Atheroma

Atheroma
Other names	atheromata (plural), atheromas (plural), atheromatous plaque, plaque
Atherosclerotic plaque from a carotid endarterectomy specimen. This shows the division of the common into the internal and external carotid arteries.
Specialty	Cardiology
Complications	Thrombosis, embolism, atherosclerosis, arteriosclerosis
Causes	Hyperlipidemia, hypertriglyceridemia, hypercholesterolemia

An atheroma, or atheromatous plaque, is an abnormal accumulation of material in the

The healthy epicardial coronary artery consists of three layers, the tunica intima, media, and adventitia.^[10][11] Atheroma and changes in the artery wall usually result in small aneurysms (enlargements) just large enough to compensate for the extra wall thickness with no change in the lumen diameter. However, eventually, typically as a result of rupture of vulnerable plaques and clots within the lumen over the plaque, stenosis (narrowing) of the vessel develops in some areas. Less frequently, the artery enlarges so much that a gross aneurysmal enlargement of the artery results. All three results are often observed, at different locations, within the same individual.^[12][13]

Over time, atheromata usually progress in size and thickness and induce the surrounding muscular central region (the media) of the artery to stretch out, which is termed remodeling. Typically, remodeling occurs just enough to compensate for the atheroma's size such that the calibre of the artery opening (lumen) remains unchanged, until about 50% of the artery wall cross-sectional area consists of atheromatous tissue.^[6]

If the muscular wall enlargement eventually fails to keep up with the enlargement of the atheroma volume, or a clot forms and organizes over the plaque, then the lumen of the artery becomes narrowed as a result of repeated ruptures, clots and fibrosis over the tissues separating the atheroma from the blood stream. This narrowing becomes more common after decades of living, increasingly more common after people are in their 30s to 40s.^{[citation needed]}

The

While clots at the rupture site typically shrink in volume over time, some of the clot may become organized into fibrotic tissue resulting in narrowing of the artery lumen; the narrowings sometimes seen on angiography examinations, if severe enough. Since angiography methods can only reveal larger lumens, typically larger than 200 micrometres, angiography after a cardiovascular event commonly does not reveal what happened.^{[citation needed]}

If the muscular wall enlargement is overdone over time, then a gross

After they accumulate large amounts of cytoplasmic membranes (with associated high cholesterol content) they are called foam cells. When foam cells die, their contents are released, which attracts more macrophages and creates an extracellular lipid core near the centre to inner surface of each atherosclerotic plaque. ^{[citation needed]}

Conversely, the outer, older portions of the plaque become more calcified, less metabolically active and more physically stiff over time.^{[citation needed]}

Veins do not develop atheromata, because they are not subjected to the same haemodynamic pressure that arteries are, unless surgically moved to function as an artery, as in bypass surgery. In fact, veins grafted to function as arteries in bypass surgeries tend to show faster formation of atheromata, while (in rabbits) arteries grafted to function as veins also do not grow atheromata.^[14]

Because artery walls enlarge at locations with atheroma,^[6] detecting atheroma before death and autopsy has long been problematic at best. Most methods have focused on the openings of arteries; while these methods are highly relevant, they totally miss the atheroma within the arterial lumen.^{[citation needed]}

Historically, arterial wall fixation, staining and thin section has been the gold standard for detection and description of atheroma, after death and autopsy. With special stains and examination, micro calcifications^[15] can be detected, typically within smooth muscle cells of the arterial media near the fatty streaks within a year or two of fatty streaks forming.

Interventional and non-interventional methods to detect atherosclerosis, specifically vulnerable plaque (non-occlusive or soft plaque), are widely used in research and clinical practice today.^{[citation needed]}

Angiography, since the 1960s, has been the traditional way of evaluating for atheroma. However, angiography is only motion or still images of dye mixed with the blood within the arterial lumen and never show atheroma; the wall of arteries, including atheroma within the arterial wall remain invisible. The limited exception to this rule is that with very advanced atheroma, with extensive calcification within the wall, a halo-like ring of radiodensity can be seen in most older humans, especially when arterial lumens are visualized end-on. On cine-floro, cardiologists and radiologists typically look for these calcification shadows to recognize arteries before they inject any contrast agent during angiograms.^{[citation needed]}

• Type I: Isolated macrophage foam cells^[10][21]
• Type II: Multiple foam cell layers^[10][21]
• Type III: Preatheroma, intermediate lesion^[10][21]
• Type IV: Atheroma^[10][21]
• Type V: Fibroatheroma^[10][21]
• Type VI: Fissured, ulcerated, hemorrhagic, thrombotic lesion^[10][21]
• Type VII: Calcific lesion^[10][21]
• Type VIII: Fibrotic lesion^[10][21]

This section needs more primary sources, specifically: Out of ten points, only 4 are referenced, and among those only one is a primary, peer-reviewed reference. Without the medical refs, it's unclear how reliable each advised approach is pertaining to treating the disease, even if it is a good general advice. Please review the contents of the section and add the appropriate references if you can. Unsourced or poorly sourced material may be challenged and removed. Find sources: "Atheroma" – news · newspapers · books · scholar · JSTOR (October 2019)

Many approaches have been promoted^{[by whom?]} as methods to reduce or reverse^[22] atheroma progression:^{[citation needed]}

• eating a diet of raw fruits, vegetables, nuts, beans, berries, and grains;^[22][23]
• consuming foods containing
  omega−3
  fatty acids such as fish, fish-derived supplements, as well as flax seed oil, borage oil, and other non-animal-based oils;
• abdominal fat reduction;
• aerobic exercise;^[22]
• inhibitors of
  statins);^[22]
• low normal
  HbA1c
  );
• micronutrient (vitamins, potassium, and magnesium) consumption;
• maintaining normal, or healthy, blood pressure levels;
• aspirin supplement
• mouse studies indicated that subcutaneous administration of oligosaccharide 2-hydroxypropyl-β-cyclodextrin (2HPβCD) can solubilize cholesterol, removing it from plaques.^[24] However, later work concluded that "treatment with 2HPβCD is ineffective in inducing atherosclerosis regression".^[25]

When a plaque is dangerous enough, it may warrant physical intervention such as

According to United States data, 2004, for about 65% of men and 47% of women, the first

Additionally, these vascular interventions are often done only after an individual is symptomatic, often already partially disabled, as a result of the disease. It is also clear that both angioplasty and bypass interventions do not prevent future heart attack.^{[citation needed]}

The older methods for understanding atheroma, dating to before World War II, relied on autopsy data. Autopsy data has long shown initiation of fatty streaks in later childhood with slow asymptomatic progression over decades.^[6]

One way to see atheroma is the very invasive and costly

Paroi artérielle et Risque Cardiovasculaire in Asia Africa/Middle East and Latin America (PARC-AALA) is another important large-scale study, in which 79 centres from countries in Asia, Africa, the Middle East, and Latin America participated, and the distribution of CIMT according to different ethnic groups and its association with the Framingham cardiovascular score was investigated. Multi-linear regression analysis revealed that an increased Framingham cardiovascular score was associated with CIMT, and carotid plaque independent of geographic differences.^[citation needed]

Cahn et al. prospectively followed-up 152 patients with coronary artery disease for 6–11 months by carotid artery ultrasonography and noted 22 vascular events (myocardial infarction, transient ischemic attack, stroke, and coronary angioplasty) within this time period. They concluded that carotid atherosclerosis measured by this non-interventional method has prognostic significance in coronary artery patients.^{[citation needed]}

In the Rotterdam Study, Bots et al. followed 7,983 patients >55 years of age for a mean period of 4.6 years, and reported 194 incident myocardial infarctions within this period. CIMT was significantly higher in the myocardial infarction group compared to the other group. Demircan et al. found that the CIMT of patients with acute coronary syndrome were significantly increased compared to patients with stable angina pectoris.^{[citation needed]}

It has been reported in another study that a maximal CIMT value of 0.956 mm had 85.7% sensitivity and 85.1% specificity to predict angiographic CAD. The study group consisted of patients admitted to the cardiology outpatient clinic with symptoms of stable angina pectoris. The study showed CIMT was higher in patients with significant CAD than in patients with non-critical coronary lesions. Regression analysis revealed that thickening of the mean intima-media complex more than 1.0 was predictive of significant CAD our patients. There was incremental significant increase in CIMT with the number coronary vessel involved. In accordance with the literature, it was found that CIMT was significantly higher in the presence of CAD. Furthermore, CIMT was increased as the number of involved vessels increased and the highest CIMT values were noted in patients with left main coronary involvement. However, human clinical trials have been slow to provide clinical & medical evidence, partly because the asymptomatic nature of atheromata make them especially difficult to study. Promising results are found using carotid intima-media thickness scanning (CIMT can be measured by B-mode ultrasonography), B-vitamins that reduce a protein corrosive,