Pathophysiological Mechanisms of Tobacco-Related CVD

Abstract

Cigarette smoking is a leading preventable risk factor for the development and progression of cardiovascular diseases (CVDs). Epidemiologic studies conclusively prove that both active smoking and secondhand smoke contribute significantly to morbidity and mortality related to CVD. Cigarette smoke is a mixture of several toxic chemicals, of which nicotine, carbon monoxide, and oxidant chemicals are most commonly implicated in the pathogenesis of cardiovascular disease. Tobacco causes endothelial dysfunction, inflammation, insulin resistance, alteration of lipid profile, hemodynamic alterations, and a hypercoagulable state. All of these act synergistically as pathobiologic mechanisms of atherothrombosis in tobacco users.

Short‐Term E‐Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice

“…However, this study neither mimicked real‐life conditions (eg, employed e‐cigarette extracts) nor used an in vivo whole‐body exposure model to investigate the effects of e‐cigarettes on platelets. It is noteworthy that thrombosis is the main mechanism of cardiovascular mortality in smokers17; smoking causes a prothrombotic state through altering fibrinolytic and thrombotic factors17, 18; smokers’ isolated platelets exhibited increased aggregation19, 20; and exposure to cigarette smoke alters the dynamics of clot formation, making them more resistant to thrombolysis as compared with clots of nonsmokers 21, 22, 23. However, whether e‐cigarettes exert similar effects is yet to be determined and warrants investigation.…”

Effect of Cigarette Smoke on Diabetic Skin and Protection with Topical Administration of Pinus halepensis Extract

“…The World Health Organization has estimated that, if current trends continue, tobacco could cause a billion deaths in the 21st Century [1]. The pathological effects of cigarette smoke (CS) inhalation have been thoroughly investigated on lungs, the cardiovascular system [2]- [4], the immune system [5] [6] and the reproductive and development systems [7] [8]. However, the cutaneous effects of CS have been comparatively less documented, even though they contribute to the morbidity and reduced quality of life associated with smoking [9].…”

Effect of Smoking Status on Monocyte Tissue Factor Activity, Carotid Atherosclerosis and Long-Term Prognosis in Metabolic Syndrome

“…Therefore, smoking impairs endothelium-dependent vasodilation of coronary arteries, reduces coronary flow reserve, and induces coronary spasm. 5, 6 The assessment of endothelium-dependent vasodilatation is widely used to evaluate endothelial function, and the 1.02; 95% CI: 1.01-1.04, P=0.039) were each significantly and independently associated with atherothrombotic events in patients with MetS ( Table 6). …”

“…1-4 Any or all of endothelial dysfunction, inflammation, and a hypercoagulable state may play a significant role in the pathogenesis and development of atherothrombotic events in smokers. [5][6][7][8] Cigarette smoke exposure seems to alter the balance of anti-thrombotic/prothrombotic factors by affecting the functions of endothelial cells (EC), platelets, fibrinogen, and coagulation factors. 8 Tissue factor (TF) is an initiator of the extrinsic coagulation cascade, and it is expressed in the peripheral blood monocytes and on macrophages in atherosclerotic plaque.…”