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Drugs for Angina Pectoris, Myocardial Infarction, and Cerebrovascular Accident Expanded Key Concepts 25.1 Coronary artery disease includes angina and myocardial infarction. It is a result of the narrowing of the arterial lumen due to atherosclerotic plaque. The narrowing of a coronary artery deprives cells of needed oxygen and nutrients, a condition known as myocardial ischemia. The plaque impairs normal vessel elasticity and the vessel is unable to dilate properly when the myocardium needs additional blood/oxygen. 25.2 The myocardium requires a continuous supply of oxygen from the coronary arteries in order to function properly. The myocardium receives no oxygen or nutrients from the blood flowing through the atria and ventricles. The high metabolic rate of the heart mandates that a continuous supply of oxygen be maintained in the coronary arteries. 25.3 Angina pectoris is the narrowing of a coronary artery resulting in a lack of sufficient oxygen to the heart muscle. Chest pain, upon emotional or physical exertion, is the most characteristic symptom. The coronary arteries can become partially occluded with plaque resulting in ischemia. Lack of sufficient oxygen to the myocardium often causes sharp chest pain upon exertion, the characteristic symptom of angina. The healthcare provider must quickly determine the cause of the pain so appropriate treatment can be administered. 25.4 Angina management may include nonpharmacologic therapies such as diet and lifestyle modifications, treatment of underlying disorders, angioplasty or surgery. Angina can often be controlled through lifestyle changes and surgical procedures. A number of lifestyle changes can reduce the deposition of plaque in the coronary arteries and help prevent coronary artery disease. 25.5 The pharmacologic goals for the treatment of angina are to terminate acute attacks and prevent future episodes. This is usually achieved by reducing cardiac workload. Reducing the workload on the heart can relieve anginal pain. Slowing the heart rate, dilating blood vessels, reducing the force of myocardial contraction or reducing blood pressure can accomplish this. 25.6 The organic nitrates relieve angina by dilating veins and coronary arteries. They are the drugs of choice for stable angina. Fast-acting organic nitrates can quickly terminate anginal pain by causing venous vasodilation, thus reducing the workload on the heart. They also dilate the coronary arteries and bring more oxygen to the heart. Long-acting nitrates can prevent acute angina episodes, but the patient may become tolerant to their protective effect. 25.7 Beta-adrenergic blockers relieve angina by decreasing the oxygen demands on the heart. They are sometimes considered first line medications for chronic angina. Beta-blockers lower blood pressure, slow the heart rate, and reduce the force of contraction, thereby reducing the workload of the myocardium. They are prescribed to reduce the frequency of acute angina episodes. 25.8 Calcium channel blockers relieve angina by dilating the coronary vessels and reducing the workload on the heart. They are drugs of first choice for treating variant angina. CCBs are effective at lowering blood pressure, thus reducing the workload on the heart. They are used to reduce the frequency of acute anginal attacks. 25.9 Glycoprotein IIb/IIIa inhibitors are antiplatelet agents for the treatment of myocardial ischemia. Glycoprotein IIb/IIIa inhibitors are drugs that exert an anticoagulant effect by occupying the glycoprotein IIb/IIIa receptor and inhibiting clot formation. They are of value in the prevention of complications associated with angina and myocardial infarction. 25.10 The early diagnosis of myocardial infarction increases the chances of survival. Early pharmacotherapy may include thrombolytics, aspirin, beta-blockers, and antidysrhythmics. Myocardial infarction is caused by a thrombus in a coronary artery and is responsible for a substantial number of sudden deaths. Fast, effective diagnosis and treatment can reduce mortality. 25.11 If given within hours after the onset of MI, thrombolytic agents can dissolve clots and restore perfusion to affected regions of the myocardium. The goal of thrombolytic therapy is to dissolve clots obstructing the coronary arteries, thus restoring circulation to the myocardium. Quick restoration of cardiac circulation has been found to reduce mortality caused by acute MI. 25.12 When given within 24 hours after the onset of myocardial infarction, beta-adrenergic blockers can improve survival. Beta-blockers have the ability to slow heart rate, decrease contractility and reduce blood pressure. These three factors reduce myocardial oxygen demand, which is beneficial for patients experiencing a recent MI. 25.13 A number of additional drugs are used to treat the symptoms and complications of acute MI. These include analgesics, anticoagulants (including aspirin), and ACE inhibitors. Aspirin and ACE inhibitors reduce mortality when given soon after the onset of an MI. Narcotic analgesics are sometimes given to reduce the pain and the anxiety associated with MI pain. 25.14 CVA is a major cause of death and disability. CVAs may be caused by a clot or by rupture of a cerebral vessel. CVA, or stroke/brain attack, is caused by either a thrombus blocking a cerebral vessel or can be a result of cerebral hemorrhage. It is a major cause of permanent disability and death. Patients can lower their risk for CVA by adopting many of the same lifestyle changes that must be adopted by persons with coronary artery disease or hypertension. 25.15 Aggressive treatment of thrombotic CVA with thrombolytics, to restore perfusion and anticoagulants, to prevent additional clots from forming can increase survival. Stroke (brain attack) is now viewed as an emergency condition requiring immediate treatment in order to improve prognosis. Thrombolytics, when given quickly after the onset of stroke, can restore some or all of the previous brain function. Some degree of stroke prevention can be achieved by using anticoagulants and by controlling blood pressure.
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