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Atherosclerosis: Difference between revisions
→Lipid-Altering therapy
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Inhibiting HMG-CoA reductase results into several mechanisms that explain the beneficial effect of using statins. One beneficial mechanism is through lowering LDL and raising HDL. This results into less lipid content in atherosclerotic plaques and improve their biologic activity. Furthermore, anti-thrombotic and anti-inflammatory condition is enhanced by other mechanisms such as increased NO synthesis and fibrinolytic antivity, inhibition of smooth muscle proliferation and monocyte recruitment, and reduced production of matrix-degrading enzymes by macrophage. Several studies suggest that other mechanisms also contribute to anti-inflammatory condition. For example, statins reduce endothelial expression of leukocyte adhesion molecules and macrophage tissue factor production by inhibiting the macrophage cytokines or by activating PPAR-α. Another anti-inflammatory working of statins, supported by clinical trials is reducing the serum level of C-reactive protein, which is a marker of inflammation. | Inhibiting HMG-CoA reductase results into several mechanisms that explain the beneficial effect of using statins. One beneficial mechanism is through lowering LDL and raising HDL. This results into less lipid content in atherosclerotic plaques and improve their biologic activity. Furthermore, anti-thrombotic and anti-inflammatory condition is enhanced by other mechanisms such as increased NO synthesis and fibrinolytic antivity, inhibition of smooth muscle proliferation and monocyte recruitment, and reduced production of matrix-degrading enzymes by macrophage. Several studies suggest that other mechanisms also contribute to anti-inflammatory condition. For example, statins reduce endothelial expression of leukocyte adhesion molecules and macrophage tissue factor production by inhibiting the macrophage cytokines or by activating PPAR-α. Another anti-inflammatory working of statins, supported by clinical trials is reducing the serum level of C-reactive protein, which is a marker of inflammation. | ||
Figure 4. Recommendations in relations to dyslipidemia. | {| class="wikitable" | ||
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General recommendations: | ! Figure 4. Recommendations in relations to dyslipidemia. | ||
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| General recommendations: | |||
* A varied and balanced diet | * A varied and balanced diet | ||
* Regular fish intake (n – 3 fatty acids) | * Regular fish intake (n – 3 fatty acids) | ||
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* The total fat intake should not be higher than 30% of calorie intake. The saturated fat intake should not be higher than 30% of total lipids | * The total fat intake should not be higher than 30% of calorie intake. The saturated fat intake should not be higher than 30% of total lipids | ||
* The cholesterol intake should be under 300 mg per day | * The cholesterol intake should be under 300 mg per day | ||
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Specific diet recommendations: | | Specific diet recommendations: | ||
* Avoid hard margarines and products of animal origin (meat, dairy products) | * Avoid hard margarines and products of animal origin (meat, dairy products) | ||
* Increase intake of omega-3 fatty acids from fish oils and certain vegetal oils | * Increase intake of omega-3 fatty acids from fish oils and certain vegetal oils | ||
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* Exercise and body weight reduction within obese group | * Exercise and body weight reduction within obese group | ||
* Normalization of glycaemia in diabetic patients | * Normalization of glycaemia in diabetic patients | ||
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==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. | |||