Association between serum cotinine levels and electrocardiographic left atrial abnormality

Irfan, Affan; Li, Yabing; Bhatnagar, Aruni; Soliman, Elsayed Z.

doi:10.1111/anec.12586

Cited by 5 publications

(3 citation statements)

References 27 publications

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“…Moreover, our results suggest that nicotine in e-cigarettes may both acutely and chronically shorten ventricular repolarization while also acutely increasing atrial pressures (indicated by P amplitude). Notably, a few studies also observed an increased P amplitude among smokers at baseline [212,213,362,363], similar to our findings in which cotinine (proxy for tobacco use) was associated with P amplitude (particularly in deep terminal negativity of the P wave in V1 [DTNPV1]) in the chronic state [364]. However, the mechanisms for abnormal P wave indices during acute and chronic exposure may differ while also carrying different prognostic value.…”

Section: Resultssupporting

confidence: 87%

The effects of nicotine and cigarette smoking on cardiac electrophysiology.

Irfan¹

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collaboration, and contribution to projects related to this dissertation. This work would not have been possible without the administrative and financial support of Marshall University's Departments of Cardiology and Clinical Translational Services. I am especially grateful to research coordinators, Melissa Marcum and Scott Wiley, for their perseverance and unwavering commitment to this research study. I am greatly indebted to, and honored by, the encouragement and guidance from Dr. Christian Mueller, who introduced me to cardiovascular research and helped take the first steps of my scientific pursuits. Lastly, I thank my dear family, especially my mother, father, brother, sister, and wife for their enduring love, support, and sacrifice.

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Section: Resultssupporting

confidence: 87%

The effects of nicotine and cigarette smoking on cardiac electrophysiology.

Irfan¹

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“…induced by nicotine exposure, implies more gateways for the SARS-CoV-2 virus. Moreover, it is possible to hypothesize that SARS-CoV-2 entry and replication may be facilitated or induced through mechanisms related to nAChR mediated-pathways, all converging to ACE2 regulation and signalling [15,25].Additionally, nicotine exposure induces a pro-thrombotic state via stimulation of tissue factor (TF) expression both in endothelial cells and smooth muscle cells [26] as well as neo-angiogenesis [27] and, finally, elevated serum cotinine levels, the metabolite of nicotine, are associated with left atrial abnormalities, a possible mechanism for increased risk of cardiovascular diseases (CVD) [28]. Importantly, post-mortem examinations of people who died with COVID-19 revealed widespread vascular abnormalities including thrombosis, microangiopathy, and a high degree of angiogenesis [29].…”

Section: Introductionmentioning

confidence: 99%

Nicotine upregulates ACE2 expression and increases competence for SARS-CoV-2 in human pneumocytes

Maggi

Rosellini²,

Spezia

et al. 2021

ERJ Open Res

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The COVID-19 pandemic has a variable degree of severity according to underlying comorbidities and life-style. Several research groups have reported an association between cigarette smoking and increased severity of COVID-19. The exact mechanism of action is largely unclear.We exposed low ACE2-expressing human pulmonary adenocarcinoma A549 epithelial cells to nicotine and assessed ACE2 expression at different times. We further used the nicotine-exposed cells in a virus neutralisation assay.Nicotine exposure induces rapid and long-lasting increases in gene and protein expression of the SARS-CoV-2 receptor ACE2, which in turn translates into increased competence for SARS-CoV-2 replication and cytopathic effect.These findings show that nicotine worsens SARS-CoV-2 pulmonary infection and have implication for public health policies.

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“…In a study of 8146 individuals that were aged 40 and above without AF, current smokers were statistically significantly more likely to present a DTNPV1 in their ECG, which was associated with an increased risk of death [ 87 ]. Also, in 4507 patients without AF, abnormal DTNPV1 was associated with elevated serum cotinine levels [ 88 ].…”

Section: Atrial Myocardium and Tobacco Smokingmentioning

confidence: 99%

Harmful Impact of Tobacco Smoking and Alcohol Consumption on the Atrial Myocardium

Ohlrogge

Frost

Schnabel

2022

Cells

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Tobacco smoking and alcohol consumption are widespread exposures that are legal and socially accepted in many societies. Both have been widely recognized as important risk factors for diseases in all vital organ systems including cardiovascular diseases, and with clinical manifestations that are associated with atrial dysfunction, so-called atrial cardiomyopathy, especially atrial fibrillation and stroke. The pathogenesis of atrial cardiomyopathy, atrial fibrillation, and stroke in context with smoking and alcohol consumption is complex and multifactorial, involving pathophysiological mechanisms, environmental, and societal aspects. This narrative review summarizes the current literature regarding alterations in the atrial myocardium that is associated with smoking and alcohol.

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Association between serum cotinine levels and electrocardiographic left atrial abnormality

Abstract: Elevated serum cotinine levels are associated with an abnormal DTNPV1. This suggests that nicotine exposure can lead to left atrial abnormalities, a possible mechanism for increased risk of CVD.

Cited by 5 publications

References 27 publications

The effects of nicotine and cigarette smoking on cardiac electrophysiology.

The effects of nicotine and cigarette smoking on cardiac electrophysiology.

Nicotine upregulates ACE2 expression and increases competence for SARS-CoV-2 in human pneumocytes

Harmful Impact of Tobacco Smoking and Alcohol Consumption on the Atrial Myocardium

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