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Atherosclerosis: Difference between revisions
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==Tabacco smoking== | ===Tabacco smoking=== | ||
Tabacco use is known to increase the risk of atherosclerosis and ischemic heart diseased based on numerous studies. Smoking is estimated to be responsible of estimated 30% of all cardiovascular diseases, and it may increase the risk even at minimal use. Tabacco smoking can lead to several mechanisms that may contribute to atherosclerosis. It enhances oxidative modification of LDL, decreases circulating HDL levels, stimulates tissue hypoxia and oxidant stress, leading to endothelial dysfunction, promotes platelet adhesiveness, increases expression of leukocyte adhesion molecules, inappropriately stimulates sympathetic nervous system, and displaces oxygen with carbon monoxide in hemoglobin. Another important component, induced by cigarette smoking is thrombosis. | Tabacco use is known to increase the risk of atherosclerosis and ischemic heart diseased based on numerous studies. Smoking is estimated to be responsible of estimated 30% of all cardiovascular diseases, and it may increase the risk even at minimal use. Tabacco smoking can lead to several mechanisms that may contribute to atherosclerosis. It enhances oxidative modification of LDL, decreases circulating HDL levels, stimulates tissue hypoxia and oxidant stress, leading to endothelial dysfunction, promotes platelet adhesiveness, increases expression of leukocyte adhesion molecules, inappropriately stimulates sympathetic nervous system, and displaces oxygen with carbon monoxide in hemoglobin. Another important component, induced by cigarette smoking is thrombosis. | ||
According to major studies, quitting smoking is one of the most effective preventive measures of cardiovascular diseases and their complications. It decreases the risk of coronary heart disease dramatically compared to those who don’t. Not only does cessation of smoking reduce risk of CVD, but also substantially reduce the risk of all-cause mortality. | |||
===Lack of physical activity / obesity=== | |||
Recent evidence shows that physical activity can lower triglyceride levels and blood pressure, raise HDL, and can also enhance insulin sensitivity and production of NO by the endothelial cells. Several prospective studies have shown that all genders can have beneficial effects from even modest activities such as walking against cardiovascular mortality. Although large scale randomized primary prevention trials are lacking, physical activity should be promoted to anyone with risk of developing atherosclerosis. | |||
===Estrogen Status=== | |||
Women and men have different risk for cardiovascular diseases throughout life. For example, at young age, men have estimated four- to fivefold higher risk than women. This difference diminishes with age, but even in the age range of 75 and 85, the incidence of coronary disease is almost twofold in men compared to woman. The age point of diminished difference between men and women is strongly related to the moment of menopause. From this observation, studies suggest that estrogen may play athero-protective roles, since the levels of estrogen decline after menopause. In premenopausal women, estrogen raises HDL levels and reduces LDL levels in blood. Experiments have also shown that estrogen can exhibit antioxidant and antithrombotic properties, and can improve endothelium-dependent vasodilatation. | |||
In the past, hormone replacement therapy has been suggested by several studies due to the findings of potential athero-protective roles of estrogen. However, the Heart and Estrogen/progestin Replacement Study, along with randomized primary prevention studies from the Women’s Health Initiative showed that such hormone replacement therapy rather increased cardiovascular risk in women. Thus hormone replace therapy is currently not recommended for reducing cardiovascular risk, due to its possible harmfulness according to current clinical trials. Further analyses are being done whether hormone replacement approaches can still be safe and effective, since some cohort studies didn’t show increased cardiovascular risk outcomes as other clinical trials, when they applied estrogen-only hormone therapy. | |||
==Co-morbidity groups== | |||
===Hypertension=== | |||
Hypertension is defined as a systolic blood pressure (SBP) ≥ 140mmHg and/or a diastolic blood pressure (DBP) ≥ 90mmHg. This elevated blood pressure substantially increases the risk of atherosclerosis, coronary heart disease, and stroke. For example, cardiovascular disease doubles for every 20 mmHg increase in SBP or every 10 mmHg increase in DBP. | |||
One of the mechanisms of hypertension in contributing to atherosclerosis is injury of vascular endothelium by elevated hemodynamic stress. Injury of endothelium may increase the permeability of the vessel wall to lipoproteins. Increased blood pressure may also increase the number of scavenger receptors on macrophages, which enhances the development of foam cells. Furthermore, increased cyclic circumferential strain in hypertensive arteries can result into promoting LDL accumulation in the intima and facilitation of their oxidative modification. As last, hypertension can contribute to atherogenesis due to the presence of Angiotensin II, which not only works as a vasoconstrictor, but also as a pro-inflammatory cytokine. | |||
===Antihypertensive therapy=== | |||
Antihypertensive therapy can either consist of lifestyle interventions or pharmacotherapy. Lifestyle modifications consist of diet, body weight reduction, increased activity, and cessation of smoking. As for diet, high consumption of fruits, vegetables, dairy products low in fat, fish oils, and potassium and reduced consumption of sodium and alcohol are recommended. | |||
The indication for pharmacotherapy depends on the severity of hypertension and on the assessment of total CVD risk. Many large trials have shown that pharmacotherapy for hypertension can substantially reduce CVD mortality and morbidity. Drug therapy is indicated when chronic SBP ≥ 160mmHg and/or DBP ≥100mmHg, or if target organ damage is present. Hypertensive patients with lower blood pressure than the previously mentioned indication are managed according to their total risk for CVD, which usually means indications for medications, since absence of other risk factors and low risk is very unusual with hypertension. | |||
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! Figure 5. Lifestyle recommendations for hypertension. | |||
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| * Weight reduction in overweight individuals | |||
* Reduction of salt consumption to < 6g daily | |||
* Restriction of alcohol intake to < 10-30g/day (men) and < 10-20g/day (women) | |||
* Regular physical activity | |||
* Smoking cessation | |||
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===Diabetes mellitus=== | |||
With estimated global incidence of 170 million people diabetes mellitus remains a large problem worldwide. Diabetes mellitus increases the risk of acute coronary events by three- to five folds and 80% of diabetic patients will face atherosclerosis-related cardiovascular diseases. Risk for atherosclerosis among diabetes group is considered as high as a group with previous myocardial infarction. | |||