HEART ATTACKS: RISKS, TREATMENT, AND PREVENTION

Myocardial infarctions or “heart attacks” are the leading cause of death in our society. In America, someone will suffer a coronary event every 26 seconds and someone will die about every minute. It is estimated that there are 900,000 heart attacks annually with almost a third of patients dying before reaching the hospital. The average age of a person suffering a heart attack is nearly 66 years old for a man and 70 years old for a woman. The prevalence is expected to increase as our population ages. In addition, those individuals who suffer a heart attack will need lifelong care and often require major adjustments to their lifestyle, work habits, and productivity.

The traditional risk factors for heart attacks include smoking, diabetes, hypertension, abnormal lipids (high LDL, low HDL, high triglycerides), male sex, and family history. There are also a number of new, potential risk factors being studied. C-reactive protein (hs CRP) is a marker of inflammation, which is quite specific for the heart. It may be particularly helpful in deciding treatment for individuals with traditionally “normal” lipid profiles. Other sub particles of cholesterol like Lp (a) and HDL fractions may also be useful in assessing risk. In addition, recent studies show that aggressive lowering of blood pressure may dramatically lower risk for heart attacks.

The heart’s main function is to pump oxygen, glucose (sugar), and other nutrients to the tissues so they have fuel to work. On average, the heart beats in excess of 100,000 times daily, rarely “missing a beat”. The blood supply to the heart is by way of 3 coronary arteries. The Latin word “corona” means crown. Thus, these arteries crown the heart. On average, the main arteries are 3-3.5mm in diameter in women and 3.5-4.5mm in men. The largest are therefore rarely greater than 1/6th of an inch in diameter. The heart pumps blood out of its main chamber, the left ventricle, into the aorta which in turn carries blood to the rest of the body. Immediately upon leaving the heart, blood flows into its own coronary arteries. Two of these arteries arise from the left side (left main) and one from the right side (right coronary artery). The blood flows down the arteries into numerous smaller branches that supply the heart muscle.

Arteries are complex pipes that have an inner lining called endothelium. This inner lining acts as a nonstick “Teflon” coating which allows blood to flow unimpeded. Through a complex process called atherosclerosis, damage can result to this endothelium. As a consequence of the risk factors above, LDL cholesterol becomes oxidized and dense, acting as a wrecking ball to the endothelium. Once the nonstick coating is damaged, other cells move in and an inflammatory process ensues.

Over time, this process results in some narrowing of the blood vessel. However, a more worrisome result is the formation of an unstable plaque that in many ways resembles a “boil” or abscess invading the endothelial lining. The irregular edges of this plaque stick out in the blood stream acting as a site for blood clots to form. The body is always in a constant seesaw battle to keep bleeding and clotting in check. But, the scales are tipped when this unstable plaque ruptures, overwhelming the artery with cholesterol and debris. The ruptured plaque and blood clot obstruct flow through the artery.

Heart attacks occur when blood supply to the heart is abruptly interrupted. When the heart muscle (myocardium) is deprived of oxygen for more than 30 minutes, death (infarction) of the heart muscle begins. Complete death of the sup¬plied heart muscle will occur in just 6-12 hours. The sooner blood supply is restored, the better. As time passes, there is greater likelihood of permanent and lasting damage to the heart and other complications.

Warning signs usually develop when a heart attack is imminent. The classic symptoms include chest pain that feels like pressure deep within the chest cavity as well as shortness of breath, discomfort in the left arm and jaw, sweating, and poor skin color. These symptoms often occur in the weeks prior to a heart attack in varying degrees as the blockage and blood clot act as a “ball-valve” causing intermittent obstruction. Symptoms occur with activity and stress, but resolve with rest. Once the artery stays completely closed, the pain and discomfort may become relentless. Unfortunately, as many as a third to one-half of patients may have no symptoms or very unusual complaints. This is especially true in elderly patients and women. Dizziness, passing out spells, stomach pain, nausea and vomiting, and just plain “feeling bad” may be symptoms of a heart attack in those individuals. As a general rule, any symptom that is unusual for an individual with risk for heart disease needs to be taken seriously.

When a heart attack occurs, prompt evaluation is essential. This process includes: an EKG (which measures the electrical activity of the heart with certain definite patterns indicating the source of injury) blood tests like CPK and troponin (which measure heart muscle enzymes released into the bloodstream following heart damage) as well as echocardiography and advanced imaging techniques (which are used to identify abnormal wall motion or injury to the heart muscle).

Heart attack victims need a number of medicines, each with a specific purpose. Platelet drugs, like aspirin and Plavix (or Effient), are given to interrupt further clotting of the blood by platelets. Heparin and similar drugs are used to prevent clotting of the blood by different mechanisms. Nitroglycerin is administered to dilate the vessel involved and allow more flow. Beta-blocker drugs are given to improve the efficiency of the heartbeat and lower the risk of possibly fatal arrhythmias. Finally, clot-busting drugs may be given to actually melt away a clot within a vessel.

Ideally, the preferred way to open the occluded vessel is mechanically. The patient is taken emergently to the heart catheterization laboratory. A very small incision is made in the groin and small catheters are threaded into the coronary arteries. Using dye and x-ray, the blockage is identified almost immediately. Subsequently, a small wire is passed across the obstruction downstream. A hollow catheter with a balloon at its tip is passed over the wire to the site of the stenosis. By inflating the balloon, the obstruction is relieved and blood flow restored. Usually, within minutes the results are dra¬matic with improvement in symptoms and the patients’ vital signs. In most cases performed today, a stent is inflated on the tip of the balloon across the blockage. It serves as a permanent metal scaffold that prevents collapse of the vessel.

Following a heart attack, the extent of injury to the heart is assessed. Depending on the degree of damage and the patients’ pump function, decisions are made regarding medications, devices, and rehabilitation. Depression is quite common and needs to be addressed. Many of the medications above become a permanent part of the patient’s medication list. In addition, other drugs such as ACE inhibitors and cholesterol lowering drugs are given to alter the plaques within the vessel, thereby lowering the risk of future heart attacks. Smoking cessation, weight loss, exercise, and changes in diet are main¬stays of treatment as well. Unfortunately, an individual who has suffered a heart attack is at risk for future events. Close monitoring of risk factors and periodic evaluation for development of further plaques is vital to prevention. There is much cause for optimism given the decline in death rates following myocardial infarctions for those patients who reach the hospital.