Atherosclerosis Facts: Symptoms, Causes, Diagnosis, Treatments and Prevention

Arteriosclerosis is a disease of the arteries, characterized by the development of “atheromatous plaque” on the walls of the arteries, which are mainly composed of fatty substances that narrows the lumen of the arteries. The risk is the more or less abrupt obstruction of the artery.



The plaque is mainly composed of fat (or “lipids”) and fibrosis.

The risk of plaque is that it may rupture or ulcerate (“unstable plaque”), causing the formation of clots (“thrombus”).

What is atheromatous plaque?

Atheromatous plaques are very common: almost all adults in the West have them.

The plaques are made up of fatty substances (or “lipids”) that are deposited on the walls of the arteries under the influence of various cardiovascular risk factors. Fibrosis is associated with them and appears as a result of various inflammatory and immunological phenomena.

A series of cardiovascular risk factors favor the appearance of these plaques, as well as their growth: hereditary factors, age, and sex, which are not modifiable, and environmental factors, which are: hypercholesterolemia, arterial hypertension, diabetes, smoking, physical activity…

These plaques are like “calcium buildup” inside a water pipe. If they’re too big, they’ll clog the arteries. The thickening process of the plaque can cause the cracking of its surface coating when it comes into contact with blood, which can trigger the formation of a clot (“thrombus”), which can be initially non-obstructive (“wall”) and then obstructive.

What are the signs of atherosclerosis?

Atherosclerosis is a silent disease: the vast majority of atherosclerotic plaques never appear and doctors say they are “asymptomatic”.

The risk is that like a “time bomb”, the progressive thickening of a plaque may be suddenly aggravated by the formation of a blood clot (“thrombus”), which will block the artery and eventually completely block the blood flow if it is large enough to block the remainder of the arterial lumen.

Plaque is considered a “clot trap” because, the arterial narrowing created by the plaque causes, the blood to accelerate with turbulence, which tends to favor the deposition of clotting elements (platelets and fibrin), which are added to the clots (“thrombus”).

Atherosclerosis will appear first in the small arteries: coronary arteries and penile arteries (internal pudendal arteries), then in the larger arteries (carotid arteries and lower limb arteries).

The appearance of these arterial problems generally occur from the age of 50, both progressively (pain such as angina pectoris, shortness of breath during exercise, instability during walking, vision problems or changes in heart rate) and sharply and brutally (heart attack).

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The risk is that the formation of a clot (“thrombus”) in an ulcerated plaque may lead to sudden obstruction: the lack of blood and oxygen is, therefore, brutal at the bottom of the obstruction, causing cell death, i.e. a “heart attack”.

How does atheromatous plaque form?

Early atherosclerosis lesions look like simple fat deposits on the inner wall of the artery. The plaques are produced later and are characterized by a scar containing collagen fibers and inflammatory cells surrounding a nucleus filled with cellular debris and fat, including cholesterol.

These plaques reshape under the influence of an inflammatory and immune response with the appearance of scars (“sclerosis”) and plaque ulcerations that trigger the aggregation of blood platelets (“thrombosis”), which can lead to a sudden blockage of the artery.

As the healing cycles of ulcers progress, atheromatous plaques grow in size and eventually block the artery lumen, which can also be suddenly blocked by a larger than average thrombus.

What causes atheromatous plaques?

Atherosclerosis is a multifactorial disease.

First, there seems to be a family or genetic predisposition to atherosclerosis: each person does not respond in the same way to different risk factors.

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There are four main risk factors that increase the likelihood of plaque development or severity. Eating disorders and excess cholesterol are the main risk factor. The study of primitive populations that were food-insecure clearly showed that when people accessed a Western-type diet, i.e. rich in calories and animal fats, blood cholesterol levels tended to rise and cardiovascular disease tended to occur.

Smoking is the second most important risk factor, especially in young women. Smoking increases the number of certain clotting factors and promotes the formation of clots. It also alters the ability of vessels to dilate and causes arterial spasms, particularly in coronary arteries. Arterial hypertension is another important risk factor due to vascular damage caused by “strokes” of hypertension. Excessive blood pressure leads to thickening and hardening of the arteries that promote the development of atherosclerosis, especially in the arteries that feed the brain. Diabetes is the fourth most important risk factor for atherosclerosis.

Abdominal obesity or “fat belly” is a minor but cumulative risk factor. As well as other risk factors: sedentariness, stress…

The thing to remember is that these risk factors are often associated and their respective risks are cumulative.

What are the complications of atheromatous plaques?

Most atheromatous plaques are stable, but the main risk is that when one of them forms a clot with arterial obstruction, often causing a dramatic acute vascular accident: about 80% of sudden deaths are caused by the rupture of an atheromatous plaque.

Depending on the position, the rupture of the plaque can cause a “myocardial infarction” in the heart, an “ischemic stroke” in the brain, “arteritis of the lower limbs” in the legs, “erectile dysfunction” in an artery of the penis, or a “mesenteric infarction” in an artery of the intestine.

Imaging tests can assess this arterial narrowing before complete blockage (arterial Doppler ultrasound, arteriography). In combination with functional tests, they allow the plaques to be observed and their dangerousness to be assessed.

Atherosclerosis can also cause dilation of a weakened part of the artery wall, called aneurysm. This dilation can burst and cause bleeding: inside the brain in the case of a cerebral artery (“hemorrhagic stroke”), or in the abdomen in the case of an aortic aneurysm (the largest artery in the heart), which can then be fatal.

Atherosclerosis Diagnosis

When is it necessary to mention the atheromatous plate?

Most of the time, atherosclerosis is silent for a long time and does not cause any signs until it is advanced enough to block an important blood vessel or cause an important aneurysm.

Of course, the existence of atheromatous plaque must be considered in the case of a perceived vascular noise (“murmur”) or in the case of “stress ischemia”: angina with chest pain at effort, shortness of breath at effort, calf cramps during walking, stomach pain during digestion or even in case of erectile dysfunction.

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But it is best not to wait for such arterial narrowing to occur before detecting atherosclerosis. This disease should be considered from the age of 50 in men (60 in women), especially in the case of a proven cardiovascular risk factor (smoking, high blood pressure, high cholesterol, diabetes), and even earlier in the case of early menopause in women or family hypercholesterolemia.

How is unstable plaque diagnosed?

The progressive accumulation of lipids in the plaque (and the softening of its fibrous layer) predisposes it to breakage. This “rapture” (or “crack”) usually results in the formation of a clot (“thrombus”) which can eventually block the arterial lumen and cause a heart attack downstream.

Atheromatous plaques may also have their lipid and cellular content gradually replaced by calcium phosphate crystals and apatite: the lesion calcifies and “calcified plaques” are observed.

Inflammation is involved in the formation and growth of a stable plaque but also plays an important role in the transformation into the unstable plaque by stimulating metalloproteinase, macrophages and thrombotic activity. C-reactive protein (CRP) is an inflammation marker that could be used to assess vascular inflammation.

The search for unstable plaque can be evaluated with other non-invasive tests such as calcium scores, coronary angiography, but the test that particularly displays this unstable plaque is called intracoronary echo endoscopy – a miniature ultrasound probe is inserted into the coronary artery through the artery of the leg or arm.

The Gist on atherosclerosis

Atherosclerosis is a general arterial disease and the discovery of plaques in one vascular site should lead to the search for plaques in other sites at risk.

Any discovery of a severe atherosclerotic lesion will lead to the search for silent lesions in other locations.

Therefore, the main sites explored are usually the coronary arteries (resting or exercise electrocardiogram, calcium score, angiogram or coronary angiography and thallium myocardial scintigraphy), the arteries of the neck to the brain (neck vessel doppler echocardiography), the abdominal artery (abdominal aorta doppler echocardiography) and the lower limbs (lower limb Doppler echocardiography). Other sites can be explored but during a more specialized evaluation.

Atherosclerosis Treatment

What can you do about atherosclerosis?

The prevention of worsening atherosclerosis consists of combating the main cardiovascular risk factors that can be modified: hypercholesterolemia, high blood pressure, smoking, diabetes, and obesity.

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The first thing to do is to correct the diet at the expense of animal fats (except fish) and in favor of fruit and vegetables with high fiber content. It is absolutely necessary to stop smoking. You should lose some weight if you are overweight and become physically active.

If you have high cholesterol or high blood pressure that is resistant to dietary changes and increased physical activity, you should consult a doctor to consider treatment. Similarly, in the case of diabetes, treatment should be introduced.

What is the treatment for atherosclerosis?

The treatment of atherosclerosis is mainly based on preventing its worsening – quitting smoking, losing weight, developing physical activity and treating hypertension, high cholesterol, and possible diabetes.

In people who have failed to balance their diet and who are at high cardiovascular risk, cholesterol medications, especially statins, help to stabilize plaque progression. Depending on their class, statins can reduce LDL cholesterol levels by 30 to 50%: we can, therefore, expect a 25% reduction in cardiovascular risk for every 1 mmol/l reduction in LDL cholesterol (the “bad” cholesterol). After a first vascular accident, the prevention of relapse from statins is systematic in addition to the diet, with more stringent treatment goals. Antihypertensive treatment is also necessary for the event of an increase in blood pressure above normal for the population.

In the case of more severe hypercholesterolemia (“autosomal familial hypercholesterolemia”), a new therapeutic pathway is emerging thanks to the identification of a key gene in the regulation of the body’s LDL cholesterol level, the PCSK-9 gene. This treatment, isolated or even combined with a statin, can drastically reduce LDL cholesterol levels and cardiovascular events in patients at very high risk (“autosomal familial hypercholesterolemia”).

What is the treatment for acute unstable plaque?

Treatment for acute thrombotic events in advanced atherosclerotic plaque is “angioplasty”. It involves inserting a balloon through a catheter into the narrowing of the artery and then inflating it to dilate the atheromatous area.

This expansion is then maintained with the use of a “stent”, a small mechanical device placed by the same catheter to prevent the artery from closing.

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This technique is widely used in the heart arteries (“coronary angioplasty”) where its success rate is remarkable: 95% for the simplest lesions and 85% for the most complex ones. Stenting angioplasty can also be used in lower limb arteries, carotid arteries, and renal arteries.

Atherosclerosis Prevention

How can atherosclerosis be prevented?

You can reduce the risk of atherosclerosis, heart disease, and stroke by adopting healthy lifestyle habits:

  • Avoid smoking and avoid second-hand smoke,
  • Physical activity,
  • A healthy diet, i.e. not abusing animal fats (except fish), especially so-called “saturated” fats and fats rich in “trans” fatty acids,
  • Maintain a normal body weight,
  • Limit alcohol consumption,
  • Reduce the stress level.

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It is also important to be tested for cardiovascular risk factors, especially if there is a family history of cardiovascular disease: it is important to know your blood pressure, possible levels of blood sugar and cholesterol so that you can establish strategies with your doctor to control them.

How can plaque breakage be avoided?

The treatment of atherosclerosis is based on the treatment of risk factors, and if an unstable plaque is suspected, the treatment should be further intensified. Only in certain cases (repeated angina pectoris, anginal pain, etc.), an unstable plaque is treated with a specific therapy.


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