Effects of Ambient Particles and Carbon Monoxide on Supraventricular Arrhythmias in a Rat Model of Myocardial Infarction

Wellenius, Gregory A.; Coull, Brent A.; Batalha, Joao R. F.; Diaz, Edgar A.; Lawrence, Joy; Godleski, John J.

doi:10.1080/08958370600945473

Cited by 14 publications

(11 citation statements)

References 34 publications

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“…Another major finding of this study is the proarrhythmogenic effect of chronic CO exposure in a healthy population. This result provides experimental support to previous reports that CO is associated with life-threatening VA in populations with cardiopathies (30,31). The arrhythmic events may have an electrical origin or a Ca 21 origin (32).…”

Section: Discussionsupporting

confidence: 90%

Carbon Monoxide Pollution Promotes Cardiac Remodeling and Ventricular Arrhythmia in Healthy Rats

André¹,

Boissière²,

Reboul³

et al. 2010

Am J Respir Crit Care Med

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Section: Discussionsupporting

confidence: 90%

Carbon Monoxide Pollution Promotes Cardiac Remodeling and Ventricular Arrhythmia in Healthy Rats

André¹,

Boissière²,

Reboul³

et al. 2010

Am J Respir Crit Care Med

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“…The carotid body sensory response to hypoxia was markedly pronounced in PM-exposed CREB A133 mice compared with vehicle-treated CREB A133 mice or PM-challenged CD1 mice ( Figures 3C and 3D), indicating that PM exposure sensitizes carotid body responses to acute hypoxia only in CHF mice, with reflexive sympathetic nervous system-mediated cardiac and respiratory arrhythmias. These findings parallel the susceptibility of patients with CHF to the adverse effects of PM exposure (14).…”

Section: Pm Mediates Heightened Carotid Body Sensitivity and Autonomisupporting

confidence: 68%

“…Multiple pathogenetic mechanisms have been hypothesized to underlie the adverse cardiac effects of PM, including induction of inflammatory cascades (10), increased levels of reactive oxygen species (ROS) (11), induced coagulation cascades (10,12), changes in blood viscosity (13), and altered autonomic function (6). In a rat model of acute myocardial infarction, PM exposure produced severe bradycardia, decreased heart rate variability (HRV), and increased ventricular arrhythmias (14). PM exposure alters the duration of the QT interval in patients with preexisting coronary disease and increases the number of discharges in patients with implanted cardiac defibrillators (15).…”

mentioning

confidence: 99%

Particulate Matter Induces Cardiac Arrhythmias via Dysregulation of Carotid Body Sensitivity and Cardiac Sodium Channels

Wang¹,

Lang²,

Moreno‐Vinasco³

et al. 2012

Am J Respir Cell Mol Biol

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The mechanistic links between exposure to airborne particulate matter (PM) pollution and the associated increases in cardiovascular morbidity and mortality, particularly in people with congestive heart failure (CHF), have not been identified. To advance understanding of this issue, genetically engineered mice (CREB A133 ) exhibiting severe dilated cardiomyopathic changes were exposed to ambient PM collected in Baltimore. CREB A133 mice, which display aberrant cardiac physiology and anatomy reminiscent of human CHF, displayed evidence of basal autonomic aberrancies (compared with wild-type mice) with PM exposure via aspiration, producing significantly reduced heart rate variability, respiratory dysynchrony, and increased ventricular arrhythmias. Carotid body afferent nerve responses to hypoxia and hyperoxia-induced respiratory depression were pronounced in PM-challenged CREB A133 mice, and denervation of the carotid bodies significantly reduced PM-mediated cardiac arrhythmias. Genome-wide expression analyses of CREB A133 left ventricular tissues demonstrated prominent Na 1 and K 1 channel pathway gene dysregulation. Subsequent PM challenge increased tyrosine phosphorylation and nitration of the voltage-gated type V cardiac muscle a-subunit of the Na 1 channel encoded by SCN5A. Ranolazine, a Na 1 channel modulator that reduces late cardiac Na 1 channel currents, attenuated PM-mediated cardiac arrhythmias and shortened PMelongated QT intervals in vivo. These observations provide mechanistic insights into the epidemiologic findings in susceptibility of human CHF populations to PM exposure. Our results suggest a multiorgan pathobiology inherent to the CHF phenotype that is exaggerated by PM exposure via heightened carotid body sensitivity and cardiac Na 1 channel dysfunction.

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“…Decreases in heart rate and HRV indices have been reported to be pronounced in senescent mice, which indicates that aging may be a susceptibility factor. 353 Using an anesthetized model of postinfarction myocardium sensitivity, Wellenius and colleagues 377 did not demonstrate an effect of 1 hour of CAP exposure on heart rate or spontaneous ventricular arrhythmias. In contrast, in a post-MI heart failure model in Sprague-Dawley rats, diesel exhaust emissions reduced HRV in both healthy and heart failure groups and increased the incidence of premature ventricular contractions.…”

Section: Vascular Dysfunction and Atherosclerosismentioning

confidence: 96%

Particulate Matter Air Pollution and Cardiovascular Disease

Brook¹,

Rajagopalan²,

Pope³

et al. 2010

Circulation

5,347

3,225

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Abstract-In 2004, the first American Heart Association scientific statement on "Air Pollution and Cardiovascular Disease" concluded that exposure to particulate matter (PM) air pollution contributes to cardiovascular morbidity and mortality. In the interim, numerous studies have expanded our understanding of this association and further elucidated the physiological and molecular mechanisms involved. The main objective of this updated American Heart Association scientific statement is to provide a comprehensive review of the new evidence linking PM exposure with cardiovascular disease, with a specific focus on highlighting the clinical implications for researchers and healthcare providers. The writing group also sought to provide expert consensus opinions on many aspects of the current state of science and updated suggestions for areas of future research. On the basis of the findings of this review, several new conclusions were reached, including the following: Exposure to PM Ͻ2.5 m in diameter (PM 2.5 ) over a few hours to weeks can trigger cardiovascular disease-related mortality and nonfatal events; longer-term exposure (eg, a few years) increases the risk for cardiovascular mortality to an even greater extent than exposures over a few days and reduces life expectancy within more highly exposed segments of the population by several months to a few years; reductions in PM levels are associated with decreases in cardiovascular mortality within a time frame as short as a few years; and many credible pathological mechanisms have been elucidated that lend biological plausibility to these findings. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM 2.5 exposure and cardiovascular morbidity and mortality. This body of evidence has grown and been strengthened substantially since the first American Heart Association scientific statement was published. Finally, PM 2.5 exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality. (Circulation. 2010;121:2331-2378.)

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Effects of Ambient Particles and Carbon Monoxide on Supraventricular Arrhythmias in a Rat Model of Myocardial Infarction

Cited by 14 publications

References 34 publications

Carbon Monoxide Pollution Promotes Cardiac Remodeling and Ventricular Arrhythmia in Healthy Rats

Carbon Monoxide Pollution Promotes Cardiac Remodeling and Ventricular Arrhythmia in Healthy Rats

Particulate Matter Induces Cardiac Arrhythmias via Dysregulation of Carotid Body Sensitivity and Cardiac Sodium Channels

Particulate Matter Air Pollution and Cardiovascular Disease

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