Each year in the United States approximately 1.1 million people experience a heart attack.  It is, in fact, the number one killer in all developed countries.  More surprising, however, is the fact that nearly a third of these victims never have any warning.  That means that there are no prior symptoms, and no recognition of the presence of heart disease.  (It seems that nearly everyone knows a person who has died suddenly, and for no apparent reason.) The cause of the heart attack, or sudden cardiac death (SCD), is generally attributable to one of two different mechanisms.  These are:
 

Arrhythmia:  Although it is a muscle, the heart is similar to a 4-cylinder automobile engine in that the firing sequence for each cylinder, or in this case, chamber, is precisely timed.  The firings, or contractions, are controlled by electrical impulses just like a real engine is.  An abnormal firing sequence, rhythm, or heartbeat is called an arrhythmia (also referred to as dysrhythmia). In most cases, the human body can tolerate an occasional arryhthmia, but there are exceptions.  A severe arrhythmia can be harmful, or even deadly.  In addition, the cause of the arrhythmia is often very difficult to determine.

The diagnosis of this condition is obtained by tracking the patient’s EKG (electrocardiogram, ECG, or heart monitor), which is a visual chart of these electrical impulses.  Because the heart may respond differently under physical stress, it is common to measure the EKG both at stress, and at rest.  The use of a treadmill, a reclining bicycle, or stress-inducing medications are common ways in which the stress is achieved.  This test is commonly referred to as a stress EKG.  In some cases, the resting EKG may need to be continually recorded for several days.

Treatment of arthythmias is done in several different ways, depending upon the extent of abnormality.  Medication may be adequate for some patients, while others may require the placement of a pacemaker.  (This is an electronic device that takes over control of the firing sequence of the heart.)  The pacemaker is typically inserted just under the skin of the chest.  A third treatment option is called ablation therapy and involves a minor physical alteration of the heart for the purpose of stopping the aberrant electrical signals that cause the arrhythmias.  A cardiac catheterization (see Testing for Heart Disease) is involved in that treatment process, where specific tissues of the heart are altered through the use of a laser (heat), an electrical impulse, or injection of small amounts of pure alcohol.

In days past it was believed that most SCD’s were caused by arrhythmias because it could be documented on the EKG’s of victims who had been monitored.  It is now more commonly accepted that most arrhythmias, which are demonstrated just prior to death, are the result of an occlusion, or closing, of a coronary (heart) artery.  (If blood flow to some of the heart muscle is inadequate, the affected tissue cannot continue the relay of electrical pulses: resulting in an arrhythmia.)  For this reason, it is now thought that arrhythmia is responsible for a relatively small percentage of the total number of heart attacks.

Coronary Occlusion:  The closure or blockage of a coronary artery, resulting in a lack of blood flow to the muscle of the heart (the myocardium), can kill the affected the tissues.  This occurrence is called a myocardial infarction. (infarction is defined as damage from being cut-off)  It is referred to in the medical community as an M.I.  If a large enough area of muscle is infarcted, the victim will die.  Conversely, if the patient is treated immediately and the blood flow can be restored, the damage may be minimal.  For this reason, most large hospital emergency rooms now administer a special clot-dissolver (streptokinase, or tissue plasminogen activator (TPA)) as soon as a heat attack is confirmed.  There are two primary mechanisms responsible for coronary occlusions:

Vasospasm:  The name itself, vasospasm, refers to a spasm of the vessel; in this case a coronary artery.  To understand this event it is important to recognize that the arteries are essentially “tubular muscles.”  As with most muscles, they can have a spasm.  (Think of this as a cramp, or Charlie Horse.)  If that occurs, and the muscle is unable to relax before the myocardium is damaged from lack of oxygen, the patient can die.  The cause of the vasospasm is not always known, however, cocaine use and thermal shock (cold) can result in this condition.   Vasospasm, like arrhythmia, is also responsible for a fairly small percentage of all SCD.

Blood Clot:  The culprit in most cardiac deaths, blood clots are typically facilitated by atherosclerosis.  (This word refers to a hardening of the vessel: in this case, the arteries.)  Like a silent accomplice, this process may spend years setting the victim up for the kill by slowly narrowing the coronary arteries with an accumulation of fatty deposits and other organic materials (plaque) along the internal vessel wall (endothelium).  In recent days, the mechanism for the formation of the clot itself has become much better understood.  The plaque can consist of both soft matter (fatty and fibrous), and hard matter (calcified).  There are three primary mechanisms by which atherosclerosis contributes to the building of a blood clot:

Stenosis:  This is the narrowing of the artery that increases the ease with which a clot can actually block the flow of blood.  Frequently, a chest pain while under exertion, called angina, is experienced by these patients long before a fatal event occurs.  Typically, the artery is more than 60% blocked by plaque before angina, or other symptoms are experienced.

Erosion:  This is the lifting-up, or breaking-off, of pieces of plaque, which leads to the formation of a clot.  These events often take place at the site of plaques that are well under 50% stenotic.

Rupture:  This occurs when an inflamed plaque releases the fluid inside.  Surprisingly, the latest estimates are that up to two thirds of all fatal heart attacks are due to a ruptured plaque.  Perhaps more importantly, about 80% of all heart attacks occur at sites that are less than 50% stenotic.

It has been demonstrated that a daily dose of common aspirin can reduce the risk of heart attack, and such a regimen is simple, and cost-effective.  The effectiveness of aspirin has been attributed to the fact that it makes platelets slippery.  Since platelets are a key building block for blood clots, this may in fact be the case.  Recently, however, this theory has been challenged.  Since aspirin is also excellent at reducing inflammation, the new thinking is that its greater effect may be in reducing the occurrence of the vulnerable “pimples”, or inflamed plaque, which can be so deadly.  In any event, aspirin therapy is helpful.  In fact, many authorities have gone so far as to recommend chewing (not swallowing) an aspirin in the event of chest pain. (While also seeking immediate medical attention.)