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Acute coronary
syndromes result from acute obstruction of a coronary artery. Consequences depend
on degree and location of obstruction and range from unstable angina
to non-ST-segment elevation MI (NSTEMI), ST-segment elevation MI
(STEMI), and sudden cardiac death. Symptoms are similar in each
of these syndromes (except sudden death) and include chest discomfort
with or without dyspnea, nausea, and diaphoresis. Diagnosis is by
ECG and the presence or absence of serologic markers. Treatment
is antiplatelet drugs, anticoagulants, nitrates, β-blockers,
and, for STEMI, emergency reperfusion via fibrinolytic drugs, percutaneous
intervention, or, occasionally, coronary artery bypass graft surgery.
In the US, about 1.5 million MIs occur annually; MI results in death for 400,000 to 500,000 people, with about half dying before they reach the hospital (see Respiratory and Cardiac Arrest: Cardiac Arrest).
Etiology
Acute coronary syndromes (ACS) usually occur when an acute thrombus forms in an atherosclerotic coronary artery. Atheromatous plaque sometimes becomes unstable or inflamed, causing it to rupture or split, exposing thrombogenic material, which activates platelets and the coagulation cascade and produces an acute thrombus. Platelet activation involves a conformational change in membrane glycoprotein IIb/IIIa receptors, allowing cross-linking (and thus aggregation) of platelets. Even atheromas causing minimal obstruction can rupture and result in thrombosis; in > 50% of cases, stenosis is < 40%. The resultant thrombus abruptly interferes with blood flow to parts of the myocardium. Spontaneous thrombolysis occurs in about 2⁄3 of patients; 24 h later, thrombotic obstruction is found in only about 30%. However, in virtually all cases, obstruction lasts long enough to produce tissue necrosis.
Rarely, these syndromes are caused by arterial embolism (eg, in mitral or aortic stenosis, infective endocarditis, or marantic endocarditis). Cocaine use and other causes of coronary spasm can sometimes result in MI. Spasm-induced MI may occur in normal or atherosclerotic coronary arteries.
Pathophysiology
Initial consequences vary with size, location, and duration of obstruction and range from transient ischemia to infarction. Measurement of newer, more sensitive markers indicates that some cell necrosis probably occurs even in mild forms; thus, ischemic events occur on a continuum, and classification into subgroups, although useful, is somewhat arbitrary. Sequelae of the acute event depend primarily on the mass and type of cardiac tissue infarcted.
Myocardial dysfunction:
Ischemic (but not infarcted) tissue has impaired contractility, resulting in hypokinetic or akinetic segments; these segments may expand or bulge during systole (called paradoxical motion). The size of the affected area determines effects, which range from minimal to mild heart failure to cardiogenic shock. Some degree of heart failure occurs in about 2⁄3 of hospitalized patients with acute MI. It is termed ischemic cardiomyopathy if low cardiac output and heart failure persist. Ischemia involving the papillary muscle may lead to mitral valve regurgitation.
MI:
MI is myocardial necrosis resulting from abrupt reduction in coronary blood flow to part of the myocardium. Infarcted tissue is permanently dysfunctional; however, there is a zone of potentially reversible ischemia adjacent to infarcted tissue.
MI affects predominantly the left ventricle (LV), but damage may extend into the right ventricle (RV) or the atria. RV infarction usually results from obstruction of the right coronary or a dominant left circumflex artery; it is characterized by high RV filling pressure, often with severe tricuspid regurgitation and reduced cardiac output. An inferoposterior infarction causes some degree of RV dysfunction in about half of patients and produces hemodynamic abnormality in 10 to 15%. RV dysfunction should be considered in any patient who has inferoposterior infarction and elevated jugular venous pressure with hypotension or shock. RV infarction complicating LV infarction may significantly increase mortality risk.
Anterior infarcts tend to be larger and result in a worse prognosis than inferoposterior infarcts. They are usually due to left coronary artery obstruction, especially in the anterior descending artery; inferoposterior infarcts reflect right coronary or dominant left circumflex artery obstruction.
Transmural infarcts involve the whole thickness of myocardium from epicardium to endocardium and are usually characterized by abnormal Q waves on ECG. Nontransmural or subendocardial infarcts do not extend through the ventricular wall and cause only ST-segment and T-wave (ST-T) abnormalities. Subendocardial infarcts usually involve the inner 1⁄3 of myocardium, where wall tension is highest and myocardial blood flow is most vulnerable to circulatory changes. These infarcts may follow prolonged hypotension. Because the transmural depth of necrosis cannot be precisely determined clinically, infarcts are usually classified by the presence or absence of ST-segment elevation or Q waves on the ECG. Volume of myocardium destroyed can be roughly estimated by the extent and duration of CK elevation.
Electrical
dysfunction:
Ischemic and necrotic cells are incapable of normal electrical activity, resulting in various ECG changes (predominantly ST-T abnormalities), arrhythmias, and conduction disturbances. ST-T abnormalities of ischemia include ST-segment depression (often downsloping from the J point), T-wave inversion, ST-segment elevation (often referred to as injury current), and peaked T waves in the hyperacute phase of infarction. Conduction disturbances can reflect damage to the sinus node, the atrioventricular (AV) node, or specialized conduction tissues. Most changes are transient; some are permanent.
Classification
Classification is based on ECG changes and presence or absence of cardiac markers in blood. Distinguishing NSTEMI and STEMI is useful because prognosis and treatment are different.
Unstable
angina (acute coronary insufficiency, preinfarction angina, intermediate syndrome) is defined as:
Also, ECG changes such as ST-segment depression, ST-segment elevation, or T-wave inversion may occur during unstable angina but are transient. Of cardiac markers, CPK is not elevated but troponin I or T may be slightly increased. Unstable angina is clinically unstable and often a prelude to MI or arrhythmias or, less commonly, to sudden death.
Non-ST-segment elevation
MI (NSTEMI, subendocardial MI) is myocardial necrosis (evidenced by cardiac markers in blood; troponin I or T and CPK will be elevated) without acute ST-segment elevation or Q waves. ECG changes such as ST-segment depression, T-wave inversion, or both may be present.
ST-segment elevation
MI (STEMI, transmural MI) is myocardial necrosis with ECG changes showing ST-segment elevation that is not quickly reversed by nitroglycerin or showing new left bundle branch block. Q waves may be present. Both troponin and CPK are elevated.
Symptoms and Signs
Symptoms of ACS depend somewhat on the extent and location of obstruction and are quite variable. Except when infarction is massive, recognizing the amount of ischemia by symptoms alone is difficult.
After the acute event, many complications can occur. They usually involve electrical dysfunction (eg, conduction defects, arrhythmias), myocardial dysfunction (eg, heart failure, interventricular septum or free wall rupture, ventricular aneurysm, pseudoaneurysm, mural thrombus formation, cardiogenic shock), or valvular dysfunction (typically mitral regurgitation). Electrical dysfunction can be significant in any form of ACS, but usually, large parts of myocardium must be ischemic to cause significant myocardial dysfunction. Other complications of ACS include recurrent ischemia and pericarditis. Pericarditis that occurs 2 to 10 wk after an MI is known as post-MI syndrome or Dressler's syndrome.
Unstable
angina:
Symptoms are those of angina pectoris (see Coronary Artery Disease: Symptoms and Signs), except that the pain or discomfort of unstable angina usually is more intense, lasts longer, is precipitated by less exertion, occurs spontaneously at rest (as angina decubitus), is progressive (crescendo) in nature, or involves any combination of these features.
NSTEMI and STEMI:
Symptoms of NSTEMI and STEMI are the same. Days to weeks before the event, about 2⁄3 of patients experience prodromal symptoms, including unstable or crescendo angina, shortness of breath, and fatigue. Usually, the first symptom of infarction is deep, substernal, visceral pain described as aching or pressure, often radiating to the back, jaw, left arm, right arm, shoulders, or all of these areas. The pain is similar to angina pectoris but is usually more severe and long-lasting; more often accompanied by dyspnea, diaphoresis, nausea, and vomiting; and relieved little or only temporarily by rest or nitroglycerin . However, discomfort may be mild; about 20% of acute MIs are silent (ie, asymptomatic or producing vague symptoms not recognized as illness by the patient), more commonly in diabetics. Some patients present with syncope. Patients often interpret their discomfort as indigestion, particularly because spontaneous relief may be falsely attributed to belching or antacid consumption. Women are more likely to present with atypical chest discomfort. Elderly patients may report dyspnea more than ischemic-type chest pain. In severe ischemic episodes, the patient often has significant pain and feels restless and apprehensive. Nausea and vomiting may occur, especially with inferior MI. Dyspnea and weakness due to LV failure, pulmonary edema, shock, or significant arrhythmia may dominate.
Skin may be pale, cool, and diaphoretic. Peripheral or central cyanosis may be present. Pulse may be thready, and BP is variable, although many patients initially have some degree of hypertension during pain.
Heart sounds are usually somewhat distant; a 4th heart sound is almost universally present. A soft systolic blowing apical murmur (reflecting papillary muscle dysfunction) may occur. During initial examination, a friction rub or more striking murmurs suggest a preexisting heart disorder or another diagnosis. Detection of a friction rub within a few hours after onset of MI symptoms suggests acute pericarditis rather than MI. However, friction rubs, usually evanescent, are common on days 2 and 3 post-STEMI. The chest wall is tender when palpated in about 15% of patients.
In RV infarction, signs include elevated RV filling pressure, distended jugular veins (often with Kussmaul's sign—see Approach to the Cardiac Patient: Veins), clear lung fields, and hypotension.
Diagnosis
ACS should be considered in men > 30 yr and women > 40 yr (younger in diabetics) whose main symptom is chest pain or discomfort. Pain must be differentiated from the pain of pneumonia, pulmonary embolism, pericarditis, rib fracture, costochondral separation, esophageal spasm, acute aortic dissection, renal calculus, splenic infarction, or various abdominal disorders. In patients with previously diagnosed hiatus hernia, peptic ulcer, or a gallbladder disorder, the clinician must be wary of attributing new symptoms to these disorders.
The approach is the same when any ACS is suspected: initial and serial ECG and serial cardiac marker measurements, which distinguish among unstable angina, NSTEMI, and STEMI. Every emergency department should have a triage system to immediately identify patients with chest pain for rapid assessment and ECG. Pulse oximetry and chest x-ray (particularly to look for mediastinal widening, which suggests aortic dissection) is also done.
ECG:
ECG is the most important test and should be done within 10 min of presentation. It is the center of the decision pathway because fibrinolytics benefit patients with STEMI but may increase risk for those with NSTEMI. Also, emergent cardiac catheterization is indicated for patients with acute STEMI but not for those with NSTEMI.
For STEMI, initial ECG is usually diagnostic, showing ST-segment elevation ≥ 1 mm in 2 or more contiguous leads subtending the damaged area (see Fig. 1: Coronary Artery Disease: Acute anterior left ventricular infarction (tracing obtained within a few hours of onset of illness). , Fig. 2: Coronary Artery Disease: Acute anterior left ventricular infarction (after the first 24 h)., Fig. 3: Coronary Artery Disease: Acute anterior left ventricular infarction (several days later)., Fig. 4: Coronary Artery Disease: Acute inferior (diaphragmatic) left ventricular infarction (tracing obtained within a few hours of onset of illness)., Fig. 5: Coronary Artery Disease: Acute inferior (diaphragmatic) left ventricular infarction (after the first 24 h)., and Fig. 6: Coronary Artery Disease: Acute inferior (diaphragmatic) left ventricular infarction (several days later).).
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Fig. 1
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Acute anterior left ventricular infarction (tracing obtained within a few hours of onset of illness).
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There is striking hyperacute ST-segment elevation in leads I, aVL, V4, and V6 and reciprocal depression in other leads.
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Fig. 2
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Acute anterior left ventricular infarction (after the first 24 h).
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ST segments are less elevated; significant Q waves develop and R waves are lost in leads I, aVL, V4, and V6.
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Fig. 3
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Acute anterior left ventricular infarction (several days later).
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Significant Q waves and loss of R-wave voltage persist. ST segments are now essentially isoelectric. The ECG will probably change only slowly over the next several months.
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Fig. 4
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Acute inferior (diaphragmatic) left ventricular infarction (tracing obtained within a few hours of onset of illness).
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There is hyperacute ST-segment elevation in leads II, III, and aVF and reciprocal depression in other leads.
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Fig. 5
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Acute inferior (diaphragmatic) left ventricular infarction (after the first 24 h).
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Significant Q waves develop with decreasing ST-segment elevation in leads II, III, and aVF.
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Fig. 6
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Acute inferior (diaphragmatic) left ventricular infarction (several days later).
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ST segments are now isoelectric. Abnormal Q waves in leads II, III, and aVF indicate that myocardial scars persist.
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Pathologic Q waves are not necessary for the diagnosis. The ECG must be read carefully because ST-segment elevation may be subtle, particularly in the inferior leads (II, III, aVF); sometimes the reader's attention is mistakenly focused on leads with ST-segment depression. If symptoms are characteristic, ST-segment elevation on ECG has a specificity of 90% and a sensitivity of 45% for diagnosing MI. Serial tracings (obtained q 8 h for 1 day, then daily) showing a gradual evolution toward a stable, more normal pattern or development of abnormal Q waves over a few days tends to confirm the diagnosis.
Because nontransmural (non–Q-wave) infarcts are usually in the subendocardial or midmyocardial layers, they do not produce diagnostic Q waves or distinct ST-segment elevation on the ECG. Instead, they commonly produce only varying degrees of ST-T abnormalities that are less striking, variable, or nonspecific and sometimes difficult to interpret (NSTEMI). If such abnormalities resolve (or worsen) on repeat ECGs, ischemia is very likely. However, when repeat ECGs are unchanged, acute MI is unlikely and, if still suspected clinically, requires other evidence to make the diagnosis. A normal ECG taken when a patient is pain free does not rule out unstable angina; a normal ECG taken during pain, although it does not rule out angina, suggests that the pain is not ischemic.
If RV infarction is suspected, a 15-lead ECG is usually recorded; additional leads are placed at V4R, and, to detect posterior infarction, V8 and V9.
ECG diagnosis of MI is more difficult when a left bundle branch block configuration is present because it resembles STEMI changes. ST-segment elevation concordant with the QRS complex strongly suggests MI as does > 5-mm ST-segment elevation in at least 2 precordial leads. But generally, any patient with suggestive symptoms and new-onset (or not known to be old) left bundle branch block is treated as for STEMI.
Cardiac
markers:
Cardiac markers are cardiac enzymes (eg, CPK-MB) and cell contents (eg, troponin I, troponin T, myoglobin) that are released into the bloodstream after myocardial cell necrosis. The markers appear at different times after injury and decrease at different rates (see Fig. 7: Coronary Artery Disease: Relative timing and levels of cardiac markers in blood after acute MI.).
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Fig. 7
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Relative timing and levels of cardiac markers in blood after acute MI.
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MGB = myoglobulin.
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Usually, several different markers are measured at regular intervals, typically q 6 to 8 h for 1 day. Newer bedside tests, which are more convenient, can be just as sensitive when done at shorter intervals (eg, time 0, 1, 3, and 6 h after presentation).
Troponins are most specific for MI but can also be elevated by ischemia without infarction; elevated levels (actual number varies with assay used) are considered diagnostic. Borderline elevated troponin levels in patients with unstable angina indicate increased risk of adverse events and thus the need for further evaluation and treatment. False positives sometimes occur in heart failure and renal failure. CPK-MB is slightly less specific. False positives occur with renal failure, hypothyroidism, and skeletal muscle injury. Myoglobin is not specific for MI but, because it increases earlier than other markers, may be an early warning sign to assist in triage of patients with nondiagnostic ECGs.
Coronary
angiography:
Coronary angiography most often combines diagnosis with percutaneous coronary intervention (PCI, ie, angioplasty, stenting). Angiography is obtained emergently for patients with STEMI, patients with persistent chest pain despite maximal medical therapy, and patients with complications (eg, markedly elevated cardiac markers, presence of cardiogenic shock, acute mitral regurgitation, ventricular septal defect, unstable arrhythmias). Patients with uncomplicated NSTEMI or unstable angina whose symptoms have resolved typically undergo angiography within the first 24 to 48 h of hospitalization to detect lesions that may require treatment.
After initial evaluation and therapy, coronary angiography may be used in patients with evidence of ongoing ischemia (ECG findings or symptoms), hemodynamic instability, recurrent ventricular tachyarrhythmias, and other abnormalities that suggest recurrence of ischemic events. Some experts also recommend that angiography be done before hospital discharge in STEMI patients with inducible ischemia on stress imaging or an ejection fraction < 40%.
Other tests:
Routine laboratory tests are nondiagnostic but, if obtained, show nonspecific abnormalities compatible with tissue necrosis (eg, increased ESR, moderately elevated WBC with a shift to the left). A fasting lipid profile should be obtained within the first 24 h for all patients hospitalized with ACS.
Myocardial imaging (see also Cardiovascular Tests and Procedures: Imaging Tests) is not needed to make the diagnosis if cardiac markers or ECG is positive. However, in patients with MI, bedside echocardiography is invaluable for detecting mechanical complications. Before or shortly after discharge, patients with symptoms suggesting an ACS but nondiagnostic ECGs and normal cardiac markers should have a stress imaging test (radionuclide or echocardiographic imaging with pharmacologic or exercise stress). Imaging abnormalities in such patients indicate increased risk of complications in the next 3 to 6 mo.
Right heart catheterization using a balloon-tipped pulmonary artery catheter (see Approach to the Critically Ill Patient: Pulmonary Artery Catheter Monitoring) can be used to measure right heart, pulmonary artery, and pulmonary artery occlusion pressures and cardiac output. This test is usually done only if patients have significant complications (eg, severe heart failure, hypoxia, hypotension).
Prognosis
Unstable
angina:
About 30% of patients with unstable angina have an MI within 3 mo of onset; sudden death is less common. Marked ECG changes with chest pain indicate higher risk of subsequent MI or death.
NSTEMI and STEMI:
Overall mortality rate is about 30%, with 50 to 60% of these patients dying before reaching the hospital (typically due to ventricular fibrillation). In-hospital mortality rate is about 10% (typically due to cardiogenic shock) but varies significantly with severity of LV failure (see Table 4: Coronary Artery Disease: Killip Classification and Mortality Rate of Acute MI* ).
Most patients who die of cardiogenic shock have an infarct or a combination of scar and new infarct affecting ≥ 50% of LV mass. Five clinical characteristics predict 90% of the mortality in patients who present with STEMI (see Table 5: Coronary Artery Disease: Mortality Risk at 30 Days in STEMI): older age (31% of total mortality), lower systolic BP (24%), Killip class > 1 (15%), faster heart rate (12%), and anterior location (6%). Mortality rate of diabetics and women tends to be higher.
Mortality rate of patients who survive initial hospitalization is 8 to 10% in the year after acute MI. Most fatalities occur in the first 3 to 4 mo. Persistent ventricular arrhythmia, heart failure, poor ventricular function, and recurrent ischemia indicate high risk. Many authorities recommend stress ECG before hospital discharge or within 6 wk. Good exercise performance without ECG abnormalities is associated with a favorable prognosis; further evaluation is usually not required. Poor exercise performance is associated with a poor prognosis.
Cardiac performance after recovery depends largely on how much functioning myocardium survives the acute attack. Scars from previous infarcts add to the acute damage. When > 50% of LV mass is damaged, prolonged survival is unusual.
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Table 4
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Killip Classification
and Mortality Rate of Acute MI*
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Class
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PAO2†
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Clinical Description
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Hospital
Mortality Rate
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1
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Normal
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No clinical evidence of left ventricular (LV) failure
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3–5%
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2
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Slightly reduced
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Mild to moderate LV failure
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6–10%
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3
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Abnormal
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Severe LV failure, pulmonary edema
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20–30%
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4
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Severely abnormal
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Cardiogenic shock: hypotension, tachycardia, mental obtundation, cool extremities, oliguria, hypoxia
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> 80%
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*Determined by repeated examination of the patient during the course of illness..
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†Determined while the patient is breathing room air.
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Modified from Killip T, Kimball JT: Treatment of myocardial infarction in a coronary care unit. A two-year experience with 250 patients. The American Journal of Cardiology 20:457–464, 1967.
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Table 5
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Mortality
Risk at
30 Days in STEMI
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Scoring
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Risk Factor
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Points
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Age ≥ 75
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3
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Age 65–74
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2
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Diabetes mellitus, hypertension, or angina
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1
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Systolic BP < 100 mm Hg
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3
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Heart rate > 100 beat/min
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2
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Killip class II–IV
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2
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Weight < 67 kg
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1
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Anterior ST-elevation or left branch bundle block
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1
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Time to treatment > 4 h
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1
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Total points possible
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0–14
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Risk
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Total Points
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Mortality Rate at 30 Days (%)
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0
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0.8
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1
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1.6
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2
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2.2
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3
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4.4
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4
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7.3
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5
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12.4
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6
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16.1
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7
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23.4
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8
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26.8
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> 8
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35.9
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STEMI = ST-segment elevation MI; TIMI = thrombolysis in MI.
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Based on data from Morrow DA et al: TIMI risk score for ST-elevation myocardial infarction: a convenient, bedside, clinical score for risk assessment at presentation. Circulation 102 (17):2031–2037, 2000 and ACC/AHA guidelines for the management of patients with acute myocardial infarction.
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Table 6
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Risk of
Adverse Events* at
14 Days in NSTEMI
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Scoring
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Risk Factor
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Points
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Age > 65
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1
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CAD risk factors (must have ≥ 3 for 1 point)
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1
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Family history
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Hypertension
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Current smoker
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High cholesterol
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Diabetes mellitus
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Known CAD (stenosis ≥ 50%)
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1
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Previous chronic use of aspirin
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1
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Two episodes of rest angina in past 24 h
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1
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Elevated cardiac markers
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1
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Risk level is based on total points: 1–2 = low; 3–4 = intermediate; 5–7 = high.
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Absolute Risk
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Total Points
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Risk of Events at 14 Days (%)*
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0 or 1
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4.7
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2
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8.3
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3
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13.2
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4
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19.9
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5
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26.2
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6 or 7
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40.9
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*Events include all-cause mortality, MI, and recurrent ischemia requiring urgent revascularization.
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CAD = coronary artery disease; NSTEMI = non-ST-segment elevation MI; TIMI = thrombolysis in MI.
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Based on data from Antman EM et al: The TIMI risk score for unstable angina/non-ST elevation MI: A method of prognostication and therapeutic decision making. JAMA 284:835–42, 2000.
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General
Treatment
Treatment is designed to relieve distress, interrupt thrombosis, reverse ischemia, limit infarct size, reduce cardiac workload, and prevent and treat complications. An ACS is a medical emergency; outcome is greatly influenced by rapid diagnosis and treatment.
Treatment occurs simultaneously with diagnosis. A reliable IV route must be established, O2 given (typically 2 L by nasal cannula), and continuous single-lead ECG monitoring started. Prehospital interventions by ambulance personnel (including ECG, chewed aspirin (325 mg), early thrombolysis when indicated and possible, and triage to the appropriate hospital) can reduce risk of mortality and complications. Early diagnostic data and response to treatment can help determine the need for and timing of revascularization (see below).
Bedside cardiac marker tests can help identify low-risk patients with a suspected ACS (eg, those with initially negative cardiac markers and nondiagnostic ECGs), who can be managed in 24-h observation units or chest pain centers. Higher-risk patients should be admitted to a monitored inpatient unit or coronary care unit (CCU). Several validated tools can help stratify risk. Thrombolysis in MI (TIMI) risk scores may be the most widely used (see Table 5: Coronary Artery Disease: Mortality Risk at 30 Days in STEMI and Table 6: Coronary Artery Disease: Risk of Adverse Events* at 14 Days in NSTEMI).
Patients with suspected NSTEMI and intermediate or high risk should be admitted to an inpatient care unit. Those with STEMI should be admitted to a CCU.
Only heart rate and rhythm recorded by single-lead ECG are consistently useful for routine, continuous monitoring. However, some clinicians recommend routine multilead monitoring with continuous ST-segment recording to identify transient, recurrent ST-segment elevations or depressions. Such findings, even in patients without symptoms, suggest ischemia and identify higher-risk patients who may require more aggressive evaluation and treatment.
Qualified nurses can interpret the ECG for arrhythmia and initiate protocols for its treatment. All staff members should know how to do CPR.
Contributing disorders (eg, anemia, heart failure) are aggressively treated.
The care unit should be a quiet, calm, restful area. Single rooms are preferred; privacy consistent with monitoring should be ensured. Usually, visitors and telephone calls are restricted to family members during the first few days. A wall clock, a calendar, and an outside window help orient the patient and prevent a sense of isolation, as can access to a radio, television, and newspaper.
Bed rest is mandatory for the first 24 h. On day 1, patients without complications (eg, hemodynamic instability, ongoing ischemia), including those in whom reperfusion with fibrinolytics or PCI is successful, can sit in a chair, begin passive exercises, and use a commode. Walking to the bathroom and doing nonstressful paperwork is allowed shortly thereafter. Recent studies have shown that patients with successful, uncomplicated primary PCI for acute MI may be ambulated quickly and be safely discharged in 3 to 4 days. If reperfusion is not successful or complications are present, patients require longer bed rest, but they (particularly elderly patients) are mobilized as soon as possible. Prolonged bed rest results in rapid physical deconditioning, with development of orthostatic hypotension, decreased work capacity, increased heart rate during exertion, and increased risk of deep venous thrombosis. Prolonged bed rest also intensifies feelings of depression and helplessness.
Anxiety, mood changes, and denial are common. A mild tranquilizer (usually a benzodiazepine) is often given, but many experts believe such drugs are rarely needed.
Reactive depression is common by the 3rd day of illness and is almost universal at some time during recovery. After the acute phase of illness, the most important tasks are often management of depression, rehabilitation, and institution of long-term preventive programs. Overemphasis on bed rest, inactivity, and the seriousness of the disorder reinforces anxiety and depressive tendencies, so patients are encouraged to sit up, get out of bed, and engage in appropriate activities as soon as possible. The effects of the disorder, prognosis, and individualized rehabilitation program should be explained to the patient.
Maintaining normal bowel function with stool softeners (eg, docusate ) to prevent straining is important. Urinary retention is common among elderly patients, especially after several days of bed rest or if atropine was given. A catheter may be required but can usually be removed when the patient can stand or sit to void.
Because smoking is prohibited, a hospital stay should be used to encourage smoking cessation. All caregivers should devote considerable effort to making smoking cessation permanent.
Although acutely ill patients have little appetite, tasty food in modest amounts is good for morale. Patients are usually offered a soft diet of 1500 to 1800 kcal/day with Na reduction to 2 to 3 g. Na reduction is not required after the first 2 or 3 days if there is no evidence of heart failure. Patients are given a diet low in cholesterol and saturated fats, which is used to teach healthy eating.
Because the chest pain of MI usually subsides within 12 to 24 h, any chest pain that remains or recurs later is investigated. It may indicate such complications as recurrent ischemia, pericarditis, pulmonary embolism, pneumonia, gastritis, or ulcer.
Drugs
Antiplatelet and antithrombotic drugs, which stop clots from forming, are used routinely. Anti-ischemic drugs (eg, β-blockers, IV nitroglycerin ) are frequently added, particularly when chest pain or hypertension is present (see Table 3: Coronary Artery Disease: Drugs for Coronary Artery Disease ). Fibrinolytics should
be used if not contraindicated for STEMI if primary PCI is not immediately available but worsen outcome for unstable angina and NSTEMI.
Chest pain can be treated with morphine or nitroglycerin . Morphine 2 to 4 mg IV, repeated q 15 min as needed, is highly effective but can depress respiration, can reduce myocardial contractility, and is a potent venous vasodilator. Hypotension and bradycardia secondary to morphine can usually be overcome by prompt elevation of the lower extremities. Nitroglycerin is initially given sublingually, followed by continuous IV drip if needed.
BP is normal or slightly elevated in most patients on arrival at the emergency department; BP gradually falls over the next several hours. Continued hypertension requires treatment with antihypertensives, preferably IV nitroglycerin , to lower BP and reduce cardiac workload. Severe hypotension or other signs of shock are ominous and must be treated aggressively with IV fluids and sometimes vasopressors (see Shock and Fluid Resuscitation: Prognosis and Treatment).
Antiplatelet
drugs:
Aspirin |
