EKG or ECG. heart failure a failure of the heart to pump sufficient blood
from the chambers into the aorta; inadequate supply of blood
reaches organs and tissues. myocardial infarction death of an area of heart muscle due to
blockage of coronary artery by blood clot and atheroma;
medical term for a heart attack or coronary thrombosis. myocardium the heart muscle. palpitation rapid heart rate; the patient feels the heartbeat.
preload the degree of ventricular muscle stretch present at the onset of myocardial contraction; often expressed as end diastolic volume or pressure.
tachycardia minute.
increase in heart rate exceeding 100 beats per

PAIN OR DISCOMFORT IN THE CHEST, THROAT, jaw, or arms caused by severe, but temporary, lack of blood and oxygen to a part of the heart muscle defines angina pectoris (see Fig. 1 in the chapter Heart Attacks). Angina is caused by coronary artery disease (CAD) but often referred to as coronary heart disease (CHD). Because obstructive coronary artery disease causes a lack of blood to reach the heart muscle (ischemia), the condition is also called ischemic heart disease (IHD). Angina affects men more commonly than women, and the underlying disease condi¬tion is not surprisingly referred to as ‘‘the widow-maker.’’

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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.