Angina
I. Size of the Problem
II. Pathophysiology
III. Diagnosis
IV. Disease Processes Causing Angina
V. Stable and Unstable Angina
VI. Nondrug Treatment
VII. Drug Treatment
VIII. Hypertension
IX. Angina Patients with Heart Failure
X. Silent Ischemia
XI. Variant Angina (Prinzmetal’s Angina)
XII. Unstable Angina/Acute Coronary Syndrome
GLOSSARY
afterload arterial impedance, restriction to blood flow delivered
from the left ventricle; force against which the myocardium
contracts in systole; a major determinant of wall stress. arrhythmia general term for an irregularity or rapidity of the
heartbeat, an abnormal heart rhythm. atheroma same as atherosclerosis, raised plaques filled with
cholesterol, calcium, and other substances on the inner wall of
arteries that obstruct the lumen and the flow of blood;
the plaque of atheroma hardens the artery, hence the term
atherosclerosis (sclerosis ¼ hardening). ejection fraction the fraction of blood ejected from the heart
into the arteries, normally this ranges from 50 to 75%; a low
ejection fraction is less than 40%; often used as a marker
of left ventricular contractility and function. electrocardiogram test used to diagnose myocardial infarction;
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- I. SIZE OF THE PROBLEM
Angina is caused by CAD. Atherosclerosis of the coronary arteries causes obstruction to blood flow and deprives the heart muscle of blood. Obstructive atherosclerotic CAD leads to stable or unstable angina, fatal or nonfatal myocardial infarction, sudden death, heart failure, arrhyth¬mias, atrial fibrillation, and thromboembolism that may cause stroke. Approximately 15 million Americans have CAD; approximately 7 million have angina and 8 million have had a heart attack. The approximate economic cost of CAD and stroke in North America is approximately $350 billion, with about $120 billion just for CAD. - II. PATHOPHYSIOLOGY A. Overview
A high blood cholesterol and other factors including a genetic background, cause damage to arteries leading to blockage by atheroma. Obstruction by atheroma occurs most often in the coronary arteries that feed the heart muscle with blood (see Fig. 1 in the chapter Heart Attacks and Fig. 1 in the chapter Atherosclerosis/Atherothrom-bosis). - III. DIAGNOSIS
A. Pain Pattern - IV. DISEASE PROCESSES CAUSING ANGINA
Atherosclerosis Atheroma is the main cause of obstruction of coronary arteries and accounts for more than 90% of cases of angina and coronary artery disease. - V. STABLE AND UNSTABLE ANGINA
There are two types of angina: stable and unstable. Angina is described as stable if the condition has been present for more than two months, or if there has been no change in the pattern of pain, particularly no change in the frequency of attacks, severity, or duration of pain. Patients with stable angina only get pain at rest with sudden emotional stress. Angina is described as unstable when angina is present for less than 60 days, or when there is an increase in the frequency, severity, and duration of pain and a change in the known precipitating factors. If pain that normally occurs only on exertion or moderate activities starts to occur on minimal activity or at rest but without emotional stress, a patient should seek urgent attention in the emergency room. - VI. NONDRUG TREATMENT A. Weight Reduction Effects
If you have angina and you lose 10–25 lb, you will certainly experience less pain, you will require a smaller dose of antianginal medication, and you may not require angioplasty or surgery. - VII. DRUG TREATMENT
In patients with stable angina treatment with drugs usually produces about a 75% improvement in symptoms and quality of life. Three groups of drugs are usually employed: nitrates, beta-blockers, and calcium blockers (calcium antagonists). Aspirin is added to prevent coronary throm¬bosis which causes heart attacks. - VIII. HYPERTENSION
Hypertension causes atheroma formation and athero¬sclerosis. A significant number of patients with angina have hypertension: blood pressure greater than 140 or pressures in the high normal range of 135–140 systolic mmHg. Hypertension causes an increased thickness of the left ventricular muscle, which requires more blood and oxygen to function. Hypertension must be aggressively controlled. The best antihypertensive agents for patients with angina are beta-blockers and ACE inhibitors. ACE inhibitors are particularly useful because they dilate the arterial circulation and rest the myocardium without stimulating the heart to beat at a faster rate or to require more oxygen. Other vasodilators that include OL1-adrenergic blockers, such as terazosin, increase heart rate and ejection velocity and are contraindicated in patients with CAD. These agents may increase the incidence of heart failure. A randomized clinical trial the HOPE study; see the Bibliography indicates that ACE inhibitors improve survival in patients with CAD. - IX. ANGINA PATIENTS WITH HEART FAILURE
Coronary artery disease leads to myocardial infarction which causes weakness of the heart muscle, and some patients over time develop heart failure. These patients are difficult to treat because they are not candidates for bypass surgery. Medical therapy must be used judiciously. Nitrates, in particular cutaneous nitrates, applied 14 h daily, plus a small dose of a beta-blocking drug along with an ACE inhibitor and a diuretic, are beneficial for many patients. Beta-blockers should be avoided in patients with severe heart failure, but those with mild-to-moderate heart failure gain major relief. Recent randomized clinical trials have shown the beta-blockers, carvedilol, metoprolol, and bisoprolol effective in reducing mortality rates and hospitalization. - X. SILENT ISCHEMIA
Myocardial ischemia without pain or symptoms is common in patients with CAD. The incidence of silent ischemia is high and the outcome unfavorable in patients with unstable angina. Interventional therapy is often recommended. Holter monitoring after noncardiac sur¬gery in patients with stable angina and post myocardial infarction patients has documented a high incidence of silent ischemia within the second to fourth day after surgery. - XI. VARIANT ANGINA (PRINZMETAL’S ANGINA)
Prinzmetal’s variant angina is caused by coronary artery spasm of undetermined etiology. Pain usually occurs at rest as opposed to typical stable angina occurring during exertion. The ECG during pain shows ST-segment elevation as opposed to typical angina showing ST-segment depression. An ECG is not necessary, however, to initiate therapy. - XII. UNSTABLE ANGINA/ACUTE CORONARY SYNDROME
A. Pathophysiology and Symptoms - BIBLIOGRAPHY
Cannon, C., and Braunwald, E. Unstable angina. In Heart Disease, sixth edition. E. Braunwald, D.P. Zipes, and P. Libby, eds. W.B. Saunders, Philadelphia, 1232–71, 2201.