Prevention


Prevention and treatment of atherosclerosis involves controlling the known modifiable risk factors. This includes weight control, physical exercise, low saturated fat intake, hypertension and hyperlipidaemia.

Lifestyle Changes

The best way to treat atherosclerosis is to prevent the continued development of the process with non-pharmaceutical methods. Lifestyle changes are the most effective way of preventing or reversing the process of atherosclerosis as well as reducing risk of developing cardiovascular disease.
  • Five means of reducing the risk of atherosclerosis include:
    • Moderate consumption of alcohol
    • Practicing regular exercise
    • Healthy diet
    • Losing weight (if overweight)
    • Cessation of smoking (if smoker)

Smoking

  • Smoking impairs production of vasodilators nitric oxide and prostacyclin, which cause damage to the endothelium. This endothelial dysfunction increases permeability in the endothelial layer allowing lipoproteins and other molecules to deposit into the arterial wall. Stopping smoking will prevent continued endothelial wall damage, thereby decreasing the susceptibility of lipoprotein deposits and build up in the subendothelial layer (Powell, 1998).

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Smoking Effects on the Heart (National Heart, Lung and Blood Institute, 2011)


Diet

  • Eating an unhealthy diet high in fat will increase the low density lipoprotein (LDL) cholesterol levels in the blood, increasing the process of atherosclerosis. High levels of LDL cholesterol in the blood increase the chance of formation of oxidized LDL (OxLDL), a major contributor to the genesis of atherosclerosis. By avoiding foods high in saturated fat (high in LDL cholesterol content) and eating small amounts of food high in unsaturated fat (high in HDL cholesterol content), it is possible to minimalize the risk of developing atherosclerosis.
  • Olive oil, wine, and certain black and green tea's are good foods to have in your diet, this is because they have a high polyphenol content. Polyphenols inhibit oxidation of LDL by seeking out superoxide anions (a free radical known to cause oxidized LDL).

Alcohol

  • Excess amounts of alcohol increases risk factors of hyperlipidaemia, liver disease and hypertension. However, moderate amounts of alcohol (1-2drinks/day of red wine) have been postulated to have beneficial cardiovascular effect due to the flavonoids (antioxidant) and increased high density lipoprotein (HDL) cholesterol levels (Srivastava, 2008).

Pharmaceuticals

Several kinds of medication may be used in treatment of atherosclerosis. Most of these medications treat the underlying cause for atherosclerosis such as high cholesterol and hypertension.

Hypertension

  • High blood pressure can cause damage to the lining in the blood vessel wall, contributing to endothelial dysfunction. In combination with hyperlipidaemia, formation of artheromatous plaques are the end result. By exercising and/or taking medication like beta blockers, angiotensin-converting enzyme (ACE) inhibitors, calcium channel blockers, and water pills (diuretics), it is possible to lower blood pressure decreasing the risk of atherosclerotic disease (Zhao, et al., 2004).
  • One Beta blocker of particular importance is Carvedilol. Carvedilol exhibits antioxidant properties and has been known to steal free oxygen radicals, which are known to be involved in the lipid peroxidation. Of all the beta blockers Carvedilol is much more powerful in the inhibition of lipid peroxidation, especially when it is initiated by iron metal ions. It also prevents the amount of antioxidants, such as Vitamin E, from becoming significantly reduced. (Feuerstein & R., 1995)

Cholesterol Medication

  • Statins (3-hydroxy-3-methylglutaryl co-enzyme A (HMG-CoA) reductase inhibitors) are the most commonly used drug to regulate cholesterol. It functions to lower LDL cholesterol levels and also increase HDL cholesterol in the blood. Statins inhibits the synthesis of hepatic (liver) cholesterol synthesis, thereby decreasing the concentration of cholesterol in the liver. This causes LDL receptors to become more susceptible to plasma LDL uptake to balance out the decrease of concentration in the liver. More LDL cholesterol uptake by the liver from the blood results in lower LDL levels (Willacy, 2010).
  • Statins such as "fluvastatin and lovastatin" attach to lipoproteins and prevent the release of free radicals from the core when it is undergoes oxidative stress. "Simvastatin" reduces the amount of macrophages and it protect the lipoproteins from becoming oxidized. (Norata, Pirillo, & Catapano, 2003)

Probucol

  • Probucol is an anti-hyperlipidemic drug which counteracts oxidation of LDL by preventing the formation of fatty streaks and reducing the amount of cholesterol and cholesterol esters in macrophages. It protects the vessel wall by reducing oxidative damage caused by free radicals and thus preventing atherogenic plaque from forming within the wall.

Surgery

There is no medication or treatment besides surgery capable of removing the plaque built up in the carotid arteries. The following are the most popular procedures recommended by surgeons.

Angioplasty

  • Angioplasty is a procedure that opens blocked or narrowed coronary arteries (National Heart, Lung and Blood Institute, 2011). A thin tube with a balloon end is threaded to the narrowed carotid artery. Once in place the balloon is inflated to push the plaque outwards against the wall of the artery. Then a small metal tube called a stent is placed in the artery to keep it open.

Coronary Artery Bypass Grafting

  • In coronary artery bypass grafting, arteries or veins from other parts of the body are used to bypass the narrowed coronary artery. This procedure includes taking part of an artery or vein vessel and using it to bridge the heart to other coronary arteries that are receiving insufficient flow due to blockage in the main artery.

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Coronary arteries bypass grafting (National Heart, Lung and Blood Institute, 2011)

Carotid Endarterectomy

  • Carotid endarterectomy is the surgical removal of plaque build up from the carotid arteries in the neck. A surgeon makes an incision in the neck and clamps all common, external, and internal carotid arteries. Then the lumen of the internal carotid artery is sliced open and the plaque is removed. The artery is closed as with all other layers opened when incision was made (Society of Vascular Surgery, 2011).

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Carotid endarterectomy (Carotid Endarterectomy, 2011)


Antioxidants

HDL

  • Higher levels of HDL can inhibit LDL oxidation because it has anti-inflammatory properties, promotes cholesterol transport back to the liver, and reduces the amount of macrophages entering the arterial wall.
  • HDL in its native state is anti-inflammatory and can remove the oxidized LDL within the wall. However, HDL has been observed to become modified itself and actually promote inflammation (Asztalos, 2004).
  • By limiting the amount of macrophages entering the endothelium, the ability of macrophages to become saturated with lipids is decreased, and this decreases the risk of foam cells from being produced to form atherogenic plaque.

Vitamin E

  • Vitamin E is one of the most prominent antioxidants studied in atherosclerosis prevention. It lowers the amount of monocytes entering the arterial wall, which causes inflammation, and decreases interactions between adhesion molecules and endothelial cells, which is a leading cause of fatty streaks and plaque formation. Vitamin E is also important as a chain-breaking antioxidant; it helps to prevent both polyunsaturated fatty acids from undergoing lipid peroxidation and modification of proteins such as Apo-B (Meydani, 2001).
  • Vitamin E inhibits the proliferation of smooth muscle cells and platelet aggregation (essentially blood clots) through it's nonantioxidant properties. These are both primary causes of atherogenic plaque formation. Vitamin E also reduces the number of ligands on monocytes and thereby reduces their adhesive interactions. (Meydani, 2001)
  • Vitamin E is still not conclusively considered a prevention because the results vary study upon study.

Vitamin E Structure
Vitamin E Structure

References


Asztalos, B. F. (2004). High-density lipoprotein metabolism and progression of atherosclerosis: new insights from the HDL Atherosclerosis Treatment Study.Current opinion in cardiology, 19(4), 385-391.

Carotid Endarterectomy. (2011, February). Retrieved November 1, 2012, from Society of Vascular Surgery: http://www.vascularweb.org/vascularhealth/Pages/carotid-endarterectomy.aspx

Catapano, A. L., Maggi, F. M., & Tragni, E. (2000). Low density lipoprotein oxidation, antioxidants, and atherosclerosis. Current opinion in cardiology,15(5), 355.

Donetti, E., Soma, M. R., Barberi, L., Paoletti, R., Fumagalli, R., Roma, P., & Catapano, A. L. (1998). Dual effects of the antioxidant agents probucol and carvedilol on proliferative and fatty lesions in hypercholesterolemic rabbits.Atherosclerosis, 141(1), 45-51.

FEUERSTEIN, G. Z., & R., R. R. (1995). Carvedilol, a novel multiple action antihypertensive agent with antioxidant activity and the potential for myocardial and vascular protection. European Heart Journal.

How Is Atherosclerosis Treated? (2011, July 1). Retrieved November 1, 2012, from National Heart, Lung and Blood Institute: http://www.nhlbi.nih.gov/health/health-topics/topics/atherosclerosis/treatment.html

How Does Smoking Affect the Heart and Blood Vessels? (2011, December 20). Retrieved November 1, 2012, from National Heart, Lung and Blood Institute: http://www.nhlbi.nih.gov/health/health-topics/topics/smo/

Meydani, M. (2001). Vitamin E and atherosclerosis: beyond prevention of LDL oxidation. The Journal of nutrition, 131(2), 366S-368S.

Norata, G., Pirillo, A., & Catapano, A. (2003). Statins and Oxidative Stress During Atherogenesis. European Journal of Cardiovascular Risk.

Powell, J. T. (1998). Vascular damage from smoking: disease mechanisms at the arterial wall. Vascular Medicine, 21-28.

Sävykoski née Huittinen, T. (2003). 2.4 Atherosclerosis. Retrieved November 1, 2012, from Oulu University Library: http://herkules.oulu.fi/isbn9514269853/html/x1017.html

Srivastava, R. (2008). Synopsis of Causation: Atherosclerosis. London: United Kingdom Ministry of Defence.

Willacy, H. (2010, December 12). Lipid-regulating Drugs. Retrieved November 1, 2012, from Patient.co.uk: http://www.patient.co.uk/doctor/lipid-regulating-drugs

Zhao, X.-Q., Morse, J. S., Dowdy, A. A., Heise, N., DeAngelis, D., Frohlich, J., et al. (2004). Safety and Tolerability of Simvastatin Plus Niacin in Patients with Coronary Artery Disease and Low High-Density Lipoprotein Cholesterol (The HDL Atherosclerosis Treatment Study). The American Journal of Cardiology Vol.93, 307-312.