How is a heart attack diagnosed?

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When there is severe chest pain, suspicion that a heart attack is occurring usually is high, and tests can be performed quickly that will confirm the heart attack. A problem arises, however, when the symptoms of a heart attack do not include chest pain. A heart attack may not be suspected, and the appropriate tests may not be performed. Therefore, the initial step in diagnosing a heart attack is to be suspicious that one has occurred.

Electrocardiogram. An electrocardiogram (ECG) is a recording of the electrical activity of the heart.

Abnormalities in the electrical activity usually occur with heart attacks and can identify the areas of heart muscle that are deprived of oxygen and/or areas of muscle that have died. In a patient with typical symptoms of heart attack (such as crushing chest pain) and characteristic changes of heart attack on the ECG, a secure diagnosis of heart attack can be made quickly in the emergency room and treatment can be started immediately. If a patient’s symptoms are vague or atypical and if there are pre-existing ECG abnormalities, for example, from old heart attacks or abnormal electrical patterns that make interpretation of the ECG difficult, the diagnosis of a heart attack may be less secure. In these patients, the diagnosis can be made only hours later through detection of elevated cardiac enzymes in the blood.

Blood tests. Cardiac enzymes are proteins that are released into the blood by dying heart muscles. These cardiac enzymes are creatine phosphokinase (CPK), special sub-fractions of CPK (specifically, the MB fraction of CPK), and troponin, and their levels can be measured in blood. These cardiac enzymes typically are elevated in the blood several hours after the onset of a heart attack. A series of blood tests for the enzymes performed over a 24 hour period are useful not only in confirming the diagnosis of heart attack, but the changes in their levels over time also correlates with the amount of heart muscle that has died.

The most important factor in diagnosing and treating a heart attack is prompt medical attention. Rapid evaluation allows early treatment of potentially life-threatening abnormal rhythms such as ventricular fibrillation and allows early reperfusion (return of blood flow to the heart muscle) by procedures that unclog the blocked coronary arteries. The more rapidly blood flow is reestablished, the more heart muscle that is saved.

Large and active medical centers often have a “chest pain unit” where patients suspected of having heart attacks are rapidly evaluated. If a heart attack is diagnosed, prompt therapy is initiated. If the diagnosis of heart attack is initially unclear, the patient is placed under continuous monitoring until the results of further testing are available.

How is a heart attack treated?

Treatment of heart attacks include:

• Anti-platelet medications to prevent formation of blood clots in the arteries
  
• Anti-coagulant medications to prevent growth of blood clots in the arteries
  
• Coronary angiography with either percutaneous transluminal coronary Angioplasty (PTCA) with or without stenting to open blocked coronary arteries
  
• Clot-dissolving medications to open blocked arteries
  
• Supplemental oxygen to increase the supply of oxygen to the heart’s muscle
  
• Medications to decrease the need for oxygen by the heart’s muscle
  
• Medications to prevent abnormal heart rhythms

The primary 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, damage to heart muscle ceases, and the patient becomes pain free. By minimizing the extent of heart muscle damage, early reperfusion preserves the pumping function of the heart. Optimal benefit is obtained if reperfusion can be established within the first 4-6 hours of a heart attack. Delay in establishing reperfusion can result in more widespread damage to heart muscle and a greater reduction in the ability of the heart to pump blood. Patients with hearts that are unable to pump sufficient blood develop heart failure, decreased ability to exercise, and abnormal heart rhythms. Thus, the amount of healthy heart muscle remaining after a heart attack is the most important determinant of the future quality of life and longevity.

Anti-platelet agents

Anti-platelet agents are medications that prevent blood clots from forming by inhibiting the aggregation of platelets. Platelets are fragments of cells that circulate in the blood. Platelets begin the formation of blood clots by clumping together (a process called aggregation). Platelet clumps are then strengthened and expanded by the action of clotting factors (coagulants) that result in the deposition of protein (fibrin) among the platelets. Aggregation of platelets occurs at the site of any injury or laceration, but it also occurs at the site of rupture of cholesterol plaques in the walls of coronary arteries. Formation of clots at the site of an injury or laceration is desirable because it prevents excessive loss of blood, but formation of clots inside coronary arteries blocks the arteries and causes heart attacks.

There are three types of anti-platelet agents—aspirin, thienopyridines, and the glycoprotein IIb/IIIa inhibitors. These agents differ in their mode of action, anti-platelet potency, speed of onset of action, and cost.

Aspirin

Aspirin inhibits the activity of the enzyme cyclo-oxygenase inside platelets. Cyclo-oxygenase is an enzyme whose activity is necessary for the formation of a chemical, thromboxane A2, that causes platelets to aggregate. Aspirin, by inhibiting the formation of thromboxane A2, prevents platelets from aggregating and thereby prevents the formation of blood clots.

Aspirin alone has its greatest impact on improving survival among patients with heart attacks. Numerous studies have shown that aspirin reduces mortality (by 25%) when given to patients with heart attacks. Aspirin is easy to use, safe at the low doses used for anti-platelet action, fast acting (with an onset of action within 30 minutes), and cheap. Aspirin is given at a dose of 160 mg to 325 mg immediately to almost all patients as soon as a heart attack is recognized. It also is continued on a daily basis indefinitely after the heart attack. The only reason for not using aspirin is a history of intolerance or allergy to aspirin.

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