 |
| Training |
|
|
| Treatment |
|
|
 |
|
|
|
Unstable Angina
General Considerations
A. BACKGROUND AND HISTORICAL PERSPECTIVE
Nearly 40 years ago, the term intermediate coronary syndrome was used to describe what is now known as the syndrome of unstable angina, which has also been given numerous other labels: preinfarction angina, status anginosus, crescendo angina, impending myocardial infarction (MI), coronary failure, acute coronary insufficiency, spasmodic angina, and atypical angina—all of which terms attest to the heterogeneity of its clinical presentation. In the current era, unstable angina is the admitting diagnosis for about 40–50% of all admissions to cardiac intensive care units.
B. CLINICAL SPECTRUM
Atherosclerotic coronary artery disease comprises a spectrum of conditions that ranges from a totally asymptomatic state at one end to sudden cardiac death at the other . It is clear that coronary artery disease, the primary cause of mortality and morbidity in much of the industrialized world, takes its toll through such acute complications (unstable coronary syndromes) as unstable angina, myocardial infarction, acute congestive heart failure, and sudden cardiac death. Also known as acute ischemic syndromes, these are the first clinical expressions of atherosclerotic coronary artery disease in 30–40% of patients with coronary artery disease.
Clinical Findings
A. SYMPTOMS AND SIGNS
Unstable angina is a clinical syndrome characterized by symptoms of ischemia, which may include classic retrosternal chest pain or such pain surrogates as a burning sensation, feeling of indigestion, or dyspnea (Table 4–2). Anginal symptoms may also be felt primarily or as radiation in the neck, jaw, teeth, arms, back, or epigastrium. In some patients, particularly the elderly, dyspnea, fatigue, diaphoresis, light-headedness, a feeling of indigestion and the desire to burp or defecate, or nausea and emesis may accompany other symptoms—or may be the only symptoms. The pain of unstable angina typically lasts 15—30 min; it can last longer in some patients. The clinical presentation of unstable angina can take any one of several forms.
Differential Diagnosis
Conditions that simulate or masquerade as unstable angina include acute myocardial infarction, acute aortic dissection, acute pericarditis, pulmonary embolism, esophageal spasm, hiatal hernia, chest wall pain, and so on. Careful attention to the history, risk factors and objective findings of ischemia (transient ST-T changes and mild elevations of troponins in particular) remain the cornerstones for the diagnosis.
A. ACUTE MYOCARDIAL InFARCTION
Although myocardial infarction often produces more prolonged pain, the clinical presentation can be indistinguishable from that of unstable angina. As stated earlier, this distinction should be considered somewhat arbitrary because abnormal myocardial technetium-99m pyrophosphate uptake, mild creatine kinase elevations detected on very frequent blood sampling, and increases in troponin-T and I levels (released from necrotic myocytes) are observed in some patients with otherwise classic symptoms of unstable angina—which represents the severe end of the continuum of acute ischemic syndromes.
B. ACUTE AORTIC DISSECTION
The pain of aortic dissection is usually prolonged and severe. It frequently begins in or radiates to the back and tends to be relatively unrelenting and often tearing in nature; transient ST-T changes are rare. An abnormal chest x-ray film showing a widened mediastinum, accompanied by asymmetry in arterial pulses and blood pressure, can provide clues to the diagnosis of aortic dissection, which can be verified by bedside echocardiography (transesophageal, with or without transthoracic echocardiography), magnetic resonance imaging (MRI), computed tomography (CT) scanning, or aortography.
C. ACUTE PERICARDITIS
Acute pericarditis may be difficult to differentiate from unstable angina. A history of a febrile or respiratory illness suggests the former. The pain of pericarditis is classically pleuritic in nature and worsens with breathing, coughing, deglutition, truncal movement, and supine posture. A pericardial friction rub is diagnostic, but it is often evanescent, and frequent auscultation may be needed. Prolonged, diffuse ST elevation that is not accompanied by reciprocal ST depression or myocardial necrosis is typical of pericarditis. Leukocytosis and an elevated sedimentation rate are common in pericarditis but not in unstable angina. Echocardiography may detect pericardial effusion in patients with pericarditis; diffuse ventricular hypokinesis may imply associated myocarditis. Regional dysfunction, especially if transient, is more likely to reflect myocardial ischemia.
D. ACUTE PULMONARY EMBOLISM
Chest pain in acute pulmonary embolism is also pleuritic in nature and almost always accompanied by dyspnea. Arterial hypoxemia is common, and the ECG may show sinus tachycardia with a rightward axis shift. Precordial ST-T wave abnormalities may simulate patterns of anterior myocardial ischemia or infarction. A high index of suspicion, combined with a noninvasive assessment of pulmonary ventilation-perfusion mismatch, evidence of lower extremity deep vein thrombosis, and possibly pulmonary angiography, is necessary to exclude the diagnosis.
E. GASTROINTESTINAL CAUSES OF PAIN
Various gastrointestinal pathologies can mimic unstable angina. These include esophageal spasm, peptic ulcer, hiatal hernia, cholecystitis, and acute pancreatitis. A history compatible with those conditions, the response to specific therapy, and appropriate biochemical tests and imaging procedures should help clarify the situation. It should be noted that these abdominal conditions may produce ECG changes that simulate acute myocardial ischemia.
F. OTHER CAUSES OF CHEST PAIN
Many patients present with noncardiac chest pain that mimics unstable angina, and sometimes no specific diagnosis can be reached. The pain may be musculoskeletal or there may be nonspecific changes on the ECG that increase the diagnostic confusion. In these patients, a definite diagnosis often cannot be reached despite careful clinical observation. When the pain has abated and the patient is stable, a provocative test for myocardial ischemia may help rule out ischemic heart disease. Although coronary angiography may provide evidence of atherosclerotic coronary artery disease, anatomic evidence does not necessarily prove an ischemic cause for the symptoms. In some patients acute myocarditis may also produce chest pain syndromes simulating unstable angina and acute myocardial infarction. Recreational drug use (cocaine and amphetamine) may also produce clinical syndromes of chest pain, sometimes related to drug-induced acute coronary syndrome precipitated by the vasoconstrictor and prothrombic effects of drugs.
Management
In treating unstable angina, the initial objective is to stratify patients for their short-term morbidity and mortality risks based on their clinical presentations . Following risk stratification, management objectives include eliminating episodes of ischemia and preventing acute myocardial infarction and death.
Prognosis
The treatment of USA/NSTEMI has evolved rapidly over the past several years resulting in improved patient outcomes. It has been difficult to obtain an accurate and precise rate of adverse events because of the heterogeneous nature of the patient population and different designs and background medications used in clinical trials. However, it is clear that with the advancement of treatment strategies, clinical event rates for refractory angina, MI, and death have reduced substantially. For example, in patients who were not treated with aspirin and heparin, the rate of refractory angina, MI, and death was 23, 12, and 1.7%, respectively, within first week of treatment and the rates became 10.7, 1.6, and 0%, respectively, if the patients were treated with aspirin and heparin. With the addition of a IIb/IIIa receptor inhibitor, the rate for refractory angina, MI, or death was 10.6, 8.3, and 6.9%, respectively, at 6 months in the PRISM-PLUS trial. With the combination of early invasive strategy, IIb/IIIa inhibitor, heparin, and aspirin, the 6-month mortality rate decreased further to 3.3% in the TACTICS-TIMI 18 trial. Even with such decreases in the event rates, a substantial number of patients still continue to suffer from USA/NSTEMI and its complications due to the high prevalence of atherosclerosis. All patients should become acquainted with risk factor modification strategies, which include lipid lowering, smoking cessation, an exercise program, diabetes control, BP control, dietary counseling, and weight control. Recently, the use of angiotensin-converting enzyme inhibitors has also been shown to reduce atherothrombotic events in patients with coronary artery disease especially in presence of diabetes. With the advancement of therapies and risk factor modification, patients' short- and long-term outcomes can be further improved. A simple mnemonic—ABCDE summarizes the long-term risk-reducing approach for patients with unstable coronary artery disease.
|
 |
Healt Tips |
|
|
|
