Cardiovascular diseases are the leading cause of death globally.   The World Health Organization lists ischaemic heart disease as the number one cause of death in the world, followed by stroke in a distant second place.  Ischaemic heart disease, also called coronary artery disease, describes the build-up of plaque (fatty material) in the heart’s arteries, causing them to narrow and reduce blood flow to the heart, which can result in acute and chronic health problems.  The building-up of plaque is called atherosclerosis, while arteriosclerosis refers to the hardening of the walls of arteries, which can also restrict blood flow.  Healthy arteries are flexible and elastic, as well as free from plaque.

What is arterial plaque?

Arterial plaque, or atherosclerosis, refers to the buildup of fats, cholesterol, and other substances on the surface cells (endothelial cells) and the innermost layers of blood vessels.  The build-up of plaque over time can restrict blood flow or can burst to trigger a blood clot.

Development of atherosclerosis

Atherosclerosis occurs in large and medium-sized arteries and is characterized by a lesion forming in a damaged area of the arterial wall, by the accumulation of lipids (fats), cholesterol, calcium, and cellular debris (from damaged and dying cells).  The lesion is covered by a very thin layer of endothelial (surface) cells, called the fibrous cap.  The lesion is infiltrated by inflammatory cells, which accelerates the atherosclerotic plaque to a point where it can suddenly rupture, forming a blood clot that cuts off blood flow to part of the heart, resulting in a heart attack.  Thrombosis (blood clots blocking the blood vessels) can be caused by either plaque rupture – when the fibrous cap fissures – or by plaque erosion due to endothelial damage.

Plaque deposits can grow to such an extent that they bulge into the artery and restrict the blood flow.  If this occurs in the coronary arteries that supply the heart with blood, it may cause chest pain during physical activity.  This condition is called angina.  If the restrictive plaque is in the arteries feeding the brain, it may cause vascular dementia with a decline in thinking skills.  If the build-up occurs in the arteries in the arms or legs, it is known as peripheral artery disease. 

Harvard warns that most ruptures stems from smaller, non-obstructive, inflamed plaques, which are not as easy to detect as the larger obstructive plaques.

When the blood clot completely blocks blood flow to the heart, it results in a heart attack, while a blockage in the arteries leading to the brain results in a stroke.  A blood clot in any part of the body can kill healthy tissue within minutes.

After disruption of the plaque, plaque healing occurs in some people (but inexplicably not in everyone) and prevents the forming of a blood clot.

Stages of plaque development – from healthy artery to heart attack:

The smooth linings of healthy arteries can become damaged by risk factors such as smoking, inactivity, diabetes, high blood pressure, infections, and inflammation.  Once the lining is damaged, it becomes susceptible to deposits of cholesterol.  Diets that are typically high in saturated fat stoke the liver to produce higher levels of low-density lipoprotein, which are particles better known as LDL cholesterol – the unhealthy kind.  Excess LDL can end up lodging in damaged areas in the arterial wall, causing plaques to grow.

Once cholesterol is deposited in arterial walls, white blood cells fight the invaders and engulf the LDL cholesterol, which then enlarge the cells and transform them into fat-laden foam cells.  Foam cells die, resulting in the release of a soft, fatty gruel and more inflammation is triggered.  The muscle cells in artery walls form a cap over the plaque lesion, with bigger plaques usually having a thicker and more substantial cap, while smaller plaques may have underdeveloped caps that rupture easily.  When a plaque ruptures, blood platelets (with clotting properties) assemble at the site and a blood clot develops, which can restrict or block the flow of blood in the artery.

Image: Harvard Medical School.

Prevention of atherosclerosis:

The treatment and prevention of atherosclerosis relies on healthy lifestyle changes, such as

  • Eating healthy foods – a mostly plant-based diet minimizes processed foods and maximizes fruit, vegetables, legumes, whole grains, nuts, and fish, while allowing moderate amounts of cheese and wine, and limited portions of red meat.  The Mediterranean diet is rated as the healthiest diet to follow.
  • Regular exercise – at least 40 minutes of aerobic activity that gets the heart and lungs pumping, for three or four days a week.  Exercise helps to lower blood sugar levels, burn body fat, lower blood pressure, and the resulting weight loss can help to lower LDL levels.
  • Quit smoking – the toxins in tobacco smoke can lower healthy HDL and increase unhealthy LDL cholesterol.  The nicotine and carbon monoxide in tobacco smoke can damage the lining of arteries and pave the way for the forming of plaque in the damaged areas.
  • Maintain a healthy weight – obesity is one of the risk factors for atherosclerosis.
  • Controlling underlying conditions – the lowering of LDL cholesterol to healthy levels plays an important part in lowering the risk of atherosclerosis, but cholesterol is only one of the risk factors for artery diseases.  Other risk factors include obesity (contributing to high blood lipid levels), high blood pressure (increasing the permeability of arterial walls and promoting the retention of LDL in arterial walls), and diabetes (driving inflammation and slowing blood flow, which accelerates atherosclerosis).

Conclusions

The danger of arterial plaque lies in the smaller lesions that quietly and invisibly do not cause any symptoms; are not easy to detect, and rupture more easily than the bigger lesions.

With intensive lifestyle changes it is possible to stop the progression and even reverse the condition to some extent, but people with advanced disease may also need medication to treat the underlying conditions and keep cholesterol, blood pressure, and blood sugar levels in a healthy range.

References:

Atherosclerotic plaque healing.  Published 27 August 2020.  New England Journal of Medicine.  USA.  (www.nejm.org)

Pathophysiology of atherosclerosis.  Chapter 12 of the handbook Cellular and molecular pathobiology of cardiovascular disease.  Michael A Seidman et al.  2014.  Elsevier Inc.  Published online October 2016 in Science Direct.  (www.sciencedirect.com)

Atherosclerosis.  Published 21 April 2015.  New England Journal of Medicine.  McMaster Pathophysiology Review.  (www.pathophys.org)

Arteriosclerosis/atherosclerosis.  Published 24 April 2018.  Mayo Clinic.  (www.mayoclinic.org)

Atherosclerosis.  Published online.  National Heart, Lung, and Blood Institute.  National Institutes of Health.  USA.  (www.nhlbi.nih.gov)

Types of thrombosis.  Published online and reviewed 29 May 2020.  Web MD.  (www.webmd.com)

Effects of native and modified low-density lipoproteins on hypertension monocyte recruitment in atherosclerosis.  Published 4 June 2007.  American Heart Association.  (www.ahajournals.org)

Avoiding atherosclerosis: the killer you can’t see.  Published February 2019.  Harvard Health Letter.    Harvard Medical School.  (www.health.harvard.edu)

The problem with plaque: even lesser amounts are still risky.  Published online.  Harvard Medical School.  (www.health.harvard.edu)

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