Serum Cotinine and Silent Myocardial Infarction in Individuals Free from Cardiovascular Disease

Brunetti, Riccardo; Hicklin, Harry E; Rackley, Justin; Ahmad, Muhammad Imtiaz; Li, Yabing; Soliman, Elsayed Z.

doi:10.1016/j.amjcard.2019.05.064

Cited by 6 publications

(3 citation statements)

References 21 publications

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“…A higher proportion of patients with AMI were found to have a history of smoking and elevated plasma cotinine levels, which is consistent with previous reports (35,36). Based on these findings, we further investigated the potential mediation effect of IgE in the association between plasma cotinine and AMI using mediation analyses.…”

Section: Discussionsupporting

confidence: 92%

Smoking, immunity, and cardiovascular prognosis: a study of plasma IgE concentration in patients with acute myocardial infarction

Zhang,

Zhu,

Meng

et al. 2023

Front. Cardiovasc. Med.

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BackgroundImmunoglobulin E (IgE) is implicated in the pathogenesis of acute myocardial infarction (AMI), and smokers often exhibit elevated plasma IgE levels. However, it remains uncertain whether the role of smoking in the development and prognosis of AMI is influenced by IgE levels. This study aimed to investigate the potential contribution of IgE in mediating the association between smoking and AMI.MethodsWe conducted a prospective study involving 348 consecutive patients with chest discomfort who underwent coronary angiography. Plasma cotinine, an alkaloid present in tobacco, and IgE levels were measured. The patients were followed up for mean 39-months to assess their long-term prognosis based on major adverse cardiac and cerebrovascular events (MACCE).ResultsOur findings indicate that patients with AMI had higher plasma levels of cotinine and IgE. Univariate analyses demonstrated a positive association between plasma cotinine (OR = 1.7, 95% CI: 1.27–2.26, P < 0.001) and IgE (OR = 2.8, 95% CI: 1.75–4.39, P < 0.001) with AMI. Receiver operating characteristics analyses showed that the combined use of cotinine and IgE (AUC: 0.677) had a larger predictive performance compared to cotinine alone (AUC: 0.639) or IgE alone (AUC: 0.657), although the improvement did not reach statistical significance. Multivariable logistic regression revealed a positive association between plasma cotinine and AMI (OR = 1.70, 95% CI: 1.04–2.78, P = 0.036). Furthermore, the inclusion of plasma IgE in the regression model led to a decrease in the OR and 95% CI of plasma cotinine (OR = 1.66, 95% CI: 1.01–2.73, P = 0.048). Process mediation analyses showed a significant indirect effect of plasma cotinine on AMI mediated through increased plasma IgE. Kaplan–Meier analysis during a mean 39-months follow-up revealed that higher plasma levels of IgE were associated with an increased risk of MACCE following AMI (P = 0.047). However, in the context of the COX regression analysis, no significant correlation was observed between IgE, cotinine and AMI.ConclusionCotinine exhibits a positive association with AMI, wherein IgE plays a mediating role. Elevated plasma levels of IgE was positively associated with AMI and poor prognosis, which further confirms the adverse role of smoking on the incidence of AMI and prognosis. (Clinical trial registration: ChiCTR2100053000).

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Section: Discussionsupporting

confidence: 92%

Smoking, immunity, and cardiovascular prognosis: a study of plasma IgE concentration in patients with acute myocardial infarction

Zhang,

Zhu,

Meng

et al. 2023

Front. Cardiovasc. Med.

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“…Alshaarawy et al found that higher serum cotinine levels were positively associated with hypertension in non-smokers, independently of various confounders [ 18 ]. Moreover, our study aligns with Affan Irfan’s and Ryan Brunetti’s research, which investigated specific cardiovascular outcomes associated with tobacco exposure, such as left atrial abnormalities and silent myocardial infarction, respectively [ 19 , 20 ].…”

Section: Discussionmentioning

confidence: 52%

Investigating the interplay of smoking, cardiovascular risk factors, and overall cardiovascular disease risk: NHANES analysis 2011–2018

Mambo,

Yang,

Mahulu

et al. 2024

BMC Cardiovasc Disord

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Background This study explores the intricate relationship between smoking, cardiovascular disease (CVD) risk factors and their combined impact on overall CVD risk, utilizing data from NHANES 2011–2018. Methods Participants were categorized based on the presence of CVD, and we compared their demographic, social, and clinical characteristics. We utilized logistic regression models, receiver operating characteristics (ROC) analysis, and the chi-squared test to examine the associations between variables and CVD risk. Results Significant differences in characteristics were observed between those with and without CVD. Serum cotinine levels exhibited a dose-dependent association with CVD risk. The highest quartile of cotinine levels corresponded to a 2.33-fold increase in risk. Smoking, especially in conjunction with lower HDL-c, significantly increases CVD risk. Combinations of smoking with hypertension, central obesity, diabetes, and elevated triglycerides also contributed to increased CVD risk. Waist-to-Height Ratio, Visceral Adiposity Index, A Body Shape Index, Conicity Index, Triglyceride-Glucose Index, Neutrophil, Mean platelet volume and Neutrophil to Lymphocyte ratio demonstrated significant associations with CVD risk, with varying levels of significance post-adjustment. When assessing the combined effect of smoking with multiple risk factors, a combination of smoking, central obesity, higher triglycerides, lower HDL-c, and hypertension presented the highest CVD risk, with an adjusted odds ratio of 14.18. Conclusion Smoking, when combined with central obesity, higher triglycerides, lower HDL-c, and hypertension, presented the highest CVD risk, with an adjusted odds ratio of 14.18.

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“…Since nicotine can be metabolized to cotinine with a metabolic halftime of about 2 h, over the course of this experiment, cotinine levels on the order of 5-10 ng/ml blood would be present. A 10 ng/ml of cotinine concentrations increase in serum is associated with a 2% increase in myocardial ischemia in humans, so a contributory role for cotinine cannot be ruled out [63].…”

Section: Discussionmentioning

confidence: 99%

Acute administration of nicotine induces transient elevation of blood pressure and increases myocardial infarct size in rats

Zhao

Dai

Carreño

et al. 2020

Heliyon

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We investigated the acute effects of nicotine on myocardial infarct size, no reflow, hemodynamics and cardiac function in an acute myocardial ischemia and reperfusion infarction rat model. Main methods: Female Sprague-Dawley rats (n ¼ 23/group) received an intravenous loading dose of nicotine at 2.0 μg/kg/min or saline control for 30 min before starting coronary artery occlusion, then followed by a maintenance dose 0.35 μg/kg/min of nicotine to the end of 30 min occlusion and 3 h reperfusion.Key findings: At baseline, there was no difference in systolic blood pressure (BP in mmHg) (nicotine, 69.0 AE 2.7; control, 69.3 AE 4.4; p ¼ NS) or diastolic BP (nicotine, 45.7 AE 3.2; control, 48.2 AE 4.2; p ¼ NS) between groups. Nicotine administration initially increased systolic BP (nicotine, 97.0 AE 8.6; control, 69.2 AE 3.3, p < 0.0001) and diastolic BP (nicotine, 65.6 AE 6.4; control, 47.4 AE 3.1, p ¼ 0.0003) at 10 min after starting injection of the loading dose; BP dropped to control levels in both groups at 30 min. During occlusion and reperfusion, the BP and heart rate were not altered by nicotine. Nicotine significantly increased myocardial infarct size as a percentage of the ischemic risk zone compared to the controls (nicotine, 54.9 AE 1.9; control, 48.6 AE 2.7, p < 0.05), but nicotine did not affect the no-reflow size and heart function. Significance: While acute nicotine only transiently elevated blood pressure, it did not affect hemodynamic parameters during coronary artery occlusion. Nicotine increased myocardial infarct size, suggesting that the increase in infarct size was not simply due to an increase in oxygen demand due to altered afterload, heart rate, or contractility, but may have been due to a more direct effect on the myocardium.

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Serum Cotinine and Silent Myocardial Infarction in Individuals Free from Cardiovascular Disease

Cited by 6 publications

References 21 publications

Smoking, immunity, and cardiovascular prognosis: a study of plasma IgE concentration in patients with acute myocardial infarction

Smoking, immunity, and cardiovascular prognosis: a study of plasma IgE concentration in patients with acute myocardial infarction

Investigating the interplay of smoking, cardiovascular risk factors, and overall cardiovascular disease risk: NHANES analysis 2011–2018

Acute administration of nicotine induces transient elevation of blood pressure and increases myocardial infarct size in rats

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