Acute Coronary Syndromes

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Chapter 18 Acute Coronary Syndromes

The term acute coronary syndrome covers a broad spectrum of clinical situations, from unstable angina to ST-segment elevation myocardial infarction (STEMI). These are, with rare exceptions (Table 18-1), a consequence of acute thrombus formation related to a disrupted coronary atherosclerotic plaque. Over the past decade, tremendous progress has been made in our understanding of the pathophysiology, classification, patient risk stratification, and management of acute coronary syndromes. However, they remain an important cause of morbidity and mortality; they were the most common cause of adult hospital admissions in the United States in 2001.

Table 18-1 Causes of Regional Myocardial Ischemia Other Than Atherosclerotic Disease

Spontaneous coronary artery dissection
Coronary emboli (thrombus, vegetations, atrial myxoma, valve leaflet calcification)
Coronary artery spasm
Coronary arteritis
Aortic dissection involving the aortic root
Transplant vasculopathy


The coronary atherosclerotic plaque is the hallmark lesion of coronary artery disease. It is located in the intima of the artery and consists of a central lipid core surrounded by a fibrous capsule which separates the core from the vessel lumen (Fig. 18-1A). Atherosclerotic plaques most likely originate from preexisting intimal lesions (intimal masses or thickenings and intimal xanthoma or fatty streaks) that are present from childhood. The majority of these intimal lesions regress or remain stable. However, in the presence of atherogenic risk factors (smoking, hypertension, hyperglycemia, dyslipidemia)—which result in endothelial cell dysfunction and inflammation—these intimal lesions can lead to the formation of atherosclerotic plaques. Endothelial cell dysfunction and inflammation are key features of this process.1,2

Thrombus Formation on Vulnerable Atherosclerotic Plaques

The underlying pathophysiologic process of acute coronary syndromes involves thrombus formation on an atherosclerotic plaque (Fig. 18-1B).3 Three separate mechanisms appear to result in thrombus formation: (1) plaque rupture; (2) plaque erosion; (3) thrombosis associated with a calcified nodule (Table 18-2).

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Table 18-2 Plaque Thrombosis: Mechanisms and Plaque Characteristics

Rights were not granted to include this table in electronic media. Please refer to the printed book.

(Figures from Naghavi M, Libby P, Falk E, et al: From vulnerable plaque to vulnerable patient: A call for new definitions and risk assessment strategies: Part I. Circulation 108:1664, 2003.)

Following plaque disruption the subendothelial connective tissue, the tissue-factor-rich lipid core, or both are exposed to blood. This results in platelet activation and aggregation and in stimulation of the coagulation cascade, eventually leading to thrombus formation. Thrombus may be limited and remain within the plaque, in which case it is clinically silent. Alternatively, thrombus formation may progress and become exposed to blood flow within the artery lumen (mural thrombus). Platelet-thrombin emboli may pass distally and cause microvascular obstruction and result clinically in a non-ST-elevation acute coronary syndrome. Further growth of the thrombus eventually leads to intraluminal obstruction with resultant macrovascular ischemia. When thrombus causes total vessel occlusion, an ST-elevation acute coronary syndrome results.

The morphologies of plaques that are at high risk for thrombus formation through these mechanisms are quite distinct.4 Furthermore, the majority of these lesions are non-flow-limiting stenoses of less than 70% diameter. Therefore, the risk for future acute coronary ischemic events appears to be dependent largely on the presence of these morphologically distinct plaques, rather than on the presence of severely stenotic lesions. The term vulnerable plaque is used to describe lesions that are prone to thrombus formation.


Patients with acute coronary syndromes usually present with symptoms consistent with myocardial ischemia at rest or on minimal exertion, typically of more than 10 minutes in duration. The classification of acute coronary syndromes attempts to incorporate several aspects of the syndrome (pathophysiology, assessment, diagnosis, risk stratification, and evidence-based therapy) into a single clinically useful paradigm.

Establishing a Working Diagnosis of Acute Coronary Syndrome

Patients with acute coronary syndromes are classified into two groups on the basis of ST-segment changes on their admission electrocardiograms (ECGs) (Fig. 18-3). This classification provides an initial working diagnosis so that appropriate therapy can be initiated.

Establishing a Final Diagnosis of Myocardial Infarction

Myocardial infarction is defined as myocyte necrosis in the setting of an acute coronary syndrome, PCI, or CABG (Table 18-3). The diagnosis of myocardial infarction in a patient with an acute coronary syndrome is based on: (1) biochemical markers; (2) evolving ECG changes; (3) clinical features.

Table 18-3 Definition of Myocardial Infarction

The European Society of Cardiology and American College of Cardiology: Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction. Eur Heart J 21:1502-1513, 2000.

CK-MB, MB fraction of creatine kinase; PCI, percutaneous coronary intervention.

Biochemical evidence of myocardial infarction involves a typical pattern of elevation followed by a gradual fall of the troponins (either I or T) or of the creatine kinase MB fraction (CK-MB) (see Table 18-6 and Fig. 18-11 in Laboratory Tests, later in the text). When using troponin T, a level above 0.03 μg/l is considered elevated; the cut-off for troponin I depends on the assay used. CK-MB increases more rapidly than the troponins and provides early evidence of myocardial infarction, but CK-MB is a less sensitive and less specific marker of myocyte damage.


Figure 18.11 Kinetic profiles of cardiac markers following ST-elevation myocardial infarction.

(From French JK, White HD: Clinical implications of the new definition of myocardial infarction. Heart 90:99-106, 2004.) ULRR, upper limit of the reference range.

The development of pathologic Q waves on the ECG in the territory of ischemia correlates with, but does not necessarily reflect, transmural (full-thickness) ventricular wall necrosis (Q wave or transmural myocardial infarction). However, this differentiation is of no benefit in patient management.

In non-ST-elevation acute coronary syndromes, and uncommonly in ST-elevation acute coronary syndromes, rapid resolution of symptoms and ECG changes occurs with no evidence of myocardial marker elevation. In this situation the diagnosis is aborted infarction (if ST elevation was present) or unstable angina.


A targeted history, a clinical examination, and investigations are needed to confirm a diagnosis of acute coronary syndrome, to exclude other causes of the presenting symptoms (Table 18-4), to risk-stratify the patient, and to initiate appropriate therapy without delay. The assessment and risk stratification of a patient should be a dynamic process throughout his or her hospitalization (Fig. 18-4).

Table 18-4 Differential Diagnosis of Symptoms Associated With Acute Coronary Syndromes

Aortic dissection
Pulmonary embolus
Peptic ulcer
Tension pneumothorax
Esophageal rupture with mediastinitis
Gastroesophageal reflux and spasm
Musculoskeletal/chest wall pain
Biliary or pancreatic pain
Cervical disk or neuropathic pain

Figure 18.4 Early triage of patients presenting with probable or possible ischemic symptoms, including chest pain. ACS, acute coronary syndrome; ECG, electrocardiogram; LBBB, left bundle branch block; PCI, percutaneous coronary intervention.

(Adapted from Braunwald E, Antman EM, Beasley JW, et al: ACC/AHA 2002 Guideline updated for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction. J Am Coll Cardio 40:1366-1374, 2002.)


An ECG should be obtained and reviewed immediately on presentation. If the initial ECG is normal or only mildly abnormal (Fig. 18-5) and there is a high clinical suspicion of myocardial infarction, serial ECGs should be performed at 5- to 10-minute intervals or, ideally, continuous ST-segment monitoring should be instituted. ECGs should be obtained every 6 to 8 hours in all other patients until an established diagnosis has been made.

ECG in ST-Elevation Acute Coronary Syndromes

The following criteria are used to define ST-segment elevation:

A patient who presents with a history consistent with acute myocardial ischemia and has an ECG with new or presumed-new LBBB should be classified and managed as having an ST-elevation acute coronary syndrome. In the setting of LBBB, the presence of one of the following ECG criteria adds independent diagnostic value: