Impact of particulate matter on the incidence of atrial fibrillation and the risk of adverse clinical outcomes: A review

Mandaglio-Collados, Darío; López-Gálvez, Raquel; Ruiz–Alcaraz, Antonio J.; López-García, Cecilia; Roldán, Vanessa; Lip, Gregory Y. H.; Marı́n, Francisco; Rivera‐Caravaca, José Miguel

doi:10.1016/j.scitotenv.2023.163352

Cited by 6 publications

(3 citation statements)

References 46 publications

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“…[145,169,170] Particulate matter exposure New-onset AF can follow exposure to particulate matter. [171][172][173][174] This can be an acute occurrence [175] Increases with known genetic risk factors.…”

Section: Exercisementioning

confidence: 99%

Fibrinaloid Microclots and Atrial Fibrillation

Kell,

Lip,

Pretorius

2024

Biomedicines

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Atrial fibrillation (AF) is a comorbidity of a variety of other chronic, inflammatory diseases for which fibrinaloid microclots are a known accompaniment (and in some cases, a cause, with a mechanistic basis). Clots are, of course, a well-known consequence of atrial fibrillation. We here ask the question whether the fibrinaloid microclots seen in plasma or serum may in fact also be a cause of (or contributor to) the development of AF. We consider known ‘risk factors’ for AF, and in particular, exogenous stimuli such as infection and air pollution by particulates, both of which are known to cause AF. The external accompaniments of both bacterial (lipopolysaccharide and lipoteichoic acids) and viral (SARS-CoV-2 spike protein) infections are known to stimulate fibrinaloid microclots when added in vitro, and fibrinaloid microclots, as with other amyloid proteins, can be cytotoxic, both by inducing hypoxia/reperfusion and by other means. Strokes and thromboembolisms are also common consequences of AF. Consequently, taking a systems approach, we review the considerable evidence in detail, which leads us to suggest that it is likely that microclots may well have an aetiological role in the development of AF. This has significant mechanistic and therapeutic implications.

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Section: Exercisementioning

confidence: 99%

Fibrinaloid Microclots and Atrial Fibrillation

Kell,

Lip,

Pretorius

2024

Biomedicines

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“…While the association between ambient air pollutants (AP) and atrial fibrillation (AF) is still a matter of debate, several systematic reviews and meta-analyses support a link between AP effects and cardiovascular diseases, including AF [7][8][9][10]. This association, alongside cardiopulmonary issues, is estimated to have contributed to 8.79 million deaths worldwide in 2018 [11], especially affecting vulnerable subpopulations.…”

Section: Introductionmentioning

confidence: 99%

“…Short-term exposure to pollutants, including PM2.5, sulfur dioxide (SO 2 ), and nitrogen dioxide (NO 2 ), increases the likelihood of AF, while prolonged exposure to PM2.5, PM10, SO2, NO2, and carbon monoxide (CO) significantly contributes to AF incidence in healthy populations. Studies also show a higher risk of mortality and stroke in pre-existing AF patients exposed to elevated PM levels [10]. Exposure to PM2.5 is linked to new-onset AF, especially in males over 60 years old with obesity and a history of hypertension or myocardial infarction [13].…”

Section: Introductionmentioning

confidence: 99%

Disruption of Atrial Rhythmicity by the Air Pollutant 1,2-Naphthoquinone: Role of Beta-Adrenergic and Sensory Receptors

Soares,

Teixeira,

Thakore

et al. 2023

Biomolecules

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The combustion of fossil fuels contributes to air pollution (AP), which was linked to about 8.79 million global deaths in 2018, mainly due to respiratory and cardiovascular-related effects. Among these, particulate air pollution (PM2.5) stands out as a major risk factor for heart health, especially during vulnerable phases. Our prior study showed that premature exposure to 1,2-naphthoquinone (1,2-NQ), a chemical found in diesel exhaust particles (DEP), exacerbated asthma in adulthood. Moreover, increased concentration of 1,2-NQ contributed to airway inflammation triggered by PM2.5, employing neurogenic pathways related to the up-regulation of transient receptor potential vanilloid 1 (TRPV1). However, the potential impact of early-life exposure to 1,2-naphthoquinone (1,2-NQ) on atrial fibrillation (AF) has not yet been investigated. This study aims to investigate how inhaling 1,2-NQ in early life affects the autonomic adrenergic system and the role played by TRPV1 in these heart disturbances. C57Bl/6 neonate male mice were exposed to 1,2-NQ (100 nM) or its vehicle at 6, 8, and 10 days of life. Early exposure to 1,2-NQ impairs adrenergic responses in the right atria without markedly affecting cholinergic responses. ECG analysis revealed altered rhythmicity in young mice, suggesting increased sympathetic nervous system activity. Furthermore, 1,2-NQ affected β1-adrenergic receptor agonist-mediated positive chronotropism, which was prevented by metoprolol, a β1 receptor blocker. Capsazepine, a TRPV1 blocker but not a TRPC5 blocker, reversed 1,2-NQ-induced cardiac changes. In conclusion, neonate mice exposure to AP 1,2-NQ results in an elevated risk of developing cardiac adrenergic dysfunction, potentially leading to atrial arrhythmia at a young age.

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