.

Methods: This was a post hoc analysis of the compariSON of various methods In evaluatIon of sarCopenia in patients with Heart Failure (SONIC-HF) study, a multicentre prospective observational study. Among 435 patients hospitalised for heart failure (median age: 81 [interquartile range 74-85] years; 41.8% female), we defined respiratory sarcopenia as the presence of both low resting diaphragm thickness, assessed using ultrasonography, and reduced percent predicted forced vital capacity (FVC), a surrogate for respiratory muscle strength. The primary outcome was 2-year all-cause mortality.

Results: Respiratory sarcopenia was observed in 47 patients (10.8%). During the 2-year follow-up, 78 patients (17.9%) died. All-cause mortality was significantly higher among patients with respiratory sarcopenia than those without (P < 0.001). In Cox proportional hazards analysis, respiratory sarcopenia was independently associated with increased mortality risk (hazard ratio: 2.51; 95% confidence interval: 1.40-4.50; P = 0.002), even after adjustment for conventional risk factors. Low diaphragm thickness or reduced percent predicted FVC alone were not associated with mortality.

Conclusions: In older patients with heart failure, respiratory sarcopenia was uncommon but associated with significantly higher mortality. Simultaneous assessment of respiratory muscle mass and function may aid in identifying high-risk individuals and enhance risk stratification beyond structural assessments alone.