Heart Attack Report

Mine is STEMI (ST-segment Elevation Myocardial Infarction).

Review Date: 5/24/2012


Heart Attack In-Depth Report

Background
The heart is the human body's hardest working organ. Throughout life it continuously pumps blood enriched with oxygen and vital nutrients through a network of arteries to all tissues of the body. To perform this strenuous task, the heart muscle itself needs a plentiful supply of oxygen-rich blood, provided through a network of coronary arteries. These arteries carry oxygen-rich blood to the heart's muscular walls (the myocardium).
A heart attack (myocardial infarction) occurs when blood flow to the heart muscle is blocked, and tissue death occurs from loss of oxygen, severely damaging a portion of the heart.


Coronary Artery Disease. Coronary artery disease is the most common cause of heart attacks. Coronary artery disease is the end result of a complex process called atherosclerosis (commonly called "hardening of the arteries"). This causes blockage of arteries (ischemia) and prevents oxygen-rich blood from reaching the heart.
HEART ATTACK
Heart attack (or myocardial infarction) is among the most serious outcome of atherosclerosis. It can occur as a result of one of two effects of atherosclerosis:
If the plaque itself develops fissures or tears. Blood platelets adhere to the site to seal off the plaque, and a blood clot (thrombus) forms. A heart attack can then occur if the blood clot completely blocks the passage of oxygen-rich blood to the heart.
If the artery becomes completely blocked after gradual buildup of plaque due to atherosclerosis. Heart attack may occur if not enough oxygen containing blood can flow through this blockage.
ANGINA
Angina, the primary symptom of coronary artery disease, is typically experienced as chest pain. There are two kinds of angina:
Stable Angina. This is predictable chest pain that can usually be managed with lifestyle changes and medications, such as low-dose aspirin.
Unstable Angina. This situation is much more serious than stable angina, and is often an intermediate stage between stable angina and a heart attack. Unstable angina is part of a condition called acute coronary syndrome.
ACUTE CORONARY SYNDROME
Acute coronary syndrome (ACS) is a severe and sudden heart condition that, although needing aggressive treatment, has not developed into a full blown heart attack. Acute coronary syndrome includes:
Unstable Angina. Unstable angina is potentially serious and chest pain is persistent, but blood tests do not show markers for heart attack.
NSTEMI (Non ST-segment Elevation Myocardial Infarction). This condition, also called non Q-wave myocardial infarction, is diagnosed when blood tests and ECGs suggest a heart attack that does not involve the full thickness of the heart muscle. The injury in the arteries is less severe than with a full-blown heart attack.
Patients diagnosed with acute coronary syndrome (ACS) may be at risk for a heart attack. Doctors use a patient's medical history, various tests, and the presence of certain factors to help predict which ACS patients are most at risk for developing a more serious condition. The severity of chest pain itself does not necessarily indicate the actual damage in the heart.
Symptoms
HEART ATTACK SYMPTOMS
Heart attack symptoms can vary. They may come on suddenly and severely or may progress slowly, beginning with mild pain. Symptoms can also vary between men and women. Women are less likely than men to experience classic chest pain, but more likely to to experience shortness of breath, nausea or vomiting, or jaw and back pain.
Common signs and symptom of heart attack include:
Chest pain. Chest pain or discomfort (angina) is the main sign of a heart attack. It can feel like pressure, squeezing, fullness, or pain in the center of the chest. Patients with coronary artery disease who have stable angina often experience chest pain that lasts for a few minutes and then goes away. With heart attack, the pain usually lasts for more than a few minutes and the feeling may go away but then come back.
Discomfort in the upper body. People who are experiencing a heart attack may feel discomfort in the arms, neck, back, jaw, or stomach.
Shortness of breath can occur with or without chest pain.
Nausea and vomiting
Breaking out in cold sweat
Lightheadedness or fainting
SYMPTOMS THAT ARE LESS LIKELY TO INDICATE HEART ATTACK
The following symptoms are less likely to be due to heart attack:
Sharp pain brought on by breathing in or when coughing
Pain that is mainly or only in the middle or lower abdomen
Pain that can be pinpointed with the top of one finger
Pain that can be reproduced by moving or pressing on the chest wall or arms
Pain that is constant and lasts for hours (although no one should wait hours if they suspect they are having a heart attack)
Pain that is very brief and lasts for a few seconds
Pain that spreads to the legs
However, the presence of these symptoms does not always rule out a serious heart event.
SILENT ISCHEMIA
Some people with severe coronary artery disease do not have angina pain. This condition is known as silent ischemia, which some doctors attribute to the brain abnormally processing of heart pain. This is a dangerous condition because patients have no warning signs of heart disease. Some studies suggest that people with silent ischemia experience higher complication and mortality rates than those with angina pain.
WHAT TO DO WHEN SYMPTOMS OCCUR
Individuals who experience symptoms of a heart attack should take the following actions:
For angina patients, take one nitroglycerin dose either as an under-the-tongue tablet or in spray form at the onset of symptoms. Take another dose every 5 minutes up to three doses or when the pain is relieved, whichever comes first.
Call 911 or the local emergency number. This should be the first action taken if angina patients continue to experience chest pain after taking the full three doses of nitroglycerin. However, only 20% of heart attacks occur in patients with previously diagnosed angina. Therefore, anyone who develops heart attack symptoms should contact emergency services.
The patient should chew an aspirin (250 - 500 mg) and be sure to tell emergency health providers so an additional dose is not given.
Patients with chest pain should go immediately to the nearest emergency room, preferably traveling by ambulance. They should not drive themselves.
Prognosis
Heart attacks may be rapidly fatal, evolve into a chronic disabling condition, or lead to full recovery. The long-term prognosis for both length and quality of life after a heart attack depends on its severity, the amount of damage sustained by the heart muscle, and the preventive measures taken afterward.
Patients who have had a heart attack have a higher risk of a second heart attack. Although no tests can absolutely predict whether another heart attack will occur, peole can avoid more heart attacks with healthy lifestyle changes and adherence to medical treatments. Two-thirds of patients who have suffered a heart attack, however, do not take the necessary steps to prevent another.
Heart attack also increases the risk for other heart problems, including heart failure, abnormal heart rhythms, heart valve damage, and stroke.
Higher Risk Individuals. A heart attack is always more serious in certain people, including:
Elderly
People with a history of heart disease or risk factors for heart disease
People with heart failure
People with diabetes
People on long-term dialysis
Women are more likely to die after a heart attack than men. The risk is highest in younger women.
Factors Occurring at the Time of a Heart Attack that Increase Severity. The presence of other conditions during a heart attack can contribute to a poorer outlook:
Arrhythmias (disturbed heart rhythms). A dangerous arrhythmia called ventricular fibrillation is a major cause of short-term death from heart attack. Arrhythmias are more likely to occur within the first 4 hours of a heat attack, and they are associated with a high mortality rate. Patients who are successfully treated, however, have the same long-term prognosis as those who do not have such arrhythmias.
Shock. This very dangerous condition is associated with very low blood pressure, reduced urine levels, and cellular abnormalities. Shock occurs in about 7% of heart attacks. The incidence has not declined over recent years, although its survival rates have improved.
Heart block, also called atrioventricular (AV) block, is a condition in which the electric conduction of nerve impulses to specialized muscles in the heart is slowed or interrupted. Although heart block is dangerous, it can be treated effectively with a pacemaker, and it rarely causes any long-term complications in patients who survive it.
Heart failure. The damaged heart muscle is unable to pump all the blood that the tissues need. Patients experience fatigue, shortness of breath, and fluid build up.
Risk Factors
The risk factors for heart attack are the same as those for coronary artery disease (heart disease). They include:
AGE
The risks for coronary artery disease increase with age. About 85% of people who die from heart disease are over the age of 65. For men, the average age of a first heart attack is 66 years.
GENDER
Men have a greater risk for coronary artery disease and are more likely to have heart attacks earlier in life than women. Women’s risk for heart disease increases after menopause, and they are more likely to have angina than men.
GENETIC FACTORS AND FAMILY HISTORY
Certain genetic factors increase the likelihood of developing important risk factors, such as diabetes, elevated cholesterol and high blood pressure.
RACE AND ETHNICITY
African-Americans have the highest risk of heart disease, in part due to their high rates of severe high blood pressure, as well as diabetes and obesity.
MEDICAL CONDITIONS
Obesity and Metabolic Syndrome. Excess body fat, especially around the waist, can increase the risk for heart disease. Obesity also increases the risk for other conditions (high blood pressure, diabetes) that are associated with heart disease. Obesity is particularly hazardous when it is part of the metabolic syndrome, a pre-diabetic condition that is significantly associated with heart disease. This syndrome is diagnosed when three of the following are present:
Abdominal obesity
Low HDL cholesterol
High triglyceride levels
High blood pressure
Insulin resistance
Unhealthy Cholesterol Levels. Low-density lipoprotein (LDL) cholesterol is the "bad" cholesterol responsible for many heart problems. Triglycerides are another type of lipid (fat molecule) that can be bad for the heart. High-density lipoprotein (HDL) cholesterol is the "good" cholesterol that helps protect against heart disease. Doctors test for a "total cholesterol" profile that includes measurements for LDL, HDL, and triglycerides. The ratio of these lipids can affect heart disease risk.
High Blood Pressure. High blood pressure, or hypertension, has long been a proven cause of coronary artery disease and heart attack. A normal blood pressure reading is 120/80 mm Hg or lower. High blood pressure is generally considered to be a blood pressure reading greater than or equal to 140 mm Hg (systolic) or greater than or equal to 90 mm Hg (diastolic). Blood pressure readings in the prehypertension category (120 - 139 systolic or 80 - 89 diastolic) indicate an increased risk for developing hypertension.
Diabetes. Diabetes, especially for people whose blood sugar levels are not well controlled, significantly increases the risk of developing heart disease. In fact, heart disease and stroke are the leading causes of death in people with diabetes. People with diabetes are also at risk for high blood pressure and unhealthy cholesterol levels, blood clotting problems, kidney disease, and impaired nerve function, all of which can damage the heart.
VASCULAR DISEASES
Peripheral artery disease (PAD), aortic aneurysm, stroke, and renal artery stenosis are vascular diseases that increase the risk for heart attack.
LIFESTYLE FACTORS
Smoking. Smoking is the most important risk factor for heart disease. Smoking can cause elevated blood pressure, worsen lipids, and make platelets very sticky, raising the risk of clots. Although heavy cigarette smokers are at greatest risk, people who smoke as few as three cigarettes a day are at higher risk for blood vessel abnormalities that endanger the heart. Regular exposure to passive smoke also increases the risk of heart disease in nonsmokers.
Alcohol. Moderate alcohol consumption (one or two glasses a day) can help boost HDL “good” cholesterol levels. Alcohol may also prevent blood clots and inflammation. By contrast, heavy drinking harms the heart. In fact, heart disease is the leading cause of death in alcoholics.
Diet. Diet plays an important role in the health of the heart, especially by reducing dietary sources of trans fats, saturated fats, and cholesterol and restricting salt intake that contributes to high blood pressure.
Physical Inactivity. Exercise has a number of effects that benefit the heart and circulation, including improving cholesterol levels and blood pressure and maintaining weight control. People who are sedentary are almost twice as likely to suffer heart attacks as are people who exercise regularly.
NSAIDS AND COX-2 INHIBITORS
All nonsteroidal anti-inflammatory drugs (NSAIDs) -- with the exception of aspirin -- carry heart risks. NSAIDs and COX-2 inhibitors may increase the risk for death in patients who have experienced a heart attack. The risk is greatest at higher dosages, but not necessarily for length of time.
NSAIDs include nonprescription drugs like ibuprofen (Advil, Motrin) and prescription drugs like diclofenac (Cataflam, Voltaren). Celecoxib (Celebrex) is currently the only COX-2 inhibitor that is available in the U.S. It has been linked to cardiovascular risks, such as heart attack and stroke. Patients who have had heart attacks should talk to their doctors before taking any of these drugs.
The American Heart Association recommends that patients who have, or who are at risk for, heart disease first try non-drug methods of pain relief (such as physical therapy, exercise, weight loss to reduce stress on joints, and heat or cold therapy). If these methods don't work, patients should take the lowest possible dose of acetaminophen (Tylenol) or aspirin. COX-2 inhibitors, such as celecoxib (Celebrex), should be the last resort.
Diagnosis
When a patient comes to the hospital with chest pain, the following diagnostic steps are usually taken to determine any heart problems, and, if present, their severity:
The patient will report all symptoms so that a health care provider can rule out either a non-heart problem or possible other serious accompanying conditions.
An electrocardiogram (ECG) reading is taken, recording the waves made by the heart. It is the key tool for determining if heart problems are causing chest pain and, if so, how severe they are.
Blood tests showing elevated levels of certain factors (troponins and CK-MB) indicate heart damage. (The doctor will not wait for results, however, before administering treatment if a heart attack is strongly suspected.)
Imaging tests, including echocardiogram and perfusion scintigraphy, help rule out a heart attack if there is any question.
ELECTROCARDIOGRAM (ECG)
An electrocardiogram (ECG or EKG) measures and records the electrical activity of the heart. The waves measured by the ECG correspond to the contraction and relaxation pattern of the different parts of the heart. Specific waves seen on an ECG are named with letters:



P. The P wave is associated with the contractions of the atria (the two chambers in the heart that receive blood from outside).
QRS. The QRS is a series of waves associated with ventricular contractions. (The ventricles are the two major pumping chambers in the heart.)
T and U. These waves follow the ventricular contractions.
Doctors use a term called the P-Q or P-R interval, which is the time taken for an electrical impulse to travel from the atria to the ventricle.
The most important wave patterns in diagnosing and determining treatment for a heart attack are called ST elevations and Q waves.
Elevated ST Segments: Heart Attack. Elevated ST segments are strong indicators of a heart attack in patients with symptoms and other indicators. They suggest that an artery to the heart is blocked and that the full thickness of the heart muscle is damaged. The kind of heart attack associated with these findings is referred to as either a Q-wave myocardial infarction or a STEMI (ST-segment elevation myocardial infarction.)
However, ST segment elevations do not always mean the patient has a heart attack. An infection in the sack around the heart (pericarditis) is another cause of ST-segment elevation.
Non-Elevated ST Segments: Angina and Acute Coronary Syndrome. A depressed or horizontal ST wave suggests some blockage and the presence of heart disease, even if there is no angina present. It occurs in about half of patients with other signs of a heart event. This finding, however, is not very accurate, particularly in women, and can occur without heart problems. In such cases, laboratory tests are needed to determine the extent, if any, of heart damage. In general, one of the following conditions may be present:
Stable Angina (blood test results or other tests show no serious problems and chest pain resolves). Between 25 - 50% of people who have angina or silent ischemia have normal ECG readings.
Acute Coronary Syndrome (ACS). This includes severe and sudden heart conditions that require aggressive treatment but have not developed into a full-blown heart attack. ACS, refers to either unstable angina or NSTEMI (non ST-segment elevation myocardial infarction) -- also referred to as non Q-wave myocardial infarction. Unstable angina is potentially serious, and chest pain is persistent, but blood tests do not show markers for heart attack. With NSTEMI, the blood tests suggest a heart attack, but most likely, injury to the heart is less serious than with a full-blown heart attack.
ECHOCARDIOGRAM
An echocardiogram is a noninvasive test that uses ultrasound images of the heart. Your doctor can see whether a part of your heart muscle has been damaged and is not moving. An echocardiogram may also be used as part of an exercise stress test, to detect the location and extent of heart muscle damage at the time of discharge or soon after you leave the hospital after a heart attack.
RADIONUCLIDE IMAGING (THALLIUM STRESS TEST)
Radionuclide procedures use imaging techniques and computer analyses to plot and detect the passage of radioactive tracers through the region of the heart. Such tracing elements are typically given intravenously. Radionuclide imaging is useful for diagnosing and determining:
Severity of unstable angina when less expensive diagnostic approaches are unavailable or unreliable
Severity of chronic coronary artery disease
Success of surgeries for coronary artery disease
Whether a heart attack has occurred
The location and extent of heart muscle damage at the time of discharge or soon after you leave the hospital after a heart attack
The procedure is noninvasive. It is a reliable measure of severe heart events and can help identify if damage has occurred from a heart attack. A radioactive isotope such as thallium (or technetium) is injected into the patient's vein. The radioactive isotope attaches to red blood cells and passes through the heart in the circulating blood. The isotope can then be traced through the heart using special cameras or scanners. The images may be combined with an electrocardiogram. The patient is tested while resting, then tested again during an exercise stress test. If the scan detects damage, more images are taken 3 or 4 hours later. Damage due to a prior heart attack will persist when the heart scan is repeated. Injury caused by angina, however, will have resolved by that time.
ANGIOGRAPHY
Angiography is an invasive test. It is used for patients who show strong evidence for severe obstruction on stress and other tests and for patients with acute coronary syndrome. In the procedure:
A narrow tube is inserted into an artery, usually in the leg or arm, and then threaded up through the body to the coronary arteries.
A dye is injected into the tube, and an x-ray records the flow of dye through the arteries.
This process provides a map of the coronary circulation, revealing any blocked areas.
Major complications include stroke, heart attacks, and kidney damage. These risks are very low (about 0.1%), however, if the procedure is done in an experienced medical center (one that performs at least 300 of these operations every year). Allergic reactions can also occur. The procedure is expensive, and 10 - 30% of patients who have this procedure have normal results.
BIOLOGIC MARKERS
When heart cells become damaged, they release different enzymes and other molecules into the bloodstream. Elevated levels of such markers of heart damage in the blood or urine may help predict a heart attack in patients with severe chest pain, and help determine treatment. Tests for these markers are often performed in the emergency room or hospital when a heart attack is suspected. Some markers include:
Troponins. The proteins cardiac troponin T and I are released when the heart muscle is damaged. Both are proving to be among the best diagnostic indications of heart attacks. They help to identify many individuals with ACS who might otherwise be misdiagnosed.
Creatine kinase myocardial band (CK-MB). CK-MB has been a standard marker, but the MB fraction is not as accurate as troponin levels, since elevated levels can appear in people without heart injury.
Treatment
Treatment options for heart attack, and acute coronary syndrome, include:
Oxygen therapy
Relieving pain and discomfort using nitroglycerin or morphine
Controlling any arrhythmias (abnormal heart rhythms)
Blocking further clotting (if possible), using aspirin or clopidogrel (Plavix), as well as possibly anticoagulant drugs such as heparin
Opening up the artery that is blocked as soon as possible, by using medicines that open up the clot or by performing angioplasty
Giving the patient beta blockers, calcium channel blockers, or angiotensin converting enzyme inhibitor drugs to help the heart muscle and arteries work better
IMMEDIATE TREATMENTS TO SUPPORT THE PATIENT
Early supportive treatments are similar for patients who have ACS or those who have had a heart attack.
Oxygen. Oxygen is almost always administered right away, usually through a tube that enters through the nose.
Aspirin. The patient is given aspirin if one was not taken at home.
Medications for Relieving Symptoms.
Nitroglycerin. Most patients will receive nitroglycerin during and after a heart attack, usually under the tongue. Nitroglycerin decreases blood pressure and opens the blood vessels around the heart, increasing blood flow. Nitroglycerin may be given intravenously in certain cases (recurrent angina, heart failure, or high blood pressure).
Morphine. Morphine not only relieves pain and reduces anxiety but also opens blood vessels, aiding the circulation of blood and oxygen to the heart. Morphine can decrease blood pressure and slow down the heart. In patients in whom such effects may worsen their heart attacks, other drugs may be used.
OPENING THE ARTERIES: EMERGENCY ANGIOPLASTY OR THROMBOLYTIC DRUGS
With a heart attack, clots form in the coronary arteries that supply oxygen to the heart muscle. Opening a clotted artery as quickly as possible is the best approach to improving survival and limiting the amount of heart muscle that is permanently damaged.
The standard medical and surgical solutions for opening arteries are:
Angioplasty, also called percutaneous coronary intervention (PCI), is the preferred emergency procedure for opening the arteries. Angioplasty should be performed promptly, preferably within 90 minutes of arriving at the hospital and no later than 12 hours after a full-thickness (STEMI) heart attack. In most cases, a stent is placed in the artery to keep it open after the angioplasty.
Thrombolytics, known as blood-clot-busting drugs, are the standard medications used to open the arteries. A thrombolytic drug needs to be given within 3 hours after the onset of symptoms.
Coronary artery bypass graft (CABG) surgery is sometimes used as an alternative to angioplasty.
Factors considered in choosing a strategy include:
How likely it is the patient is having a heart attack
Patient's age (preferably less than age 75 years)
Presence of risk factors for bleeding or history of recent bleeding
Elapsed time since symptoms began (preferably fewer than 12 hours)
Whether a patient needs to be transported in order to have angioplasty
Blood pressure level
History of stroke or cancer
Which and how many coronary arteries are blocked
THROMBOLYTICS
Thrombolytic, also called clot-busting or fibrinolytic, drugs are recommended as alternatives to angioplasty. These drugs dissolve the clot, or thrombus, responsible for causing artery blockage and heart-muscle tissue death.
Generally speaking, thrombolysis is considered a good option for patients with full-thickness (STEMI) heart attacks when symptoms have been present for fewer than 3 hours. Ideally, these drugs should be given within 30 minutes of arriving at the hospital if angioplasty is not a viable option. Other situations where it may be used include when:
Prolonged transport will be required
Too long of a time will pass before a catheterization lab is available
PCI procedure is not successful or anatomically too difficult
Thrombolytics should be avoided or used with great caution in the following patients after heart attack:
Patients older than 75 years
When symptoms have continued beyond 12 hours
Pregnant women
People who have experienced recent trauma (especially head injury) or invasive surgery
People with active peptic ulcers
Patients who have been given prolonged CPR
Current users of anticoagulants
Patients who have experienced any recent major bleeding
Patients with low ST segments
Patients with a history of stroke
Patients with uncontrolled high blood pressure, especially when systolic is higher than 180 mm Hg
Specific Thrombolytics. The standard thrombolytic drugs are recombinant tissue plasminogen activators or rt-PAs. They include alteplase (Activase) and reteplase (Retavase) as well as a newer drug tenecteplase (TNKase).
Thrombolytic Administration. The sooner that thrombolytic drugs are given after a heart attack, the better. The benefits of thrombolytics are highest within the first 3 hours. They can still help if given within 12 hours of a heart attack.
Complications. Hemorrhagic stroke, usually occurring during the first day, is the most serious complication of thrombolytic therapy, but fortunately it is rare.
REVASCULARIZATION PROCEDURES: ANGIOPLASTY AND BYPASS SURGERY
Percutaneous coronary intervention (PCI), also called angioplasty, and coronary artery bypass graft surgery are the standard operations for opening narrowed or blocked arteries. They are known as revascularization procedures.
Emergency angioplasty/PCI is the standard procedure for heart attacks but should be performed within 90 minutes or no later than 12 hours following a heart attack. Studies have shown that balloon angioplasty and stenting fails to prevent heart complications in patients who receive the procedure 3 - 28 days after a heart attack.
Coronary bypass surgery is typically used as elective surgery for patients with blocked arteries. It may occasionally be used after a heart attack if angioplasty or thrombolytics fail or are not appropriate. It is usually not performed for several days to allow recovery of the heart muscles.
Most patients who meet the criteria for either thrombolytic drugs or angioplasty do better with angioplasty (although only in centers equipped to do this procedure).
Angioplasty/PCI involves procedures such as percutaneous transluminal coronary angioplasty (PTCA) that help open the blocked artery. A typical angioplasty procedure involves the following steps:
The cardiologist threads a narrow catheter (a tube) containing a fiber into the blocked vessel.
The cardiologist opens the blocked vessel using balloon angioplasty, in which a tiny deflated balloon is passed through the catheter to the vessel.
The balloon is inflated to compress the plaque against the walls of the artery, flattening it out so that blood can once again flow through the blood vessel freely.
The balloon is inflated to compress the plaque against the walls of the artery, flattening it out so that blood can once again flow through the blood vessel freely.
To keep the artery open afterwards, doctors use a device called a coronary stent, an expandable metal mesh tube that is implanted during angioplasty at the site of the blockage. The stent may be bare metal or it may be coated with a drug that slowly releases medication.
Once in place, the stent pushes against the wall of the artery to keep it open. Stenting is improving results in patients with heart attack who have emergency angioplasty. It also significantly prevents reclosure and reduces heart attack rates in patients with ACS.
Complications occur in about 10% of patients (about 80% of complications occur within the first day). Best results occur in hospital settings with experienced teams and backup. Women who have angioplasty after a heart attack have a higher risk of death than men.
Reclosure and Blockage During or After Angioplasty. Narrowing or reclosure of the artery (restenosis) often occurs during or shortly after angioplasty. It can also occur up to a year after surgery, requiring a repeat angioplasty procedure.
Drug-eluting stents, which are coated with sirolimus (Rapamune) or paclitaxel (Taxol), can help prevent restenosis. They may be better than bare metal stents for patients who have experienced a STEMI heart attack, but they can also increase the risks of blood clots.
It is very important for patients who have drug-eluting stents to take aspirin and clopidogrel (Plavix) for at least 1 year after the stent is inserted, to reduce the risk of blood clots. Clopidogrel, like aspirin, helps to prevent blood platelets from clumping together. If for some reason patients cannot take clopidogrel along with aspirin after angioplasty and stenting, they should receive a bare metal stent instead of a drug-eluting stent. In rare cases, a drug called ticlopidine is used instead of clopidogrel.
Coronary Artery Bypass Graft Surgery (CABG). Coronary artery bypass graft surgery (CABG) is the alternative procedure to angioplasty for opening blocked arteries in patients with severe angina, particularly those who have two or more blocked arteries. It is a very invasive procedure, however:
The chest is opened, and the blood is rerouted through a lung-heart machine.
The heart is stopped during the procedure.
Segments of veins or arteries taken from elsewhere in the patient's body are fashioned into grafts, which are used to reroute the blood. The blood vessel grafts are placed in front of and beyond the blocked arteries, so the blood flows through the new vessels around the blockage.
Mortality rates with this procedure after a heart attack are much higher (6%) than when it is used electively (1 - 2%). How or when it should be used after a heart attack is controversial.
TREATMENT FOR PATIENTS IN SHOCK OR WITH HEART FAILURE
Severely ill patients, particularly those with heart failure or who are in cardiogenic shock (a dangerous condition that includes a drop in blood pressure and other abnormalities), will be monitored closely and stabilized. Oxygen is administered, and fluids are given or replaced when it is appropriate to either increase or reduce blood pressure. Such patients may be given dopamine, dobutamine, or both. Other treatments depend on the specific condition.
Heart failure. Intravenous furosemide may be administered. Patients may also be given nitrates, and ACE inhibitors, unless they have a severe drop in blood pressure or other conditions that preclude them. Clot-busting drugs or angioplasty may be appropriate and life-saving in many of these patients, although heart failure patients are less likely to receive these treatments.
Cardiogenic Shock. A procedure called intra-aortic balloon counterpulsation (IABP) can help patients with cardiogenic shock when used in combination with thrombolytic therapy. IABP involves inserting a catheter containing a balloon, which is inflated and deflated within the artery to boost blood pressure. Left ventricular assist devices and early angioplasty might also be considered.
TREATMENT OF ARRHYTHMIAS
An arrhythmia is a deviation from the heart's normal beating pattern caused when the heart muscle is deprived of oxygen and is a dangerous side effect of a heart attack. A very fast or slow rhythmic heart rate often occurs in patients who have had a heart attack, and is not usually a dangerous sign.
Premature beats or very fast arrhythmias called tachycardia, however, may be predictors of ventricular fibrillation. This is a lethal rhythm abnormality, in which the ventricles of the heart beat so rapidly that they do not actually contract but quiver ineffectually. The pumping action necessary to keep blood circulating is lost.
Preventing Ventricular Fibrillation. People who develop ventricular fibrillation do not always experience warning arrhythmias, and to date, there are no effective drugs for preventing arrhythmias during a heart attack.
Potassium and magnesium levels should be monitored and maintained.
Intravenous beta blockers followed by oral administration of the drugs may help prevent arrhythmias in certain patients.
Treating Ventricular Fibrillation.
Defibrillators. Patients who develop ventricular arrhythmias are given electrical shocks with defibrillators to restore normal rhythms. Some studies suggest that implantable cardioverter-defibrillators (ICDs) may prevent further arrhythmias in heart attack survivors of these events who are at risk for further arrhythmias.
Antiarrhythmic Drugs. Antiarrhythmic drugs include lidocaine, procainamide, or amiodarone. Amiodarone or another antiarrhythmic drug may be used afterward to prevent future events.
Managing Other Arrhythmias. People with an arrhythmia called atrial fibrillation have a higher risk for stroke after a heart attack and should be treated with anticoagulants such as warfarin (Coumadin). Other rhythm disturbances called bradyarrhythmias (very slow rhythm disturbances) frequently develop in association with a heart attack and may be treated with atropine or pacemakers.
Secondary Prevention
Patients can reduce the risk for a second heart attack by following secondary prevention measures. No one should be discharged from the hospital with these issues being addressed and appropriate medications prescribed. Lifestyle choices, particularly dietary factors, are equally important in preventing heart attacks and must be strenuously adhered to.
Blood Pressure. Aim for a blood pressure of less than 130/80 mm Hg.
Cholesterol. LDL (“bad”) cholesterol should be substantially less than 100 mg/dL. If triglycerides are greater than or equal to 200 mg/dL, then non-HDL-C should be less than 130 mg/dL. Nearly all patients who have had a heart attack should receive a prescription for a statin drug before being discharged from the hospital. It is also important to control dietary cholesterol by reducing intake of saturated fats to less than 7% of total calories. Increased omega-3 fatty acid consumption (by eating more fish or taking fish oil supplements) can help reduce triglyceride levels.
Exercise. Exercise for 30 - 60 minutes 7 days a week (or at least a minimum of 5 days a week.)
Weight Management. Combine exercise with a healthy diet rich in fresh fruits, vegetables and low-fat dairy products. Your body mass index (BMI) should be 18.5 - 24.8. Waist circumference is also an important measure of heart attack risk. Men’s waist circumferences should be fewer than 40 inches (102 centimeters) and women’s should be fewer than 35 inches (89 centimeters).
Smoking. It is essential to stop smoking. Also, avoid exposure to second-hand smoke.
Antiplatelet Drugs. Your doctor may recommend you take aspirin (75 - 81 mg) on a daily basis. If you have had a drug-coated stent inserted, you must take clopidogrel (Plavix) along with aspirin for at least 1 year following surgery. (Aspirin is also recommended for some patients as primary prevention of heart attack.)
Other Drugs. Your doctor may recommend that you take an ACE inhibitor or beta blocker drug on an ongoing basis. It is also important to have an annual influenza (“flu”) vaccination.
Medications
ASPIRIN AND OTHER ANTI-CLOTTING DRUGS
Anti-clotting drugs that inhibit or break up blood clots are used at every stage of heart disease. They are generally classified as either antiplatelets or anticoagulants. Appropriate anticlotting medications are started immediately in all patients. Such drugs are sometimes used along with thrombolytics, and also as on-going maintenance to prevent a heart attack. All anti-clotting therapies carry the risk of bleeding, which can lead to dangerous situations, including stroke.
Anti-Platelet Drugs. These drugs inhibit blood platelets from sticking together, and therefore help to prevent clots. Platelets are very small disc-shaped blood cells that are important for blood-clotting.
Aspirin. Aspirin is an antiplatelet drug. An aspirin should be taken immediately after a heart attack begins. It can be either swallowed or chewed, but chewing provides more rapid benefit. If the patient has not taken an aspirin at home, it will be given at the hospital. It is then continued daily. Using aspirin for heart attack patients has been shown to reduce mortality. It is the most common anti-clotting drug, and most people with heart disease are advised to take it daily in low dose on an ongoing basis.
Clopidogrel (Plavix), a thienopyridine, is another type of anti-platelet drug. Clopidogrel is started either immediately or right after percutaneous intervention is performed for patients with heart attacks. It is also begun after thrombolytic therapy. Patients who receive a drug-eluting stent should take clopidogrel along with aspirin for at least 1 year to reduce the risk of clots. Patients admitted for unstable angina should receive clopidogrel if they are unable to take aspirin. Clopidogrel should also be given to patients with unstable angina for whom an invasive procedure is planned. Even for conservatively treated patients, Clopidogrel should be started and continued for up to 1 year. Some patients may need to take clopidogrel on an ongoing basis.
Glycoprotein IIb/IIIa Inhibitors. These powerful blood-thinning drugs include abciximab (ReoPro), eptifibatide (Integrilin), tirofiban (Aggrastat), and lamifiban. They are administered intravenously in the hospital and are used with angioplasty and stent placement. They are proving to be helpful for ACS patients with NSTEMI (non ST-segment elevation myocardial infarction), particularly when invasive procedure is planned or patients are still unstable after receiving aspirin and clopidogrel.
Anticoagulant Drugs. Anticoagulants thin blood. They include:
Heparin is usually begun during or at the end of treatment with thrombolytic drugs and continued for at least 2 days if not the whole time in the hospital.
Fondaparinux (Arixtra) is a newer blood thinner that may be used, but its exact role remains unclear.
Warfarin (Coumadin).
Direct thrombin inhibitors, such as argatroban (Novastan), danaparoid (Orgaran), lepirudin (Refludan), and bivalirudin (Angiomax). A clear benefit for these drugs over heparin has not been shown. They also carry an increased risk for bleeding.
All of these drugs pose a risk for bleeding.
BETA BLOCKERS
Beta blockers reduce the oxygen demand of the heart by slowing the heart rate and lowering pressure in the arteries. They are effective for reducing deaths from heart disease. Beta blockers are often given to patients early in their hospitalization, sometimes intravenously. Patients with heart failure or who are at risk of going into cardiogenic shock should not receive intravenous Beta blockers. Long-term oral beta blocker therapy for patients with symptomatic coronary artery disease, particularly after heart attacks, is recommended in most patients. [For more information, see In-Depth Report #03: Coronary artery disease.]
These drugs include propranolol (Inderal), carvedilol (Coreg), bisoprolol (Zebeta), acebutolol (Sectral), atenolol (Tenormin), labetalol (Normodyne, Trandate), metoprolol (Lopressor, Toprol-XL), and esmolol (Brevibloc).
Administration During a Heart Attack. The beta blocker metoprolol may be given through an IV within the first few hours of a heart attack to reduce the destruction of heart tissue.
Prevention After a Heart Attack. Beta blockers taken by mouth are also used on a long-term basis (as maintenance therapy) after a first heart attack to help prevent future heart attacks.
Side Effects. Beta blocker side effects include fatigue, lethargy, vivid dreams and nightmares, depression, memory loss, and dizziness. They can lower HDL (“good”) cholesterol. Beta blockers are categorized as non-selective or selective. Non-selective beta blockers, such as carvedilol and propranolol, can narrow bronchial airways. Patients with asthma, emphysema, or chronic bronchitis, should not take these beta blockers.
Patients should not abruptly stop taking these drugs. The sudden withdrawal of Beta blockers can rapidly increase heart rate and blood pressure. The doctor may want the patient to slowly decrease the dose before stopping completely.
STATINS AND OTHER CHOLESTEROL AND LIPID-LOWERING DRUGS
After being admitted to the hospital for acute coronary syndrome or a heart attack, patients should not be discharged without statins or other cholesterol medicine unless their LDL ("bad") cholesterol is below 100 mg/dL. Some doctors recommend that LDL should be below 70 mg/dL. [For more information, see In-Depth Report #23: Cholesterol.]
ANGIOTENSIN CONVERTING ENZYME INHIBITORS
Angiotensin converting enzyme (ACE) inhibitors are important drugs for treating patients who have had a heart attack, particularly for patients at risk for heart failure. ACE inhibitors should be given on the first day to all patients with a heart attack, unless there are medical reasons for not taking them. Patients admitted for unstable angina or acute coronary syndrome should receive ACE inhibitors if they have symptoms of heart failure or evidence of reduced left ventricular fraction echocardiogram. These drugs are also commonly used to treat high blood pressure (hypertension) and are recommended as first-line treatment for people with diabetes and kidney damage.
ACE inhibitors include captopril (Capoten), ramipril (Altace), enalapril (Vasotec), quinapril (Accupril), benazepril (Lotensin), perindopril (Aceon), and lisinopril (Prinivil, Zestril).
Side Effects. Side effects of ACE inhibitors are uncommon but may include an irritating cough, excessive drops in blood pressure, and allergic reactions.
CALCIUM CHANNEL BLOCKERS
Calcium channel blockers may provide relief in patients with unstable angina whose symptoms do not respond to nitrates and beta blockers, or for patients who are unable to take beta blockers.
Rehabilitation
PHYSICAL REHABILITATION
Physical rehabilitation is extremely important after a heart attack. Patients with recent episodes of acute coronary syndrome also generally need some sort of supervised exercise training. Rehabilitation may include:
Leg exercises may start as early as the first day. The patient usually sits in a chair on the second day, and begins to walk on the second or third day.
Most patients undergo low-level exercise tolerance tests early in their recovery.
After 8 - 12 weeks, many patients, even those with heart failure, benefit from supervised exercise programs. Health care providers should give the patient schedules for low-level aerobic home-activity. Strength (resistance) training is also important. Tai Chi, a Chinese martial art, appears to be very beneficial and safe for people after a heart attack. In general, the risk for serious heart events during rehabilitation is very low.
Patients generally return to work in about 1 - 2 months, although timing can vary depending on the severity of the condition.
Sexual activity after a heart attack has a very low risk and is believed to be safe, particularly in people who had exercised regularly before the attack. In any case, the feelings of intimacy and love that accompany healthy sex can help offset depression, a far greater risk for a future attack.
EMOTIONAL REHABILITATION
Major depression occurs in many patients who have ACS or who have had heart attacks. Studies suggest that depression is a major predictor for increased mortality in both women and men. (One reason may be that depressed patients are less likely to comply with their heart medications.)
Psychotherapeutic techniques, especially cognitive behavioral therapies, are very helpful. For some patients, certain types of antidepressant drugs may be appropriate.

An ECG is a helpful aid in the diagnosis of heart disease. It records the electrical activity of the heart, giving the physician a picture of how the heart is functioning

While the patient is awake and pain-free (local anesthesia), a catheter is inserted into an artery at the top of the leg (the femoral artery). The procedure begins with the doctor injecting some local anesthesia into the groin area and putting a needle into the femoral artery (the blood vessel that runs from the heart down the leg). Once the needle is inserted, a guide wire is placed through the needle, into the blood vessel. Following this step, the guide wire is left in the blood vessel and the needle is removed. A large needle called an introducer is then placed over the guide wire and the guide wire is removed.

Once the catheter is placed in the opening, or ostium, of one of the coronary arteries, the doctor injects dye and takes a series of x-rays of the artery. Areas of narrowing or blockage in the coronary artery can be seen on the x-rays.

References
Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE Jr, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-Elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction) developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine. J Am Coll Cardiol. 2007 Aug 14;50(7):e1-e157.
Antman EM. ST-Elevation myocardial infarcation: management. In: Libby P, Bonow RO, Mann DL, Zipes DP, eds. Libby: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Saunders; 2007:chap 51.
Antman EM, Bennett JS, Daugherty A, Furberg C, Roberts H, Taubert KA. Use of nonsteroidal antiinflammatory drugs: an update for clinicians: a scientific statement from the American Heart Association. Circulation. 2007 Mar 27;115(12):1634-42. Epub 2007 Feb 26.
Antman EM, Hand M, Armstrong PW, Bates ER, Green LA, Halasyamani LK, Hochman JS, et al. 2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: developed in collaboration With the Canadian Cardiovascular Society endorsed by the American Academy of Family Physicians: 2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee. Circulation. 2008 Jan 15;117(2):296-329. Epub 2007 Dec 10.
Cannon CP and Braunwald E. Unstable angina and non-ST elevation myocardial infarction. In: Libby P, Bonow RO, Mann DL, Zipes DP, eds. Libby: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Saunders; 2007:chap 53.
Eisenstein EL, Anstrom KJ, Kong DF, Shaw LK, Tuttle RH, Mark DB, et al. Clopidogrel use and long-term clinical outcomes after drug-eluting stent implantation. JAMA. 2007 Jan 10;297(2):159-68. Epub 2006 Dec 5.
Goodman SG, Menon V, Cannon CP, Steg G, Ohman EM, Harrington RA; et al. Acute ST-segment elevation myocardial infarction: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest. 2008 Jun;133(6 Suppl):708S-775S.
Hirsch A, Windhausen F, Tijssen JG, Verheugt FW, Cornel JH, de Winter RJ; Invasive versus Conservative Treatment in Unstable coronary Syndromes (ICTUS) investigators. Long-term outcome after an early invasive versus selective invasive treatment strategy in patients with non-ST-elevation acute coronary syndrome and elevated cardiac troponin T (the ICTUS trial): a follow-up study. Lancet. 2007 Mar 10;369(9564):827-35.
Hulten E, Jackson JL, Douglas K, George S, Villines TC. The effect of early, intensive statin therapy on acute coronary syndrome: a meta-analysis of randomized controlled trials. Arch Intern Med. 2006 Sep 25;166(17):1814-21.
Hochman JS, Lamas GA, Buller CE, Dzavik V, Reynolds HR, Abramsky SJ, et al. Coronary intervention for persistent occlusion after myocardial infarction.N Engl J Med. 2006 Dec 7;355(23):2395-407. Epub 2006 Nov 14.
Hochman JS, Sleeper LA, Webb JG, Dzavik V, Buller CE, Aylward P, et al. Early revascularization and long-term survival in cardiogenic shock complicating acute myocardial infarction. JAMA. 2006 Jun 7;295(21):2511-5.
King SB 3rd, Smith SC Jr, Hirshfeld JW Jr, Jacobs AK, Morrison DA, Williams DO;et al. 2007 Focused Update of the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: 2007 Writing Group to Review New Evidence and Update the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention, Writing on Behalf of the 2005 Writing Committee. Circulation. 2008 Jan 15;117(2):261-95. Epub 2007 Dec 13.
Krumholz HM, Anderson JL, Bachelder BL, Fesmire FM, Fihn SD, Foody JM, et al. ACC/AHA 2008 performance measures for adults with ST-elevation and non-ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Performance Measures (Writing Committee to develop performance measures for ST-elevation and non-ST-elevation myocardial infarction): developed in collaboration with the American Academy of Family Physicians and the American College of Emergency Physicians: endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation, Society for Cardiovascular Angiography and Interventions, and Society of Hospital Medicine. Circulation. 2008 Dec 9;118(24):2596-648. Epub 2008 Nov 10.
Lloyd-Jones DM, Liu K, Tian L, Greenland P. Narrative review: Assessment of C-reactive protein in risk prediction for cardiovascular disease. Ann Intern Med. 2006 Jul 4;145(1):35-42.
Spaulding C, Henry P, Teiger E, Beatt K, Bramucci E, Carrie D, et al. Sirolimus-eluting versus uncoated stents in acute myocardial infarction. N Engl J Med. 2006 Sep 14;355(11):1093-104.
Wang TJ, Gona P, Larson MG, Tofler GH, Levy D, Newton-Cheh C, et al. Multiple biomarkers for the prediction of first major cardiovascular events and death. N Engl J Med. 2006 Dec 21;355(25):2631-9.