Nicotine Addiction and Coronary Artery Disease: Impact of Cessation Interventions

Abstract

Cigarette smoking is the leading preventable cause of death worldwide, and a considerable proportion of smoking-related fatalities are attributable to coronary artery disease (CAD). The detrimental effects of smoking span all stages in the development of CAD ranging from the early functional alterations in the endothelium and the microcirculation to the late clinicopathological manifestations of atherosclerotic plaques. Smoking results in the generation of free radicals and increased oxidative stress which plays a central role in the pathogenetic mechanisms leading to atherosclerotic disease. It causes reduced nitric oxide bioavailability and lipid peroxidation which are crucial initial steps of plaque formation. Furthermore, smoking enhances leukocyte and platelet activation and promotes local and systemic inflammation, which contribute to plaque progression and maturation. Finally, alterations in fibrinolytic and prothrombotic factors create a pro-thrombogenic environment which harbours the risk of plaque rupture and thrombosis. In smokers, the cessation of smoking is the most important intervention for cardiovascular risk reduction. Total mortality can be reduced by 36% which is comparable to established modern secondary preventive therapies. Nonetheless, non-aided cessation attempts are notoriously poor with a success rate of less than 10%. Patient counselling and pharmacological therapies are important aides for smoking cessation and can improve success rates by two to threefold. However, there is still need for improved strategies of smoking cessation to reduce the high socioeconomic impact of smoking.

Secondary Prevention of Atherosclerotic Cardiovascular Disease in Older Adults

“…Tobacco smoking has multiple deleterious effects that include increased generation of free radicals, reduced nitric oxide bioavailability, enhanced leukocyte and platelet activation, and prothrombotic alterations in coagulation factors (93). Clinical and laboratory manifestation of tobacco smoking include increases in heart rate, inflammatory markers, and plasma catecholamines, and reduced flow-mediated arterial dilation and HDL-cholesterol.…”

Smokers making a quit attempt using e-cigarettes with or without nicotine or prescription nicotine replacement therapy: Impact on cardiovascular function (ISME-NRT) - a study protocol

“…Smoking is the leading, preventable death-cause worldwide [2], being responsible for almost 650,000 deaths in the E.U. annually [3].…”

“…Smoking cessation could reduce total cardiovascular disease (CVD) mortality by 36% [2]. This is because the vascular endothelium plays a major role in cardiovascular health and disease (e.g.…”

“…This is because the vascular endothelium plays a major role in cardiovascular health and disease (e.g. systemic and pulmonary hypertension, coronary heart disease and stroke; [4], and cigarette smoking has been associated with endothelial dysfunction in otherwise healthy adults [5] – with its detrimental effects ranging from early functional endothelial alterations to late clinico-pathological manifestations of atherosclerotic plaques [2]. The negative effects upon cardiovascular function are not limited to smokers; passive smoking increases heart disease death-risk by almost 30% [6].…”

Nicotine-Induced Morphological Changes in Rat Aorta: The Protective Role of Melatonin

“…Our experimental study involved rats treated with nicotine, which causes endothelial dysfunction [Chalon et al, 2000;Paganelli et al, 2001;Rodella et al, 2010a] and which in turn precedes atherosclerotic lesions [Gaemperli et al, 2010]. Furthermore, nicotine accelerates the growth of atherosclerotic plaques in a mouse model of atherosclerosis [Heeschen et al, 2001], an effect caused by nicotine-induced VSMC proliferation [Cucina et al, 2000].…”