An atheroma is the accumulation of degenerative material that is reversible in the inner lining of the artery wall. The material consists of most macrophage cells, or debris, containing lipids, calcium and a number of fibrous connective tissues. The accumulation of the material forms a swelling in the arterial wall, which can infiltrate the arterial channel, narrow it down and restrict blood flow. Atheroma occurs in atherosclerosis, which is one of three subtypes of arteriosclerosis (which is atherosclerosis, arteriosclerosis and Monckeberg arteriolosclerosis).
In the context of heart or arterial problems, atheromata is usually referred to as atheromatous plaque . This is a pathological condition found in most humans.
Veins do not develop atheromata, as they do not experience the same hemodynamic pressure as the arteries, unless surgery is removed as an artery, as in bypass surgery. Accumulation (swelling) is always in the intima tunica, between the endothelium layer and the middle layer of smooth muscle of the artery wall. While the early stages, based on gross appearance, are traditionally termed striped by pathologists, they are not composed of fat cells but the accumulation of white blood cells, especially macrophages, which have taken low-density lipoprotein (LDL) oxidizers. Once they accumulate large amounts of cytoplasmic membranes (with high cholesterol related content) they are called foam cells. When the foam cells die, the contents are released, which attract more macrophages and create extracellular lipid nuclei near the center to the surface in any atherosclerotic plaque. In contrast, the older exterior of the plaque becomes more calcified, less metabolically active and more physically stiffer over time.
Video Atheroma
Signs and symptoms
For most people, the first symptoms occur due to the development of atheroma in the heart arteries, most often resulting in a heart attack and subsequent disability. However, the heart arteries, because (a) they are small (from about 5 mm to microscopic), (b) they are hidden deep inside the chest and (c) they never stop moving, has become a target organ that is difficult to trace. , especially clinically in still asymptomatic individuals. In addition, all mass-enforced clinical strategies focus on (a) minimal cost and (b) the overall safety of the procedure. Therefore, existing diagnostic strategies for detecting atheroma and tracking response to treatment are limited. The most commonly dependable method, the patient's symptoms and the heart stress test, does not detect any symptoms of the problem until the atheromatous disease is highly advanced because the arteries are enlarged, not narrowed in response to the increased atheroma. It is a plaque rupture, producing debris and clots that block the flow of blood downstream, sometimes also locally (as seen on the angiogram), which reduces/stops blood flow. However, these events occur suddenly and are not previously revealed either by stress testing, stress tests or angiograms.
Maps Atheroma
Mechanism
A healthy epicardial coronary artery consists of three layers, intima, media, and adventitia. Atheroma and alterations in the artery wall usually result in a large (enlarged) small aneurysm to compensate for the extra wall thickness without alteration in the lumen diameter. Ultimately, however, usually as a result of rupture of vulnerable plaques and clots in the lumen above the plaque, stenosis (narrowing) of blood vessels develops in some areas. More rarely, the arteries dilate so much that enlarged aneurysm enlarges from the arteries. All three results are often observed, in different locations, within the same individual.
Stenosis and closure
Over time, atheromata usually develop in size and thickness and induce the central region of the muscles surrounding the arterial (medium) arteries to stretch, called remodeling, usually enough to compensate their size so that the calibration of the artery (lumens) remains unchanged until it is usually more than 50% of the area Cross-sectional artery walls consist of atheromatous tissue.
If the muscle wall enlargement ultimately fails to keep up with the enlargement of the volume of the atheroma, or the clump form and set on the plaque, the lumen of the artery becomes narrowed as a result of repeated rupture, lumps & amp; fibrosis above the tissue that separates the atheroma from the bloodstream. This narrowing becomes more common after decades of life, increasingly common after people aged 30 to 40 years.
The endothelium (cell monolayer inside the blood vessels) and covering the tissue, termed fibrous stamp, atheroma separated from the blood in the lumen. If the rupture (see vulnerable plaque) of the endothelium and fibrous stamp occurs, then (a) the bath debris of the plaque combined with (b) platelet and freeze response (for both debris and at the breaking location) occurs within the fraction of a second.
The breakdown of results in both (a) bath debris occluding smaller downstream vessels (debris greater than 5 microns is too large to pass through the capillaries)) combined with (b) platelets and accumulated clots upon rupture (injury/repair response) resulting in narrowing , sometimes closing, lumen.
Downstream tissue damage occurs due to (a) downstream microvascular closure and/or (b) lumen closure of the rupture, both resulting in a loss of blood flow to the downstream capillary microvasulature. This is the main mechanism of myocardial infarction, stroke or other cardiovascular disease related problems.
While clots in ruptured locations usually shrink in volume over time, some clots may become organized into fibrotic tissue resulting in narrowing of the lumen of the artery; narrowing is sometimes seen on angiographic examination, if it is severe enough. Because the angiography method can only reveal larger lumens, typically & gt; & gt; 200 microns, angiography after cardiovascular events usually do not reveal what happened.
Artery enlargement
If the muscle wall muscles overload over time, then a rough enlargement of the artery results, usually for decades of life. This is a less common result. Atheroma in aneurysm enlargement (swelling of blood vessels) can also rupture and accumulate atheroma flakes and clot down in the downstream. If the arterial enlargement continues up to 2 to 3 times the regular diameter, the wall often becomes weak enough that only with pulse pressure, loss of wall integrity may occur causing sudden bleeding (bleeding), major symptoms and weakness; often a quick death. The main stimulus for aneurysm formation is pressure atrophy from structural support of the muscle layer. The main structural proteins are collagen and elastin. This causes thinning and wall balloons allowing rough enlargement to occur, as is common in the abdominal area of ​​the aorta.
Diagnosis
Because the arterial wall is enlarged at the site with atheroma, detecting atheroma before death and autopsy has long been problematic. Most methods have focused on opening the arteries; is highly relevant, but actually loses atheroma in the artery walls.
Historically, the fixation of arterial walls, staining and thin sections has become the gold standard for the detection and description of atheroma, after death and autopsy. With staining and special examination, micro-calcification can be detected, usually in smooth muscle cells from the artery medium near the fat line in a year or two of fatty layer formation.
Interventional and non-interventional methods for detecting atherosclerosis, especially plaque prone (non-occlusive or soft plaques), are widely used in current clinical research and practice.
Measurement of Carotid Scan intima-media thickness (CIMT can be measured by B-mode ultrasound) has been recommended by the American Heart Association as the most useful method for identifying atherosclerosis and may now be the gold standard for detection.
IVUS is the most sensitive method today that detects and measures further atheromas in living individuals, although it is not usually used until decades after atheroma begins to develop due to cost and invasion of the body.
CT scans use a higher state of the art spiral higher resolution, or higher speed EBT, the machine has become the most effective method for detecting calcification present in plaque. However, the atheroma should be advanced enough to have a large enough calcification region in it to create a large area of ​​Hounsfield ~ 130 units that can be detected by the CT scanning software as distinct from other surrounding tissues. Usually, the area begins to occur in the heart arteries about 2-3 decades after atheroma begins to develop. Therefore, the detection of plaque that is much smaller than the previous one may be being developed by some companies, such as Image Analysis. The presence of smaller plaques, spotty may actually be more dangerous to develop into acute myocardial infarction.
Arterial ultrasound, especially the carotid artery, with measurements of arterial wall thickness, offers a way to track some disease progression. In 2006, the thickness, commonly referred to as IMT for intima-medial thickness, was not measured clinically although it has been used by some researchers since the mid-1990s to track changes in artery walls. Traditionally, clinical carotid ultrasound estimates only the degree of restriction of blood lumen, stenosis, due to very severe disease. The National Institute of Health undertakes a five-year, $ 5 million research, led by medical researcher Kenneth Ouriel, to study intravascular ultrasound techniques on atherosclerotic plaque. Progressive doctors have begun to use IMT measurements as a way to measure and track disease progression or stability in each patient.
Angiography, since the 1960s, has become a traditional way of evaluating atheroma. However, angiography is only movement or still image of dye mixed with blood with arterial lumen and never shows atheroma; artery walls, including atheromas with arterial walls remain invisible. The only exception to this rule is that with a highly advanced atheroma, with extensive calcification within the walls, a halo-like radiodensity ring can be seen in most older humans, especially when the lumens of the arteries are visualized. In cine-floro, cardiologists and radiologists usually look for these calcified shadows to identify the arteries before they inject the contrast agent during the angiogram.
Classification of lesions
- Type I: An isolated macrophage foam cell
- Type II: Multiple layers of foam cells
- Type III: Preatheroma, intermediate lesion
- Type IV: Atheroma
- Type V: Fibroatheroma
- Type VI: Fissured, ulcerated, hemorrhagic, thrombotic lesions
- Type VII: Calcification lesion
- Type VIII: Fibrotic lesions
Treatment
Many approaches have been promoted as a method to reduce or reverse the development of atheroma:
- eat foods from raw fruits, vegetables, nuts, nuts, fruits, and seeds;
- consume foods containing omega-3 fatty acids such as fish, fish derived supplements, and linseed oil, borage oil, and other non-animal oils;
- abdominal fat reduction;
- aerobic exercise;
- cholesterol synthesis inhibitors (known as statins);
- normal low blood glucose levels (glycosylated hemoglobin, also called HbA1c);
- consumption of micronutrients (vitamins, potassium, and magnesium);
- maintaining normal, or healthy blood pressure levels;
- aspirin supplements
- cyclodextrin can dissolve cholesterol, remove it from plaque
History of research
In developed countries, with improved public health, infection control and increased life span, the atheroma process has become an increasingly important problem and burden for society. Atheromata continues to be a major basis for disability and death, despite the tendency for gradual improvement since the early 1960s (adjusted for patient age). Thus, improvement efforts towards better understanding, treating and preventing problems continue to grow.
According to US data, 2004, for about 65% of men and 47% of women, the first symptoms of cardiovascular disease are myocardial infarction (heart attack) or sudden death (death within an hour of symptom onset).
A large number of arterial flow disruption events occur in locations with a lumenal narrowing of less than 50%. Cardiac stress tests, traditionally the most common non-invasive testing method for limiting blood flow, generally only detect luminal constriction of ~ 75% or more, although some doctors recommend methods of nuclear pressure that can sometimes detect as little as 50%.
The sudden nature of pre-existing atheroma complications, vulnerable plaques (non-occlusive or soft plaques), has led, since the 1950s, to the development of intensive care units and complex medical and surgical interventions. Angiography and then cardiac stress tests are initiated to visualize or indirectly detect stenosis. Next is a bypass operation, to pinch the transplanted vein, occasionally the artery, around recent stenosis and angioplasty, now including the stent, the latter being a drug-coated stent, to stretch the more open stenosis.
However, despite these medical advances, with success in reducing angina symptoms and reducing blood flow, the incidence of atheroma rupture remains a major problem and still sometimes results in sudden disability and death despite the fastest, massive and skilled medical and surgical interventions available only. today. According to some clinical trials, bypass surgery and angioplasty procedures have the best effect, if any, on improving overall survival. Usually death bypass surgery is between 1 and 4%, of angioplasty between 1 and 1.5%.
In addition, this vascular intervention is often performed only after a person has symptoms, often partially disabled, as a result of the disease. It is also clear that both angioplasty and bypass intervention do not prevent future heart attacks.
The older method to understand atheroma, dating before World War II, depends on autopsy data. Autopsy data has long been demonstrated in early childhood fatigue initiation with progressive progressive symptoms for decades.
One way to look at atheroma is a highly invasive and costly IVUS ultrasound technology; this gives us an intimate volume right inside plus a central media layer about 2.5 cm (1 inch) long artery. Unfortunately, it does not provide information about the structural strength of the arteries. Angiography does not visualize atheroma; it just makes the blood flow in the veins visible. Alternative methods that are not physically or less invasive and less expensive per individual test have been used and continue to be developed, such as those using computed tomography (CT, led by electron beam tomography forms, given greater velocity) and magnetic resonance imaging (MRI). The most promising since the early 1990s was EBT, detecting calcification in atheroma before most individuals begin to have clinically known symptoms and weaknesses. Interestingly, statin therapy (to lower cholesterol) does not slow the rate of calcification as determined by CT scan. Imaging of the coronary artery walls of MRI, although currently limited to studies, has demonstrated the ability to detect thickening of blood vessel walls in high-risk individuals without symptoms. As a non-invasive ionizing free radiation technique, MRI-based techniques can have future use in monitoring disease progression and regression. Most visualization techniques used in the study, they are not widely available for the majority of patients, have significant technical limitations, have not been widely accepted and are generally not covered by medical insurance operators.
From human clinical trials, it has become increasingly clear that a more effective treatment focus is to slow, stop and even partially reverse the process of atheroma growth. There are several prospective epidemiological studies including the Atherosclerosis Risk Study in Society (ARIC) and Heart Health Study (CHS), which has supported a direct correlation of Carotid Intima-Media (CIMT) thickness with myocardial infarction and stroke risk in patients without cardiovascular disease. history of the disease. ARIC studies were performed on 15,792 individuals between 5 and 65 years in four different regions of the US between 1987 and 1989. Baseline CIMT was measured and measurements were repeated at 4- to 7-year intervals with carotid B mode ultrasonography in this lesson. The CIMT increase correlates with an increased risk for CAD. CHS began in 1988, and the association of CIMT with the risk of myocardial infarction and stroke was investigated in 4,476 subjects <65 years. At the end of approximately six years of follow-up, CIMT measurements correlated with cardiovascular events.
Parvée artÃÆ'Â © rielle et Risque Cardiovasculaire in Asia Africa/Middle East and Latin America (PARC-AALA) is another important large-scale study, in which 79 centers from countries in Asia, Africa, Middle East and Latin America participate, and the distribution of CIMT according to different ethnic groups and their relationship to Framingham cardiovascular scores were investigated. Multi-linear regression analysis revealed that an increase in Framingham cardiovascular scores was associated with CIMT, and carotid plaque was independent of geographical differences.
Cahn et al. prospectively followed up 152 patients with coronary artery disease for 6-11 months with carotid artery ultrasonography and recorded 22 vascular events (myocardial infarction, transient ischemic attack, stroke, and coronary angioplasty) in this period. They conclude that carotid atherosclerosis as measured by this non-intervention method has a prognostic significance in patients with coronary arteries.
In the Rotterdam Study, Bots et al. following 7,983 patients & gt; 55 years for an average period of 4.6 years, and reported 194 incidents of myocardial infarction within this period. CIMT was significantly higher in the myocardial infarction group than in the other groups. Demircan et al. found that CIMT patients with acute coronary syndrome increased significantly compared with patients with stable angina pectoris.
It has been reported in another study that a maximum CIMT value of 0.956 mm has a sensitivity of 85.7% and a specificity of 85.1% for predicting CAD angiography. The study group consisted of patients treated at outpatient cardiology clinics with symptoms of stable angina pectoris. Research shows CIMT is higher in patients with significant CAD than in patients with non-critical coronary lesions. Regression analysis revealed that an average thickening of intima-media complexes over 1.0 was a significant predictor of CAD in our patients. There was a significant increase in CIMT with the number of coronary arteries involved. In accordance with the literature, it was found that CIMT was significantly higher in the presence of CAD. Furthermore, CIMT increases as the number of involved vessels increases and the highest CIMT value is recorded in patients with major left coronary involvement. However, clinical trials in humans are slow to provide clinical & amp; medical evidence, in part because the asymptomatic nature of atheromata makes them very difficult to learn. Promising results were found using a scanning of carotid intima-media thickness (CIMT can be measured by B-mode ultrasonography), B-vitamins that reduce corrosive proteins, homocysteine ​​and that reduce the volume and thickness of carotid artery neck plaques, even at end -stage disease.
Source of the article : Wikipedia
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