BACKGROUND
Ambient air pollution is an established cardiovascular risk factor, but its relation to arrhythmia-related outcomes has been synthesised less comprehensively than other cardiovascular endpoints.
OBJECTIVE
We conducted a systematic review and meta-analysis of studies examining ambient air pollution and arrhythmia-related outcomes.
METHODS
Primary meta-analyses were restricted to short-term particulate matter associations standardised to 10 μg/m3. Secondary analyses examined broader short-term models on the original study scale, long-term models were analysed separately, and an exploratory global multilevel model was used to account for multiple effect estimates within studies.
RESULTS
Thirty-two studies represented over 34 million participants or analysed cases across designs. In the primary analyses, short-term PM2.5 exposure standardised to 10 μg/m3 was associated with atrial fibrillation (4 studies; pooled relative risk [RR] 1.045, 95% CI 1.025-1.066; I2=0.66%) and with sudden cardiac arrest or sudden cardiac death (7 studies; RR 1.052, 1.031-1.075; I2=49.0%). Short-term PM10 exposure standardised to 10 μg/m3 was associated with sudden cardiac arrest or sudden cardiac death (3 studies; RR 1.024, 1.012-1.036; I2=0%). Expanded short-term analyses yielded similar pooled estimatesLong-term PM2.5-AF estimates were highly heterogeneous (pooled ratio 1.077, 95% CI 1.002-1.158; I2=99.9%), limiting interpretation. Additional sensitivity models yielded directionally consistent estimates.
CONCLUSIONS
Short-term exposure to particulate air pollution was associated with risks of atrial fibrillation and sudden cardiac arrest/sudden cardiac death. Given the observational evidence base, findings should be interpreted cautiously and viewed as consistent with, rather than definitive evidence of, an association between particulate exposure and arrhythmia-related events.
Andrea Matteucci, Luca Sgarra, M. Bonanni et al.· Heart Rhythm· 1 citation
Lipoprotein(a) [Lp(a)] has emerged as a major, genetically determined, contributor to residual cardiovascular risk. Accumulating evidence from epidemiological studies, human genetics, and Mendelian randomization has unequivocally established elevated Lp(a) as an independent risk factor for atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve stenosis (CAVS). Lp(a) consists of a low-density lipoprotein-like particle in which apolipoprotein(a) is covalently linked to apolipoprotein B100. This unique structure confers proatherogenic, pro-inflammatory, and antifibrinolytic properties, largely mediated by oxidized phospholipids and the structural homology of apolipoprotein(a) with plasminogen. Circulating Lp(a) concentrations are genetically determined and remain relatively stable throughout life with minimal influence from lifestyle interventions. Conventional lipid-lowering therapies have little or no meaningful effect on circulating Lp(a) concentrations, leaving an important component of residual cardiovascular risk unaddressed. In contrast, RNA-based therapeutics targeting hepatic LPA expression have demonstrated reductions in circulating Lp(a) of up to 80–90% and are currently being evaluated in phase 3 cardiovascular outcome trials. This narrative review summarizes the molecular biology, genetics, epidemiology, pathophysiological mechanisms, and clinical relevance of Lp(a), and critically examines current and emerging therapeutic strategies aimed at reducing Lp(a)-mediated cardiovascular risk.
Lucio Giuseppe Granata, Simona Giubilato, Francesca Campanella et al.· Frontiers in Medicine· 0 citations
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