Causes of arteriosclerosis

Written by Tang Li
Cardiology
Updated on September 13, 2024
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The etiology of arteriosclerosis has not been fully determined, and studies indicate that arteriosclerosis is a multifactorial disease, caused by multiple factors acting at different stages, which are referred to as risk factors. The primary risk factors include the following:

First, age and gender. Clinically, it is more common in middle-aged and elderly people over forty years old. After the age of forty-nine, the progression is fast, but early arteriosclerotic changes have also been found in autopsy of some young adults and even children. In recent years, clinical onset age tends to be younger. Compared to men, the incidence rate in women is lower, because estrogen has a protective effect against arteriosclerosis. Therefore, the incidence rate in women increases rapidly after menopause. Age and gender are unchangeable risk factors.

Second, abnormal lipid levels, with abnormal lipid metabolism being the most important risk factor for arteriosclerosis.

Third, hypertension, as the incidence of arteriosclerosis in patients with hypertension is significantly higher. Sixty to seventy percent of patients with coronary arteriosclerosis have hypertension, and patients with hypertension are three to four times more likely to have arteriosclerosis compared to those with normal blood pressure.

Fourth, smoking, as the incidence and mortality rate of coronary arteriosclerosis in smokers are two to six times higher than in non-smokers, and it correlates positively with the number of cigarettes smoked daily. Secondhand smoke is also a risk factor.

Fifth, diabetes and glucose intolerance, where not only is the incidence of arteriosclerosis in diabetic patients several times higher than in non-diabetics, but the progression of the disease is also rapid.

Sixth, obesity, defined as being more than twenty percent over the standard weight or a BMI greater than twenty-four. Obesity is also a risk factor for arteriosclerosis.

Seventh, family history, where a family history of coronary heart disease, diabetes, hypertension, and hyperlipidemia significantly increases the incidence of coronary heart disease.

Various theories have been proposed to explain the pathogenesis of coronary arteriosclerosis from different perspectives. These include the lipid infiltration theory, thrombosis theory, and smooth muscle cell clonal theory. In recent years, the endothelial damage response theory has gained more support, suggesting that the disease results from various risk factors ultimately damaging the arterial intima, and the formation of arteriosclerosis lesions is an inflammatory, fibro-proliferative response of the arteries to endothelial damage.

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The earliest lesions of arteriosclerosis

The earliest lesion of atherosclerosis is the formation of lipid spots and streaks. The so-called lipid spots are small yellow dots that appear on the arterial intima. Under pathological observation, these are small areas of macrophages containing lipid droplets, forming a cluster of foam cells. As this small yellow dot develops, it gradually turns into a yellow streak made up of layers of macrophages containing lipids. The intima also comprises smooth muscle cells and lipids, as well as an infiltration of T cells, resembling a yellow streak on the intima.

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The difference between arteriosclerosis and atherosclerosis

Arteriosclerosis is the most common and most important among a group of vascular diseases called arteriosclerosis. The common characteristics of various arteriosclerosis include thickening, hardening, loss of elasticity, and narrowing of the arterial walls. The characteristic of arteriosclerosis is that the affected arterial lesions start from the intima, with various lesions coexisting, including local accumulation of papyraceous and complex carbohydrates, proliferation of fibrous tissue, and formation of plaques due to calcification, along with gradual degradation of the arterial media. Secondary lesions include intraplaque hemorrhage, plaque rupture, and local thrombosis formation. Modern cellular and molecular biology techniques show that arteriosclerotic lesions are characterized by migration of macrophages, proliferation of smooth muscle cells, and abundant formation of fibrous, collagen, elastic fibers, and proteoglycans as connective tissue matrices, as well as intra- and extracellular lipid accumulation. Because the lipid accumulation in the intima appears yellow and mushy, it is called arteriosclerosis. Although arteriosclerosis is only one type of arteriosclerosis, it is commonly referred to simply as arteriosclerosis due to its frequent occurrence and significant clinical relevance.

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Is coronary arteriosclerosis serious?

The severity of arterial atherosclerosis is related to the location of the lesion and the narrowing it causes in the coronary arteries. This is because if the blood flow through the coronary arteries is insufficient to meet the metabolic demands of the heart muscle, it can lead to ischemia and hypoxia of the heart muscle, causing angina. Severe and prolonged ischemia can lead to myocardial necrosis, or myocardial infarction. When there is significant narrowing in the coronary artery lumen, for instance more than 50%-75%, the situation can be compensated during rest. However, during exercise or rapid heart rate or emotional excitation, the oxygen demand of the heart muscle increases. This may result in mild or transient myocardial oxygen supply, or an imbalance between supply and demand. Another scenario involves unstable atherosclerotic plaques that rupture, erode, or bleed, leading to platelet aggregation or thrombus formation, causing a rapid worsening of luminal narrowing. This results in a decreased supply of oxygen to heart muscle, leading to acute coronary syndrome, which is very severe. In fact, the degree of coronary artery atherosclerosis is positively correlated with plaque stability, plaque location, and the elasticity of the coronary artery.

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What tests are used for arteriosclerosis?

If arteriosclerosis is in the early stages, we need to understand the situation with lipids and blood sugar, so lipid and blood glucose tests should be done. Later on, when some atheromatous plaques appear, examinations such as color Doppler ultrasound and cardiac echocardiography can be done to assess blood flow and the degree of narrowing in the vessels. For some severe narrowings, consider conducting a CTA, MRI, or angiography, which can non-invasively understand the lesions of arteriosclerosis. For some patients, if there is a need for interventional treatment, invasive, selective arterial angiography can be performed to understand the condition of the lesions. Therefore, different tests can be chosen at different stages.

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The difference between arteriosclerosis and atherosclerosis.

Arteriosclerosis and atherosclerosis are two different concepts. Arteriosclerosis is a type of vascular disease within arteriosclerosis, but atherosclerosis is more commonly significant clinically. Hence, it is customarily referred to simply as arteriosclerosis, generally implying atherosclerosis. The causes of arteriosclerosis are numerous, but they share common characteristics including thickening, hardening, loss of elasticity, and narrowing of the arterial walls. Atherosclerosis is characterized by lesions starting in the innermost layer of the artery, involving local accumulation of lipids, complex carbohydrates, fibrous tissue proliferation, and calcification forming plaques, along with a gradual degeneration of the innermost layer. The lipid accumulation gives the inner layer a yellowish, porridge-like appearance, hence the name atherosclerosis.