Finally getting a chance to sit down after another long work day, the electrical contractor, sinks into his easy chair. “This business is killing me,” he says to his wife as she rocks their newborn baby. “My accounts payable can’t collect.”
He rubs his left shoulder and complains “My neck and back are so sore.” Assuming the pain is muscular from working on the construction site, he ignores it for days. The next week is similar but a new pain extends to the front of his chest. “Kyle, you keep rubbing your shoulder. You should get that checked out,” says his wife.
After a week of chest and back discomfort unrelieved by Tylenol, 43-year-old, 6 foot, 260 pound Kyle Hansen goes to a walk-in clinic, where his blood pressure measures 210/98 and his chief complaint is persistent chest and left-shoulder discomfort for 1 week. The workup in the clinic is for acute chest pain but there’s much more needed for Mr. Hansen.
As the healthcare professional, what would you do first? Is this a medical emergency? What diagnostic tests should be completed? How could this be a heart problem when he’s so young? What were the patient’s risk factors? How common is this?
This scenario is all too common for coronary artery disease.
The heart supplies the whole body with life-giving oxygen, but how does the heart receive that oxygen? The blood supply to the heart muscles comes via the coronary arteries located on the outer surface (epicardium) of the heart. Heart muscle requires a constant supply of oxygen and nutrients, and blockage of the coronary arteries can lead to serious and even critical heart problems.
When atherosclerosis, a disease that narrows the arteries, begins to limit blood flow through the coronary arteries, the condition is called coronary artery disease (CAD), coronary heart disease (CHD) or atherosclerotic heart disease (AHD).
The result of limiting the heart’s blood supply is ischemia, and CAD is sometimes called ischemic heart disease (IHD). Technically, ischemic heart disease is a broader category than coronary artery disease because there are a variety of ways that the blood supply to the heart can be limited, but atherosclerosis is by far the most common cause of ischemic heart disease (Antman et al., 2008).
The term arteriosclerosis, is often mistakenly used for atherosclerosis. Arteriosclerosis is the stiffening or hardening of the arterial walls and atherosclerosis is the narrowing of the arterial lumen due to plaque buildup. Atherosclerosis, then, is a specific kind of arteriosclerosis (Nordvist, 2015).
Atherosclerosis leads to the buildup of fatty deposits called plaque in the walls of large arteries. All the major arteries are susceptible to atherosclerosis, including the aorta, coronary, carotid, vertebral, cerebral, iliac, and femoral arteries. When atherosclerosis blocks arteries in the limbs, the condition is called peripheral artery disease (PAD); when it blocks the central arteries, the condition is called cardiovascular disease.
Atherosclerotic symptoms that appear from blockages in any artery warn the likelihood of atherosclerosis in other arteries; therefore, the appearance of peripheral artery disease makes the presence of CAD more likely, even in patients without symptoms of CAD. A person with CAD has a 1 in 3 chance of having blocked leg arteries (Mitchell & Schoen, 2009).
Once they are present, atherosclerotic plaques in the coronary arteries gradually thicken. The bulging plaques narrow the arterial lumens and reduce the amount of blood that is delivered to the heart muscles. In addition, clots form on the surface of some of the plaques. Occasionally, the clots, along with pieces of plaque, are dislodged and travel downstream, obstructing smaller arteries, which can cause an embolism (an obstruction in a blood vessel).
Whether by the gradual thickening of plaque or the sudden formation of a thromboembolus (obstruction of a blood vessel by an embolus), atherosclerosis reduces the perfusion of the heart. Heart muscle that does not get sufficient oxygen and nutrients becomes ischemic, and ischemic heart muscle contracts weakly or irregularly. Ischemic heart muscle can also stop contracting, and if deprived of oxygen and nutrients for an extended time, heart muscle will die, causing a heart attack or even sudden cardiac death. The irony is that sudden cardiac death isn’t sudden, as it has been developing for years.
Ischemic heart disease causes more deaths and disability and incurs greater economic costs than any other illness in the developed world and is likely to become the most common cause of death worldwide by 2020 (Antman et al., 2008).
If the heart becomes ischemic, an uncomfortable feeling called angina pectoris is likely. Angina pectoris (or, simply, angina) is a deep chest discomfort that is usually described as squeezing, heaviness, aching, or pressure underneath the sternum. This discomfort can sometimes also be felt along the shoulder, arm, neck, jaw, or upper back.
The name angina pectoris was coined in 1768 in one of the first written descriptions of the symptoms of CAD. This description was in a medical paper discussing “a disorder of the breast [chest] marked with strong and peculiar symptoms, considerable for the kind of danger belonging to it, and not extremely rare. The seat of it, and sense of strangling and anxiety with which it is attended, may make it not improperly be called angina pectoris” [Latin, anguish and choking of the chest] (Silverman & Wooley, 2008). That this condition was specifically a disease of the heart, however, was not agreed upon until the late 1800s, over a century later.
Typical angina is a chronic condition; it occurs with exercise and it is relieved by rest. At first, physicians did not connect angina with clogged coronary arteries because it was thought that blockages of a coronary artery were always fatal. The assumption of lethality came from the observation that autopsies of patients who died of heart attacks frequently found that the patient had blocked coronary arteries, and in the nineteenth century the left anterior descending (LAD) coronary artery was even called “the artery of sudden death” (Silverman & Wooley, 2008).
By 1920, however, it had become clear that obstructions of the coronary arteries could produce a range of effects, not all of which were fatal, and by 1930 “nonfatal myocardial infarction,” or heart attack, was becoming a common diagnosis. Today, angina is recognized as a symptom of CAD that can cause ischemic heart problems along a spectrum from reduced coronary blood flow to total coronary artery blockage and from a temporary self-limiting chest ache to sudden cardiac death.
If a coronary artery has gradually become narrowed, it can usually still deliver sufficient blood to the heart to support normal pumping when the person is at rest. When the heart beats more rapidly and forcefully, such as during stress or exercise, it requires more oxygen. A time will come when the heart needs more oxygen than a narrowed artery can deliver, and at this point the heart muscle becomes ischemic and cardiac tissue may die.
An individual who has narrowed coronary arteries may be asymptomatic at rest but with exercise can experience angina, or chest pain. When the person stops exercising and returns to a resting state, the angina will subside after a few minutes. This condition of predictable, exercise-dependent angina that is relieved by rest is the form of CAD called stable angina.
More serious forms of CAD are called acute coronary syndromes. Acute coronary syndromes occur when a coronary artery suddenly becomes obstructed by clots or pieces of atherosclerotic plaque, causing the heart muscle to receive insufficient oxygen even at rest. Acute coronary syndromes occur unpredictably: the person might be exercising, but could also be relaxing, watching TV, or even sleeping.
Angina from an acute coronary syndrome tends to feel more severe than stable angina, and it usually does not ease with a few minutes of rest or even with sublingual nitroglycerin tablets. Acute coronary syndromes cause ischemia to threaten the viability and function of heart muscle.
When the obstruction causes an acute coronary syndrome but lasts for only a brief time and no significant heart necrosis occurs, it is called an episode of unstable angina. In other cases, the ischemia is substantial and persistent, causing heart muscle death, and the acute coronary syndrome is called a myocardial infarction (MI).
Myocardial infarction is one of a number of serious consequences of CAD, which also causes heart failure, arrhythmias, and sudden cardiac death. In the United States, CAD is the leading cause of death for both men and women (CDC, 2016a). Fortunately, early treatment can significantly reduce the likelihood that a patient will develop life-threatening complications.
Lifestyle changes are the first-line treatment for CAD. People with coronary atherosclerosis should stop smoking, eat reduced-calorie, low-fat/high-fiber diets, and exercise regularly. Diabetes, hypertension, high levels of blood cholesterol, and excess body fat are all CAD risk factors and, if present, should be aggressively controlled. This plan is used both to prevent and to treat CAD.
Medications are usually part of the management of CAD. Medications are also given to reduce the heart’s workload and prevent blood clots. Beta-blockers, calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors, or antiplatelet drugs such as aspirin may be used. When a patient’s coronary arteries have already become significantly narrowed or obstructed, treatment may extend beyond medicines and require surgical reopening of the artery (angioplasty) or bypassing the blockage with arterial or venous grafts (Schoen & Mitchell, 2009; NHLBI, 2016a).
In our earlier scenario, Mr. Hansen was diagnosed with CAD and angina. What symptoms did he present with, and what were his risk factors? His symptoms of hypertension and chest pain are classic for CAD and angina, but because the chest pain wasn’t relieved by rest it was unstable. A quick 12-lead ECG demonstrated a non-STEMI. He was given nitroglycerine, oxygen, and morphine for chest pain. He was sent by ambulance to the hospital for a full workup, angiogram, and treatment. His risk factors included BMI >30, hypertension, high-fat diet, male gender, age >40 and stress. So is Mr. Hansen the rare case? What additional tests and procedures will be done at the hospital? What are the statistics for CAD in men and women like Mr. Hansen?