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The Pharmacologic Management of Coronary Artery Disease: A Brief Overview

George DeMaagd, PharmD, BCPS
Published Online: Sunday, February 1, 2004   [ Request Print ]

Coronary artery disease (CAD), often referred to as ischemic heart disease, includes a broad spectrum of disease. The American College of Cardiology (ACC) and the American Heart Association (AHA) have provided guidelines for the management of CAD. Publications available include guidelines on chronic stable angina (CSA) and acute coronary syndromes (ACSs). ACSs include unstable angina (UA), non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).1-3

Chronic Stable Angina

The pathophysiology of CSA is best described as the formation of fibrous plaques protruding into the lumen, restricting blood flow, and leading to anginal symptoms. The pharmacotherapeutic goals include treating and preventing symptoms in addition to preventing future cardiac events and death (Table 1). Symptom management includes the use of nitroglycerin (NTG) sublingual or spray, beta-blockers (BBs), nondihydropyridine calcium channel blockers (CCBs), and long-acting nitrates. Other therapies used to prevent future cardiac events include antiplatelet agents, aspirin (ASA), or clopidogrel. Angiotensin-converting enzyme inhibitors (ACEIs) are recommended for patients with a history of diabetes or left ventricular (LV) dysfunction. Concurrent disease state management includes controlling lipids, blood pressure, and blood glucose in diabetics.1,4,5

Acute Coronary Syndromes

Unstable Angina and Non-ST-Segment Elevation Myocardial Infarction

UA and NSTEMI are considered ACSs and are difficult to differentiate clinically. Objectively, NSTEMI patients present with elevated cardiac enzymes and electrocardiographic (ECG) changes (ST-segment depression), features not usually seen with UA. The pathophysiology of these syndromes is best described as a disruption of plaque in the lumen of the artery, resulting in decreased coronary blood flow.2

The pharmacotherapy of UA and NSTEMI (Table 2) includes drugs to relieve symptoms and myocardial ischemia, including NTG, morphine sulfate (MS), and intravenous BBs. In patients with normal LV function, CCBs may be alternatives if there is inadequate response or a contraindication to BBs. Management also requires a greater focus on anticoagulant and antiplatelet therapies, including administration of ASA 325 mg, chewed on arrival in the emergency room. Clopidogrel may be an alternative antiplatelet agent if there are contraindications to aspirin. More recent evidence supports the combination of ASA with clopidogrel for up to 9 months, especially in hospitalized patients not receiving percutaneous coronary intervention (PCI).2,3 Some patients receiving PCI also may receive this combination if they are at a low risk for bleeding. In patients undergoing coronary artery bypass grafts (CABG),6 clopidogrel should be discontinued 1 week prior to the procedure.2,3,6

The glycoprotein IIb/IIIa inhibitors (Table 3) and unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) may be added to ASA and clopidogrel, especially in patients who will undergo catheterization and PCI. In patients not undergoing PCI, the guidelines2 specify patient types and choice of agents that may be used. If patients have a history of heparin-induced thrombocytopenia, the direct thrombin inhibitors (Table 4) may be used as an alternative to UFH or LMWH.2

Post-ACS pharmacotherapy should include ASA (75-160 mg) and/or clopidogrel, BBs, or a CCB in most patients. ACEIs are recommended especially in patients with hypertension, LV dysfunction, or diabetes.4 Lipid-lowering therapies also are recommended for some patients.2,5

The complexity of treating patients with ACS involves a series of decisions and risk stratifications made in the emergency room and the cardiac catheterization laboratory. Decisions may involve conservative strategies versus revascularization procedures.3,6

ST-Segment Elevation Myocardial Infarction

The pathophysiology of STEMI is best described by plaque rupture in the vessel lumen, thrombus formation, occlusion, and an interruption of blood flow. The resultant progressive cell necrosis requires urgent revascularization. STEMI patients present objectively with elevation of cardiac enzymes and ST segment elevation on ECG.7

Pharmacotherapy (Table 3) includes a dose of ASA 325 mg chewed, intravenous NTG, and MS if needed. Intravenous BBs are recommended within 12 hours, with a switch to oral BBs once the patient is stable. Heparin is initiated in most patients, using UFH or LMWH. Initiation of ACEIs also is recommended within 24 hours of presentation. After initial evaluation, a decision is made to treat with intervention (eg, PCI or CABG)3,6 or with thrombolytic therapy. Post-MI management of STEMI will include ASA, oral BBs, ACEIs, and HMGCoA reductase inhibitors (Tables 3 and 4).5,7

Post-MI patients may receive warfarin, especially if they have concurrent atrial fibrillation or an LV thrombus. Other therapies may include the use of scheduled nitrates for postinfarction ischemia or amiodarone when antiarrhythmic therapy is indicated.7

Variant Angina (Prinzmetal's Angina)

Another form of angina unrelated to plaque formation and disruption in the arteries has vasospasm as its primary etiology. Management includes identifying risk factors (eg, smoking) and pharmacotherapy with NTG and CCBs. BBs should be avoided due to potential exacerbation secondary to unopposed alpha constriction on the vessels.2

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