Heart Disease in Women: Different Than in Men?
Heart Disease in Women: Different Than in Men?
In CHD, plaque forms on or within the inner lining of the coronary arteries, reducing the flow of oxygenrich blood to the heart and causing fatigue. Plaque consists of fat, cholesterol, calcium, and other substances found in the blood. Over time, plaque hardens and may rupture. Hardening plaque deposits can partially or totally restrict blood flow to the heart, causing chest pain (angina), pressure, or discomfort. The most common cause of a heart attack is when plaque ruptures and a blood clot forms on its surface. A large blood clot can partially or totally block blood flow through an artery, causing heart tissue to die. A portion of the clot also can break loose and enter systemic blood circulation. The circulating clot may lodge in a smaller blood vessel and restrict blood flow to areas beyond the clot. Over time, ruptured plaque hardens and further narrows coronary arteries. In addition to angina and heart attack or MI, CHD can lead to heart failure, arrhythmias, and sudden cardiac arrest.
In CAD, blood-vessel lumen becomes narrowed and blood can no longer flow freely to the muscle cells. The narrowing of the vessels is caused by the development of atheromas (fatty tumors in the intimal lining of the vessels), attracting platelets and immune factors and causing swelling and the development of larger deposits in the intima. The lumen also loses its natural elasticity and becomes unable to respond to normal stimuli to dilate or constrict to meet the needs of the tissues.
The diseased heart may function without noticeable problems until increases in activity or other stresses place a demand on it to beat faster or harder. Normally, the heart would stimulate blood vessels to dilate and deliver more blood when this occurs, but the narrowed vessels are unable to respond and cannot supply the blood needed by the working heart. The heart muscle then becomes hypoxic. This imbalance between oxygen supply and demand manifests as pain or angina pectoris (meaning "suffocation of the chest"). Although the heart muscle does not contain pain fibers, a chemical called substance P is released from ischemic myocardial cells, and pain is felt whenever substance P reacts with pain receptors in the heart. This pain does not result in heart-muscle damage. If a coronary vessel becomes completely occluded and is unable to deliver blood to the cardiac muscle, the area of the heart muscle that depends on that vessel for oxygen becomes ischemic and then necrotic. This event is a myocardial infarction, and the pain associated with it can be excruciating.
CHD
In CHD, plaque forms on or within the inner lining of the coronary arteries, reducing the flow of oxygenrich blood to the heart and causing fatigue. Plaque consists of fat, cholesterol, calcium, and other substances found in the blood. Over time, plaque hardens and may rupture. Hardening plaque deposits can partially or totally restrict blood flow to the heart, causing chest pain (angina), pressure, or discomfort. The most common cause of a heart attack is when plaque ruptures and a blood clot forms on its surface. A large blood clot can partially or totally block blood flow through an artery, causing heart tissue to die. A portion of the clot also can break loose and enter systemic blood circulation. The circulating clot may lodge in a smaller blood vessel and restrict blood flow to areas beyond the clot. Over time, ruptured plaque hardens and further narrows coronary arteries. In addition to angina and heart attack or MI, CHD can lead to heart failure, arrhythmias, and sudden cardiac arrest.
In CAD, blood-vessel lumen becomes narrowed and blood can no longer flow freely to the muscle cells. The narrowing of the vessels is caused by the development of atheromas (fatty tumors in the intimal lining of the vessels), attracting platelets and immune factors and causing swelling and the development of larger deposits in the intima. The lumen also loses its natural elasticity and becomes unable to respond to normal stimuli to dilate or constrict to meet the needs of the tissues.
The diseased heart may function without noticeable problems until increases in activity or other stresses place a demand on it to beat faster or harder. Normally, the heart would stimulate blood vessels to dilate and deliver more blood when this occurs, but the narrowed vessels are unable to respond and cannot supply the blood needed by the working heart. The heart muscle then becomes hypoxic. This imbalance between oxygen supply and demand manifests as pain or angina pectoris (meaning "suffocation of the chest"). Although the heart muscle does not contain pain fibers, a chemical called substance P is released from ischemic myocardial cells, and pain is felt whenever substance P reacts with pain receptors in the heart. This pain does not result in heart-muscle damage. If a coronary vessel becomes completely occluded and is unable to deliver blood to the cardiac muscle, the area of the heart muscle that depends on that vessel for oxygen becomes ischemic and then necrotic. This event is a myocardial infarction, and the pain associated with it can be excruciating.
