A Heart Attack (Myocardial Infarction, or MI) occurs when a coronary artery is completely obstructed and no blood flows past the obstruction. As a result, that part of the heart muscle dies. This obstruction is caused by a clot and occurs in an artery that previously had an atherosclerotic plaque.
According to the American Heart Association, more than one million heart attacks occur per year in the U.S.
Some people think that every episode of chest pain or angina is actually a heart attack. This is not correct; angina is reversible and does not cause death of the heart muscle cells. Some people think that when you have a heart attack your heart stops beating. Although heart attacks can lead to this, the proper term for when the heart stops beating is cardiac arrest.
Chest pain is obviously the most common symptom of an MI. The chest pain of an MI is similar to that of angina but is usually more severe and lasts longer. Typically, it is described as tightness, squeezing, pressure, aching or heaviness. The pain is located in the substernal (front and center) part of the chest and can radiate to the left arm, back, neck or jaw. Associated symptoms include shortness of breath, nausea, vomiting, profuse sweating and sometimes a feeling of impending doom.
To confirm the diagnosis of an MI, an EKG and blood tests are performed.
During an MI, the EKG goes through a series of abnormalities. The initial abnormality is called a hyperacute T wave. This is a T wave that is taller and more pointed than the normal T wave. The abnormality lasts for a very short time, and then elevation of the ST segment occurs. This is the hallmark abnormality of an acute MI. It occurs when the heart muscle is being injured by a lack of blood flow and oxygen and is also called a current of injury. This is followed by T wave inversions. Over time, when the heart muscle cells actually die, these abnormalities are replaced with Q waves. However, not everyone with an MI has an abnormal EKG. In fact the initial EKG may not show ST elevation in up to 40% of patients having an MI. When a Q wave develops after an MI, it is called a Q-wave MI and usually corresponds to a transmural MI (entire thickness of the heart muscle wall has died). When a Q wave does not develop after an MI, it is called a non-Q-wave MI and usually corresponds to non transmural heart muscle death or a subendocardial MI(heart muscle just under the inner lining of the heart has died). An EKG can not only tell a physician if an MI is present but can also show the approximate location of the heart attack and often which artery is involved. When the EKG abnormalities mentioned above occur in certain of the 12 EKG leads, then the MI can be localized to a certain region of the heart. For example, see the table below:
|EKG leads||Location of MI||Coronary Artery|
|II, III, aVF||Inferior MI||Right Coronary Artery|
|V1-V4||Anterior or Anteroseptal MI||Left Anterior Descending Artery|
|V5-V6, I,aVL||Lateral MI||Left Circumflex Artery|
|ST depression in V1, V2||Posterior MI||Left Circumflex Artery or Right Coronary Artery|
Note: there are many anatomic variations that may alter the exact artery involved in any particular person.
- Lab tests
Certain blood tests read as "abnormal" after an MI has occurred because when heart muscle cells die, the chemicals in these cells are released into the blood. This does not occur instantly and usually takes several hours and it is why your doctor cannot always tell you if you are having an MI on the spot. Because results can take some time to develop, you may need to be admitted to the hospital to have a series of EKGs and blood tests to catch the abnormalities when they happen in order to determine if an MI has occurred.
These chemicals are called markers of MI and include CPK, CPK-MB, Troponin, and Myoglobin. Some of these markers occur in other cells and can limit their usefulness in diagnosing an MI.
|Lab Test||Begins to rise||Peak||Duration||Found in|
|CPK||4-8 hours||48-72 hours||Heart, Brain, Skeletal Muscle|
|CPK-MB||3-4 hours||12-24 hours||48 hours||Heart|
|Myoglobin||1-2 hours||4-6 hours||24 hours||Heart, Skeletal Muscle|
|Troponin||3-6 hours||12-24 hours||1 week||Heart|
Treatment of MI
Initially a patient is placed on a cardiac monitor because of the risk of cardiac arrhythmias which can occur during an MI. Ventricular fibrillation is one such arrhythmia and is a frequent cause of death in patients with MI who do not survive to reach the hospital. Approximately 250,000 people die per year of a heart attack before reaching a hospital. Ventricular fibrillation causes death in a few minutes if untreated. Patient's are also placed on oxygen and intravenous lines are started. The chest pain of a heart attack is treated with Nitroglycerin (either sublingually or intravenously). Morphine is given if nitroglycerin is unable to relieve the pain. An aspirin should be given at this time as well. Beta-blockers and ACE inhibitors are given after MI's because they both are known to reduce mortality after an MI.
Streptokinase, TPA (Tissue Plasminogen Activator), and Reteplase are thrombolytic medications that dissolve blood clots in the coronary artery that causes the MI. These medications clearly decrease death from heart attacks. It is crucial that this medication be given quickly, as soon as an MI is diagnosed. If this medication is delayed, the cell death is permanent and cannot be reversed even if blood flow is restored by dissolving the clot. There is a common saying in medicine that "time is muscle" which means that the longer the heart muscle is without blood flow before thrombolytic medications can dissolve the clot, the more heart muscle dies. There is much controversy about which medication is the most effective. There are several contraindications to the use of these medications:
- active internal bleeding
- history of a stroke
- cancer or aneurysm of the brain
- recent brain or spinal surgery
- known bleeding disorder
- severe hypertension.
These medications have complications. Bleeding is the most common complication and usually occurs at I.V. sites. If the bleeding happens in the brain, it can cause a stroke and possibly death.
Another treatment for MI is angioplasty. The obstruction is mechanically opened with a balloon during cardiac catheterization. Many cardiologists believe that this therapy has advantages over thrombolytics. However, an angioplasty must be performed within 60 minutes of the MI in a center that does a high volume of these procedures, to be most effective. Less than 20% of U.S. hospital have this capability.
Obviously, there are many complications of heart attacks. Some of the more common ones are:
- Arrhythmias - variation from the normal heartbeat
- premature ventricular beats
- ventricular tachycardia
- ventricular fibrillation
- Accelerated idioventicular rhythm
- AV node block
- supraventricular tachycardia
- Heart failure - The inability of the heart to pump out enough blood to meet the needs of the body. If 20-25% of the left ventricle becomes damaged from an MI, heart failure will result. Death usually results if over 40% of the heart is infarcted.
- Cardiac rupture - The heart bursts open, rupture of papillary muscle (attaches to Mitral valve) or rupture of the Ventricular Septum (wall between right and left Ventricle)
- Aneurysm of the left ventricle
- Blood clots
- Repeat MI
Following a Miocardial Infarction (MI), several days of rest in the hospital are advised. A cardiac rehabilitation program should be a part of the recovery from an MI and includes an exercise program and education about heart disease and risk factors. A stress test is often performed at some point after an MI to assess the degree of ischemia and tolerance for exercise. If repeated episodes of chest pain and ischemia occur, you may need a cardiac catheterization to determine if an angioplasty or a coronary artery bypass graft is necessary.
Some medications that are given to post-MI patients include aspirin, beta-blockers, and ACE inhibitors.
After reading this article, one thing that you are probably thinking is this: "I don't want atherosclerosis!" One of the best parts about this disease is that there are things you can do to lower your risk factors. These include:
- quitting smoking
- reducing cholesterol levels
- reducing blood pressure
- losing weight
Hopefully this article has provided some insight into how the most common diseases of the heart work. Perhaps this can be an impetus to control the risk factors that can lead to heart disease. If you do develop CAD, then having a background knowledge will help immeasurably in your treatment.
For more information on heart disease and related topics, check out the links on the next page.
- Heart Health Quiz
- How Your Heart Works
- 10 Types of Heart Drugs
- 5 Facts About Women's Heart Health
- Top 10 Ways to Avoid a Heart Attack
- How Congestive Heart Failure Works
- How Diagnosing Heart Disease Works
- Why is aspirin good for your heart?
- What is open heart surgery and a bypass operation?
More Great Links
- American Heart Association
- The Heart: An Online Exploration
- National Heart, Lung, and Blood Institute (NHLBI)
About the Author
Dr. Carl Bianco, M.D. is an Emergency Physician practicing at Dorchester General Hospital in Cambridge, MD, located on the Eastern Shore of Maryland. Dr. Bianco attended Medical school at Georgetown University School of Medicine and he received his undergraduate degree from Georgetown University majoring in nursing and pre-med. He Completed an internship and residency in Emergency Medicine at Akron City Hospital in Akron, Ohio.