Myocardial Infarction (heart attacks)

A heart attack is an event that results in permanent heart damage or death. It is also known as a myocardial infarction, because part of the heart muscle (myocardium) may literally die (infarct). A heart attack occurs when one of the coronary arteries becomes severely or totally blocked, usually by a blood clot. When the heart muscle does not receive the oxygen-rich blood that it needs, it will begin to die. The severity of a heart attack usually depends on how much of the heart muscle is injured or dies during the heart attack.

Someone’s chance of surviving a heart attack depends on the treatment that is given within the first hour of the heart attack. Immediate treatment for a heart attack should always include professional emergency medical intervention, including a call to 9-1-1 if the patient lives in an area with such access. While waiting for help to arrive or on the way to the hospital, patients are often told to begin chewing aspirin, which has been shown to inhibit blood clots.

After a heart attack, people will need from two weeks to more than six weeks of recovery time, depending the severity of the attack. Cardiac rehabilitation programs are strongly recommended to help people get back on their feet quickly and safely.

The American Heart Association estimates that in 2006, about 700,000 Americans will suffer a new heart attack and about 500,000 will have a recurrent attack. Additionally, another 175,000 silent first heart attacks will occur. The average age for a first heart attack is 65.8 years for men and 70.4 years for women.

About heart attacks

A heart attack occurs when the supply of oxygen-rich blood to the heart is disrupted, usually by a blood clot in one of the coronary arteries that supply the heart with blood. The heart is composed of a special kind of muscle that never rests and therefore has high oxygen requirements. When the heart muscle is deprived of oxygen for even a brief period of time, the myocardial tissue begins to die (infarct). Medically, heart attacks are known as myocardial infarctions.

Coronary artery disease is the leading cause of heart attacks in the United States , accounting for more than half of all cardiovascular events in men and women under the age of 75. Atherosclerosis is the leading cause of coronary artery disease. Sometimes called "hardening of the arteries," atherosclerosis is characterized by fatty plaque deposits that gradually block arteries, causing them to lose their suppleness. A blood clot can form after such a plaque deposit ruptures.

Heart attacks can occur both with and without warning signals. Many people experience episodes of cardiac ischemia before a heart attack. Ischemia describes a lack of oxygen-rich blood. Ischemia may have no symptoms (silent ischemia) or it may be accompanied by a type of chest pain known as angina. In many cases, angina occurs at predictable times, usually during periods of activity when the heart's oxygen requirements are increased, such as after exercise. If the angina occurs at irregular or unpredictable times, and is not associated with exertion, it is known as unstable angina. This is a dangerous warning sign that a heart attack may be imminent.

Depending upon the severity of the attack and of the subsequent scarring, as well as how rapidly the person gets access to medical service, a heart attack can lead to:

  • Full recovery, occurring in the majority of patients
  • Heart failure , a chronic condition in which at least one chamber of the heart is not pumping well enough to meet the body’s demands
  • Electrical instability of the heart, which can cause a potentially dangerous abnormal heart rhythm (arrhythmia)
  • Cardiac arrest , in which the heart stops beating altogether, resulting in sudden cardiac death in the absence of immediate medical attention
  • Cardiogenic shock , a condition in which damaged heart muscle cannot pump normally and enters a shock-like state that is often fatal
  • Death

The location of the damage in the heart muscle is also important. Because different coronary arteries supply different areas of the heart, the severity of the damage depends upon which artery was blocked, how much it was blocked and how much of the heart muscle depended on that blocked artery.

A heart attack is not the same thing as cardiac arrest, even though many people use the terms interchangeably. Cardiac arrest occurs when the heart actually stops beating and pumping blood. It is usually caused by an abnormal heart rhythm that causes the heart's main pumping chambers (e.g., ventricles) to quiver and contract irregularly (ventricular fibrillation). The term “massive heart attack” is also mistakenly used to describe cardiac arrest, but they are not the same thing. A heart attack may lead to cardiac arrest, but these are separate events.

Atherosclerosis and heart attack

Atherosclerosis is the single most deadly disease in the United States . At one time, researchers used to think of arteries as roughly analogous to plumbing pipes. In recent years, however, our understanding of arteries, and arterial disease, has been greatly enhanced. In fact, arteries are muscular organs that contract along with the heart to enhance blood flow and help maintain blood pressure.

Arteries are highly sensitive to a number of chemicals and hormones that help regulate their function. These chemicals act upon, and are sometimes excreted by, the inner lining of the artery, or the endothelium. Researchers have learned that long before atherosclerosis becomes clinically apparent, this thin layer of cells has already been damaged and the earliest plaque deposits have already formed. Indeed, atherosclerosis often begins in early childhood, and it rarely is limited to the coronary arteries. In most cases, if a person has atherosclerotic plaque deposits in their coronary arteries, other arteries are also affected.

The underlying defect, or cause, of atherosclerosis often remains unknown. However, researches have made great strides forward in understanding the process by which damage to the endothelial cells early in life can later evolve into a heart attack as an adult. It is now thought that the atherosclerotic process is mediated by immune-related inflammation. LDL cholesterol molecules also play an important role.

According to this theory, arteries are damaged, which provokes a local immune response at the site of the injury. White blood cells gather at the site of the injury and begin to secrete chemical messengers that cause inflammation. This is a normal immune system reaction that occurs in an inappropriate place. At the same time, the protective endothelial layer has been compromised, allowing LDL "bad" cholesterol cells to migrate into the inner layer of the artery. This further aggravates the injury, which causes more white blood cells to gather. Other fatty materials in the bloodstream (e.g., triglycerides) also begin to gather at the injury. Together, these materials combine to form a lipid foam. This foam forms fatty streaks.

Over time, these fatty streaks grow larger, eventually attracting circulating blood platelets and evolving into plaque deposits on the inside of the artery wall. Not all plaque deposits pose the same threat. Some plaque deposits develop a relatively hard "shell" of minerals in a process called calcification. These types of plaque are considered to be stable plaques. They are less likely to rupture and cause a heart attack. Other types of plaque are known as unstable plaques, which (in comparison to stable plaques) have the following:

  • A larger fatty core
  • More white blood cells encased within
  • A thinner, softer, more unpredictable coating that might be stripped off without warning

The exact trigger of a plaque rupture is unknown. However, it can occur as a result of a strong, fast blood flow, especially during heavy exertion or emotional stress, when the coating is thin and the core of fat/white blood cells is particularly full.

During a plaque rupture, the fatty core of the plaque deposit is exposed to circulating blood, while pieces of the plaque shower downstream into the artery. At this point, several different things might happen. The site of the plaque rupture might attract platelets, which start a clotting cascade and form a blood clot (thrombosis). This blood clot may grow big enough to obstruct blood flow. Alternatively, it may break off and travel down the artery until it becomes lodged in a smaller artery. Finally, the pieces of the plaque may themselves become trapped in an artery, blocking blood flow. Any of these scenarios results in a heart attack. The severity of the attack will depend on which coronary artery is blocked, how dependent the heart muscle was on that source of blood supply and how severe the blockage is.

Researchers have found that almost 80 percent of first-time heart attack patients had ruptured plaque located both where the heart attack occurred and at other, distant sites. Researchers concluded that a heart attack is often not the result of one, discrete area of plaque damage. It may be separate areas of plaque rupture that combine to make the heart less stable and therefore vulnerable to a heart attack, a concept known as (pancoronaritis).

Heart attacks may also be caused by a coronary artery spasm, a temporary constriction of an artery in the heart.

Researchers are still looking for the underlying cause of atherosclerosis. In all likelihood, atherosclerosis is a multifactorial disease, meaning that several factors come together to launch and sustain the disease. The most important among these is probably genetics. Although an "atherosclerosis gene" has not been identified, the disease is known to run in families and there is clearly a strong genetic component. Researchers have found that patients whose parents have had a heart attack before age 60 have a higher risk for developing coronary artery disease at a young age. Patients (average age 19) whose parents had early heart attacks can have thicker artery walls and worse artery function than is normal for their age.

Beyond genetics, a number of other factors may serve to either promote atherosclerosis or interrupt the disease process. These factors are known as risk factors if they promote the disease. Risk factors can be either controllable (e.g., diet, exercise and smoking) or uncontrollable (e.g., age, gender). So far, researchers have found that:

  • Patients with unstable plaque deposits are at greater risk for a heart attack than those with compact, calcified plaque deposits. Some researchers have tried to develop methods to determine the degree of calcification, which may help predict the risk of heart attack.
  • The risk of plaque rupture appears to increase in the morning hours, which may explain why more heart attacks occur between 6 a.m. and noon .
  • People with chronic kidney disease tend to have high blood pressure, which places added stress on waste-removing filters in the kidney (nephrons). Uncontrolled high blood pressure also contributes to heart disease through a process known as remodeling, where there is enlargement and weakening of the heart’s left ventricle (left ventricular hypertrophy) and increased risk of heart attack. Research has found that heart attack survival decreases even with mild to moderate kidney disease.
  • People with metabolic syndrome have been found to have double the risk for heart attack and stroke when compared to people without the syndrome. The characteristics of metabolic syndrome are elevated fasting blood glucose levels, abdominal obesity, high LDL (“bad”) cholesterol levels, high triglyceride levels and high blood pressure.
  • Researchers have found a connection between infection and increased risk of heart attack. Infectious diseases, such as influenza, destabilize plaque and increase risk of plaque rupture. In some studies, influenza vaccines have been shown to reduce the risk of plaque rupture among the elderly, thus reducing the risk of heart attack and stroke.

Totally vs. partially blocked arteries

It is interesting to note that a totally blocked artery is generally considered less of a threat in terms of a future heart attack than a partially or almost totally blocked artery. This is because there is no potential for further damage with the totally blocked vessel. The areas of the heart formerly supplied by that vessel are permanently scarred or “dead,” with no need for an oxygen-rich blood supply. Surgical bypass of a totally blocked artery that supplies a “dead” area of the heart may serve little or no purpose. Instead, the goal of the physician and the patient is to prevent further damage in those areas in which good or partial function still exists.

Signs and symptoms of heart attacks

Just as some people experience no symptoms during silent ischemia, some people can have a silent heart attack without knowing it. Up to 25 percent of heart attacks are symptom-free. Of course, the absence of symptoms does not mean the absence of damage to the heart muscle. Unfortunately, people having a silent heart attack are unaware that they need to seek proper treatment immediately, and additional heart-related events or damage may occur.

However, the majority of people who suffer a heart attack experience symptoms that are often severe and frightening. Recognizing these symptoms and realizing their importance is crucial. The vast majority (90 percent or more) of heart attack-related deaths in younger patients (below age 55) occur outside of the hospital, and medical experts believe this is often due to their not understanding the situation. Younger people tend to ignore symptoms, whereas an older person may be more willing to call 9-1-1 at the first sign of trouble. Whatever the case, the sooner the symptoms of a heart attack are recognized and appropriate treatment is administered, the better the outlook for survival – both in the near future and over the long term. Symptoms of a heart attack may include:

  • Chest pain that is unrelieved by rest and often spreads or radiates through the upper body to the arms, neck, shoulders or jaw
  • Chest-area pressure, discomfort or squeezing sensation that may be either constant or intermittent
  • Shortness of breath or shallow breathing
  • Heart palpitations, in which the heartbeat is fast, strong or obviously irregular
  • Abnormally weak and/or fast pulse
  • Fainting (syncope) or loss of consciousness
  • Feeling tired or fatigued
  • Sweating, often heavy and often cold
  • Nausea or upset stomach
  • Gray facial color

Women tend to have different heart attack symptoms than men. Although they may experience shortness of breath, weakness, unusual fatigue and cold sweats, they may not experience chest pain. They may instead feel pain high in the abdomen or chest, or in the back, neck or jaw. They may also experience dizziness. Women have also reported symptoms of unusual fatigue, sleep disturbances, shortness of breath, indigestion and anxiety in the weeks leading up to their heart attack. For more information, see Heart Attacks & Women.

Although one or a combination of these symptoms may indicate the onset of a heart attack, they may be due to other conditions as well. As a general rule, it is better to be safe than sorry (see When to Call a Doctor). If a heart attack is suspected and any of these symptoms are present, this may indeed be a sign of a serious lack of oxygen–rich blood supply to the heart. Emergency medical help should be sought immediately. Physicians usually advise stricken individuals to first call 000, then to chew an aspirin (“regular” aspirin) and wash it down with a glass of water while waiting for help to arrive.

Diagnosis methods for heart attacks

When a patient has symptoms of a heart attack, the physician will promptly evaluate the patient’s medical history and run tests such as:

  • Electrocardiogram (ECG). A recording of the heart’s electrical activity as a graph, or series of wave lines, on a moving strip of paper or video monitor. The highly sensitive electrocardiograph machine helps detect heart irregularities, disease and damage by measuring the heart’s rhythms and electrical impulses.
  • Blood tests . These can be used to detect the presence of certain markers that are released following a heart attack. These include troponin, creatine phosphokinase (CK) and creatine kinase MB.

Once the patient is stabilized, the final diagnosis of whether the patient actually had a heart attack can take several days. Tests that may be run during this time include:

  • Radionuclide imaging . A branch of nuclear medicine that introduces small, harmless amounts of radioactive materials (“tracers”) into the body. A special gamma camera is then used to scan the radioactive tracers and create visual images of the heart.

Echocardiogram of the heart. This test uses sound waves to track the structure and function of the heart. A moving image of the patient’s beating heart is played on a video monitor, allowing the physician to study the heart’s thickness, size and function. The image also shows the motion pattern and structure of the four heart valves. During this test, a Doppler ultrasound may also be done to evaluate blood flow within the heart, revealing any potential leakage (regurgitation) or narrowing (stenosis) of the heart valves. Treatment options for heart attacks

A heart attack is not a one-time, one-moment occurrence. It is a process that occurs over a period of a few hours. With each minute that goes by, less oxygen reaches the surrounding heart muscle and the risk of permanent damage rises. Therefore, someone’s chance of surviving a heart attack depends on the treatment that is given within the first hour of the heart attack. The vast majority (about 90 percent) of heart attack patients who reach the hospital alive survive the event.

Immediate treatment for a heart attack should always include professional emergency medical intervention, including a call to 9-1-1 if possible. If the person goes into cardiac arrest, immediate death may be avoided if someone on the scene can administer CPR (cardiopulmonary resuscitation) within the first five minutes following the attack. CPR does not restart a heart in cardiac arrest, but it can keep a victim alive until help arrives. Of course, CPR is NOT a substitute for emergency paramedic or hospital treatment.

People who believe they are experiencing a heart attack are urged to let an ambulance or friend/family member take them to the hospital, rather than driving themselves. While waiting for help to arrive or on the way to the hospital, patients are often told to begin chewing aspirin, which inhibits blood clots and has been shown to reduce the risk of death and the degree of damage associated with a heart attack.

Information has circulated around the Internet about the use of repeated coughing during a heart attack. With some life-threatening arrhythmias, which could be caused by a heart attack, frequent, recurrent and vigorous coughing may help to maintain the circulation of the blood and stabilize the heartbeat. Therefore, it may be a useful aid during a heart attack if a patient begins to feel faint and may pass out. However, this would not be helpful in the absence of a life-threatening arrhythmia and should not be routinely used.

Upon arrival at a hospital or other emergency care facility, someone experiencing a heart attack may be given medications to prevent further blood clots and to take the strain off the heart. These medications include beta blockers, calcium channel blockers, anticoagulants and nitrates. The patient may also be given medications known as clot busters, the only medications able to dissolve an existing blood clot. Clot busters have been hailed by patients and physicians as somewhat of a miracle drug when given in time and in the right amounts. All clot busters must only be given to carefully selected patients following very specific guidelines.

Treatment for a heart attack may also include one or more procedures to open any blocked coronary arteries, including:

  • Balloon angioplasty . A catheter-based procedure in which a balloon-tipped catheter is inserted into coronary artery and rapidly inflated in order to press plaque back against the vessel wall.
  • Stenting . A procedure in which a wire-mesh tube is inserted through a catheter and permanently implanted in an artery to hold it open. Stenting is usually performed right after a balloon angioplasty, while the catheter is still in place.
  • Coronary artery bypass graft (CABG). A surgery that increases blood flow to the heart by re-routing the blood flow around the blocked portion of an artery with a bypass graft. A section of a blood vessel from another part of the body (e.g., the leg or chest) is relocated and grafted above and below the damaged portion of the coronary artery to form an open channel around the blockage. Traditional bypass surgery requires the use of a heart-lung machine. However, alternative strategies are becoming more widely available

Physicians determine the type of treatment needed based on the patient’s current condition and the underlying cause of his or her heart attack.

After a heart attack, patients are typically hospitalized for a few days following the attack. During this time, they are closely monitored for any abnormalities in heartbeat or other functions, as well as for signs of other heart-related trauma (e.g., chest pain or shortness of breath). Additional blood tests are taken to confirm the diagnosis and monitor the patient's progress. Patients will most likely be educated about the need for lifestyle modifications, including the need for a heart-healthy diet, exercise and stress management. These have been shown to lower the risk of additional damage to the heart.

After a few days in the hospital, most patients are sent home if there are no serious after-effects. Specific recovery times vary from patient to patient, but a general guideline is offered for patients whose heart attacks are classified as mild, moderate or severe, based on the amount of damage that was done. This guideline is as follows:

Severity of Heart Attack

Amount of Time before Returning to Work or Engaging in Strenuous Activity (including having sex)

Mild

2 weeks

Moderate

Up to 4 weeks

Severe

6 weeks or longer


Other after-effects of a heart attack may be emotional in nature. Fear of a future attack, fear of physical activity (including having sex), and even mild or moderate depression are all normal and common feelings following the trauma of a heart attack. Patients are encouraged to discuss their concerns with their physician, and to also discuss their sex-related fears with their spouse/partner. Appropriate treatment and suggestions vary from patient to patient. One excellent strategy for feeling more comfortable with physical activity is to join a cardiac rehabilitation program. It is important to remember that feelings of anger, depression, resentment and fear are not uncommon. Sharing these concerns with a physician or other trained health professional (e.g., a therapist) can be a very important step on the road to recovery from a heart attack.

There are a number of medications that a physician may prescribe for someone who has had a heart attack. These medications include:

  • Antiplatelets (e.g., aspirin and clopidogrel). Drugs that help prevent the formation of blood clots. They are almost always prescribed, unless the patient has a history of gastrointestinal bleeding, peptic ulcer disease or allergy to that drug. Oftentimes, aspirin and clopidogrel will be prescribed for up to 12 months, after which time, aspirin will be continued as a monotherapy, possibly for life.
  • Beta blockers . Drugs that reduce pulse rate, lower blood pressure and allow the heart to pump less vigorously while still meeting the body’s needs. Research suggests that they can help maintain a normal heart rhythm and reduce the risk of further cardiac events or sudden cardiac death. Once prescribed, the drugs are taken for life. They might not be prescribed for patients who have a history of asthma, insulin-dependent diabetes, severe peripheral vascular disease or a very slow heart rate (bradycardia). There has been concern that prolonged use of beta blockers may impair sexual function and bring on symptoms of depression. However, studies have found no greater incidence of sexual dysfunction and depression in people taking beta blockers when compared to people given an inactive pill, or placebo.
  • ACE inhibitors . Drugs that reduce vascular resistance of the arteries and relieve some of the strain on the heart, allowing the heart to pump more efficiently. Because they help the left ventricle to pump out oxygen-rich blood, they are often prescribed if the left ventricle was damaged during the heart attack and is no longer functioning normally. The drugs will continue to be taken for life.
  • Cholesterol-reducing drugs. Drugs that are prescribed if the heart attack survivor has high levels of lipids (e.g., cholesterol and triglycerides) to reduce the risk of another heart attack or other cardiovascular event. These drugs may be prescribed for life, or until there is evidence that the patient can maintain lower lipid levels with diet and exercise alone. Statins, for example, have shown benefit when given to heart attack patients before being released from the hospital, lowering the risk of mortality in the year following the attack.

All four of these types of drugs can safely be taken together, even over the long term. However, the use of multiple medications after a heart attack may not provide additional benefits