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Cardiology Services
Chest pain is one of the most common complaints that will bring a patient to the Emergency Department. Seeking immediate care may be lifesaving, and considerable public education has been undertaken to get patients to access medical care when chest pain strikes. While you may be worried about a heart attack, there are many other causes of pain in the chest that the healthcare provider will need to consider. Some diagnoses are life threatening, while others are less dangerous. Deciding the cause of chest pain is sometimes very difficult and may require blood tests, x–rays, CT scans and other tests to sort out the diagnosis. Often though, a careful history taken by the healthcare provider may be all that is needed to find the answer. The key to diagnosis remains history. Learning about the nature of the pain will give the healthcare provider direction as to what are reasonable diagnoses to consider, and what are reasonable to exclude. Understanding the quality and quantity of the pain, its associated symptoms and the risk factors for disease, can help the care provider assess the probability of what potential diagnoses should be considered and which should be discarded. Differential diagnosis is a thought process that healthcare providers use to consider and then eliminate potential causes for an illness. As more information is gathered, either from history and physical examination or testing, the potential diagnosis list is narrowed until the final answer is achieved. As well, the patient's response to therapy can expand or narrow the differential diagnosis list. In patients with chest pain, many potential diagnoses may exist, and the healthcare provider will want to first consider those that are life-threatening. Tests to rule out heart attack, pulmonary embolus, or aortic dissection may not be necessary; when clinical skill and judgment may be all that is needed to consider or discard a diagnosis. You may be asked a variety of questions to help the healthcare provider understand the patient's pain. Patients use different words to describe pain, and it is important that the healthcare provider get an accurate impression of the situation. The concept of ruling out a diagnosis is difficult for some patients to understand. Instead of proving what is happening, the healthcare provider is sometimes charged with proving that a life-threatening diagnosis is not present. "Proving what isn't" takes time and technology. A combination of blood tests and imaging studies may take hours to confirm or refute a diagnosis.
The worry for patients and healthcare providers is that any chest pain may originate from the heart. Angina is the term given to pain that occurs because blood vessels to the heart muscle narrow and decrease the amount of oxygen that can be delivered to the heart itself. This can cause the classic symptoms of chest pressure or tightness with radiation to the arm or neck associated with shortness of breath and sweating. Unfortunately, many people don't present with classic symptoms, and the pain may be difficult to describe - or in some people may not even be present. Instead of angina or typical chest pressure, their anginal equivalent (symptom they get instead of chest pain) may be indigestion, shortness of breath, or weakness and malaise. Women and the elderly are at higher risk for having atypical presentation of heart pain. If one of the blood vessels to the heart (coronary artery) completely occludes (becomes blocked), then the muscle it supplies blood to is at risk of dying. This is a heart attack or myocardial infarction. In most circumstances, this pain is more intense than routine angina, but again, there are many variations in signs and symptoms. The diagnosis of angina is a clinical one. After the healthcare provider takes a careful history and assesses the potential risk factors, the diagnosis is either reasonably pursued or else it is considered not to be present. If angina is the potential diagnosis, further evaluation may include electrocardiograms (EKG or ECG) and blood tests. Cardiac enzymes can be measured in the bloodstream when heart muscle is irritated or damaged. If these chemicals are not present, it may be reasonable to perform imaging studies of the heart in a variety of ways depending on the patient's past history:
The purpose of making the diagnosis of angina is restore normal blood supply to heart muscle before a heart attack occurs and permanent muscle damage occurs. Aside from minimizing risk factors by controlling blood pressure, cholesterol, and diabetes, and stopping smoking, medications can be used to make the heart beat more efficiently (for example, beta blockers), to dilate blood vessels (for example, nitroglycerin) and to make blood less likely to clot (aspirin). An acute heart attack (myocardial infarction) is a true emergency, since complete blockage of blood supply will cause part of the heart muscle to die and be replaced by scar tissue. This lessens the ability of the heart to pump blood to meet the body's needs. As well, injured heart muscle is irritable and can cause electrical disturbances like ventricular fibrillation, a condition in which the heart jiggles like Jello and cannot beat in a coordinated fashion. This is the cause of sudden death in heart attack. The cause of an acute heart attack is the rupture of a cholesterol plaque in a coronary artery. This causes a blood clot to form and occlude the artery. The treatment for heart attack is emergent restoration of blood supply. Two options include use of a drug like TPA or TNK to dissolve the blood clot (thrombolytic therapy) or emergency heart catheterization and using a balloon to open up the blocked area (angioplasty) and keeping it open with a mesh cage called a stent. A heart attack is a layperson's term for a sudden blockage of a coronary artery. This blockage, which doctors call a coronary artery occlusion, may be fatal, but most patients survive it. Death can occur when the occlusion leads to an abnormal heartbeat (severe arrhythmia) or death of heart muscle (extensive myocardial infarction). In both of these situations, the heart can no longer pump blood adequately to supply the brain and other organs of the body. Almost all heart attacks occur in people who have coronary artery disease (coronary atherosclerosis). So, this photo essay will review the structure (anatomy) of the normal coronary artery, the structural abnormalities (pathology) of the coronary artery in atherosclerosis, and the effect of these abnormalities on the heart.
The coronary arteries carry blood to the heart to supply oxygen and necessary nutrients. As seen in Figure 1, the wall of a coronary artery has 3 distinct layers: the inner (intima), middle (media), and outer (adventitia) layers. The wall of the artery surrounds the lumen of the artery, which is the channel through which blood flows. Figure 1: Normal Coronary Artery Cross-sectional Microscopic View
In Figure 1, smooth muscle is red, and connective (supporting) tissue is black (elastic) or blue (collagen). The intima is best seen in the close-up view in Figure 1. It is composed of a layer of so-called endothelial cells that covers the artery's inner (lumenal) surface, connective (supporting) tissue (collagen and elastin), and a layer of compact elastic tissue called the internal elastic lamina (IEL). In the past, the intima was thought to be simply a passive layer whose major purpose was to serve as a barrier. Now, however, we know that the endothelial cells actually keep track of the pressure, flow, and "health" of the artery. Moreover, endothelial cells secrete chemicals that can adjust the function of the artery (e.g., vasodilator chemicals to widen and vasoconstrictors to narrow it) and growth of the artery wall (e.g., growth factors). The media (M) is a layer made up primarily of smooth muscle cells (SMCs). The muscle can contract and relax to control the blood pressure and flow in the artery. Elastic tissue and collagen in the media, along with elastic tissue in the IEL, increase the elasticity and strength of the wall of the artery, as the artery contracts and relaxes. The adventitia is a layer of connective tissue and cells (e.g., SMCs) that produce this connective tissue. The adventitia contains potent factors, including one called tissue thromboplastin, that promote blood clotting. The clots are useful when the artery becomes injured because they can limit excessive bleeding from the injured artery.
What happens to the coronary artery in atherosclerosis? In coronary artery disease (coronary atherosclerosis), injury to the intima of the artery leads to the formation of plaques, which are regions of thickening on the inner lining of the artery. How then do the plaques form? In response to the injury, the smooth muscle cells (SMCs) from the media and perhaps from the adventitia move (migrate) into the intima. In the intima, these SMCs reproduce themselves (divide) and make (synthesize) connective tissue. These processes of migration, division, and synthesis, which collectively are referred to as intimal proliferation (buildup), cause thickening of the intima. When cholesterol, other fats, and inflammatory cells, such as white blood cells, enter the proliferating, thickened intima, the result is an atherosclerotic plaque. Then, as these plaques grow, they accumulate scar (fibrous) tissue and abundant calcium. (Calcium is the hard material in our teeth and bones.) Hence, the plaques are often hard, which is why atherosclerosis is sometimes referred to as "hardening of the arteries." Who gets coronary artery plaques and what happens to the plaques? Most adults in industrialized nations have some plaques (atherosclerosis) on the inner (lumenal) surface of their coronary arteries. Autopsy studies of young soldiers who died in World War II, the KOrean War, and the Vietnam War showed that even young adults in their 20s usually have coronary arteries that exhibit localized (focal) thickening of the intima. This thickening is the beginning of intimal proliferation and plaque formation. The distribution, severity (amount of plaque), and rate of growth of the plaques in the coronary arteries vary greatly from person to person. Figure 2 shows a coronary artery with an uneven (asymmetric), stable atherosclerotic plaque. A stable plaque may grow slowly, but has an intact inner (lumenal) surface with no clot (thrombus) on this surface. Figure 2: Coronary Artery with Stable Atherosclerotic Plaque Cross-sectional Microscopic View
Rupture of a stable plaque in a coronary artery is the initial pathological event leading to a heart attack. When the rupture occurs, a clot suddenly forms in the lumen (channel) of the artery at the site of the rupture. Bleeding into the plaque often accompanies the rupture. The clot then blocks (occludes) the artery and thereby decreases the blood flow to the heart. This sequence of events in the coronary arteries is the basic problem in over 75% of people who suffer a heart attack. In some patients, more often women, there is just an erosion or ulceration of the plaque surface, rather than a full rupture that leads to clot formation in the coronary artery. Figure 3 shows an atherosclerotic plaque rupture and a clot in a coronary artery. Figure 3: Rupture of Atherosclerotic Plaque in Coronary Artery Cross-sectional Microscopic View
What happens to the heart muscle after a person survives a Heart Attack? According to medical studies, 50% to 75% of people survive their first heart attack The others die during the heart attack because the decreased coronary blood flow causes a severe abnormal heart rhythm or extensive death of heart muscle. Figure 4 shows the heart of a patient who died 5 days after a heart attack. The photos show his myocardial infarction as it appears on the surface of the left ventricle and when the heart is sliced to view the muscle wall. About 90% of myocardial infarctions involve only the left ventricle (LV), which pumps oxygen-rich blood that comes from the lungs to the entire body. The other 10% also involve the right ventricle (RV), which pumps the blood to the lungs. Figure 4: Myocardial Infarction Caused by Heart Attack Views of Heart Surface and Slice Across Heart
How is a heart attack treated? Treatment of heart attacks include:
Anti–platelet agents are medications that prevent blood clots from forming by inhibiting the aggregation of platelets. Platelets are fragments of cells that circulate in the blood. Platelets begin the formation of blood clots by clumping together (a process called aggregation). Platelet clumps are then strengthened and expanded by the action of clotting factors (coagulants) that result in the deposition of protein (fibrin) among the platelets. Aggregation of platelets occurs at the site of any injury or laceration, but it also occurs at the site of rupture of cholesterol plaques in the walls of coronary arteries. Formation of clots at the site of an injury or laceration is desirable because it prevents excessive loss of blood, but formation of clots inside coronary arteries blocks the arteries and causes heart attacks. There are three types of anti–platelet agents –– aspirin, thienopyridines, and the glycoprotein IIb/IIIa inhibitors. These agents differ in their mode of action, anti–platelet potency, speed of onset of action, and cost.
Anti–coagulants Coagulants (clotting factors) are proteins produced by the liver. Clotting factors are responsible for "cementing" clumps of platelets together to form a stronger and larger clot. Anti–coagulants such as intravenous or subcutaneous heparin, subcutaneous low molecular weight heparin, and oral warfarin (Coumadin), prevent the formation of blood clots either by inhibiting the production of clotting factors or by interfering with the action of the clotting factors.
While anti–platelet agents and anti–coagulants prevent the formation of blood clots, they cannot dissolve existing blood clots and hence cannot be relied upon to open blocked arteries rapidly. Clot–dissolving drugs (also called fibrinolytic or thrombolytic medications) actually dissolve blood clots and can rapidly open blocked arteries. Intravenous administration of clot–dissolving drugs such as tissue plasminogen activator (TPA) or TNK can open up to 80% of acutely blocked coronary arteries. The earlier these drugs are administered, the greater the success at opening the artery and the more effective the preservation of heart muscle. If clot–dissolving drugs are given too late (more than six hours after the onset of the heart attack), most of the muscle damage already may have occurred. If a hospital does not have a catheterization laboratory with the ability to perform PTCA, or if there are logistic reasons why PTCA will be delayed, clot–dissolving drugs can be promptly administered to achieve reperfusion. PTCA then may be performed in patients who fail to respond to the clot–dissolving drugs. (If prompt PTCA and stenting are available, it has been demonstrated that they are preferable to clot–dissolving drugs to open arteries.) Nitrates Nitroglycerin is the most common nitrate used in the treatment of heart attacks. It can be given sublingually (under the tongue), as a spray, as a paste applied over skin, and intravenously. Intravenous nitroglycerine has a rapid onset of action and is commonly used in the initial (first 48 hours) treatment of heart attacks. Nitroglycerine is a vasodilator (blood vessel dilator), which opens arteries by relaxing the muscular wall of the artery. Nitroglycerine dilates coronary arteries as well as other blood vessels throughout the body. By dilating blood vessels, nitroglycerine lowers blood pressure, decreases the work that the heart must do, lowers the demand by the heart for oxygen, prevents coronary artery spasm, improves blood flow to the heart muscle, and potentially minimizes the size of the heart attack. Nitroglycerine is especially helpful in patients with heart attacks who also have heart failure or high blood pressure. Angiotensin converting enzyme (ACE) inhibitors, another class of blood vessel dilators, often are given orally after a large heart attack to improve the healing of heart muscle. Examples of ACE inhibitors include captopril (Capoten), enalapril (Vasotec), lisinopril (Zestril and Prinivil), and ramipril (Altace). These medications lower the blood pressure and reduce the workload of the heart, thereby helping the damaged heart muscle to recover. They are especially helpful in patients who have recovered from heart attacks but have high blood pressure, heart failure, major damage to the left ventricle, and diabetes mellitus. For additional information, please see the ACE Inhibitors article. Beta–blockers Beta–blockers such as propranolol (Inderal), metoprolol (Lopressor, Toprol XL), andatenolol (Tenormin) usually are given early during a heart attack and are continued long–term. Beta blockers antagonize the action of adrenaline and relieve stress on the muscles of the heart. Beta–blockers decrease the workload of the heart by slowing the heart rate and decreasing the force of contraction of heart muscle. Decreasing the workload decreases the demand for oxygen by the heart and limits the amount of damage to the heart muscle. Long–term administration of beta–blockers following a heart attack has been shown to improve survival and reduce the risk of future heart attacks. Beta–blockers also improve survival among patients with heart attacks by decreasing the incidence of life–threatening abnormal heart rhythms, for example, ventricular fibrillation. Beta–blockers can be given intravenously in the hospital and then can be taken orally for long–term treatment. Oxygen
Interventional cardiologists are the physician specialists who perform diagnostic cardiac catheterizations and emergency angioplasty procedure to treat emergency heart attack patients. FMH interventional cardiologists have collectively performed thousands of these procedures, and Dr. Mark Turco, Medical Director of FMH Interventional Cardiology Services is Fellowship trained - as are all of the FMH interventional cardiologists - and is also the Director of the Center for Cardiac and Vascular Research at Washington Adventist Hospital. Meet the FMH Interventional Cardiologists:
Cardiac catheterization (also called cardiac cath or coronary angiogram) is a procedure that allows your doctor to "see" how well your heart is functioning. The test involves inserting a long, narrow tube, called a catheter, into a blood vessel in your arm or leg, and guiding it to your heart with the aid of a special X-ray machine. Contrast dye is injected through the catheter so that X-ray movies of your valves, coronary arteries and heart chambers can be created. Why Do I Need a Cardiac Catheterization? Your doctor uses cardiac cath to:
Most people will need to have a routine chest X-ray , blood tests and electrocardiogram performed within 2 weeks before the procedure. You can wear whatever you like to the hospital. You will wear a hospital gown during the procedure. Leave all valuables at home. If you normally wear dentures, glasses or a hearing assist device, plan to wear them during the procedure. Your doctor or nurse will give you specific instructions about what you can and cannot eat or drink before the procedure. Ask your doctor what medications should be taken on the day of your test. You may be told to stop certain medications, such as Coumadin (warfarin, a blood thinner). If you have diabetes, ask your doctor how to adjust your medications the day of your test. Tell your doctor and/or nurses if you are allergic to anything, especially iodine, shellfish, X-ray dye, latex or rubber products (such as rubber gloves or balloons) or penicillin-type medications. You may or may not return home the day of your procedure. Bring items with you (such as robe, slippers and toothbrush) to make your stay more comfortable. When you are able to return home, arrange for someone to bring you home.
The cateterization procedure usually takes about 30 minutes, but the preparation and recovery time add several hours. Plan on being at the hospital all day for the procedure.
You will be given a hospital gown to wear. A nurse will start an intravenous (IV) line in your arm so that medications and fluids can be administered through your vein during the procedure. The cardiac catheterization room is cool and dimly lit. You will lie on a special table. If you look above, you will see a large camera and several TV monitors. You can watch the pictures of your cardiac cath on the monitors. The nurse will clean your skin (and possibly shave) the site where the catheter will be inserted (arm or groin). Sterile drapes are used to cover the site and help prevent infection. It is important that you keep your arms and hands down at your sides and not disturb the drapes. Electrodes (small, flat, sticky patches) will be placed on your chest. The electrodes are attached to an ECG that charts your heart's electrical activity. You will be given a mild sedative to help you relax, but you will be awake and conscious during the entire procedure. The doctor will use a local anesthetic to numb the insertion site.
When the catheter is in place, the lights will be dimmed and a small amount of dye (or "contrast material") will be injected through the catheters into your arteries and heart chambers. The contrast material outlines the vessels, valves and chambers.
The X-ray camera will be used to take photographs of the arteries and heart chambers. You will be asked to hold your breath while the X-rays are taken. When all the photos have been taken, the catheter will be removed and the lights will be turned on. After your procedure you will be taken to the Intensive Care Unit. You will be asked to lie flat for several hours. Before leaving the hospital you will be given instructions about medications, physician activity, and follow up care.
Here are some important links to FMH programs specifically designed for cardiac patients. Click on the prompts below to find out more information. |
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