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Diagnosis &Treatment Of Heart Attack
By peace | May 23, 2006
A blockage in the heart’s arteries may reduce or completely cut off the blood supply to a portion of the heart. This can cause a blood clot to form and totally stop blood flow in a coronary artery, resulting in a heart attack (also called an acute myocardial infarction or MI).
How is a heart attack diagnosed?
The initial diagnosis of a heart attack is made by a combination of clinical symptoms and characteristic electrocardiogram (ECG) changes. An ECG is a recording of the electrical activity of the heart, and can detect areas of ischemic heart muscle (muscle which is deprived of oxygen) and/or dead tissue in the heart. However, confirmation of a heart attack can only be made hours later through detection of elevated cardiac enzymes in the blood. Cardiac enzymes are muscle proteins which are released into the blood circulation by dying heart muscles when their surrounding membranes dissolve. Such enzymes include creatine kinase (CK), special subforms of CK, and troponin.
Achieving PROMPT MEDICAL ATTENTION is the THE MOST IMPORTANT FACTOR for an improved prognosis with a heart attack. Rapid evaluation allows early treatment of potentially life-threatening arrhythmias, and permits early “reperfusion” (return of blood flow) of the heart muscle. The sooner that reperfusion is established, the smaller the resultant heart attack will be. Large and active cardiac centers often have a “chest pain unit”, where patients are rapidly screened for the presence of a heart attack, and prompt therapy is initiated. If the diagnosis of heart attack is initially unclear, the patient is observed in a monitored setting, until the results of further testing are available.
What are the treatment options for a heart attack?
The immediate goal of treatment is to quickly open the blocked artery and restore blood flow to the heart muscle; a process called “reperfusion.” Once the artery is open, the heart attack is generally halted and the patient becomes pain free. Early reperfusion minimizes the extent of heart muscle damage and preserves the pumping function of the heart. Delay in establishing reperfusion can result in irreversible death to the heart muscle cells and reduced pumping force of the remaining heart muscle. The amount and health of the remaining heart muscle is the major determinant of the future quality of life and longevity for a patient after a heart attack. Optimal benefit is obtained if reperfusion can be established in the first 4- 6 hours of a heart attack.
Balloon angioplasty of the coronary artery, or percutaneous transluminal coronary angioplasty (PTCA), is a relatively new procedure introduced in the late 1970’s. PTCA is a non-surgical procedure that relieves narrowing and obstruction of the arteries to the muscle of the heart (coronary arteries). This allows more blood and oxygen to be delivered to the heart muscle. PTCA is accomplished with a small balloon catheter inserted into an artery in the groin or arm, and advanced to the narrowing in the coronary artery. The balloon is then inflated to enlarge the narrowing in the artery. When successful, PTCA can relieve chest pain of angina improve the prognosis of patients with unstable angina, and minimize or stop a heart attack without having the patient undergo CABG surgery.
The most direct method of opening a blocked artery, provided the hospital has a cardiac catheterization facility, is to perform an immediate coronary angiogram and PTCA (percutaneous transluminal coronary angioplasty). Under X-ray guidance, a tiny plastic catheter with a balloon at the end is advanced over a fine guide wire to the blockage site and inflated, thus pushing the clot and plaque out of the way. PTCA can be effective in opening up to 95% of arteries, usually within 60 minutes. In addition, the angiogram allows evaluation of the status of the other coronary arteries, so that long- term treatment plans may be formulated.
Recently, it has been demonstrated that the placement of a coronary stent (a tiny hollow cylinder) at the time of PTCA results in even better long term outcomes, with a lower recurrence rate and lower risk of repeat heart attack. These results may be further enhanced by the addition of newer “super aspirins” (potent blood thinners that work to antagonize the blood-clotting effects of platelets in the blood and in the cholesterol plaque), which are given at the time of PTCA or coronary stenting.
As an alternative to PTCA or stenting for an acute heart attack, certain clot dissolving medicines (thrombolytic agents) such as Streptokinase & Urokinase given intravenously can successfully open up to 80% of acutely occluded coronary arteries. The earlier these agents are administered, the better the success at opening the artery, and the more effective the preservation of heart muscle. If thrombolytic administration is given too late (more than 6 hours after the onset of the heart attack), most of the muscle damage may have already occurred.
When there will be a potential delay in the ability to perform PTCA, either if the hospital does not have a catheterization laboratory with the ability to perform PTCA, or if there are logistic reasons why PTCA will be delayed, thrombolytic therapy is then be promptly administered to allow prompt reperfusion. PTCA may then be performed in patients who fail to respond to thrombolytic therapy. Thrombolytic therapy carries a significant bleeding risk, such that some patients are not candidates for this therapy (patients with recent surgery or major trauma, recent stroke, bleeding ulcer, or other related conditions.
Anti-platelet agents, like aspirin, reduce the tendency of platelets in the blood to clump and clot. These agents work in conjunction with the above-mentioned reprefusion therapies to decrease the possibility of recurrent closure of the artery and improves the chances of survival.
Heparin, is given intravenously or as a subcutaneous injection in the hospital as a blood-thinning agent to prevent blood clots and to maintain an open artery during the initial 24-72 hours.
Nitroglycerin a vasodilator (blood vessel dilator), which opens the blood vessel by relaxing the muscular wall of the blood vessel, is given intravenously to prevent blood vessel spasm and to potentially minimize the size of the heart attack. ACE (angiotensin converting enzyme) inhibitors, another class of vasodilators, are often given orally after a large heart attack to improve the heart muscle healing process. Examples of ACE inhibitors include captopril (Capoten), enalapril (Vasotec), lisinopril (Zestril and Prinvil). These medications reduce the stress load to the heart, thereby helping the damaged heart muscle to recover.
Beta blocking agents, such as propanalol, metprolol and atenelol, are also often given during the acute heart attack to decrease the amount of muscle damage. Long-term administration of these agents following a heart attack has been shown to improve survival and reduce the risk of future heart attacks.
Oxygen is also commonly administered during the acute phase of a heart attack, as are narcotics such as morphine; these agents aid in the reduction of discomfort and actually help minimize the amount of heart damage.
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