Air Pollution and Cardiac Arrhythmias: From Epidemiological and Clinical Evidences to Cellular Electrophysiological Mechanisms

Zhang, Shuguang; Lü, Weigang; Wei, Zhiqiang; Zhang, Henggui

doi:10.3389/fcvm.2021.736151

Cited by 21 publications

(13 citation statements)

References 199 publications

(257 reference statements)

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“…Finally, according to our previous research review (Zhang et al, 2021), CO was also known to affect multiple cellular pathways other than the ion channels in this study. The present study mainly considered arrhythmias caused by changes in ionic currents directly induced by CO, without considering the mitochondrial toxicity of CO and some other complicated electrophysiological remodeling induced by cellular ischemia.…”

Section: Potential Limitations Of This Studymentioning

confidence: 77%

In silico assessment of pharmacotherapy for carbon monoxide induced arrhythmias in healthy and failing human hearts

et al. 2022

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Background: Carbon monoxide (CO) is gaining increased attention in air pollution-induced arrhythmias. The severe cardiotoxic consequences of CO urgently require effective pharmacotherapy to treat it. However, existing evidence demonstrates that CO can induce arrhythmias by directly affecting multiple ion channels, which is a pathway distinct from heart ischemia and has received less concern in clinical treatment.Objective: To evaluate the efficacy of some common clinical antiarrhythmic drugs for CO-induced arrhythmias, and to propose a potential pharmacotherapy for CO-induced arrhythmias through the virtual pathological cell and tissue models.Methods: Two pathological models describing CO effects on healthy and failing hearts were constructed as control baseline models. After this, we first assessed the efficacy of some common antiarrhythmic drugs like ranolazine, amiodarone, nifedipine, etc., by incorporating their ion channel-level effects into the cell model. Cellular biomarkers like action potential duration and tissue-level biomarkers such as the QT interval from pseudo-ECGs were obtained to assess the drug efficacy. In addition, we also evaluated multiple specific IKr activators in a similar way to multi-channel blocking drugs, as the IKr activator showed great potency in dealing with CO-induced pathological changes.Results: Simulation results showed that the tested seven antiarrhythmic drugs failed to rescue the heart from CO-induced arrhythmias in terms of the action potential and the ECG manifestation. Some of them even worsened the condition of arrhythmogenesis. In contrast, IKr activators like HW-0168 effectively alleviated the proarrhythmic effects of CO.Conclusion: Current antiarrhythmic drugs including the ranolazine suggested in previous studies did not achieve therapeutic effects for the cardiotoxicity of CO, and we showed that the specific IKr activator is a promising pharmacotherapy for the treatment of CO-induced arrhythmias.

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Section: Potential Limitations Of This Studymentioning

confidence: 77%

In silico assessment of pharmacotherapy for carbon monoxide induced arrhythmias in healthy and failing human hearts

et al. 2022

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“…For every 10 g/cm3 increase in annual mean PM2.5 exposures, there are increases of 16 to 31% documented at a variety of concentrations (Crouse et al, 2012;Alexeeff et al, 2021;Shah et al, 2015). Increased risk of both atrial fibrillation and ventricular arrhythmias have been also linked to air pollution (Varieur et al, 2022;Zhang et al, 2021).…”

Section: Air Pollution and Cardiovascular Diseasementioning

confidence: 99%

Air pollution and cardiovascular diseases

hamed

2022

Journal of Environmental Studies

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It is well known that air pollution is a major risk factor for noninfectious diseases and that it contributes more to global morbidity and mortality than all other known environmental risk factors collectively. Still, guidelines for the prevention of cardiovascular illnesses have almost exclusively concentrated on individual behavioral and metabolic risk factors, and pollution reduction has been overlooked in programs for the control of cardiovascular disease. This is a significant oversight since including pollution reduction into the prevention of cardiovascular disease could result in millions of lives being saved. The focus of this review is to try to summarize the evidence supporting a strong link between the risk of cardiovascular diseases and cardiovascular risk factors with air pollution through a spectrum of exposure levels, possible mechanisms that increase cardiovascular risk are described, and evidence supporting the effects of air pollution on cardiovascular health is investigated, and some knowledge gaps that could help improve the rising cardiovascular morbidity and mortality linked to air pollution are discussed.

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“…In addition to inflammation, PM 2.5 can also promote oxidative stress, metabolic dysfunction, alteration of lipid metabolism, and autonomic dysfunction. All these mediators in turn can adversely affect the cardiac contractile function and heart rate [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Consequential Impact of Particulate Matter Linked Inter-Fibrillar Mitochondrial Dysfunction in Rat Myocardium Subjected to Ischemia Reperfusion Injury

Sivakumar

Alasmari

Ali

et al. 2022

Biology

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A previous study has reported that exposure to PM2.5 from diesel exhaust (diesel particulate matter (DPM)) for 21 days can deteriorate the cardiac recovery from myocardial ischemia reperfusion injury (IR), where the latter is facilitated by the efficiency of mitochondrial subpopulations. Many investigators have demonstrated that IR impact on cardiac mitochondrial subpopulations is distinct. In the present study, we decipher the role of PM2.5 on IR associated mitochondrial dysfunction at the subpopulation level by administrating PM2.5 directly to isolated female rat hearts via KH buffer. Our results demonstrated that PM2.5 administered heart (PM_C) severely deteriorated ETC enzyme activity (NQR, SQR, QCR, and COX) and ATP level in both IFM and SSM from the normal control. Comparatively, the declined activity was prominent in IFM fraction. Moreover, in the presence of IR (PM_IR), mitochondrial oxidative stress was higher in both subpopulations from the normal, where the IFM fraction of mitochondria experienced elevated oxidative stress than SSM. Furthermore, we assessed the in vitro protein translation capacity of IFM and SSM and found a declined ability in both subpopulations where the inability of IFM was significant in both PM_C and PM_IR groups. In support of these results, the expression of mitochondrial genes involved in fission, fusion, and mitophagy events along with the DNA maintenance genes such as GUF1, LRPPRC, and HSD17-b10 were significantly altered from the control. Based on the above results, we conclude that PM2.5 administration to the heart inflicted mitochondrial damage especially to the IFM fraction, that not only deteriorated the cardiac physiology but also reduced its ability to resist IR injury.

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Air Pollution and Cardiac Arrhythmias: From Epidemiological and Clinical Evidences to Cellular Electrophysiological Mechanisms

Cited by 21 publications

References 199 publications

In silico assessment of pharmacotherapy for carbon monoxide induced arrhythmias in healthy and failing human hearts

In silico assessment of pharmacotherapy for carbon monoxide induced arrhythmias in healthy and failing human hearts

Air pollution and cardiovascular diseases

Consequential Impact of Particulate Matter Linked Inter-Fibrillar Mitochondrial Dysfunction in Rat Myocardium Subjected to Ischemia Reperfusion Injury

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