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Plendil (Felodipine)

###table###Plendil(Felodipine)
HEART DISEASE: WHAT, IN FACT, HAPPENED TO MY HEART?
The most dramatic of acute heart events is a “heart attack,” known as a myocardial infarction (MI). This term refers to permanent damage to the heart caused by interruption in blood flow to the heart muscle itself, resulting in loss of heart muscle and its replacement by scar. The heart is a muscle like any other muscle in the body; in order to pump effectively, it must receive oxygen; this is delivered by blood vessels that run across the outer surface of the heart and are known as the coronary arteries. Much like the structure of a tree, large coronary arteries, which represent the trunks of a branching arterial system, divide into major branches that run on the outer surface of the heart, and then divide into many smaller branches, and ultimately into small “twigs,” which supply blood and oxygen to the heart muscle cells themselves. Not surprisingly, if any of these large trunks or branches become obstructed or blocked, blood cannot flow, and the portion of heart muscle that normally receives blood and oxygen through these branches will suffer permanent damage. If such permanent damage occurs, it is called a heart attack.
Almost all patients who have heart attacks do so because they have coronary atherosclerosis, or hardening of the arteries to the heart, which is a very slowly evolving process, taking many decades, resulting in a buildup of cholesterol, calcium and scar tissue on the inside of an artery, gradually choking off its blood supply. In response to this injury inside the blood vessel itself, the body may respond by producing a blood clot; this can be the “last straw,” resulting in the sudden blockage of an artery that has been already narrowed by the “atherosclerotic” (hardening) process. If such a blood clot forms, the muscle cells downstream from the narrowing and acute blockage (occlusion) fail to receive enough blood, and the consequence is one or more of: chest discomfort, tightness, pain, shortness of breath or nausea, otherwise known as myocardial ischemia (lack of enough blood to the heart). If this clot spontaneously dissolves or is promptly treated and dissolves, a heart attack may not actually occur, but the threat of heart attack prompts hospitalization, investigation, and often treatment. If blood flow is interrupted for a sufficiently long period of time, permanent damage to the heart muscle cells can occur.
Many patients with “hardening of the arteries” have chest discomfort or shortness of breath when they are active. This is known as angina, and it results from an increased need for oxygen by the exercising heart muscle that cannot be supplied by the narrowed artery. This is analogous to what occurs when several lanes of a highway are blocked by construction—off-peak traffic can flow almost normally, but the increased flow of traffic during rush hour creates major traffic jams. Such patients have symptoms during physical or emotional stress, but these subside with rest. A predictable pattern of chest discomfort with activity, and which subsides with rest, is known as stable angina.
A heart attack or unstable angina is suspected when pain occurs at rest or without provocation. A “heart attack” is the result of complete blockage of an artery, which leads to irreversible heart damage. This damage may be very minor or more severe, depending on the size of the artery and the amount of muscle that it supplies, and the period of time it is blocked. Administering a “clot buster,” or thrombolytic agent, early after the onset of pain can considerably limit heart damage. It is this opportunity to treat patients early— often expressed by cardiologists with the saying “Time is muscle”— that makes it very important for patients to understand the warning signs of a heart attack and to consult a doctor or go to an emergency room immediately rather than waiting.
Unstable angina is a warning from the heart, a “yellow light,” that there is fairly major shortage of blood flow, but fortunately it produces minimal to no permanent damage. The signal the heart is sending out is that the narrowing is fairly severe, often temporary and due to a blood clot that significantly but not completely blocks blood flow. Medications and bed rest can lead to these clots dissolving and the situation returning to the status quo, or the blockage may become more severe but still not complete. Patients with unstable angina can be treated and spared future heart events, with no heart damage having been done.
With either a heart attack or unstable angina, patients are invariably admitted to a hospital, usually to a coronary care unit (CCU —a type of intensive care unit where there is close and continuous nursing and medical supervision) and are treated with medications to dissolve clots in the arteries, prevent further clotting and reduce the work of the heart. Sometimes, attempts are made to immediately “open up” the blocked artery using tubes and balloons inserted directly into the heart’s arteries, a procedure known as balloon angioplasty. Rarely, emergency bypass surgery may be performed. During the hospital stay, patients receive drug therapy, stabilization and treatment of any complications that may occur.
Fortunately, over 90 percent of patients admitted to hospitals with acute heart attacks survive without major complications, and often are hospitalized for only five to seven days. During the initial period, there will not be any major tests in most instances, but patients are treated, closely monitored and stabilized. Prior to discharge from the hospital, a patient may undergo tests to assess the potential risk for a repeat heart attack or future serious heart events. These tests often include an ultrasound of the heart (echocardiogram), an exercise test or X-ray imaging of the blood flow to the heart {thallium or Cardiolite® imaging), and sometimes coronary angiography (an X ray of the blood vessels to the heart).
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