CHAPTER 52 Acute Coronary Syndrome

Acute coronary syndrome (ACS) is usually diagnosed in the emergency department based on history, physical examination, abnormalities on ECG, and elevations of cardiac serum biomarkers. According to the American Heart Association (AHA) and American College of Cardiology (ACC), high-risk patients recognized as having ACS should undergo early invasive coronary angiography and angiographically directed revascularization.¹ The ultimate goal is to reperfuse and salvage any viable myocardium immediately. Other imaging modalities play minimal role in the evaluation of these patients. ACS is just one of many possible diagnoses when patients present to the emergency department with acute chest pain, however. Other considerations range from acute life-threatening conditions, such as pulmonary embolism, tension pneumothorax, or aortic dissection, to conditions with less morbidity and mortality, such as gastroesophageal reflux or costochondritis.

Acute chest pain accounts for approximately 6 million emergency department visits annually, and is the second most common reason for patients to present to the emergency department in the United States.² Although most emergency department physicians and cardiologists have a low threshold for diagnosing ACS, 2% to 5% of patients are misdiagnosed and discharged inappropriately.³ In these patients, the mortality rate is 1.7 to 1.9 times greater than in patients who are hospitalized. Most patients who are inappropriately discharged with ACS have a nondiagnostic initial assessment. Various noninvasive imaging modalities are available to evaluate patients with acute, but indeterminate, chest pain in the emergency department.

DEFINITION

ACS refers to any group of clinical symptoms compatible with acute myocardial ischemia. Acute myocardial ischemia is precipitated by coronary artery disease (CAD), resulting in chest pain owing to the lack of blood supply to the myocardium. When patients present with chest pain, an ECG is usually performed. The ECG may show myocardial infarction (MI) with or without ST segment elevation. Patients with ischemia-related discomfort but without ST segment elevation are classified as having either unstable angina or non–ST segment elevation myocardial infarction (NSTEMI). Unstable angina is unexpected chest pain or discomfort that usually occurs while at rest. The discomfort may be more severe and prolonged than typical angina, or may be an initial episode of angina. NSTEMI usually progresses to subendocardial acute MI. Patients who have ST segment elevation myocardial infarction (STEMI) are likely to go on to develop a transmural acute MI. ACS is a spectrum of clinical diagnoses, ranging from unstable angina to NSTEMI to STEMI. Other conditions may mimic ACS, and these need to be excluded.

PREVALENCE AND EPIDEMIOLOGY

In the most recent National Hospital Discharge Survey by the National Center for Health Statistics, there were approximately 1.4 million unique hospitalizations because of ACS in the United States in 2005.⁴ ACS is a major cause of morbidity and mortality in Western countries. The prevalence of ACS increases with age and predominates in men among patients younger than 70 years. In patients older than 70 years, the incidence occurs with equal frequency in men and women. Other risk factors that predispose patients to ACS include diabetes mellitus, smoking, hypertension, hypercholesterolemia, hyperlipidemia, a prior cerebrovascular event, inherited metabolic or connective tissue disorder, cocaine or amphetamine use, and occupational stress.

ETIOLOGY AND PATHOPHYSIOLOGY

Atherosclerosis is the most common culprit leading to acute myocardial ischemia because it decreases the blood supply to a portion of myocardium. At first, even in the setting of atherosclerotic coronary plaques, the coronary arteries permit adequate blood flow to counterbalance myocardial demand. As myocardial demand increases, such as during exercise or stress, the decrease in blood supply may become clinically significant, resulting in angina. Initially, the angina may develop during exertion and resolve at rest, and this is termed stable angina.

Many atherosclerotic plaques are composed of rich foam cells (lipid-laden macrophages), inflammatory cells, and a thin fibrous cap. Such plaques are susceptible to sudden rupture or erosion, exposing the thrombogenic surfaces of the plaques, and allowing platelet aggregation and thrombus formation to occur. Distal microembolization of thrombi may also result. These events usually are not limited to one particular coronary artery, but affect other coronary arteries as well.

Less common causes of acute myocardial ischemia include intense focal epicardial coronary spasm (Prinzmetal angina), cardiac emboli, and arterial inflammation caused by or related to infection. Rarely, myocardial ischemia may occur secondary to increased myocardial demand, particularly sepsis, fever, tachycardia, thyrotoxicosis, or anemia. These precipitating conditions usually occur in patients who have underlying stable CAD.

MANIFESTATIONS OF DISEASE

Clinical Presentation

The typical presentation is characterized by substernal tightness, pressure, squeezing, or heaviness with or without pain radiating to the neck or arm. The chest pain, or angina, can be new in onset and can cause marked limitation of physical activity. The pain may be initiated either at rest or during exertion. Unstable angina may last more than 20 minutes during rest or be signified by a change compared with previous angina, with increasing length, frequency, or onset with less exertion. Atypical chest pain, such as epigastric pain or stabbing or pleuritic chest pain, is a common manifestation of myocardial ischemia. Symptoms other than chest pain, such as dyspnea, nausea or vomiting or both, palpitations, syncope, or cardiac arrest, also can be observed. Atypical presentations are more common in patients who are older, diabetic, and female.

Physical examination findings are frequently unremarkable. Signs of hypotension or congestive heart failure, such as new murmurs, gallops, or rales, may be present.

ECG findings of ST segment or T wave changes and elevated serum cardiac biomarkers, especially cardiac troponins, indicate ACS. The results of ECG are often nonspecific, however, and serum cardiac biomarkers, such as creatine kinase MB (CK-MB) isoenzyme and cardiac troponins, may not be useful in patients who present to the emergency department less than 4 to 5 hours after the onset of their symptoms.

Imaging Indications and Algorithm

Although complicated algorithms exist for classifying risk with regard to indications for noninvasive imaging, chest pain can be categorized into three general groups. The first group comprises patients with life-threatening conditions, in particular high-risk patients diagnosed with ACS based on the history and physical examination, ECG findings, and elevated troponins. These patients immediately undergo coronary angiography and angiographically directed revascularization. Emergent medical and surgical intervention is also required for other life-threatening conditions, such as pulmonary embolism, aortic dissection, and tension pneumothorax.

The second group comprises patients who present with acute chest pain that does not require immediate invasive intervention or imaging, such as gastroesophageal reflux disease or costochondritis. These patients are usually triaged and discharged quickly with a recommendation for outpatient follow-up.

The third group comprises patients who usually present to the emergency department with acute chest pain that is indeterminate for ACS because of a nondiagnostic history, physical examination, or ECG. These patients are considered a diagnostic challenge and often require further noninvasive imaging, including chest radiography, echocardiography, multidetector CT, MRI, and radionuclide perfusion imaging as part of further work-up.

Imaging Technique and Findings

Radiography

Conventional chest radiography is the imaging modality used initially for screening noncardiac etiologies of acute chest pain, including pneumonia, pneumothorax, or rib fractures. Chest pain of cardiac origin also can be indirectly evaluated using chest radiography. Coronary arterial stenosis may be hinted by coronary artery calcification, which is seen in the “coronary triangle”—the mid-upper portion of the left cardiac silhouette on the frontal chest radiograph. In addition, circumferential calcifications may be seen within the expected location of myocardial wall, suggesting prior MI (Fig. 52-1). On the lateral chest radiograph, “tram-track” hyperdensities along the aortic arch correspond to atherosclerotic calcifications in the aorta, which can be independently correlated with coronary heart disease.⁵

FIGURE 52-1 A 58-year-old man presented to the emergency department with chest pain. Posteroanterior and lateral chest radiographs show a circumferential thin band of calcification (arrows) in the left mid-anterior myocardium, likely representing prior MI.

Atherosclerotic calcifications overlying the borders of the heart may also indicate previous episodes of MI.⁶^,⁷ Specifically, hyperdensity or calcifications of the left heart border, often curvilinear, may signify prior infarction of the left ventricular anterolateral wall. Focal outpouching of the left heart border may also represent postinfarct myocardial pseudoaneurysm or aneurysm.⁸

Chest radiography may not only indicate coronary heart disease and prior MI, but it may also be indicative of acute myocardial ischemia. Acute myocardial ischemia may manifest as mild to severe congestive heart failure, ranging from cephalization of blood flow to the upper lobes on erect chest radiography to diffuse interstitial or alveolar pulmonary edema.