A heart attack (also known as a myocardial infarction or MI) is the death of heart muscle from the sudden blockage by a blood clot in a coronary artery that supplies blood to the heart. Blockage of a coronary artery deprives the heart muscle of blood and oxygen, causing injury to the heart muscle. Injury to the heart muscle causes chest pain and pressure. If blood flow is not restored within 20 to 40 minutes, irreversible death of the heart muscle will begin to occur. Muscle continues to die for 6 to 8 hours at which time the heart attack usually is "complete." The dead heart muscle is replaced by scar tissue.

Click here to view interactive photos of hearts that have suffered a heart attack.

Treatment of heart attacks includes:

• Antiplatelet medications to prevent formation of blood clots in the arteries
• Anticoagulant 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
• Cardiac surgery

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 pain improves. 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 to 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.

Antiplatelet 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 antiplatelet agents -- aspirin, thienopyridines, and the glycoprotein IIb/IIIa inhibitors. These agents differ in their mode of action, antiplatelet potency, speed of onset of action, and cost. For more, please read the Aspirin and Antiplatelet Medications article.

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 antiplatelet 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.

Aspirin is taken daily following a heart attack to reduce the risk of another heart attack. (Preventing further heart attacks is called secondary prevention, while preventing the first heart attack is called primary prevention). The ideal daily dose of aspirin for secondary prevention has not been established. Some doctors recommend 160 mg; others recommend 81 mg. The reason for this difference has to do with aspirin's occasional long-term side effect of bleeding (for example from stomach ulcers). Even though the risk of major bleeding with long-term, moderate dose aspirin (325 mg/day) is low (less than 1%), this risk can be lowered slightly by using an even lower dose (160 or 81 mg/day).

Aspirin also benefits patients with forms of coronary heart disease other than heart attacks. Aspirin has been shown to reduce heart attacks and improve survival in the following patients:

• Aspirin improves survival among patients with unstable angina. Patients with unstable angina experience chest pains at rest or with minimal exertion. These patients have critically narrowed coronary arteries and are at imminent risk of having a heart attack.
• Aspirin improves survival among patients with stable exertional angina. (These are patients who experience chest pain only with exertion.)
• Aspirin prevents formation of blood clots at the site of the PTCA (see below).
• Aspirin prevents the formation of blood clots that can occlude surgical bypass grafts. (Occlusion of bypass grafts can lead to heart attacks.)
• Aspirin in low doses (81 mg/day) has been shown to prevent first heart attacks (primary prevention).

Thienopyridines such as ticlopidine (Ticlid), clopidogrel (Plavix), and prasugrel (Effient), inhibit the ADP receptor on the surface of platelets. Inhibiting the ADP receptors on the platelets prevent the platelets from aggregating and causing blood clots to form. The theinopyridines are more potent antiplatelet agents than aspirin. Clopidogrel (Plavix) and prasugrel (Effient) are used far more commonly than ticlopidine (Ticlid) because ticlopidine can, in rare instances, cause low platelet and/or white blood cell counts. These agents play an important role in the treatment of heart attacks and are used in the following situations:

• Clopidogrel or prasugrel is used instead of aspirin in patients who have an allergy to aspirin.
• Clopidogrel or prasugrel are often given together with aspirin in treating heart attacks. Studies have shown that the combination of aspirin and clopidogrel is more effective than aspirin alone in improving survival and limiting damage to heart muscle among patients with heart attacks.
• Clopidogrel or prasugrel is given together with aspirin to patients undergoing PTCA with or without coronary stenting (see later discussion). Studies have shown that the combination of aspirin and clopidogrel is more effective than aspirin alone in preventing formation of blood clots that can re-occlude the coronary artery unblocked by PTCA and in preventing blood clots within recently placed stents.
• After a heart attack or after PTCA, aspirin is given indefinitely. The optimal duration of clopidogrel has not been established, and duration of use by physicians varies from weeks to months.

Patients who receive the combination of clopidogrel and aspirin are more likely than patients who receive aspirin alone to develop complications of major bleeding following coronary artery bypass surgery. Therefore, ideally, clopidogrel should be stopped 3 to 7 days before surgery.

The glycoprotein IIb/IIIa inhibitors such as abciximab (Reopro) and eptifibatide (Integrilin) prevent aggregation of platelets by inhibiting the glycoprotein receptors on the platelets. They are the most potent antiplatelet agents, approximately 9 times more potent than aspirin, and 3 times more potent than the thienopyridines. The glycoprotein IIb/IIIa inhibitors are also the most expensive antiplatelet agents. The currently FDA-approved glycoprotein IIb/IIIa inhibitors have to be given intravenously. They usually are given along with aspirin and heparin. They are quick acting; their maximal antiplatelet effects are achieved within minutes of infusion. These inhibitors have become important in the treatment of patients with heart attacks, patients with unstable angina, and patients undergoing PTCA with or without stenting. Numerous studies have shown that glycoprotein IIb/IIIa inhibitors:

• Decrease the size of the blood clot blocking the coronary arteries, thus improving blood flow, limiting damage to heart muscle, and improving survival among patients with heart attacks
• Decrease the incidence of heart attacks and improve survival among patients with unstable angina
• Prevent the formation of blood clots inside coronary stents and in coronary arteries unblocked by PTCA, thus decreasing the incidence of heart attacks and improving survival, specifically, when given intravenously at the time of PTCA and stenting and followed by oral aspirin and clopidogrel

The major risk of glycoprotein IIb/IIIa inhibitors is bleeding. Therefore, patients on heparin, aspirin, and glycoprotein IIb/IIIa inhibitors have to be monitored closely for bleeding. Recent studies have demonstrated equal efficacy of abciximab and eptifibatide. Eptifibatide is shorter acting than abciximab. In the event of major bleeding, the antiplatelet effect of eptifibatide can be reversed within hours of stopping the intravenous infusion, while the antiplatelet effect of abciximab will last much longer. Sometimes, transfusions of platelets are necessary to treat major bleeding due to abciximab.

An uncommon side effect of glycoprotein IIb/IIIa inhibitors is the development of low platelet counts (thrombocytopenia). Thrombocytopenia can increase the risk for bleeding and, in rare instances, may actually cause blood to clot. Thus, patients receiving glycoprotein IIb/IIIa inhibitors should have their platelet counts monitored closely.

Coagulants (clotting factors) are proteins produced by the liver. Clotting factors are responsible for "cementing" clumps of platelets together to form a stronger and larger clot. Anticoagulants such as intravenous or subcutaneous heparin, subcutaneous low molecular weight heparin, and oral warfarin (Coumadin), prevent the formation of blood clots either by inhibiting the production of clotting factors or by interfering with the action of the clotting factors.

Heparin prevents the formation and growth of blood clots by inhibiting the action of clotting factors that cement the clumps of platelets together. Heparin is given either intravenously or as a subcutaneous (under the skin) injection.

Heparin commonly is given intravenously, usually with aspirin, antiplatelet agents, or fibrinolytic (clot-dissolving) medications for treating heart attacks. Intravenous heparin is given (usually with aspirin or an antiplatelet agent) to patients with heart attacks who are undergoing PTCA with or without stenting. Heparin also is given to patients who are at risk of developing blood clots within the chambers (atria and ventricles) of the heart. (For example, patients with atrial fibrillation can develop blood clots in the atria. Patients with large heart attacks and major damage to the heart muscle also can develop blood clots in the ventricles.) Heparin's anticoagulant effect is fast acting (beginning shortly after the start of the infusion) and dose-related (greater with higher doses). The duration of heparin treatment for heart attacks is approximately 48 hours.

Heparin's major side effect is bleeding, and the most serious bleeding complication is intracranial hemorrhage (bleeding into the brain). The risk of bleeding is higher with higher doses. Thus, patients receiving heparin will undergo frequent blood testing to measure APPT levels. The APPT level is a measure of the degree of anticoagulation. The goal is to keep the patient's APPT level in a safe range and to avoid abnormally high APPT levels that signify excessive anticoagulation and a greater risk of bleeding. If there is bleeding, heparin has the advantage of having a short duration of action and its anticoagulant effects disappear rapidly after stopping the intravenous infusion.

Low molecular weight heparins such as enoxaparin (Lovenox) and dalteparin (Fragmin), are sub-fractions of heparin with longer-lasting effects than heparin. They can be given every 12 to 24 hours as subcutaneous injections (like insulin). Studies have shown enoxaparin and dalteparin to be equivalent to intravenous heparin in patients with many conditions such as heart attacks, unstable angina, and blood clots in the veins or arteries of the lungs. The effects of low molecular weight heparins generally wear off after 6 to 12 hours. They are not used in place of intravenous heparin in patients undergoing PTCA or stenting.

Warfarin (Coumadin) prevents the formation of blood clots by inhibiting the production of clotting factors by the liver. Warfarin must be taken orally and is slow acting; it can take days to achieve an adequate anticoagulant effect. Warfarin's anticoagulant effect is dose-related, that is, its effect is greater with larger doses.

Because of its slow onset of action, Coumadin is not commonly used immediately for the treatment of heart attacks. Instead, it is used orally on a long-term basis in selected patients after heart attacks to prevent blood clots. For example, patients with atrial fibrillation or patients with major damage to ventricular muscle will take warfarin daily on a long-term basis to prevent blood clots in the atria and ventricles, respectively. Warfarin also is commonly used to prevent blood clots in veins of the legs in patients who are likely to develop them.

The risk with warfarin is abnormal bleeding, and the risk of bleeding is higher with higher doses. Thus, patients on warfarin should have their blood tested frequently (often weekly) to measure their prothrombin time and INR. Like APPT, the prothrombin time and INR measure the degree of anticoagulation. The goal of treatment is to keep the prothrombin time and INR in a safe range, avoiding excessively high prothrombin time and INR levels that indicate too much anticoagulation and a greater risk of bleeding. The effects of warfarin may be increased or decreased greatly by many other medications or foods, and it is crucial to review these medications and foods with the doctor.

Warfarin has a long duration of action, and its anticoagulation effect can last several days after it is stopped. Therefore, transfusions of clotting factors and/or vitamin K (to stimulate the liver to produce the clotting factors depleted by treatment with warfarin) must be given to reverse the anticoagulation in the event of serious bleeding.

Direct thrombin inhibitors are newer oral anticoagulants that have recently been introduced, such as rivaroxaban (Xarelto) and dabigatran (Pradaxa), which don't require the monitoring and dietary restrictions of warfarin, and their role is under investigation.

While antiplatelet agents and anticoagulants prevent the formation of blood clots, they cannot dissolve existing blood clots and hence cannot be relied upon to open blocked arteries rapidly. Clot-dissolving drugs (also called fibrinolytic or thrombolytic medications) actually dissolve blood clots and can rapidly open blocked arteries. Intravenous administration of clot-dissolving drugs such as tissue plasminogen activator (TPA) or TNK can open up to 80% of acutely blocked coronary arteries. The earlier these drugs are administered, the greater the success at opening the artery and the more effective the preservation of heart muscle. If clot-dissolving drugs are given too late (more than 6 hours after the onset of the heart attack), most of the muscle damage already may have occurred.

If a hospital does not have a catheterization laboratory with the ability to perform PTCA, or if there are logistic reasons why PTCA will be delayed, clot-dissolving drugs can be promptly administered to achieve reperfusion. PTCA then may be performed in patients who fail to respond to the clot-dissolving drugs. (If prompt PTCA and stenting are available, it has been demonstrated that they are preferable to clot-dissolving drugs to open arteries.)

Clot-dissolving drugs increase the risk of bleeding enough so that some patients cannot be treated with them, for example, patients with recent surgery or major trauma, recent stroke, bleeding ulcer, or other conditions that increases the risk of bleeding.

Coronary angiography and percutaneous transluminal coronary angioplasty (PTCA) is the most direct method of opening a blocked coronary artery. The procedures are performed in the catheterization laboratory in a hospital. Under X-ray guidance, a tiny plastic catheter with a balloon on its end is advanced over a guide wire from a vein in the groin or the arm and into the blocked coronary artery. Once the balloon reaches the blockage, it is inflated, pushing the clot and plaque out of the way to open the artery. PTCA can be effective in opening up to 95% of arteries. In addition, the angiogram (X-ray pictures taken of the coronary arteries) allows evaluation of the status of the other coronary arteries so that long-term treatment plans may be formulated.

For optimal benefits, coronary angiography and PTCA should be performed as soon as possible. Most cardiologists recommend that the time interval between the patient's arrival at the hospital and the deployment of the angioplasty balloon to open the artery should be less than 60 to 90 minutes.

For best results, the coronary angiogram and PTCA should be performed by an experienced cardiologist in a well-equipped cardiac catheterization laboratory. The cardiologist is considered experienced if he or she performs more than 75 such procedures a year. The catheterization laboratory personnel are considered experienced if the facility performs more than 200 such procedures a year.

It also is important that there be a surgical team to perform immediate open-heart surgery (coronary artery bypass grafting) in the event that PTCA is unsuccessful in opening the blocked artery or if there is a serious complication of PTCA. For example, in a small number of patients, PTCA cannot be performed because of technical difficulties in passing the guide wire or the balloon across the narrowed arterial segment. Open-heart surgery also will be necessary if there is a serious complication such as coronary artery injury during PTCA or an abrupt closure of the coronary artery shortly after PTCA. These complications may occur in a small percentage of patients.

The most serious complication of PTCA is an abrupt closure of the coronary artery within the first few hours after PTCA. Abrupt coronary artery closure (that can lead to further heart damage) occurs in some patients after simple balloon angioplasty (without stenting). Abrupt closure is due to a combination of tearing (dissection) of the inner lining of the artery, blood clotting at the site of the balloon, and constriction (spasm) or elastic recoil of the artery at the site where the balloon is inflated. Individuals at an increased risk for abrupt closure include women, patients with unstable angina, and patients having heart attacks.

The risk of abrupt closure of the coronary arteries can be reduced if:

• Aspirin is given during or after PTCA to prevent blood clotting. In fact, virtually all patients are maintained on aspirin indefinitely after PTCA to prevent arterial clots.
• Anticoagulants such as intravenous heparin or bivalirudin are given during PTCA to further prevent blood clotting.
• Combinations of nitrates and calcium channel blockers are used to minimize coronary artery spasm (see discussion that follows).
• Coronary artery stents are deployed to minimize coronary artery closure.
• The glycoprotein IIb/IIIa inhibitors are given.

Coronary artery stents are small hollow cylinders that can be deployed over the angioplasty balloons and left within the coronary arteries to keep the arteries open. Stents help prevent abrupt closure of arteries shortly after PTCA. They also prevent restenosis (recurrent narrowing of the arteries) several months after PTCA.

Coronary stents decrease the risks of arterial dissections, elastic recoil, and artery spasm that can occur after PTCA and cause re-occlusion of the artery. Studies have shown that the incidence of abrupt coronary artery closure after PTCA has declined dramatically with the introduction of coronary stents.

Coronary stents also help to keep the coronary arteries open in the longer-term. After a successful PTCA, a significant percentage of patients will develop recurrent narrowing (restenosis) at the site of inflation of the balloon, usually within 6 months following PTCA. Restenosis may or may not be accompanied by symptoms such as angina. Thus, restenosis often is detected by exercise stress tests performed 4 to 6 months after PTCA. The widespread use of coronary stents has reduced this incidence of restenosis. The introduction of coated stents (stents that are coated with chemicals to further reduce restenosis) has reduced the incidence of restenosis to well under 10% and has been a major improvement in treatment.

Patients with coronary artery stents usually are maintained on full doses of daily aspirin. For the first 4 to 12 weeks after the placement of stents, patients are given an additional antiplatelet drug such as clopidogrel or prasugrel because the metal surface of the stents may promote the formation of blood clots in the first several weeks after the stent is inserted. With medicated stents, aspirin and clopidogrel or prasugrel are continued for a year or longer.

Nitroglycerin is the most common nitrate used in the treatment of heart attacks. It can be given sublingually (under the tongue), as a spray, as a paste applied over skin, and intravenously. Intravenous nitroglycerine has a rapid onset of action and is commonly used in the initial (first 48 hours) treatment of heart attacks. Nitroglycerine is a vasodilator (blood vessel expander), that opens arteries by relaxing the muscular wall of the artery. Nitroglycerine dilates coronary arteries as well as other blood vessels throughout the body. By dilating blood vessels, nitroglycerine lowers blood pressure, decreases the work that the heart must do to pump blood, lowers the demand by the heart for oxygen, prevents coronary artery spasm, improves blood flow to the heart muscle, and potentially minimizes the size of the heart attack. Nitroglycerine is especially helpful in patients with heart attacks who also have heart failure or high blood pressure.

The common side effects of nitrates are headaches and low blood pressure. Low blood pressure can cause weakness, dizziness, and, sometimes, even fainting. Nitrates should not be given in patients who have taken medicines for erectile dysfunction such as sildenafil (Viagra) and vardenafil (Levitra) in the preceding 24 hours, since severe low blood pressure may result. Nitrates should not be given in patients who have taken tadalafil (Cialis) in the preceding 36 to 48 hours because the effects of Cialis last longer than either sildenafil or vardenafil.

Angiotensin converting enzyme (ACE) inhibitors, another class of blood vessel dilators, often are given orally after a large heart attack to improve the healing of heart muscle. Examples of ACE inhibitors include captopril (Capoten), enalapril (Vasotec), lisinopril (Zestril and Prinivil), and ramipril (Altace). These medications lower the blood pressure and reduce the workload of the heart, thereby helping the damaged heart muscle to recover. They are especially helpful in patients who have recovered from heart attacks but have high blood pressure, heart failure, major damage to the left ventricle, and diabetes mellitus. For additional information, please see the ACE Inhibitors article.

Beta blockers such as propranolol (Inderal), metoprolol (Lopressor, Toprol XL), and atenolol (Tenormin) usually are given early during a heart attack and are continued long-term. Beta blockers antagonize the action of adrenaline and relieve stress on the muscles of the heart. Beta blockers decrease the workload of the heart by slowing the heart rate and decreasing the force of contraction of heart muscle. Decreasing the workload decreases the demand for oxygen by the heart and limits the amount of damage to the heart muscle. Long-term administration of beta blockers following a heart attack has been shown to improve survival and reduce the risk of future heart attacks. Beta blockers also improve survival among patients with heart attacks by decreasing the incidence of life-threatening abnormal heart rhythms, for example, ventricular fibrillation. Beta blockers can be given intravenously in the hospital and then can be taken orally for long-term treatment.

The side effects of beta blockers are wheezing (worsening of breathing in patients with asthma), abnormally slow heart rate, and exacerbation of heart failure (especially in patients with significant damage to their heart muscle); however, in patients with chronic heart failure, beta blockers have recently been demonstrated to be helpful in decreasing symptoms and prolonging life. For more, please read the Beta Blockers article.

Oxygen also is 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.

In some patients, PTCA can be technically difficult or dangerous to perform. In others, PTCA and clot-dissolving medications may fail to achieve reperfusion or maintain open arteries. These patients may be considered for coronary artery bypass grafting surgery. For more information, please see the Coronary Artery Bypass Graft article.

Heart attack patients are monitored in the hospital for 3 or more days prior to discharge home. Rhythm disturbances, shortness of breath due to heart failure, or recurrent chest pain are reasons for further therapy such as balloon angioplasty or coronary stenting, additional medications, or bypass surgery.

Patients gradually increase their activity under observation. Before discharge, a low-level exercise stress test may be performed to detect important residual narrowing in the coronary arteries, exercise-induced cardiac rhythm abnormalities, and heart muscle failure, and to help guide the doctor in prescribing an activity regimen after hospitalization. An abnormal stress test prior to hospital discharge following a heart attack predicts a high risk for subsequent cardiac events; if the patient has not yet had a coronary angiogram, an abnormal pre-discharge stress test is a strong reason for doing angiography. Since most patients usually receive angiography early, the use of pre-discharge stress testing has declined.

Before resuming full activity or work, several weeks may be needed for the heart muscle to heal. After a small heart attack (little damage to heart muscle), patients usually can resume normal activities after 2 weeks. These activities include returning to work as well as normal sexual activity. A moderate heart attack (moderate damage to heart muscle) requires limited, gradually increasing activity for up to 4 weeks, while a large heart attack (much damage to heart muscle) may result in a recovery period of 6 weeks or longer. These time frames are necessary in order for the dead heart muscle to substantially complete the scarring process. During this healing period, patients should avoid vigorous exertion and heavy lifting (over 20 pounds) or any strenuous activity that causes shortness of breath or undue fatigue.

Cardiac rehabilitation typically begins during hospitalization and continues during the months following a heart attack. Cardiac rehabilitation programs provide a helpful transition to a safe and full return to a normal lifestyle. In addition, cardiac rehabilitation allows the prescription of a long-term exercise program tailored to each patient and helps patients and their families adjust to lifestyle changes and the difficult and conflicting emotions that often follow a heart attack.

• Take aspirin and beta blockers (propranolol, metoprolol, atenolol) that have been shown to reduce the chances of a second heart attack and improve survival.
• Stop smoking cigarettes.
• Reduce excess weight and exercise regularly.
• Control blood pressure and diabetes.
• Follow a diet that is low in cholesterol (less than 200 mg daily) and saturated fat (less than 7% of total calories). For more, please see the Therapeutic Lifestyle Changes (TLC) Daily Food Guide, Eating Heart Healthy.
• Reduce LDL (bad) cholesterol and increase HDL (good) cholesterol. Reduction of LDL cholesterol to a value below 80 mg/dl, particularly with the statin group of medications, has been demonstrated to prevent further heart attacks. Patients with low HDL (less than 35 mg/dl) are encouraged to exercise regularly and to take medications to increase HDL. For more in-depth information about cholesterol, LDL, and HDL, please see the Cholesterol article.
• Take ACE inhibitors that aid the healing process and improve long-term survival in selected patients, particularly those with major damage to heart muscle.
• Eat a diet rich in omega-3-fatty acids by eating more fish or take fish oil supplements. (See the fish oil article). High intake of omega-3-fatty acids decreases the risk of sudden death from heart attacks.
• Undergo further testing. In the months following a heart attack, further cardiac stress testing, with or without nuclear or echocardiographic imaging, may be prescribed to determine if additional therapy will be necessary to prevent future heart attacks. In addition, special testing may be required to evaluate the risk of developing cardiac arrhythmias. All such testing should be discussed with the doctor.