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Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice
Published on: January 16, 2015
The cardiovascular pathology of smoking
1Department of Pathology, University of Texas Health Science Center, San Antonio 78284.
Insights
Cigarette smoking significantly worsens atherosclerosis and cardiovascular disease risk by affecting cholesterol, blood pressure, and promoting thrombosis. Fortunately, quitting smoking rapidly reverses these harmful effects, reducing disease risk.
Area of Science:
- Cardiovascular Science
- Atherosclerosis Research
Background:
- Atherosclerosis, a key factor in heart disease, peripheral vascular disease, and stroke, develops over decades.
- Risk factors like high LDL cholesterol, low HDL cholesterol, and hypertension correlate with advanced atherosclerosis and clinical disease.
- Cigarette smoking is a known risk factor for cardiovascular and peripheral vascular diseases.
Purpose of the Study:
- To investigate the association between cigarette smoking and the severity of atherosclerosis.
- To explore the physiological mechanisms by which smoking may accelerate atherogenesis and thrombosis.
- To examine the reversibility of smoking-induced cardiovascular risks.
Main Methods:
- The study reviews existing literature on atherosclerosis, risk factors, and the physiological effects of cigarette smoking.
- Correlations between smoking status, atherosclerosis severity in different vascular beds, and cardiovascular disease risk are analyzed.
- Physiological responses to smoking, including effects on lipid profiles, coagulation, and inflammation, are examined.
Main Results:
- Smoking is linked to more severe coronary atherosclerosis, but this alone doesn't fully explain the increased coronary heart disease risk.
- Smoking is strongly associated with severe abdominal aortic atherosclerosis, aligning with increased risk of aortic aneurysm and peripheral vascular disease.
- Smoking induces detrimental physiological changes, including reduced HDL cholesterol, increased fibrinogen, and elevated white blood cell counts.
Conclusions:
- Cigarette smoking exacerbates atherosclerosis and cardiovascular disease risk through multiple physiological pathways.
- The observed physiological changes induced by smoking likely contribute to accelerated atherogenesis and increased thrombosis risk.
- Cessation of smoking leads to a rapid decrease in cardiovascular disease risk, indicating the reversibility of smoking-induced damage.
Abstract:
Atherosclerosis, the process underlying coronary heart disease, peripheral vascular disease, and stroke, begins in childhood and progresses through several stages to result in clinically manifest disease in middle age and later. Elevated plasma low-density lipoprotein cholesterol levels, lowered high-density lipoprotein cholesterol levels, and elevated blood pressure are associated with more extensive and more severe atherosclerosis and also with greater risk of clinical disease. Cigarette smoking is firmly established as a risk factor for coronary heart disease and peripheral vascular disease. It is associated with more severe coronary atherosclerosis, but not enough to account for the twofold or greater risk of coronary heart disease among smokers. Smoking is associated with much more severe atherosclerosis of the abdominal aorta, which is consistent with the much greater risk of aortic aneurysm and peripheral vascular disease among smokers. Smoking induces a wide variety of physiologic responses, some of which appear likely to be involved in accelerating atherogenesis or increasing the probability of thrombosis. These responses include reduction in plasma high-density lipoprotein cholesterol concentration, elevation in plasma fibrinogen concentration, and elevation in white blood cell count. The rapid amelioration of the risk of cardiovascular disease after cessation of smoking suggests that these processes are readily reversible.
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