2/1/17: FEBRUARY IS NATIONAL HEART MONTH; Focus on the Scourge of Atherosclerosis: ‘Hardening’ and ‘Narrowing’ of Arteries

In honor of National Heart Month, I will be writing exclusively about the heart, heart disease, and heart health in February. Some of what I write will be a little repetitive for those of you have been reading my blogs and tidbits for some time, but the material is worth repeating.

I start with atherosclerosis, which is a bedrock cause of extensive damage to the cardiovascular system. For the content that follows, I have borrowed liberally from my book, “Our Parents in Crisis: Confronting Medical Errors, Ageist Doctors, and Other Healthcare Failings.”

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A Chronic Inflammation

Although the exact cause of atherosclerosis is unknown, it unquestionably starts with damage or injury to the intimal layer of an artery, after which inflammation and biochemical changes occur in the cells. Evidence of the atherosclerotic process can be detected in a person within the first 10 years of life. Already, fat buildup is occurring.

(The intima is the innermost layer of the arterial walls’ three layers. The middle layer, which consists of smooth muscle and elastic connective tissue, is the media; the outermost layer is the adventitia, a connective-tissue layer that contains the vasa vasorum (tiny blood vessels) that nourish the outer half of the arterial walls. The intima is a thin layer of connective tissue covered on the inner surface by endothelial cells.)

You may think of atherosclerosis as a chronic inflammation within the walls of medium and large arteries.

As the Mayo Clinic explains: “[Platelets] often clump at the injury site to try to repair the artery, leading to inflammation. Over time, fatty deposits made of cholesterol and other cellular waste products also build up at the injury and harden.” (1)

When fatty deposits grow and arterial walls thicken, cells within the wall layers die, leaving behind a fatty paste called atheroma. To contain this damage, fibroblasts form fibrous (hard) connective-tissue capsules around the atheroma. We refer to such capsules as fibrous or fatty plaques. (2) (Fibroblasts are connective-tissue cells that produce collagen and other fibers.)

Fatty plaques may completely or partially block arterial blood flow, or they may break free of the wall and enter the bloodstream as clots. Plaque-thickened arterial walls—i.e., narrowed arteries—resist blood flow, increasing the heart’s afterload requirement so that it pumps harder. When afterload increases, the systolic blood pressure rises, creating the risk of hypertension.

The afterload is the amount of pressure that the heart’s two ventricles must work against during systole, when they are contracting in order to pump blood out to the lungs and the rest of the body.

Upon encountering the force of increased blood pressure, inner layers of arterial walls weakened by plaque deposits and connective-tissue proliferation may balloon out into a bulge called an aneurysm. Aneurysms can form in any large artery, rupture, and cause severe internal bleeding. In a cerebral artery, this bleeding is a stroke. (I discussed aneurysms and strokes in my Jan. 14, 2017 blog.)

While we are all prone to atherosclerosis, also called arterial sclerosis, several prominent risk factors seem to accelerate its process. They include high blood pressure; high low-density lipoprotein (LDL) cholesterol; smoking and other nicotine sources; and type 2 diabetes. Obesity, poor physical fitness, and stress further contribute to its progression. A family history of early heart disease, over which you have no control, is also considered a risk factor for atherosclerosis, as is age. I’ll look at the aging heart and arteries in another blog this month.

According to cardiac surgeon and Georgetown University Professor David L. Pearle, atherosclerosis is a systemic disease.

“If it’s present,” he says, “it’s going to be present in all of your body’s arteries.” (3) But consequences differ depending on which arteries are affected.

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Consequences in the Body

I’ve already looked at the consequences of atherosclerosis in the brain (Jan. 14). If plaque-thickened walls obstruct cerebral arterial blood flow, an ischemic stroke may occur. The rupture of an aneurysm of a cerebral arterial wall causes a hemorrhagic (bleeding) stroke. Atherosclerosis also may affect the two big carotid arteries that carry blood to the brain, compromising them and leading to a stroke. I’ll now examine the consequences of atherosclerosis in other arteries, most significantly, in the heart.

In the Coronary Arteries

Coronary artery disease (CAD) exists whenever atherosclerotic plaques have narrowed or obstructed any of the heart’s four big arteries, which feed its circulation. Like all organs and tissues in the body, the heart needs oxygen-rich blood to survive.

The two main coronary arteries, designated as right and left, are branches of the aorta (see below for more about aorta). They, in turn, branch off into smaller arteries. The right coronary artery supplies blood to the smaller right side of the heart, which pumps blood to the lungs only. The left coronary artery supplies blood to the larger and more muscular left side of the heart. It branches into the left anterior descending artery and the circumflex artery.

When plaques prevent your heart from getting the blood it needs, you may experience chest pains called angina pectoris. Angina sufferers say the pain feels like “Someone is standing on my chest.”

Angina can be a recurring problem, in which case it is considered stable, or a sudden, acute concern. If the pain is sudden, time is of the essence. Call 911 immediately. The angina may signal a myocardial infarction (MI), commonly called a heart attack.

An infarct is an area of tissue that has died (necrotized) because its blood supply has been obstructed. Thus, an MI refers to the death of oxygen-deprived heart-muscle tissue. Once dead, these cells will not be replaced. If the heart survives, it will be weaker. Non-infarcted tissue will try to compensate for the loss.

A lesser known condition called coronary microvascular disease (MVD) results when atherosclerosis affects the heart’s tiny arteries. Plaque doesn’t cause blockages in these vessels, but patients with MVD, most of whom are women, are at an increased risk for a heart attack. They also suffer angina and other debilitating symptoms. (4)

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CAD Treatment Alternatives

Many treatment options exist for coronary artery disease and stable angina, depending on their severity. They include lifestyle changes, such as an altered diet, a program of exercise, and a cessation of smoking, and a variety of medications.

According to Dr. Pearle, there are about 110 to 120 antihypertensive drugs on the market in the United States. Cardiologists also may prescribe drugs that inhibit blood-clotting, reduce arrhythmias, and lower blood-cholesterol levels (such as statins, which I’ll discuss later this month). Coronary artery disease can be managed long-term.

The same luxury does not exist with unstable angina, which is a crisis.

Depending on the occlusion of arterial blood in the heart, says Pearle, there may be a window of only about 90 minutes between your first sudden chest pains and surgery to save your life. The window for using clot-busting drugs, such as tissue plasminogen activator (tPA), which I discussed in my Jan. 14, 2017 blog, is only 30 minutes.

For decades now, the gold-standard surgical procedures for preventing or halting a myocardial infarction have been the angioplasty, also known as percutaneous coronary intervention (PCI), and the bypass. Angioplasty and bypass can be used to repair renal arteries and restore blood flow to the kidneys, as well.

In an angioplasty, the surgeon uses tube-like catheters, including one that expands like a balloon, to open up a blocked or narrowed artery and inserts a mesh tube called a stent to keep the artery open. In a bypass, the surgeon transplants or “grafts” a blood vessel from another part of the body or uses a synthetic tube of some kind to route the blood around the problem vessel. Once an artery is bypassed, it no longer functions.

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The Renal and Peripheral Arteries

The development and accumulation of fatty plaques in your two renal arteries—one leading to each kidney—can reduce blood flow to the kidneys, increasing blood pressure and injuring tissue. Renal atherosclerosis can lead to progressive kidney dysfunction and failure.  

More than 450 gallons of blood pass every day through your renal arteries, which branch off of your abdominal aorta and account for about 21 percent of your cardiac output. The aorta is a massive artery that originates in the heart and has ascending and descending portions. The descending aorta transports blood to the chest area and ends in the abdomen, where it divides into two smaller arteries that feed the legs and branch into other arteries.  

Renal artery stenosis (RAS) is the narrowing of one or both renal arteries. Just like with CAD, RAS can be treated with lifestyle changes and medications. If this therapy proves insufficient, surgery may be done.

An atherosclerotic blockage in major arteries in the legs, arms, and/or pelvis leads to peripheral artery disease (PAD), aka peripheral vascular disease, a disorder suffered by about 30 percent of older Americans. PAD, which is characterized by severe pain, skin ulcerations, lameness (claudication), and numbness in the extremities, elevates the risk of blood clots.

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Statin medications

Statin medications, which were first approved in the late 1980s, lower the levels of cholesterol and triglycerides in the blood and, thus, address atherosclerosis. These drugs have their proponents and their detractors; they can cause severe adverse effects.

Recently, the U.S. Preventive Services Task Force recommended that healthy people between the ages of 40 and 75 who have no history of cardiovascular disease (CVD) or even high cholesterol, but who have an increased risk of developing CVD, take a low to moderate-dose statin for prevention. I will look at the USPSTF’s new guidelines in my next heart blog. If you’d like a preview, please turn back to my July 24, 2016, blog or my 4/30/16 Tidbit item and read how a 10-year CVD risk is calculated.  

Ann, 2/1/17

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1. “Causes of Atherosclerosis,” Mayo Clinic at http://www.mayoclinic.com/health/arteriosclerosis-atherosclerosis/DS00525/DSECTION=causes.

2. “The Physiology and Pathology of Aging,” by David A. Sandmire, M.D., in Gerontology for the Health Care Professional, ed. Regula H. Robnett and Walter C. Chop (Sudbury, Mass.: Jones and Bartlett Publishers, 2nd ed., 2010), p. 83

3. David L. Pearle, M.D., lecture on “Cardiology,” Georgetown University Mini-Medical School, March 20, 2012.

4. “What is Coronary Microvascular Disease?,” National Heart Lung and Blood Institute, at http/www.nhlbi.nih.gov/health/health-topics/topics/cmd.

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