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BIOC33H3 (127)
Lecture

Coronary Artery Disease and Acute Coronary Syndrome

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Department
Biological Sciences
Course
BIOC33H3
Professor
Stephen Reid
Semester
Fall

Description
Chapter 34:Coronary Artery Disease and Acute Coronary Syndrome  Coronary artery disease (CAD) is a type of blood vessel disorder included in the general category of atherosclerosis.  Atherosclerosis is characterized by a focal deposit of cholesterol and lipids within the intimal wall of the artery. Inflammation and endothelial injury play a central role in the development of atherosclerosis.  CAD is a progressive disease that develops in stages and when it becomes symptomatic, the disease process is usually well advanced.  Normally some arterial anastomoses or connections, termed collateral circulation, exist within the coronary circulation. The growth and extent of collateral circulation are attributed to two factors: (1) the inherited predisposition to develop new blood vessels (angiogenesis), and (2) the presence of chronic ischemia.  Many risk factors have been associated with CAD. o Nonmodifiable risk factors are age, gender, ethnicity, family history, and genetic inheritance. o Modifiable risk factors include elevated serum lipids, hypertension, tobacco use, physical inactivity, obesity, diabetes, metabolic syndrome, psychologic states, and homocysteine level.  Elevated serum lipid levels are one of the four most firmly established risk factors for CAD.  Lipids combine with proteins to form lipoproteins and are vehicles for fat mobilization and transport. The different types of lipoproteins are classified as high-density lipoproteins (HDLs), low-density lipoproteins (LDLs), and very-low-density lipoproteins (VLDLs).  HDLs carry lipids away from arteries and to the liver for metabolism. High serum HDL levels are desirable.  HDL levels are increased by physical activity, moderate alcohol consumption, and estrogen administration.  Elevated LDL levels correlate most closely with an increased incidence of atherosclerosis and CAD.  Hypertension, defined as a BP greater than or equal to 140/90 mm Hg, is a major risk factor in CAD.  Tobacco use is also a major risk factor in CAD. The risk of developing CAD is two to six times higher in those who smoke tobacco than in those who do not.  Obesity is defined as a body mass index (BMI) of less than 30 kg/m . The increased risk for CAD is proportional to the degree of obesity. o Diabetes, metabolic syndrome, and certain behavioral states (i.e., stress) have also been found to be contributing risk factors for CAD. CORONARY ARTERY DISEASE  Prevention and early treatment of CAD must involve a multifactorial approach and needs to be ongoing throughout the lifespan  A complete lipid profile is recommended every 5 years beginning at age 20. Persons with a serum cholesterol level greater than 200 mg/dl are at high risk for CAD.  Management of high-risk persons starts with controlling or changing the additive effects of modifiable risk factors. o A regular physical activity program should be implemented. o Therapeutic lifestyle changes to reduce the risk of CAD include lowering LDL cholesterol by adopting a diet that limits saturated fats and cholesterol and emphasizes complex carbohydrates (e.g., whole grains, fruit, vegetables). o Low-dose aspirin is recommended for people at risk for CAD. Aspirin therapy is not recommended for women with low risk for CAD before age 65. Common side effects of aspirin therapy include GI upset and bleeding. For people who are aspirin intolerant, clopidogrel (Plavix) can be considered.  If levels remain elevated despite modifiable changes, drug therapy is considered. o Statin drugs work by inhibiting the synthesis of cholesterol in the liver. Liver enzymes must be regularly monitored. o Niacin, a water-soluble B vitamin, is highly effective in lowering LDL and triglyceride levels by interfering with their synthesis. Niacin also increases HDL levels better than many other lipid-lowering drugs. o Fibric acid derivatives work by accelerating the elimination of VLDLs and increasing the production of apoproteins A-I and A-II. o Bile-acid sequestrants increase conversion of cholesterol to bile acids and decrease hepatic cholesterol content. The primary effect is a decrease in total cholesterol and LDLs. o Certain drugs selectively inhibit the absorption of dietary and biliary cholesterol across the intestinal wall.  The incidence of cardiac disease is greatly increased in the elderly and is the leading cause of death in older persons. Strategies to reduce CAD risk are effective in this age group but are often underprescribed.  Aggressive treatment of hypertension and hyperlipidemia will stabilize plaques in the coronary arteries of older adults, and cessation of tobacco use helps decrease the risk for CAD at any age. CHRONIC STABLE ANGINA  Chronic stable angina refers to chest pain that occurs intermittently over a long period with the same pattern of onset, duration, and intensity of symptoms. o Angina is rarely sharp or stabbing, and it usually does not change with position or breathing. Many people with angina complain of indigestion or a burning sensation in the epigastric region. o Anginal pain usually lasts for only a few minutes (3 to 5 minutes) and commonly subsides when the precipitating factor is relieved. Pain at rest is unusual.  The treatment of chronic stable angina is aimed at decreasing oxygen demand and/or increasing oxygen supply and reducing CAD risk factors. o In addition to antiplatelet and cholesterol-lowering drug therapy, the most common drugs used to manage chronic stable angina are nitrates.  Short-acting nitrates are first-line therapy for the treatment of angina. Nitrates produce their principal effects by dilating peripheral blood vessels, coronary arteries, and collateral vessels.  Long acting nitrates are also used to reduce the incidence of anginal attacks.  -Adrenergic blockers are the preferred drugs for the management of chronic stable angina.  Calcium channel blockers are used if -adrenergic blockers are contraindicated, are poorly tolerated, or do not control anginal symptoms. The primary effects of calcium channel blockers are (1) systemic vasodilation with decreased SVR, (2) decreased myocardial contractility, and (3) coronary vasodilation.  Certain high-risk patients (e.g., patients with diabetes) with chronic stable angina may benefit from the addition of an angiotensin- converting enzyme (ACE) inhibitor.  Common diagnostic tests for a patient with a history of CAD or CAD include a chest x-ray, a 12-lead ECG, laboratory tests (e.g., lipid profile); nuclear imaging; exercise stress testing, and coronary angiography. ACUTE CORONARY SYNDROME  Acute coronary syndrome (ACS) develops when ischemia is prolonged and not immediately reversible. ACS encompasses the spectrum of unstable angina, non–ST- segment-elevation myocardial infarction (NSTEMI), and ST-segment-elevation myocardial infarction (STEMI).  ACS is associated with deterioration of a once stable atherosclerotic plaque. This unstable lesion may be partially occluded by a thrombus (manifesting as UA or NSTEMI) or totally occluded by a thrombus (manifesting as STEMI).  Unstable angina (UA) is chest pain that is new in onset, occurs at rest, or has a worsening pattern. UA is unpredictable and represents an emergency.  Myocardial infarction (MI) occurs as a result of sustained ischemia, causing irreversible myocardial cell death. Eighty percent to 90% of all MIs are due to the development of a thrombus that halts perfusion to the myocardium distal to the occlusion. Contractile function of the heart stops in the infracted area(s). o Cardiac cells can withstand ischemic conditions for approximately 20 minutes. It takes approximately 4 to 6 hours for the entire thickness of the heart muscle to infarct. o Infarctions are described based on the location of damage (e.g., anterior, inferior, lateral, or posterior wall infarction). o Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration is the hallmark of an MI. The pain is usually described as a heaviness, pressure, tightness, burning, constriction, or crushing. o Complications after MI  The most common complication after an MI is dysrhythmias, and dysrhythmias are the most common cause of death in patients in the prehospital period.  HF is a complication that occurs when the pumping power of the heart has diminished.  Cardiogenic shock occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe left ventricular failure. When it occurs, it has a high mortality rate.  Papillary muscle dysfunction may occur if the infarcted area includes or is adjacent to the papillary muscle that attaches to the mitral valve. Papillary muscle dysfunction causes mitral valve regurgitation and is detected by a systolic murmur at the cardiac apex radiating toward the axilla.  Papillary muscle rupture is a rare but life-threatening complication that causes massive mitral valve regurgitation, resulting in dyspnea, pulmonary edema, and decreased CO.  Ventricular aneurysm results when the infarcted myocardial wall becomes thinned and bulges out during contraction.  Pericarditis may occur 2 to 3 days after an acute MI as a common complication of the infarction.  Primary diagnostic studies used to determine whether a person has UA or an MI include an ECG and serum cardiac markers. Drug Therapy  Initial management of the patient with chest pain includes aspirin, sublingual nitroglycerin, morp
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