Arteriosclerosis (Arterioscleroses)

Blausen 0227 Cholesterol[1]

Arteriosclerosis is defined as the pathological condition in which the walls of arteries thicken, harden and lose their elasticity.

Arteriosclerosis develops due to the following process: vascular.

Presentation

There is not a clinical manifestation for arteriosclerosis until plaques begin to seriously reduce blood flow to a main organ. Obviously, the nature of the clinical signs depends on the organ affected, as follows:

  • Heart: The signs are chest pain together with shortness of breath, sweating, nausea, dizziness and palpitations.
  • Brain: Dizziness and confusion, coupled with weakness or a complete paralysis of one side of the body. There can be a severe numbness of a part of the body, while vision can be lost or severely reduced. Mobility problems include difficulty in walking (like staggering or veering), and in-coordination in the movement of hands and arms, which are usually followed by impaired speech or complete inability to speak. If this episode lasts less than 24 hours it is clinically called transient ischemic attack; if it lasts for longer than 24 hours, causing much more severe consequences for the brain, it is clinically called stroke.
  • Abdomen: Dull or cramping pain in the middle of the abdomen, usually starting from 15 to 30 minutes after a meal. If the intestinal arteries are completely blocked, vomiting, diarrhea and abdominal swelling occur. 
  • Legs: Cramping pain in the leg muscles, especially while performing physical exercises. When the narrowing is severe, pain at rest, cold toes and feet, pale or bluish skin, and hair loss might occur. 

Workup

The first step in the diagnosis of arteriosclerosis is the study of the family history, to see if this presents previous cases of heart diseases, stroke, other circulatory problems and high levels of blood cholesterol. Furthermore, the habits of the subjects in term of smoking, diet, and physical activity need to be evaluated, and general physical examination to measure weight and size performed. Blood tests are indicated, to measure the level of cholesterol and glucose in the blood and make sure the subject is not diabetic, which is classically followed by a blood pressure test. The ankle-brachial index test by measuring blood pressure at the level of ankles and at the level of the arms may be helpful. A marked difference between these two readings generally suggest the presence of peripheral arterial disease. Other important tests include:

  • Electrocardiogram to measure the electrical activity of the heart and detect the presence of a heart disease.
  • Ultrasound to detect the presence of a blockage in the blood vessels. 
  • Angiography
  • CT scan
  • Ophthalmoscopy to examine blood vessels at the back of the eye and detect hardening of blood vessels in the retina (very sensitive to changes in blood pressure). 

Treatment

The treatment of arteriosclerosis is largely based on preventive measures. In particular, drug therapy plays a particular important role in preventing underlying conditions fostering plaque formation. The most important drugs used include statins/antihyperlipidemics to reduce cholesterol levels, ACE inhibitors and calcium channel blockers to reduce blood pressure, and anti-coagulant factors.

The worst cases of arteriosclerosis require more aggressive measures, especially various type of surgery such as:

  • Angioplasty and stent placement: The stent in this position keeps the artery open preventing re-narrowing .
  • Coronary artery bypass surgery: This is the preferred treatment for those suffering from severe ventricular dysfunction or diabetes mellitus [9].
  • Endarterectomy: Surgical removal of the plaque from the blocked or narrowed artery. The procedure has become widely used since it was first employed back in the 1950’ [10].
  • Thrombolytic therapy:

Prognosis

Prognosis of arteriosclerosis can be good provided that certain preventive measures are followed through life. As previously said, the condition is currently one of the most common causes of death in the US and the rest of the world, both in man and women, especially when it occurs as coronary artery complications. But it can be prevented, even in individuals genetically programmed for this type of disease, if subjects follow a healthy lifestyle, observe a low-fat diet, and take LDL-cholesterol lowering medications.

Etiology

There is great disagreement among experts regarding the causes of arteriosclerosis, and its etiology still remains unknown. However, there seems to be multiple factors that give their contribution to the development of this condition. These can be both genetic and acquired in nature, might foster or inhibit the arteriosclerosis development, and include processes like coagulation, inflammation, intimal injury, lipid metabolism, and increased proliferation of smooth muscle cells.

According to statistical data gathered so far, the most common risk factors include habits such as smoking and dietary deficiencies of antioxidants [3], the development of pathological conditions like hyperlipidemia, diabetes mellitus, and hypertension, as well as a clear family history of previous episodes of cardiovascular complications. In any case, the major event of plaque progression is undoubtedly thrombosis, or the formation of a blood clot in the lumen of the blood vessels, which can be caused by three different morphologies: rupture, erosion, and calcified nodule. Another possible etiological factor is low vitamin level in childhood, as vitamin D deficiency in children could be linked to hardening of arteries in more advanced ages [4] [5]. Anyway, the role of this compound is the arteriosclerosis development is not completely understood, and many studies still need to be done.

Epidemiology

As previously said, arteriosclerosis remains one of the most common causes of death despite the advancements of science and medicine, both in developed and poor countries [6] [7]. In the USA, AS affecting coronaries is responsible for around 1 of every 6 deaths, for a total of 400,000 individuals dying each year. Around 1.1 million of people are annually affected by myocardial infarction, 40% of which turn out to be fatal. 75% of the acute myocardial infarctions is due to plaque rupture, followed by the cases caused by coronary thrombosis open link for erosion and calcified nodules [8].

The incidence of rupture varies according to the decade of life, and in men appear to peak when they are in their 40s and while in women when they are in their 50s. In women, plaque rupture is also responsible for around 80% of the cases of coronary thrombi, and these appear to have a strong correlation with the level of circulating cholesterol. Furthermore, in the cases of acute myocardial infarction and sudden coronary death, plaque erosions largely appear in individuals younger than 50 and are responsible for the majority of the cases of acute coronary thrombi in premenopausal women.

Sex distribution
Age distribution

Pathophysiology

The lesion of arteriosclerosis begins as a fatty streak due to a local accumulation of lipid-laden foam cells in the artery intimal layer. This happens when a turbulent blood flow has triggered an endothelial dysfunction and the inhibition of nitric oxide production, which result in the production of adhesion molecules to recruit and bind inflammatory cells, with a mechanism which is still largely unknown. In the process, other molecules are also produced and these include proinflammatory cytokines, chemotactic proteins, and vasoconstrictors. The consequence of all this is the binding of monocytes and T cells, their migration to the subendothelium space, and the stimulation of a local inflammatory response. Lipids in the blood, especially low-density lipoproteins, bind this initial mass of cell forming the lipid-laden foam cells which then result in the fatty streak. This then evolves in a atherosclerotic plaque when 3 other components are added: lipids, inflammatory and smooth muscle cells, and pieces of connective tissue matrix containing thrombi with various stages of organization and Ca deposition.

These plaques can be stable or unstable. Stable plaques develop over several decades, until they cause stenosis or occlusion. The unstable plaques, instead, can be easily eroded or ruptured, causing thrombosis, occlusion or infarction much earlier than the appearance of a significant stenosis itself. For this reason these plaques are responsible for the majority of the clinical events. The stability of plaques depends on many factors, like composition, artery wall stress, size, location and configuration in relation to the blood flow. When plaques reach a certain size, reduced blood flow and complete occlusion occur.

Prevention

The prevention of arteriosclerosis is based on lifestyle changes aimed at promoting good circulation and avoiding the development of the condition. These measures include avoiding cigarette smoking, maintaining a healthy weight, following a healthy diet, practicing regular physical exercises, controlling blood pressure on a regular basis, and trying to keep cholesterol levels low.

Summary

The immediate consequence of arteriosclerosis is the gradual buildup of fatty plaques, cholesterol and organic debris on the internal walls of arteries, which in turn reduce the blood vessels lumen and restrict the blood flood and oxygen supply towards the body organs. The drastic decrease can become so severe to create a complete occlusion and bring about fatal medical problems like myocardial infarction and stroke. Arteriosclerosis was known in the past with other names, such as arterial-capillary fibrosis or endarteritis, until it got its official scientific term at the end of the ninetieth century thanks to the work of the English physicians Henry Gawen Sutton and Sir William Withey Gull [1], who firstly coined it. Due to the modern style of life and diet, this condition has now become so common to be considered one of the important causes of death in the twentieth century [2].

Patient Information

Arteriosclerosis is a pathological condition in which the walls of the arteries thicken, harden, and lose their elasticity. This creates the condition for the formation of a gradual buildup of fatty plaques, cholesterol and cellular debris which finally result in a complete occlusion of the artery. The clinical signs of arteriosclerosis depend on the organs affected, which generally include brain, heart, abdomen, and legs.

Although now arteriosclerosis is one of the most common causes of death in the developed countries, due to a bad lifestyle and diet, it can be prevented by measures such as avoiding cigarette smoking, maintaining a healthy weight, following a healthy diet, practicing regular physical exercises, controlling blood pressure on a regular basis, and trying to keep cholesterol levels low.

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References

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  3. Burke AP, Farb A, Pestaner J, et al. Traditional risk factors and the incidence of sudden coronary death with and without coronary thrombosis in blacks. Circulation. 2002 Jan 29. 105(4):419-24. 
  4. Juonala M, Voipio A, Pahkala K, Viikari JS, Mikkilä V, Kähönen M, et al. Childhood 25-OH Vitamin D Levels and Carotid Intima-Media Thickness in Adulthood: The Cardiovascular Risk in Young Finns Study. J Clin Endocrinol Metab. 2015 Feb 10. jc20143944.
  5. Davenport L. Childhood Vitamin D Levels Linked to Later Atherosclerosis. Medscape Medical News. Available at http://www.medscape.com/viewarticle/839936#vp_2. Accessed: March 10, 2015. 
  6. Roger VL, Go AS, Lloyd-Jones DM, et al. Heart disease and stroke statistics--2012 update: a report from the American Heart Association. Circulation. 2012 Jan 3. 125(1):e2-e220.
  7. Celermajer DS, Chow CK, Marijon E, Anstey NM, Woo KS. Cardiovascular disease in the developing world: prevalences, patterns, and the potential of early disease detection. J Am Coll Cardiol. 2012 Oct. 2;60(14):1207-16. 
  8. Arbustini E, Dal Bello B, Morbini P, et al. Plaque erosion is a major substrate for coronary thrombosis in acute myocardial infarction. Heart. 1999 Sep. 82(3):269-72. 
  9. Eagle, KA; Guyton RA; Davidoff R et al. ACC/AHA 2004 guideline update for coronary artery bypass graft surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1999 Guidelines for Coronary Artery Bypass Graft Surgery). Circulation 110 (14): e340–437. 
  10. Thompson JE. The Evolution of Surgery for the Treatment and Prevention of Stroke. Stroke 1996 27 (8): 1427–1434.

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Media References

  1. Blausen 0227 Cholesterol, CC BY 3.0

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