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Why Is Coronary Artery Disease Treated Differently Now?
 

Coronary artery disease (CAD), also known as coronary heart disease, is the most common type of heart disease. It affects millions of Americans and is the leading cause of death in the United States in both men and women.

For the past years, there is a major shift of thinking about CAD and its treatments. Debates continue among cardiovascular specialists about who to test for CAD, how to test them, who needs to be treated for CAD, and how to treat them. It is believed that by sticking in the traditional way of thinking and treatment methods, doctors might possibly cause many of their patients to both under treatment and overtreatment.

Traditionally, CAD happens when there is buildup of plaque (known as atherosclerosis) in the inner walls of arteries that supply blood to the heart muscle. As atherosclerosis grows, the blood flow to the heart will be restricted and the heart will become starved of oxygen. Over time, CAD can weaken the heart muscle, causing heart failure and arrhythmias. If the plaque ruptures, heart attack or sudden cardiac death could result.

Since the focus is on blockages, it is obvious that cardiologists will tend to insist on cardiac catheterizations as the only adequate diagnostic test. If the condition is not serious, stenting might be used. But for extensive or difficult blockages, they might involve cardiac surgeon.

On the other hand, evidence has shown that CAD is more than just about blockages. CAD is believed to be a chronic and progressive disease. Arteries may appear normal on cardiac catheterization with the presence of some plaques. Women especially can have widespread CAD that produces a narrowing of the coronary arteries without any actual blockages. Moreover, the plaque that ruptures and causes a heart attack are often not the one that cause blockages prior to rupture and is often considered as insignificant on cardiac catheterization. Hence, the important thing about CAD is about the presence of coronary artery plaques that often do not cause significant blockages, and not about the presence of specific blockages.

Undoubtedly, actual blockages can cause angina and heart attack, and it is important to treat specific blockages. However, focusing on treating blockages alone is often unnecessary or insufficient to adequately treat CAD. In fact, intensive therapy that is based on statins together with aggressive risk-factor modification can halt or even reverse CAD. It is also possible to reduce the likelihood of rupture of plaques by stabilizing them. Moreover, exercise, smoking cessation, weight loss, blood pressure control and cholesterol control are especially important.

First of all, the doctors must decide whether their patients are likely to have active CAD so that they can direct appropriate therapy accordingly. This can mostly be accomplished noninvasively. A simple assessment of risk should be started to decide whether one’s risk is low, intermediate or high. No further intervention is needed for people in the low-risk categories. For people in the high-risk categories, aggressive treatment with statins and risk factor modification should be carried out because these individuals are most likely to have plaques, whereas for people in the intermediate-risk categories, noninvasive testing with EBT scanning (calcium scans) could be recommended. If calcium deposits on the coronary arteries are found, which indicates plaques are present, they should then be treated aggressively.

A general consensus among health experts is that people in the high-risk category should have a stress thallium test. If the test indicates there is a major blockage, cardiac catheterization should be suggested. A stress test or cardiac catheterization should also be given to people who have symptoms of angina, irrespective of whichever category they belong to. Using surgery or stenting to relieve blockages can be very effective in treating angina, and can sometimes improving survival, too.

With the changing in perspective about CAD, treatment aimed at stopping or reversing chronic CAD and at stabilizing plaques to prevent them from rupture becomes very important regardless of whether significant blockages are present or not.

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