International journal of cardiology. Cardiovascular risk and prevention · 2026
Influence of cigarette smoking on cardio-inflammatory biomarkers among healthy individuals or cardiopulmonary disorder patients: systematic review and meta-analysis.
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Hassanpour Hossein, Nasiri Leila, Mojtahed Marzieh, Karimi-Shayan Tahereh, Vaez-Mahdavi Mohammad-Reza
Аннотация
BACKGROUND: Cigarette smoking is a leading cause of cardiopulmonary disease through chronic inflammation, but individual studies on its effects on cardio-inflammatory biomarkers have yielded inconsistent results. This meta-analysis synthesizes evidences of smoking on cardio-inflammatory biomarkers.
METHODS: A systematic search was conducted across PubMed, Scopus, Web of Science, and MagIran up to April 22, 2026. Case-control studies measuring the effect of smoking on specific blood biomarkers (CK-MB, E-selectin, P-selectin, TnI, TnT, hsCRP, ICAM-1, VCAM-1, NT-proBNP) were included. Data were analyzed using a random effects model to calculate unstandardized mean differences. Subgroup analyses were performed by smoking status, gender, and health status. A total of 55 studies comprising 116,147 participants were included.
RESULTS: Meta-analysis revealed that smoking was associated with significant increases in CK-MB levels, E-selectin, ICAM-1, NT-proBNP, hsCRP, P-selectin, TnI, and TnT. For VCAM-1, the analysis was inconclusive due to wide confidence intervals. Subgroup analysis showed that current smokers had widespread biomarker elevations, whereas former smokers showed significant changes only in hsCRP and P-selectin. Gender-specific analyses indicated more pronounced biomarker elevations in males. By health status, smoking elevated six biomarkers in healthy individuals but only ICAM-1 and hsCRP in those with cardiopulmonary disease. This study confirms that smoking promotes a pro-inflammatory state and subclinical heart damage, as shown by a distinct biomarker profile. The impact varies by exposure and sex, being most severe in current smokers and males, with lingering effects after cessation.
CONCLUSION: These findings provide a mechanistic link for smoking-related cardiopulmonary risk and reinforce the importance of cessation programs.
METHODS: A systematic search was conducted across PubMed, Scopus, Web of Science, and MagIran up to April 22, 2026. Case-control studies measuring the effect of smoking on specific blood biomarkers (CK-MB, E-selectin, P-selectin, TnI, TnT, hsCRP, ICAM-1, VCAM-1, NT-proBNP) were included. Data were analyzed using a random effects model to calculate unstandardized mean differences. Subgroup analyses were performed by smoking status, gender, and health status. A total of 55 studies comprising 116,147 participants were included.
RESULTS: Meta-analysis revealed that smoking was associated with significant increases in CK-MB levels, E-selectin, ICAM-1, NT-proBNP, hsCRP, P-selectin, TnI, and TnT. For VCAM-1, the analysis was inconclusive due to wide confidence intervals. Subgroup analysis showed that current smokers had widespread biomarker elevations, whereas former smokers showed significant changes only in hsCRP and P-selectin. Gender-specific analyses indicated more pronounced biomarker elevations in males. By health status, smoking elevated six biomarkers in healthy individuals but only ICAM-1 and hsCRP in those with cardiopulmonary disease. This study confirms that smoking promotes a pro-inflammatory state and subclinical heart damage, as shown by a distinct biomarker profile. The impact varies by exposure and sex, being most severe in current smokers and males, with lingering effects after cessation.
CONCLUSION: These findings provide a mechanistic link for smoking-related cardiopulmonary risk and reinforce the importance of cessation programs.