More than 1 million people in the United States suffer heart attacks every year, and about 34 percent of them die as a result of those heart attacks, according to the American Heart Association. A heart attack is a manifestation of coronary artery disease. Coronary artery disease is caused by plaque accumulation in the vessels that supply blood to the heart. Plaque is the hallmark feature of atherosclerosis.
Features
Atherosclerosis forms in most larger arteries throughout the body. The plaque that is the result of the atherosclerotic process is composed of lipids, cholesterol and other similar compounds, as well as inflammatory and smooth muscle cells, connective tissue and calcium, according to the Merck Manuals Online Medical Library. As the plaque becomes more pronounced in the coronary artery, symptoms of coronary artery obstruction may begin to develop, including chest pain during exertion, shortness of breath and progressive inability to exercise.
Time Frame
The atherosclerotic plaque begins in adolescence and first appears as fatty streaks containing lipids, protein and certain cells. Over time, according to the Cleveland Clinic, more lipid is added as well as layers of connective tissue and smooth muscle, forming a fibrous cap. The fibrous cap can become unstable and rupture, spilling contents out into the lumen of the coronary artery, which attract clot-producing cells and substances in the body and lead to a heart attack. Plaques eventually become hard with progressive calcium deposition and obstruct blood flow to the heart muscle.
Considerations
At one time, atherosclerosis was considered a cholesterol problem. Although elevated cholesterol is a risk, atherosclerosis is now considered an inflammatory disease, according to Libby and Theroux in a June 2005 article published in "Circulation." It is now believed that atherosclerosis begins as healing of an inflammatory injury to the lining of blood vessels. Widespread systemic inflammation from other conditions such as diabetes, autoimmune diseases, obesity and smoking accelerate plaque formation. Measurement of C-reactive protein, a marker of inflammation, is used in assessing the risk of atherosclerotic disease.
Diagnosis
Diagnosis of atherosclerosis begins with a careful history and physical exam looking for signs and symptoms of atherosclerotic coronary artery disease. Blood tests can identify the presence of possible risk factors for atherosclerotic disease. Signs of heart damage may sometimes be seen on an EKG, a heart tracing, but a sound wave test of the heart, called an echocardiogram, is better at visualizing depressed heart function because of blocked arteries. According to the Cleveland Clinic, stress tests are useful in both the diagnosis and risk stratification of coronary artery disease from atherosclerosis. Cardiac catheterization, a test in which small tubes are placed into the coronary arteries and injected with dye to look for obstruction, is considered the gold standard in diagnosing coronary artery disease from atherosclerosis.
Prevention/Solution
Modifiable risk factors for atherosclerosis include smoking, diabetes, hypertension, obesity, high cholesterol and physical inactivity. Controlling these risk factors is important in slowing the progression of atherosclerosis. Once the diagnosis is made, anti-inflammatory medications such as aspirin may be prescribed as well as medications for symptom relief. Statins, a type of cholesterol-lowering drug, are often used, not only to treat high cholesterol, but also to decrease inflammation. Schoenhagen and colleagues reported in a June 2006 article published in "Circulation" that statins, when used in high doses, can actually reverse plaque formation. Surgical intervention may be required to improve blood flow to the heart muscle.
References
- American Heart Association: Cardiovascular Disease Statistics
- The Merck Manuals Online Medical Library: Artherosclerosis
- Cleveland Clinic: Coronary Artery Disease
- "Circulation": Pathophysiology of Coronary Artery Disease'; P. Libby and P. Theroux; June 2005
- "Circulation": Determinants of Arterial Wall Remodeling During Lipid-Lowering Therapy; P. Schoenhagen et. al.; June 2006
