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Definition of Coronary Artery Disease
Atherosclerosis of the coronary arteries that reduces blood flow to the heart. About 14 million Americans have Coronary Artery Disease (CAD), though many of them do not know it until heart attack strikes.
Coronary Artery Disease (CAD) causes 1.2 million heart attacks and more than 600,000 deaths in the United States every year.
Autopsy findings show that two thirds of women and nearly half of men who lose their lives to sudden cardiac death had unsuspected CAD. Although CAD is more common in people age 60 and older, it is becoming increasingly common among younger people. Genetic factors may underlie Coronary Artery Disease (CAD) in some people, though most often Coronary Artery Disease (CAD) is an acquired condition that is the direct consequence of lifestyle factors such as cigarette smoking, eating habits, and physical inactivity.
Heart attack is a life-threatening emergency. Call 911 immediately with symptoms or when heart attack is possible. Many people delay, wanting to be sure. Waiting can be fatal.
CAD, like generalized atherosclerosis, develops over decades. Many cardiologists believe CAD begins in childhood. The most commonly affected coronary arteries are the left anterior descending (LAD), the circumflex, and their branches. These coronary arteries provide the blood supply for most of the heart muscle, including nearly all of the left ventricle. CAD may affect the right coronary artery as well. Cardiologists classify CAD according to the number of occluded coronary arteries. A coronary artery can be 70 percent occluded before the restricted blood flow impairs cardiac function, though cardiologists believe reduced OXYGENATION begins with about 50 percent occlusion. The heart’s ability to develop collateral circulation, the growth of new arteries, allows CAD to worsen without overtly affecting cardiac function.
CAD develops when atherosclerotic plaque infiltrates the arterial intima, the innermost layer of the arterial wall, and accumulates into deposits called atheromas. The atheromas cause the arterial wall to thicken, reducing its elasticity and thus its ability to contract and expand in response to blood flow needs. Atheromas also protrude into the channel of the artery, reducing the artery’s interior diameter (lumen) and reducing the volume of blood the artery can transport. These factors converge to restrict blood flow to the heart, particularly with exertion (such as during physical exercise), and deprive segments of the heart of adequate oxygenation. The result is ischemia, or tissue hypoxia. Typically the ischemia eases with rest, as the heart’s demand for oxygen diminishes.
Symptoms and Diagnostic Path
The key symptom of Coronary Artery Disease (CAD) is angina pectoris, a pressurelike discomfort or pain originating in the central chest and often radiating up the arm into the jaw and through the shoulder area to the back. At this stage, medical or surgical interventions can head off CAD-induced heart attack. For many people, however, the first indication of CAD is heart attack, which can occur when an atherosclerotic coronary artery ruptures or a blood clot lodges in a section of a coronary artery where CAD has narrowed the passageway. The resulting blockage, or occlusion, interrupts blood flow to a portion of the heart and the heart tissue dies.
Cardiac catheterization and angiogram provide definitive diagnosis. These procedures allow the cardiologist to visualize the path of blood through the coronary arteries, highlighting constricted or blocked areas. Severe CAD also causes arrhythmia (disturbance of the heart’s electrical activity), which a person may experience as palpitations and that show up on electrocardiogram (ecg). Exercise stress test, particularly radionuclide testing, reveals the functional limitations resulting from the Coronary Artery Disease (CAD). Echocardiogram often reveals the dysfunction of the walls of the heart served by diseased coronary arteries, as well as decreased heart function if there has already been damage, and with Doppler ultrasound may show restrictions in the flow of blood.
Some cardiologists use magnetic resonance imaging (mri) to visualize the structure and function of the coronary arteries and the rest of the heart. MRI also detects new collateral circulation (angiogenesis). However, anyone who has a pacemaker, implantable cardioverter defibrillator (icd), stents, aneurysm clips, or other internal metallic objects cannot undergo MRI. An advantage of MRI is its ability to represent dimensional cross-sections of the areas of suspected atherosclerotic accumulation. This reveals the extent to which the Coronary Artery Disease (CAD) has caused the arterial wall to thicken.
A variation of CT scan, electron beam computed tomography (ebct) scan, can detect calcification in the arterial walls. Calcification indicates longstanding accumulations of plaque that have solidified within the intima, a sign of well-established CAD that, while perhaps not causing symptoms, is significant enough to pose the risk of heart attack. Of equal, and perhaps greater, concern to cardiologists is the accumulation of soft, unstable atherosclerotic plaque, sometimes called vulnerable atheroma. These soft accumulations appear to cause continued irritation to the arterial wall, with resulting clot formation and the risk that the atherosclerotic plaques will rupture, spilling particles and debris into the blood circulation.
Treatment Options and Outlook
Although coronary artery bypass graft (cabg) remains the leading treatment for CAD in the United States, cardiologists are moving toward less invasive approaches. CABG is an open heart surgery with numerous risks and complications. A number of studies in the late 1990s and early 2000s raised questions as to whether CABG provides a clear benefit over other treatment alternatives such as angioplasty, aggressive lipid-lowering therapy, and significant lifestyle modifications. Cardiologists now implement the latter two methods after CABG, and there is increasing evidence that they are equally effective without CABG.
Angioplasty, a cardiac catheterization procedure in which a balloon at the tip of a catheter compresses the occlusion, remains a popular intervention because it is far less invasive than CABG, requires minimal recovery time, and results in immediate improvement of coronary circulation. However, restenosis (return of the atherosclerotic narrowing) is more the norm than the exception and occurs in a fourth to a third of people within six months. Angioplasty with stent placement (a tiny springlike device that remains at the site of the occlusion to hold pressure against the arterial wall) fares somewhat better. Treatment options and recommendations continue to evolve as new medications and technologies become available.
The most significant long-term consequence of CAD is damage following heart attack, which may or may not improve with CABG. Left ventricular ejection fraction (lvef), a calculation of the percent of blood that leaves the heart with each contraction of the left ventricle, projects the extent of disability resulting from heart attack due to CAD. LVEF above 60 percent generally correlates with little loss of cardiovascular function except with extreme physical exertion. Most people with an LVEF greater than 40 percent can return to work and normal activities. LVEF that drops below 40 percent limits the heart’s capacity to meet the body’s oxygen needs during moderate physical exertion, and below 20 percent restricts nearly all physical activity.
Major Risk Factors for Coronary Artery Disease (CAD)
|Major Risk Factors for Coronary Artery Disease (CAD)|
|age 50 or older||cigarette smoking|
|diabetes||family history of young heart attack|
|obesity||peripheral vascular disease (pvd)|
Risk Factors and Preventive Measures
The most clear-cut early warning sign for the development of CAD is hyperlipidemia (elevated cholesterol and triglycerides blood levels). Hyperlipidemia indicates dysfunction with the body’s lipid synthesis and storage mechanisms, which typically results in accumulations of fatty acids along the inner arterial walls. These accumulations irritate and inflame the artery’s intima, establishing the foundation for atherosclerotic plaque development. Numerous studies show that lowering blood lipid levels reduces atherosclerotic accumulations, slowing the progression of CAD. Diabetes, hypertension, and obesity accelerate the progression of CAD. The prevalence of CAD in young people alarms health experts, who emphasize that it is never too early to implement a hearthealthy lifestyle.
An important understanding about Coronary Artery Disease (CAD) is that it is a chronic, lifelong cardiovascular condition. Even with CABG or angioplasty, the disease process continues. Treatments aim to slow the progression but so far are not able to prevent it. Lifestyle changes are imperative for people who want to enjoy extended life expectancy as well as quality of life. Though the outlook for controlling CAD has never been brighter, CAD remains a major health concern. Lifestyle modifications to improve cardiovascular health, in combination with medical interventions such as aspirin therapy and medications to regulate heart function, can significantly impede CAD’s progression.
See also CARDIOVASCULAR DISEASE PREVENTION; COENZYME Q10; DIABETES AND CARDIOVASCULAR DISEASE; DIET AND CARDIOVASCULAR HEALTH; PHYSICAL EXERCISE AND CARDIOVASCULAR HEALTH; SMOKING AND CARDIOVASCULAR DISEASE; STROKE.
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