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Transcript
Pharmacotherapy of Coronary Artery Disease Molly Roberts, PharmD Candidate 2007 Epidemiology Coronary artery disease is the number one killer or males and females in America. People who Disease State Definition survive a heart attack have a 1.5-15 times higher chance of illness and death than the rest of the population. Both men and women have a substantial risk of another heart attack, sudden death, angina pectoris, heart failure and stroke. Successful treatment of chronic stable angina may prevent myocardial infarction and death as well as reduce symptoms of angina and occurrence of ischemia thereby improving the quality of life. Coronary artery disease (CAD), also called coronary heart disease (CHD), ischaemic heart disease, and atherosclerotic heart disease, is the end result of the accumulation of atheromatous plaques within the walls of the arteries that supply the myocardium. While the symptoms and signs of coronary heart disease are noted in the advanced state of disease, most individuals with coronary heart disease show no evidence of disease for decades as the disease progresses before the first onset of symptoms, often a "sudden" heart attack, finally arise. After decades of progression, some of these atheromatous plaques may rupture and (along with the activation of the blood clotting system) start limiting blood flow to the heart muscle. Pathophysiology Limitation of blood flow to the heart causes ischemia of the myocardial cells. When myocardial cells die from lack of oxygen MI. This leads to heart muscle damage, heart muscle death and later scarring without heart muscle regrowth. Myocardial infarction usually results from the sudden occlusion of a coronary artery when a plaque ruptures, activating the clotting system and atheroma-clot interaction fills the lumen of the artery to the point of sudden closure. The typical narrowing of the lumen of the heart artery before sudden closure is typically 20%, according to clinical research completed in the late 1990s and using IVUS examinations within 6 months prior to a heart attack. High grade stenoses as such exceeding 75% blockage, such as detected by stress testing, were found to be responsible for only 14% of acute heart attacks the rest being due to plaque rupture/ spasm. The events leading up to plaque rupture are only partially understood. Myocardial infarction is also caused, far less commonly, by spasm of the artery wall occluding the lumen, a condition also associated with atheromatous plaque and CHD. Clinical Presentation Many episodes of ischemia do not cause symptoms of angina (silent ischemia). STABLE ANGINA Chest pain or complaining of “heaviness, pressure, squeezing, discomfort, tightness, or constriction” Chest discomfort usually begins and ends gradually, is diffuse, and radiates Precipitated by exertion, emotional upset, cold weather, or heavy meals. Pain brought on by exertion usually abates 5-10 min after cessation of activity. Some pts (elderly, diabetics) with stable angina may not present with pain, but with “anginal equivalent’ symptoms such as shortness of breath, fatigue, dizziness, light-headedness, nausea, or diaphoresis Patients commonly have a normal PE (unless currently in chest pain: S4, paradoxically split S2, or mitral regurgitation murmur may be noted) UNSTABLE ANGINA New-onset angina Angina at rest Increased frequency of angina Increased severity of angina Increased duration of angina Molly Roberts, PharmD Candidate 2007 University of Maryland School of Pharmacy Pharmacotherapy Presentation – Pharmaceutical Care Rotation Happy Harry’s Pharmacy Patient Care Center, Perryville, MD Risk Factors Diagnosis Pain occurring with decreasing levels of exertion Pain less promptly relieved with nitroglycerin Patients commonly have a normal PE (unless currently in chest pain: S4, paradoxically split S2, or mitral regurgitation murmur may be noted) Risk factors that can be modified: Smoking: complete cessation; no exposure to environmental tobacco smoke Blood Pressure: less than 140/90mmHg or less than 130/80mmHg if the patient has diabetes or CKD Lipid Management: LDL-C should be less than 100mg/dL, and it is reasonable to aim for a level less than 70mg/dL. If triglycerides are equal to or greater than 200mg/dL, non-HDL-C should be less than 130mg/dL, and it is reasonable to aim for a level less than 100mg/dL Physical Activity: 30-60 minutes seven days a week (minimum five days per week) Weight Management: BMI - 18.5 to 24.9 kg/m2; waist circumference – men less than 40 inches, women less than 35 inches Diabetes Management: HbA1c levels less than 7 percent Risk factors that cannot be modified: Age: men older than 45 years old and women older than 55 years old are at a higher risk Family History: heart disease diagnosed before age 55 in father or brother; diagnosed before age 65 in mother or sister. Potential risk factors: High blood levels of C-reactive protein (CRP), which shows in the presence of inflammation. No single test to diagnose CAD. EKG for any chest pain thought to be ischemic in etiology. Most pts with unstable angina have EKG changes (most commonly ST segment depression and T-wave inversion). In patients presenting with chest pain, a detailed symptom history, focused physical examination, and directed risk-factor assessment should be performed. With this information, the clinician should estimate the probability of significant CAD (i.e., low, intermediate, or high). The following tests may be necessary: Echocardiogram Exercise Stress Test: useful in establishing diagnosis and provides prognostic info Chest x-ray Cardiac catheterization: gold standard of diagnosing CAD; however, very invasive Coronary angiography Nuclear heart scan Fasting glucose test Fasting lipoprotein profile Hemoglobin Desired Therapeutic Outcomes* *Reference of Guidelines Used Stable Angina: Reduce risk of MI and death and thereby increase the “quantity” of life Reduce symptoms of angina and the occurrence of ischemia, which should improve the quality of life Unstable Angina: Reduce risk of death or MI/(re)infarction Immediate relief of pain/ischemia ACC/AHA 2002 guideline update for the management of patients with chronic stable angina: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Molly Roberts, PharmD Candidate 2007 University of Maryland School of Pharmacy Pharmacotherapy Presentation – Pharmaceutical Care Rotation Happy Harry’s Pharmacy Patient Care Center, Perryville, MD Treatment Options** (Non-drug and Drug Therapy – include all therapeutic classes/agents available and preferences per treatment guidelines) **See Treatment Options Table Non-Drug Therapy: Eat a healthy diet to prevent or reduce high blood pressure and high cholesterol and to maintain a healthy weight Quit smoking, if you smoke Exercise, as directed by your doctor Lose weight, if you are overweight or obese Reduce stress For the first time, flu shots are recommended in patients with chronic cardiovascular disease. Treat underlying medical conditions that may aggravate myocardial ischemia such as hypertension, tachycardia, fever, thyrotoxicosis, anemia, or hypoxemia Modification of activities that exacerbated angina (cold weather, postprandial exercise) Drug Therapy for Stable Angina: Aspirin/Antiplatelet therapy BB CCB Nitroglycerin Long-acting nitrates Drug Therapy for Unstable Angina: Bed rest with continuous ECG monitoring for ischemia and arrhythmia detection in patients with ongoing rest pain Aspirin/antiplatelet therapy NTG Supplemental O2 Morphine PRN BB ACEI Nondihydropyridine CCB (verapamil or diltizem) Monitoring (Efficacy and Toxicity Parameters) Additional Treatment of Risk Factors: Treatment of hypertension according to JNC VI Management of diabetes LDL-lowering therapy in patients with documented or suspected CAD and LDL cholesterol greater than or equal to 130 mg/dL, with a target LDL of less than 100mg/dL Indices of Therapeutic Effect: Stable Angina: Decrease frequency of chest pain and TNG administration Increase exercise tolerance Unstable Angina: Relieve chest pain and improvement of pattern of pain No evolution to MI For complete monitoring parameters for individual agents/classes see Pharmacological Treatment Options Chart. Molly Roberts, PharmD Candidate 2007 University of Maryland School of Pharmacy Pharmacotherapy Presentation – Pharmaceutical Care Rotation Happy Harry’s Pharmacy Patient Care Center, Perryville, MD