Acute Myocardial Infarction
Christopher M. Huff
I. EPIDEMIOLOGY.
Acute myocardial infarction (MI) is the leading cause of death in North America and Europe. Each year, an estimated 785,000 Americans will sustain a new MI, and another 470,00 will have a recurrent MI. An American has an acute MI every 25 seconds, and someone dies of an MI every minute. In 2007, coronary heart disease caused one out of every six deaths. The incidence and mortality with acute MI have declined dramatically over the last 30 years, with the advent of the coronary care unit, fibrinolytic therapy, catheter-based reperfusion, and statin therapy. The aging of the population in advanced economies, as well as the global increased incidence of diabetes and obesity, will however, increase the sequelae of atherosclerotic coronary artery disease in the future (1).
II. PATHOPHYSIOLOGY.
In most patients, coronary plaque rupture is the initiating event of acute MI. Rupture of the fibrous cap of a coronary atheroma exposes the underlying subendothelial matrix to formed elements of circulating blood, leading to activation of platelets, thrombin generation, and thrombus formation. Erosion of a coronary plaque without rupture can also lead to thrombus formation and is estimated to cause up to 25% of MIs. Acute coronary syndrome (ACS) is a dynamic process that involves cyclical transitioning among complete vessel occlusion, partial vessel occlusion, and reperfusion. Occlusive thrombus in the absence of significant collateral vessels most often results in acute ST-segment elevation myocardial infarction (STEMI). The pathophysiology of STEMI and non—ST-segment elevation myocardial infarction (NSTEMI) is similar, and this explains the substantial overlap in ACSs with regard to ultimate outcome, extent of necrosis, and mortality rates. The recognition of ST-segment elevation is particularly important because it generally mandates the need for emergent reperfusion therapy.
III. DEFINITION.
A 2007 expert consensus document (2) redefined acute MI as the detection of a rise and/or fall in cardiac troponin with at least one value above the 99th percentile of the upper reference limit (URL) utilizing an assay with < 10% coefficient of variation at the level of detection, together with evidence of ischemia. Ischemia was defined as any symptom of ischemia, electrocardiographic changes suggestive of new ischemia, development of pathologic Q waves on electrocardiogram (ECG), or imaging evidence of infarction. Included in the definition were sudden cardiac death (SCD) with evidence of myocardial ischemia (new ST elevation, left bundle branch block [LBBB], or coronary thrombus) and biomarker elevation > 3× URL for post—percutaneous coronary intervention (PCI) patients or > 5× URL for postcoronary artery bypass grafting (post-CABG) patients. Documented stent thrombosis was recognized in this new definition as well (Table 1.1). Established MI was defined as any one criterion that satisfies the following: development of new pathologic Q waves on serial ECGs, imaging evidence of MI, or pathologic findings of healed or healing MI.
TABLE 1.1 Clinical Classification of Different Types of Myocardial Infarction | ||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ||||||||||||||
IV. CLINICAL DIAGNOSIS.
In any patient with a clinical history of chest pain suspected to be of cardiac origin, an ECG should be obtained within 10 minutes of presentation and interpreted promptly to determine eligibility for reperfusion therapy. If the ECG demonstrates acute ST-segment elevation or new LBBB, emergent reperfusion treatment with primary PCI or fibrinolysis is indicated. During this evaluation period, a targeted medical history and physical examination should be performed. If the patient’s history is compatible with cardiac ischemia and the ECG does not meet the criteria for reperfusion therapy, the patient may have unstable angina or NSTEMI. These syndromes are discussed in Chapter 2.
A. Signs and symptoms
1. The classic symptoms are severe, crushing substernal chest pain described as a squeezing or constricting sensation with frequent radiation to the left arm, often associated with an impending sense of doom. The discomfort is similar to that of angina pectoris, but it is typically more severe, of longer duration (usually > 20 minutes), and is not relieved with rest or nitroglycerin. Peak intensity is usually not instantaneous, as it would be with pulmonary embolism or aortic dissection.
a. The chest discomfort may radiate to the neck, jaw, back, shoulder, right arm, and epigastrium. Pain in any of these locations without chest pain is possible. Myocardial ischemic pain localized to the epigastrium is often misdiagnosed as indigestion. Acute MI can occur without chest pain, especially among postoperative patients, the elderly, and those with diabetes mellitus.
b. If the pain is sudden, radiates to the back, and is described as tearing or knifelike, aortic dissection should be considered.
2. Associated symptoms may include diaphoresis, dyspnea, fatigue, light-headedness, palpitations, acute confusion, indigestion, nausea, or vomiting. Gastrointestinal symptoms are especially common with inferior infarction.
B. Physical examination.
In general, the physical examination does not add much to the diagnosis of acute MI. However, the examination is extremely important in excluding other diagnoses that may mimic acute MI, in risk stratification, in the diagnosis of impending heart failure, and in serving as a baseline examination to monitor for mechanical complications of acute MI that may develop.
1. Risk stratification, which aids in treatment decisions and counseling patients and families, is based in part on age, heart rate, and blood pressure and on the presence or absence of pulmonary edema and a third heart sound.
2. The mechanical complications of mitral regurgitation and ventricular septal defect are often heralded by a new systolic murmur (see Chapter 3). Early diagnosis of these complications relies on well-documented examination findings at baseline and during the hospital course.
V. DIFFERENTIAL DIAGNOSIS.
The differential diagnosis of ST elevation includes conditions with comorbid ischemia such as acute aortic dissection involving the root, conditions with ST elevation but no ischemia such as left ventricular (LV) hypertrophy or early repolarization abnormality, and conditions with chest pain but no ischemia such as myopericarditis (Table 1.2). The most common differential diagnostic considerations are discussed in the following text.
A. Pericarditis.
Chest pain that is worse when the person is supine and improves when the person is sitting upright or slightly forward is typical of pericarditis. Care must be taken in excluding acute MI, however, because pericarditis can complicate acute MI. The electrocardiographic abnormalities of acute pericarditis may also be confused with acute MI. Diffuse ST-segment elevation is the hallmark of acute pericarditis, but this finding may be seen in acute MI that involves the left main coronary artery or a large “wraparound” left anterior descending artery. PR-segment depression, peaked T waves, or electrocardiographic abnormalities out of proportion to the clinical scenario may favor the diagnosis of pericarditis. The ST-segment elevations in pericarditis are often concave, whereas the ST-segment elevations in acute MI are usually convex. Reciprocal ST depression does not occur in pericarditis, except in leads aVR and V1. Early T-wave inversion is not a feature of acute pericarditis. Echocardiography may be useful, not in evaluating pericardial effusion, which may occur in either condition, but in documenting the lack of wall motion abnormalities in the setting of ongoing pain and ST elevation.
B. Myocarditis.
As with pericarditis, the symptoms and electrocardiographic findings of myocarditis may be similar to those of acute MI. Echocardiography is less useful in differentiating this syndrome from acute MI, because segmental LV dysfunction may be encountered in either condition. A complete history often reveals a more insidious onset and associated viral syndrome with myocarditis.
TABLE 1.2 Differential Diagnostic Considerations for ST-Segment Elevation Myocardial Infarction | ||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ||||||||||||||||||||||||
C. Acute aortic dissection.
Sharp, tearing chest pain that radiates through the chest to the back is typical of aortic dissection (see Chapter 26). This type of radiation pattern should be investigated thoroughly before administration of antithrombotic, antiplatelet, or fibrinolytic therapy. Proximal extension of the dissection into either coronary ostium can account for acute MI. A chest radiograph may reveal a widened mediastinum. Transthoracic echocardiography may reveal a dissection flap in the proximal ascending aorta. If it does not, a more definitive diagnosis should be obtained with transesophageal echocardiography (TEE), computerized tomography (CT), or magnetic resonance imaging (MRI).
D. Pulmonary embolism.
Shortness of breath associated with pleuritic chest pain but without evidence of pulmonary edema suggests pulmonary embolism. Echocardiography helps to rule out wall motion abnormalities and may identify right ventricular (RV) dilatation and dysfunction in the setting of pulmonary embolism.
E. Esophageal disorders.
Gastroesophageal reflux disease, esophageal motility disorders, and esophageal hyperalgesia can cause chest pain, the character of which is very similar to cardiac ischemic pain. These disorders can often coexist in patients with coronary disease, thereby complicating the diagnosis. A workup for coronary disease should precede evaluation of esophageal disorders. Symptoms that may be suggestive but not diagnostic of chest pain of an esophageal origin include postprandial symptoms, relief with antacids, and lack of radiation of pain.
F. Acute cholecystitis
can mimic the symptoms and ECG findings of inferior acute MI, although the two can coexist. Tenderness in the right upper quadrant, fever, and an elevated leukocyte count favor cholecystitis, which can be diagnosed by means of hepatobiliary iminodiacetic acid (HIDA) scanning.
VI. LABORATORY EXAMINATION (Fig. 1.1)
A. Troponins.
Troponin T and troponin I assays are particularly useful in the diagnosis and management of unstable angina and NSTEMI because of their high sensitivity, ability to be used and interpreted rapidly at bedside, and nearly universal availability. Currently, the lag time between occlusion and detectable elevations in serum levels limits their usefulness in the diagnosis of acute STEMI; however, the development of high-sensitivity troponin T assays may allow for more rapid detection of myocardial necrosis. Also, data have suggested that a single troponin T concentration measured 72 hours after acute MI may be predictive of MI size, independent of reperfusion (3). Troponin elevation in the absence of ischemic heart disease can be found in congestive heart failure (CHF), aortic dissection, hypertrophic cardiomyopathy, pulmonary embolism, acute neurologic disease, cardiac contusion, or drug toxicity.
B. Creatine kinase (CK).
An elevated level of CK is rarely helpful in making the diagnosis of acute MI for a patient with ST-segment elevation. Because it usually takes 4 to 6 hours to see an appreciable rise in CK levels, an initial normal value does not exclude recent complete occlusion. CK and CK-MB (creatine kinase myocardial band) levels can be elevated in the presence of pericarditis and myocarditis, which may cause diffuse ST-segment elevation. CK levels are more helpful in gauging the size and timing of acute MI than in making the diagnosis. CK levels peak at 24 hours, but the peak CK level is believed to occur earlier among patients who undergo successful reperfusion. False-positive results of CK elevation occur in a variety of settings, including skeletal muscle disease or trauma (e.g., rhabdomyolysis).
C. Myoglobin.
Damaged cardiac myocytes rapidly release this protein into the bloodstream. Peak levels occur between 1 and 4 hours, allowing for early diagnosis of acute MI. However, myoglobin lacks cardiac specificity, thereby limiting its clinical utility. Studies have indicated that it might play a role in risk stratification after reperfusion therapy (4).
 FIGURE 1.1 Timing of biomarker release after acute myocardial infarction. AMI, acute myocardial infarction; CK, creatine kinase; CK-MB, creatine kinase myocardial band; CV, coefficient of variation. (Reprinted from Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction—executive summary. J Am Coll Cardiol. 2007; 50:652—726, with permission from Elsevier.) |
VII. DIAGNOSTIC TESTING
A. Electrocardiography
1. Definitive electrocardiographic diagnosis of acute MI requires ST elevation of 1 mm or more in two or more contiguous leads, often with reciprocal ST depression in the contralateral leads. In leads V2-V3, 2 mm of ST elevation in men and 1.5 mm in women are required for accurate diagnosis.
2. ECG subsets. ST-segment elevations can be divided into subgroups that may be correlated with the infarction-related artery and risk of death. These five subgroups are listed in Table 1.3 and illustrated in Figure 1.2.
3. Left bundle branch block
a. New LBBB in the setting of symptoms consistent with acute MI may indicate a large, anterior wall acute MI involving the proximal left anterior descending coronary artery and should be managed as acute STEMI.
b. In the absence of an old ECG or in the presence of LBBB at baseline, the diagnosis of acute STEMI can be made with > 90% specificity on the basis of the criteria listed in Table 1.4 and illustrated in Figure 1.3.
c. Right bundle branch block (RBBB) may complicate interpretation of ST elevation in leads V1 through V3. RBBB does not, however, obscure ST-segment elevation.
B. Echocardiography
may be helpful in the evaluation of LBBB of undetermined duration in that the lack of regional wall motion abnormality in the presence of continuing symptoms makes the diagnosis of acute MI unlikely. It is worth noting that abnormal septal motion is often observed in the setting of LBBB even in the absence of ischemia.
TABLE 1.3 Acute Myocardial Infarction: Electrocardiogram Subsets and Correlated Infarct-Related Artery and Mortality | |||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| |||||||||||||||||||||||||||||||||||
VIII. RISK STRATIFICATION.
It is possible and useful to estimate the risk of death of a patient with acute MI. The estimate can aid in making treatment decisions and recommendations and in counseling patients and families. Five simple baseline parameters have been reported to account for > 90% of the prognostic information for 30-day mortality. These characteristics are given in descending order of importance: age, systolic blood pressure, Killip classification (Table 1.5), heart rate, and location of MI (Table 1.3, Fig. 1.2) (5). In addition, various risk models have been created to improve risk prediction.
A. The Thrombolysis in Myocardial Infarction (TIMI) risk score
incorporates eight variables obtained from the history, physical examination, and ECG (Table 1.6). In patients treated with fibrinolysis, a TIMI score of 9 or greater predicts a 30-day mortality of approximately 35%. In patients with a TIMI score of 0 or 1, the 30-day mortality rate is < 2%. The strongest predictor of poor prognosis is advanced age (where age ≥ 75 years receives 3 points and age 65 to 74 years receives 2 points). Other variables that predict a poor prognosis include hypotension, Killip class II—IV at presentation, tachycardia, history of diabetes or hypertension, anterior ST elevation (also complete LBBB), low body weight, and a time to treatment of > 4 hours.
 FIGURE 1.2 Continued |
 FIGURE 1.2 Continued |
 FIGURE 1.2 Continued |
 FIGURE 1.2 Continued |
 FIGURE 1.2 Electrocardiographic subsets of acute myocardial infarction (MI). A: Large anterior MI with conduction disturbance (proximal left anterior descending [LAD] coronary artery). B: Anterior MI without conduction disturbance (mid-LAD). C: Lateral MI (distal LAD, diagonal branch, or left circumflex branch). D: Large inferior MI with reciprocal changes (proximal right coronary artery [RCA]). E: Small inferior MI (distal RCA). (From Topol EJ, Van de Werf FJ. Acute myocardial infarction: early diagnosis and management. In: Topol EJ, ed. Textbook of Cardiovascular Medicine. New York: Lippincott-Raven; 2002, with permission.)”. |
TABLE 1.4 Electrocardiographic Criteria for the Diagnosis of Acute Myocardial Infarction in the Presence of Left Bundl e Branch Block | ||||||||||
|---|---|---|---|---|---|---|---|---|---|---|
| ||||||||||
B. The Global Registry of Acute Coronary Events (GRACE) score
is used to predict in-hospital mortality in patients with ACS. Risk is calculated based on Killip class, heart rate, systolic blood pressure, creatinine level, age, presence or absence of cardiac arrest at admission, presence or absence of cardiac biomarkers, and ST-segment deviation. Patients with a score of ≤ 60 have a ≤ 0.2% probability of in-hospital mortality, whereas patients with a score of ≥ 250 have a ≥ 52% probability of in-hospital mortality.
IX. THERAPY
A. Prior to reperfusion
1. Aspirin. Immediate administration of aspirin is indicated for all patients with acute MI, unless there is a clear history of true aspirin allergy (not intolerance). Aspirin therapy conveys as much mortality benefit as streptokinase (SK), and the combination provides additive benefit (6). The dose should be four 81 mg chewable tablets (for more rapid absorption) or one 325 mg nonchewable tablet. If oral administration is not possible, a rectal suppository can be given. If true aspirin allergy is present, clopidogrel monotherapy is the best alternative. In STEMI patients who undergo PCI, aspirin should be continued indefinitely. According to the 2011 ACCF/AHA/SCAI PCI guidelines, after PCI it is reasonable to use 81 mg of aspirin as opposed to higher maintenance doses (16).
2. Oxygen. Supplemental oxygen by means of nasal cannula should be given to all patients with suspected MI. Administration through a face mask or endotracheal tube may be necessary for patients with severe pulmonary edema or cardiogenic shock.
3. Nitroglycerin. It is worthwhile to give sublingual nitroglycerin (0.4 mg) to determine whether the ST-segment elevation represents coronary artery spasm while arrangements for reperfusion therapy are being initiated. Patients should be questioned about recent use of a phosphodiesterase inhibitor (PDE) because administration of nitroglycerin within 24 hours of a PDE may cause life-threatening hypotension. A meta-analysis performed before the age of routine reperfusion suggested a mortality benefit with intravenous nitroglycerin (8), although routine use of oral nitrates after MI had no benefit in two large randomized trials in the modern era. Nitroglycerin can be useful in the management of acute MI complicated by CHF, ongoing symptoms, or hypertension. A 30% reduction in systolic blood pressure can be expected with appropriately
aggressive dosing (10 to 20 µg/min with 5 to 10 µg/min increases every 5 to 10 minutes). Intravenous therapy can be continued for 24 to 48 hours, after which time patients with heart failure or residual ischemia can transition to oral or topical therapy with an appropriate nitrate-free interval to avoid tachyphylaxis.
aggressive dosing (10 to 20 µg/min with 5 to 10 µg/min increases every 5 to 10 minutes). Intravenous therapy can be continued for 24 to 48 hours, after which time patients with heart failure or residual ischemia can transition to oral or topical therapy with an appropriate nitrate-free interval to avoid tachyphylaxis.
 FIGURE 1.3 Electrocardiogram displays all of the criteria for the diagnosis of acute myocardial infarction (MI) in the setting of left bundle branch block (LBBB): ST-segment elevation > 1 mm, concordant with QRS in lead II (5 points); ST-segment depression > 1 mm in leads V2 and V3 (3 points); and ST-segment elevation > 5 mm, discordant with QRS in leads III and VF (2 points). A score of 10 points indicates an extremely high likelihood of inferior MI. (From Sgarbossa EB, Wagner G, 1997, with permission.) |
TABLE 1.5 30-Day Mortality Based on Hemodynamic (Killip) Class | ||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ||||||||||||||||||||||||
TABLE 1.6 TIMI Risk Model for Prediction of Short-Term Mortality in ST-Segment Elevation Myocardial Infarction Patients | ||||||||||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ||||||||||||||||||||||||||||||||||||||||||
4. Platelet P2Y12 receptor antagonists should be used routinely in all patients with STEMI regardless of whether or not PCI is performed (9). Currently, the three agents recommended for treatment of STEMI are clopidogrel, prasugrel, and ticagrelor. Clopidogrel and prasugrel are thienopyridines that irreversibly inhibit the platelet adenosine diphosphate P2Y12 receptor, and Ticagrelor is a reversible direct inhibitor of this same receptor. In patients in whom PCI is planned, a loading dose should be given prior to or at the time of PCI. The recommended loading dose of clopidogrel is 600 mg. This is largely based on results of a meta-analysis that included more than 25,000 patients undergoing PCI. The meta-analysis demonstrated that when compared to 300 mg, a 600 mg clopidogrel loading dose reduces MACE without an increase in major bleeding. (10). The recommended loading dose of prasugrel is 60 mg (9). Prasugrel is considered to be superior to clopidogrel in onset of action and potency of platelet inhibition; in addition, its metabolism is not influenced by cytochrome P450 genetic polymorphisms. The TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel—Thrombolysis In Myocardial Infarction) investigators compared efficacy and safety of prasugrel versus clopidogrel in patients with moderate- to high-risk ACS undergoing PCI. The primary end point was a composite of death due to cardiovascular causes, nonfatal MI, or nonfatal stroke. Patients who received prasugrel had a significant reduction in the primary end point compared with patients who received clopidogrel (9.9% vs. 12.1%; hazard ratio [HR] 0.81; 95% confidence interval [CI], 0.73 to 0.90; p < 0.001). This difference was primarily driven by a reduction in nonfatal MI (7.3% for prasugrel vs. 9.5% for clopidogrel; HR 0.76; 95% CI, 0.67 to 0.85; p < 0.001). The risk of TIMI major bleeding was higher with the use of prasugrel (2.4% vs. 1.8%; HR 1.32; 95% CI, 1.03 to 1.68; p = 0.03), though the net clinical benefit end point, which included all-cause mortality, ischemic events, and major bleeding events, still favored the use of prasugrel (11). Based on subgroup analysis, diabetics derived a greater benefit with prasugrel as compared with clopidogrel, whereas post hoc analysis showed that patients 75 years of age or older or patients with a body weight of < 60 kg derived no net clinical benefit from prasugrel. Post hoc analysis also showed net harm in patients treated with prasugrel who had a history of a transient ischemic attack or stroke, and therefore prasugrel should be avoided in these patients (11). Ticagrelor is given as a 180 mg loading dose. Platelet inhibition with ticagrelor occurs faster and is more potent than clopidogrel. The efficacy and safety of ticagrelor was compared to clopidogrel in the PLATO (Platelet Inhibition And Patient Outcomes)trial. At one year, patients who received ticagrelor had a significant reduction in the composite endpoint of death from vascular causes, MI, or stroke, without an increase in major bleeding. Of note, patients who receive ticagrelor should not be treated with high dose aspirin, which has been associated with worse outcomes in these patients (12). Currently, guidelines do not endorse one agent over another except in patients who have received fibrinolysis. In these patients, clopidogrel is the thienopyridine of choice, at a loading dose of 300 mg if fibrinolysis was performed within 24 hours of administration (13). This is based on results of the CLARITY-TIMI 28 (Clopidogrel as Adjunctive Reperfusion Therapy— Thrombolysis in Myocardial Infarction) trial, which showed pretreatment with clopidogrel to be safe and effective without increased bleeding among patients treated with fibrinolytic therapy, with many receiving subsequent PCI (∽57%). The composite end point of cardiovascular death, reinfarction or revascularization, was reduced from 14.1% to 11.6% (p = 0.03) by clopidogrel pretreatment (9,13). In patients receiving a stent (BMS or drug-eluting stent [DES]), thienopyridine therapy should be continued for at least 1 year (9).
The maintenance dose of clopidogrel and prasugrel is 75 mg daily and 10 mg daily, respectively. The maintenance dose for prasugrel is 90 mg twice a day. An important consideration is the increased risk of major bleeding during surgery. It is currently recommended that clopidogrel and ticagrelor be held for 5 days and prasugrel be held for 7 days prior to CABG, unless the need for urgent revascularization outweighs the risk of potential excessive bleeding (9).
The maintenance dose of clopidogrel and prasugrel is 75 mg daily and 10 mg daily, respectively. The maintenance dose for prasugrel is 90 mg twice a day. An important consideration is the increased risk of major bleeding during surgery. It is currently recommended that clopidogrel and ticagrelor be held for 5 days and prasugrel be held for 7 days prior to CABG, unless the need for urgent revascularization outweighs the risk of potential excessive bleeding (9).
5. Parenteral anticoagulants. Unless there is a contraindication, all STEMI patients should receive antithrombotic therapy. Traditionally, this has been accomplished with unfractionated heparin (UFH). The dose of UFH is 60 U/kg as a bolus (maximum 4,000 U), followed by 12 U/kg/h infusion (maximum 1,000 U/h) to achieve a partial thromboplastin time of 45 to 65 seconds (7). Based on the GUSTO I (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries) trial, heparin should be given as an adjunct to patients who receive thrombolysis with alteplase, but should not be given to patients who receive streptokinase unless the patient has recurrent ischemia or there is another indication for anticoagulant therapy (14). The use of UFH as adjunctive therapy with reteplase and tenecteplase (TNK) has been validated in GUSTO III and ASSENT 2 (Assessment of the Safety and Efficacy of a New Thrombolytic), respectively. Low-molecular-weight heparin (LMWH) is an alternative to UFH and should be preferred in patients undergoing fibrinolysis. The ASSENT 3 trial tested the efficacy of various antithrombotic regimens in conjunction with weightbased TNK. TNK plus enoxaparin was superior to TNK plus UFH in reducing the composite end point of death, in-hospital reinfarction, or in-hospital refractory ischemia (15). Similarly, the ExTRACT-TIMI 25 (Enoxaparin and Thrombolysis Reperfusion for Acute Myocardial Infarction Treatment — Thrombolysis in Myocardial Infarction) trial randomized STEMI patients undergoing fibrinolysis to either enoxaparin throughout the index hospitalization or UFH for 48 hours. The primary end point was death or nonfatal MI at 30 days. The enoxaparin group had a significant reduction in the primary end point, most of which was due to a significant reduction in the rate of reinfarction (3.0% vs. 4.5%). The enoxaparin group was also less likely to undergo urgent revascularization (2.1% vs. 2.8%). It is worth noting that duration of therapy differed between the two groups. Although UFH was only administered for 48 hours, LMWH therapy was continued for a mean of 7 days (16). Patients undergoing PCI after treatment with LMWH may need additional dosing in the cardiac catheterization laboratory, depending on the time at which the last dose was administered. If the last dose was within 8 hours, no additional enoxaparin should be given. If the last dose was given 8 to 12 hours earlier, an intravenous dose of 0.3 mg/kg should be given. If it has been > 12 hours since that last dose, an additional 1 mg/kg dose should be administered subcutaneously. LMWH should be avoided in patients > 75 years old or in patients with significant renal insufficiency (22). The 2009 focused update of the ACC/AHA STEMI guidelines added bivalirudin as an acceptable anticoagulant in patients undergoing primary PCI (9). The 2011 ACCF/AHA/SCAI PCI guideline confirmed this with a class I recommendation for bivalirudin during PCI (17
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
