Heart Attack (Myocardial Infarction)

A myocardial infarction or heart attack occurs when the sudden blockage of a coronary artery, usually because of blood clot, causes damage and death to heart muscle.

A myocardial infarction (myo=muscle + cardium=heart + infarction=death) or heart attack occurs when the sudden blockage of a coronary artery, usually because of blood clot, causes damage and death to heart muscle.

The heart is an electric pump with the purpose of sending oxygen-rich blood through the arteries of the body to every organ and cell to allow them to function.

The heart is a muscle and needs a constant supply of oxygen. There are three main arteries to the heart, the left anterior descending (LAD), the right anterior descending (RAD), and the circumflex. Together, they branch out into tinier and tinier arterioles and capillaries to provide oxygen to every muscle cell in the heart.

If the arteries narrow enough, some heart muscle cells may not receive enough blood supply and fail to pump blood as efficiently. Also, a heart muscle that lacks enough blood supply gets irritated and that can affect the electrical activity of the heart.

Symptoms of a heart attack or MI may include chest discomfort often described as a pain, pressure or tightness associated with shortness of breath, sweating and nausea. The goal for medical care is to restore blood supply back to the heart as soon as possible -- that time is measured in minutes. The longer the heart muscle cells fail to get oxygen delivered, the more likely permanent damage will occur. Dead heart muscle is eventually replaced by scar tissue, and the risk of both short- and long-term complications increase for sudden death and heart failure.

What is a ‘widowmaker’ heart attack?

All heart attacks are an emergency and can be life threatening. A widowmaker is a type of heart attack, which is deadlier than most others.

A widowmaker heart attack occurs when the left ascending artery that supplies blood to the left ventricle, the thickest and strongest part of the heart and responsible for pumping blood to the whole body, is completely blocked because of blood clot. There is no blood flow or oxygen delivery to a large part of the heart causing many muscle cells to die.

In addition to weakening the heart, the widowmaker can also make the heart muscle irritable, increasing the risk of abnormal electrical activity like ventricular fibrillation (VFib). VFib is the cause of sudden cardiac death. Normally the heart beats rhythmically, but in VFib, every cell of the ventricle generates its own electrical signal, not allowing a unified beating of the heart. Instead, the heart muscle fibrillates, or jiggles like a bowl of Jell-O, stopping the heart from beating and pumping blood to the body.

The immediate death rate in the hospital from a widowmaker heart attack is about 12% and longer mortality is 27%.

Atherosclerosis

Atherosclerosis is a gradual process where fats and cholesterol build up inside and on the walls of an artery. These are called plaques. Often known as hardening of the arteries, these plaques narrow the inner channel (lumen) of the artery decreasing the amount of blood flow that can get through.

Plaque can build up in any artery of the body. If the plaque involves leg arteries, the decreased blood supply to the leg muscles can cause claudication or pain the legs with activity. Plaque buildup in arteries of the neck or brain can lead to stroke. Plaque that builds up in the arteries of the heart lead to heart attack.

Atherosclerosis takes time to become clinically significant. An artery needs to be narrowed by 50 to 70 percent before symptoms develop. Therefore, this disease can remain silent (causing no symptoms or health problems) for years or decades. Atherosclerosis can begin as early as the teenage years, but symptoms or health problems usually do not arise until later in adulthood. The risk factors for developing atherosclerosis include cigarette smoking, high blood pressure, high cholesterol and triglycerides, diabetes mellitus, family history, and older age.

Atherosclerosis of the coronary arteries is known by many names, including atherosclerotic heart disease (ASHD), coronary artery disease (CAD), atherosclerotic cardiovascular disease (ASCVD), and coronary heart disease (CHD). Regardless of the name, narrowing of the coronary arteries may lead to angina, heart attack, heart failure, abnormal heart rhythms, and sudden cardiac death.

Atherosclerosis and angina pectoris

Angina pectoris, or angina, is the term used for chest pain that occurs when the blood and oxygen supply to the heart muscle cannot keep up with its needs to function. When a coronary artery is narrowed by more than 50 to 70 percent, arteries may not be able to increase the supply of blood to the heart muscle during exercise or other periods of high demand for oxygen. Just like legs that get tired and sore when you run too fast, not enough oxygen to the heart muscle causes pain or angina. This situation is called as myocardial ischemia (isch=holding back + emia=blood)

Angina pain in the chest can be described by the patient in many ways. It may be an intense pain or ache, pressure, heaviness, or squeezing across the chest. This pain may travel to the neck, jaw and teeth, to either shoulder and down the arm, or to the back. Symptoms that might be associated with the chest discomfort include shortness of breath, nausea, sweating, or lightheadedness.

Some patients experience the equivalent of angina, but without the pain. Instead they may complain only of shortness of breath or early fatigue. This is especially true in patients with diabetes, who may experience little or no discomfort or pain at all.

Angina can be classified in many ways depending upon what situations might bring on the chest pain.

Exertional angina is pain that occurs with activity or a stressful situation. It should resolve when the patient stops and rests or takes medication like nitroglycerin to treat the anginal attack.

Rest angina occurs when the patient is sedentary, not moving, or wakens the patient from sleep.

Stable angina describes the situation where the angina is predictably reproducible with a specific activity level, for example when the patient has onset of chest pain after walking quickly for a mile, and then resolves almost immediately with rest.

Unstable angina occurs at rest or while sleeping, when one would expect that the work the heart might be expected to do would be minimal.

Episodes are never normal and need to be reported to and evaluated by a health care provider.

Atherosclerosis and heart attack

When the surface of a cholesterol plaque in a coronary artery ruptures, a blood clot may form on its surface, completely damming the flow of blood in the artery beyond the clot. The lack of oxygen immediately causes the affected heart muscle tissue to suffer (myocardial ischemia), become irritable, and have difficulty contracting. If the situation is not reversed quickly, heart muscle will begin to die.

Some patients do not have previous symptoms that might warn them that a heart attack might occur. There may be no warning symptoms of chest pain, shortness of breath, or fatigue. If these symptoms do exist, they should not be ignored.

The pain of a heart attack can be experienced and described in many ways.

• Chest discomfort might be pain, fullness, tightness, or squeezing. They all should be considered the same, as potentially coming from the heart.
• Jaw ache or pain, toothache
• Shortness of breath
• Nausea, vomiting, upper abdomen discomfort
• Heartburn and/or indigestion
• Sweating
• Discomfort radiating to the shoulder and down the arm. Either arm can be affected, but more often it is the left
• Upper back pain
• General malaise (vague feeling of illness)
• Symptoms that don’t appear serious or severe and are ignored

Even though the symptoms of a heart attack at times can be vague and mild, it is important to remember that heart attacks producing no symptoms or only mild symptoms can be just as serious and life-threatening as heart attacks that cause severe chest pain. Too often patients attribute heart attack symptoms to "indigestion," "fatigue," or "stress," and consequently delay seeking prompt medical attention.

Chest pain should not be ignored. In people who do not have the diagnosis of coronary artery disease or angina, it may be very difficult to decide whether the chest tightness, shortness of breath, and nausea is due to a heart condition or some other cause.

Seek medical attention immediately or call 911 for help

It is very important to seek prompt medical attention in the presence of new symptoms that may suggest a heart attack. Early diagnosis and treatment saves lives, and delays in reaching medical assistance can be fatal. A delay in treatment may lead to a permanently weakened heart due to heart muscle damage.

Sudden cardiac death is always a concern for health care providers. Monitoring for heart rhythm abnormalities, like ventricular fibrillation, is one of the first steps in caring for a patient with chest pain. That monitoring begins with paramedics on scene and continues throughout the care provided.

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<strong>High blood pressure (hypertension)

High blood pressure is a risk factor for developing atherosclerosis and heart attack. Both high systolic pressure (the blood pressure as the heart contracts) and high diastolic pressure (the blood pressure as the heart relaxes) increase the risk of a heart attack.

Medications to treat high blood pressure and keep it controlled decreases the risk of heart attack and stroke.

Tobacco use (smoking)

Cigarette smoking is a major controllable risk factor in preventing heart disease. Men who smoke a pack of cigarettes per day have 3 times the chance of having a heart attack. That risk in women who smoke increases to 6 times the non-smoking population.

When a patient stops smoking, their risk drops 50% in the first year after quitting smoking and after two years, the risk returns to that of a nonsmoker.

Diabetes (diabetes mellitus)

Diabetes is a major risk factor for atherosclerosis and can affect all the arteries in the body. Diabetic patients, or those with elevated blood sugars or glycosylated hemoglobin (H1C), not treated with insulin or other medications are at higher risk for reduced blood flow to their heart (heart attack), legs (claudication), and brain (stroke).

Other complications of poorly-controlled diabetes include peripheral neuropathy, altering their ability to feel pain, and chronic kidney disease (which can be another risk factor for heart attack).

Patients with diabetes may lower their risk of heart attack by controlling blood sugar levels, getting regular exercise, weight control, diet, and if needed, medication including insulin.

Male sex

Men are more likely to suffer heart attacks than women. As people get older, the risk of heart attack becomes the same for men and women.

Family history of heart disease

Individuals with a family history of coronary heart disease have an increased risk of a heart attack. The risk is highest if there is a first degree relative (parent or sibling) who has a heart attack at an early age: male younger than 55, female younger than 65.

It is important to know your family medical history. Many times, those details get lost, forgotten, or were never shared.

Coronary heart disease and heart attack do not discriminate by sex. Women have the same risks of having heart disease as men, and the risk factors for developing CAD in women are the same as in men. They include the following:

• High blood cholesterol
• High blood pressure
• Smoking cigarettes
• Diabetes mellitus
• Family history of coronary heart disease

Sudden death

When a person dies in the first minutes or hours after having a heart attack, it is most likely due to ventricular fibrillation, a heart rhythm disturbance.

The heart is a two-stage electric pump. Normally, an electric signal is generated by specialized cells in the upper chamber of the heart (atrium) and then spreads along the electrical pathways to the ventricle to allow all the heart muscle cells to contract in sync, and pump blood to the body.

When a heart attack occurs, heart muscle cells that lose their blood supply can become irritable and beat chaotically instead of together with the other muscle cells. Instead of generating a heartbeat, the ventricle fibrillates and no oxygen is delivered to the body. This is sudden death.

The treatment for sudden death is the same regardless of whether the patient collapses at home or in the hospital.

Outside the hospital, bystander CPR, calling 911 for help, and the use of an automatic external defibrillator (AED), increases the chance of survival.

The AED delivers an electrical shock (defibrillation) to the patient in VFib that may return the heart to normal rhythm and restore a heartbeat. CPR helps maintain some circulation in the body while attempts are made to defibrillate the heart.

In hospital (and in ambulances), the heart attack patient may be on a monitor to continually check the heart rate and rhythm. If there are warning signs, medication can be used to try to stabilize the electrical activity of the heart and prevent VFib. If VFib does occur, CPR and defibrillation remain the first steps to restore a heartbeat.

Heart failure

Heart muscle that loses its blood supply and is damaged because of a heart attack, is replaced by scar tissue. Depending upon how much muscle is damaged, the heart may no longer be able to beat as strongly and efficiently as before. The heart may not be able to pump blood to all corners of the body and supply the oxygen that is needed for normal function.

Symptoms of heart failure include fatigue, shortness of breath, cough, and swelling in the feet and ankles.

The diagnosis of a heart attack begins with patient history (family history, symptoms) and a high index of suspicion that a heart attack is happening. There is urgency to start the treatment as soon as possible. This is a medical emergency because heart muscle begins to suffer and die almost immediately.

Whether in the emergency department or in the ambulance, the first steps are the same. Diagnosis and treatment happen at the same time when the suspicion is high for a heart attack.

Electrocardiogram (EKG, ECG)

The first step in the diagnosis of an heart attack is an electrocardiogram. The EKG maps the electrical activity of the heart by using patches or leads on the chest that can sense electricity. Each EKG usually has 12 leads that “look” at the heart’s electrical patterns from different directions.

Heart muscle that is losing its blood supply does not conduct electricity in the same way as normal heart muscle. These changes in the electrical pattern in the heart may be detected on the EKG, confirming the diagnosis. However, it may take many minutes for the changes to occur, so repeated EKG tracings may be done to see whether the EKG’s electrical pattern is evolving over time.

Sometimes the EKG can appear to be normal even when a heart attack and heart muscle damage is occurring.

Blood tests

Regardless of what the EKG may show, blood tests are performed if the diagnosis of heart attack is considered. Heart muscle cells that are stressed or injured leak chemicals into the bloodstream that can be measured.

Troponin is now the preferred blood test to evaluate whether the cause of a patient’s complaints is a heart attack. It is not normally found in the blood, and its presence may confirm the diagnosis. This is especially important if the EKG is normal. However, it may take time for the levels of troponin in the blood stream to rise to a level where they can be measured. Depending upon the hospital, its lab and the clinical situation, the troponin blood test may have to be repeated after a few hours.

If the patient’s history, physical exam, and EKG confirm the diagnosis of heart attack, time is of the essence to try to re-establish blood flow to the heart muscle, either by removing the blood clot in the artery, or by dissolving it with medication.

If the EKG does not confirm a heart attack, the diagnosis will depend on the troponin lab test and supportive care will begin to protect the heart from damage.

In some patients, a heart attack may occur even when coronary arteries are not occluded. In approximately 6 percent, the heart catheterization reveals normal heart arteries, yet blood tests confirm heart damage.

A heart attack is a medical emergency. The goal is to open the blocked coronary artery and return blood supply to the heart muscle and limit any potential damage or complication.

The first step that a patient, family member or bystander can do is to call 911 or seek medical care immediately.

Hospitals that are capable of percutaneous cardiac intervention (PCI), the ability of having a cardiologist perform a cardiac catheterization, identify the blocked artery, and then open it.

The PCI includes heart catheterization where dye is injected into the coronary arteries to find the blockage, potential removal of clot fragments, inserting a balloon to open the artery, and stenting where a small cage is placed across a narrowed portion of the artery to prevent it from narrowing again.

The goal is to perform that catheterization and open the blocked artery within 120 minute or two hours of the patient arriving to the hospital door. Most hospitals train to bring that target time to less than 60 minutes.

During that time from door to cath lab, much needs to be done. The diagnosis must be made (remember that conditions other than heart attack can cause chest pain), the patient needs to be prepared for the procedure, and the cath lab and the team need to get ready. As well, other supportive medical treatments will occur simultaneously.

If there is a delay for any reason, an alternative to heart catheterization is fibrinolytic therapy (fibrin=clot + lytic=dissolve). Intravenous medication (e.g., Alteplase, Tenecteplase) may be considered.

However, not all hospitals have the capabilities to perform heart catheterization. At those hospitals, the time frame expectations are no different, except that transport time to a PCI hospital must be considered when deciding to use a fibrinolytic.

Patients who have been treated with fibrinolytic therapy will still need a heart catheterization to deal with their heart issue.

While the patient is being prepared for the heart catheterization, other medications are used to protect the heart, including the following:

• Aspirin is used as an antiplatelet medication. Platelets help form blood clots and aspirin makes platelets less sticky.
• Nitroglycerin dilates blood vessels, and its goals is to increase blood flow to the heart muscle.
• Beta blockers (metoprolol) counter some of the effects of adrenalin in the body, slow the heart and make it beat more efficiently. This lessens the oxygen requirements for heart muscle cells.
• Other medications may be used before or during the heart catheterization to treat for clot prevention and heart function.
• The patient’s heart will be continually monitored, and should any heart rhythm disturbances be observed, medication will be used to control them and to prevent VFib.

Hormone therapy in women to decrease the risk of coronary artery disease is NOT recommended. The HERS studies did not show any benefit to estrogen treatment.

Women’s Health Initiative (WHI) trial results

Based upon the Women’s Health Initiative (WHI), the increased risk of coronary artery disease applies to older women who are more than 10 years past menopause.

While there is an increased risk of blood clots in the leg or to the lung, that risk is very small in otherwise healthy postmenopausal women. The risk increases if a clotting disorder, like factor V Leiden, is present.

The use of estrogen therapy for menopause symptoms may be reasonable with minimal risk, but patients should check with their health care provider. Those at risk for complications include patients with coronary artery disease, stroke, history of blood clots, liver disease, and breast cancer.

Every patient and every heart attack are different. Depending upon the initial health status of the patient, underlying medical conditions, and the size and severity of the heart attack, each patient will have a different journey in recovery.

Cardiac rehabilitation will help maximize outcome and the potential that each patient will reach. The goal is to return the patient to the same level of activity as before the heart attack. This may require significant changes in lifestyle to minimize risk of future heart damage.

The rehabilitation time is measured in months.