Pathophysiology of Coronary artery disease

Coronary artery disease (CAD) also known as atherosclerotic heart disease, atherosclerotic cardiovascular disease, coronary heart disease, or ischemic heart disease (IHD), is the most common type of heart disease and cause of heart attacks. The disease is caused by plaque building up along the inner walls of the arteries of the heart, which narrows the arteries and reduces blood flow to the heart.

Angina (chest pain) that occurs regularly with activity, after heavy meals, or at other predictable times is termed stable angina and is associated with high grade narrowings of the heart arteries. The symptoms of angina are often treated with betablocker therapy such as metoprolol or atenolol. Nitrate preparations such as nitroglycerin, which come in short-acting and long-acting forms are also effective in relieving symptoms but are not known to reduce the chances of future heart attacks. Many other more effective treatments, especially of the underlying atheromatous disease, have been developed.

Angina that changes in intensity, character or frequency is termed unstable. Unstable angina may precede myocardial infarction. About 80% of chest pains have nothing to do with the heart.

This condition is chronic and begins when a person is an adolescent and then it slowly progresses throughout their life. Coronary artery disease pathophysiology revolves around a few theories. One widely accepted theory is that this condition occurs when the body is trying to heal itself as a result of endothelial injury. Inflammation is also beginning to be accepted as a critical component of potential plaque instability and atherosclerosis activity. Patients who have been diagnosed with established coronary artery disease and have several of the causes and/or risk factors as well are at a much higher risk of experiencing a cerebrovascular accident, myocardial infarction, and other vascular events in the future.

Elevated C-reactive protein levels, and other elevated biochemical markers, indicate a higher risk of experiencing a vascular event in the future and it indicates an increased likelihood of vascular inflammation. This marker may also indicate the need for aggressive preventative measures due to the patient having a quickly advancing coronary artery disease.

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