Pharmacotherapy of Coronary Artery Disease – Stable Angina



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 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. |

| | |

|Disease State |Coronary artery disease (CAD), also called coronary heart disease (CHD), ischaemic heart disease, and atherosclerotic heart disease, is the|

|Definition |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. |

|Patho-physiology |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 |

| |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 |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. |

|Diagnosis |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 |Stable Angina: |

|Outcomes* |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 |

|*Reference of |Cardiology/American Heart Association Task Force on Practice Guidelines |

|Guidelines Used | |

|Treatment Options** |Non-Drug Therapy: |

| |Eat a healthy diet to prevent or reduce high blood pressure and high cholesterol and to maintain a healthy weight |

|(Non-drug and Drug |Quit smoking, if you smoke |

|Therapy – include all |Exercise, as directed by your doctor |

|therapeutic |Lose weight, if you are overweight or obese |

|classes/agents |Reduce stress |

|available and |For the first time, flu shots are recommended in patients with chronic cardiovascular disease. |

|preferences per |Treat underlying medical conditions that may aggravate myocardial ischemia such as hypertension, tachycardia, fever, thyrotoxicosis, |

|treatment guidelines) |anemia, or hypoxemia |

| |Modification of activities that exacerbated angina (cold weather, postprandial exercise) |

| | |

| |Drug Therapy for Stable Angina: |

| |Aspirin/Antiplatelet therapy |

| |BB |

| |CCB |

|**See Treatment Options|Nitroglycerin |

|Table |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) |

| | |

| |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 |

|Monitoring |Indices of Therapeutic Effect: |

| |Stable Angina: |

|(Efficacy and Toxicity |Decrease frequency of chest pain and TNG administration |

|Parameters) |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. |

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