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How Coronary Artery Disease Causes Heart Failure


Coronary artery disease (CAD) can prevent your heart muscle from getting enough blood flow and oxygen. Over time, your heart muscle may be weakened or damaged because of reduced blood flow, which can lead to heart failure .

How does CAD damage my heart suddenly? CAD can damage your heart muscle suddenly if you have a significant heart attack. A heart attack happens when a tear develops in a plaque inside one of your coronary arteries and a blood clot forms over the tear. (This is similar to what happens when you cut your skin and your blood forms a clot and scab.) This clot can completely block your coronary artery and cut off the flow of blood to your heart muscle so that your heart muscle does not get any oxygen. If your heart muscle goes without oxygen for long enough, the area of muscle that is normally supplied by the blocked coronary artery will die.

How does a heart attack cause sudden systolic heart failure? If a heart attack damages a very large area of heart muscle, it is possible that the ability of your heart to pump blood will be suddenly limited to such a degree that you develop systolic heart failure. This is a fairly uncommon complication of heart attacks and usually occurs only with the blockage of the left main coronary artery, which supplies most of the left ventricle with blood, or with the blockage of the left anterior descending coronary artery, which supplies the anterior wall and some of the lateral wall of the left ventricle (a very large area).

A heart attack also can cause sudden heart failure if it damages the mitral valve and causes sudden mitral valve regurgitation. This means that blood from the left ventricle leaks back into the left atrium during each heart contraction. The mitral valve is anchored to the heart muscle by small muscles called the papillary muscles. If a heart attack damages the papillary muscles, you can have severe mitral valve regurgitation and sudden heart failure, even if the overall size of the heart attack is relatively small.

How does CAD damage my heart gradually? Ischemia is the medical term for what happens when your heart muscle doesn't get enough oxygen. Ischemia may happen only once in a while, such as when you are exercising and your heart muscle needs more oxygen than it normally does. In such cases, you may feel chest pain or discomfort (angina), but your heart muscle recovers if the ischemia goes away. Ischemia can also be ongoing (chronic) if your coronary arteries are so narrowed that they limit blood flow to your heart all the time. This chronic lack of oxygen can gradually damage portions of your heart muscle. In some cases, your heart may have numerous tiny heart attacks that you never even feel.

How does this gradual damage cause systolic heart failure? Chronic ischemia can allow your heart muscle to get just enough oxygen to stay alive but not enough oxygen to work normally. Like a heart attack, ongoing poor blood flow to the heart muscle reduces the heart's ability to contract and causes it to pump less blood during each beat. The less blood your heart pumps out to your body, the less blood it is actually pumping back to itself through the coronary arteries. The end result is that heart failure makes ischemia worse, which in turn makes heart failure worse.

How else can CAD gradually cause systolic heart failure? If you have a substantial heart attack that injures a large area of the heart muscle, you may eventually develop heart failure, even if it does not occur suddenly. This happens most commonly after you have had a heart attack involving the anterior wall of the heart. After a large area of the anterior wall is destroyed, the percentage of blood pumped with each beat (ejection fraction) can be significantly less. As a result, the heart attempts to change its shape to maximize its pumping efficiency, a process referred to as left ventricular remodeling. Initially, the changes made to the heart wall (myocardium) are beneficial. Over time, however, the left ventricle dilates and increases in size, which makes the heart less able to pump.

CAD also can cause gradual systolic heart failure by causing mitral valve regurgitation. If a heart attack partially damages one of the papillary muscles related to the mitral valve, the valve may not close properly, and blood may leak back into the left atrium when the left ventricle contracts. Over time, this results in:

  • The left ventricle pumping harder to move the extra blood that has returned to it from the left atrium.
  • The ventricle stretching and enlarging to hold the larger volume of blood.
  • Gradual weakening of the left ventricle, which may cause heart failure.

Atrial fibrillation (AF) is an irregular heart rhythm in which chaotic electrical impulses in the top chambers of the heart (atria) prevent synchronized, effective contraction of the atria. CAD can cause this abnormal heartbeat (arrhythmia) when a heart attack causes decreased left ventricular function and a resulting increase in left ventricular (LV) pressure. This increased LV pressure is transmitted to the left atrium. This causes the left atrium to stretch over time, which can cause AF. The development of AF can cause heart failure or can make it worse because the left atrium no longer contracts properly, which can significantly limit delivery of blood to the left ventricle and result in worsening heart failure.

How does CAD cause diastolic heart failure? All of the functions of your heart muscle depend on getting enough blood to the heart muscle. In the same way that poor blood supply (ischemia) can decrease your heart's ability to contract, it can also decrease the heart's ability to relax properly and fill with blood. This is called diastolic dysfunction. If you also have systolic heart failure, your heart rate may increase to compensate for the reduced ejection fraction of the left ventricle, and this can further decrease the left ventricle's ability to fill with blood.


By Healthwise Staff
Primary Medical Reviewer E. Gregory Thompson, MD - Internal Medicine
Specialist Medical Reviewer Robert A. Kloner, MD, PhD - Cardiology
Last Revised August 5, 2010

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