IV-9 Circulation December 13. 2005 3. Normal or nondiagnostic changes in ST segment or T TABLE 1. Fibrinolytic Therapy: Contraindications al waves(Box 13) are inconclusive and require further risk Cautions for Fibrinolytic Use in STEMI From ACC/AHA 2004 stratification. This classification includes patients with Guideline Update normal ecgs and those with St-segment deviation of <0.5 mm(0.05 mv) or T-wave inversion of <0.2 my. Absolute Contraindications Serial cardiac studies (and functional testing)are Any prior intracranial hemorrhage appropriate Known structural cerebral vascular lesion(eg, AVM) Cardiac biomarkers Known malignant intracranial neoplasm(primary or metastatic) New cardiac biomarkers. which are more sensitive than the Ischemic stroke within 3 months eXcept acute ischemic stroke within myocardial muscle creatine kinase isoenzyme( CK-MB),are 3 hours useful in diagnosis, risk stratification, and determination of prognosis. An elevated level of troponin correlates with an Active bleeding or bleeding diathesis(excluding menses increased risk of death, and greater elevations predict greater Significant closed head trauma or facial trauma within 3 months risk of adverse outcome. 106 Patients with increased troponin Relative Contraindications levels have increased thrombus burden and microvascular History of chronic, severe, poorly controlled hypertension embolization Severe uncontrolled hypertension on presentation(SBP >180 mm Hg or Cardiac biomarkers should be obtained during the initial DBP >110 mm Hgt evaluation of the patient, but therapeutic decisions and History of prior ischemic stroke >3 months, dementia, or known reperfusion therapy for patients with STEMI should not be intracranial pathology not covered in contraindications delayed pending the results of these tests. Important limita tions to these tests exist because they are insensitive during Traumatic or prolonged(10 minutes) CPR or major surgery the first 4 to 6 hours of presentation unless continuous Recent(within 2 to 4 weeks) internal bleeding persistent pain has been present for 6 to 8 hours. For this reason cardiac biomarkers are not useful in the prehospital Noncompressible vascular punctures setting. 107-112 For streptokinase/anistreplase: prior exposure (5 days ago) or prior Serial marker testing(CK-MB and cardiac troponin)over allergic reaction to these agents time improves sensitivity for detection of myocardial infarc- Pregnancy tion but remains insensitive in the first 4 to 6 hours. 113, 114 Current use of anticoagulants: the higher the INR, the higher the risk of ST-Segment Elevation MI (Figure 1, Boxes 5 Through 8) AVM indicates arteriovenous malformation; SBP, systolic blood pressure, Patients with STEMI usually have complete occlusion of an DBP, diastolic blood pressure, and INR, International Normalized Ratio reperfusion therapy through administration of fibrinolytics or dein ie as advisory for clinical decision making and may not be all-inclusive epicardial coronary vessel. The mainstay of treatment is fOuld be an absolute contraindication in low-risk patients with myocardial (pharmacologic reperfusion) or primary PCI (mechanical reperfusion). Providers should rapidly identify patients STEMI and quickly screen them for indications and contra- indications to fibrinolytic therapy and PCI. dentifies a population at increased risk for MACE. Patients The first physician who encounters a patient with AMI with ischemic-type pain and ECGs consistent with NSTEMI and direct its administration(see Tables I and 2). If the fibrinolytic therapy, and fibrinolysis may be harmful. l tm should be able to determine the need for reperfusion theral or normal or nondiagnostic ecgs do not benefit fro patient meets the criteria for fibrinolytic therapy, a door-to- Although many patients will not have ACs(ie, the ECG needle time(needle time is the beginning of infusion of a change is due to an alternative diagnosis, such as LV fibrinolytic agent)<30 minutes is desired. Results of cardiac biomarkers do not delay the administration of fibrinolytic antiplatelet, antithrombin, and antianginal therapy. These percentage of patients who present early with STEMI. Con- patients usually have a partially or intermittently occluding thrombus. Clinical features can correlate with the dynamic sultation with a cardiologist or the patient's personal physI- nature of clot formation and degradation, eg, waxing and cian delays therapy, is associated with increased hospital mortality rates, and is recommended only in equivocal or waning clinical sympton hospitals with capabilities for angiogra- Serial cardiac markers are often obtained during evalua phy and PCi should have a clear protocol directing ED triage and initial management. Confusion about the method of during evaluation, elevation of cardiac troponin pal int tion, including CK-MB and cardiac troponins. At any point reperfusion, eg fibrinolysis or PCL, delays definitive therapy. patient at increased risk for MACE. Studies have shown tha patients with increased troponin are best managed with UA and NSTEMI (Figure 1, Boxes 9 Through 17) strategy of small-molecule glycoprotein(GP)IIb/Illa inhibi In the absence of ST-segment elevation, patients with ische- tor therapy and an early invasive strategy(cardiac catheter mic-type chest pain can present with ST-segment depression ization with possible revascularization). Troponin serves or nondiagnostic or normal ECGs. ST-segment depression an additional and incremental adjunct to the ECG. Physicians3. Normal or nondiagnostic changes in ST segment or T waves (Box 13) are inconclusive and require further risk stratification. This classification includes patients with normal ECGs and those with ST-segment deviation of 0.5 mm (0.05 mV) or T-wave inversion of
0.2 mV. Serial cardiac studies (and functional testing) are appropriate. Cardiac Biomarkers New cardiac biomarkers, which are more sensitive than the myocardial muscle creatine kinase isoenzyme (CK-MB), are useful in diagnosis, risk stratification, and determination of prognosis. An elevated level of troponin correlates with an increased risk of death, and greater elevations predict greater risk of adverse outcome.106 Patients with increased troponin levels have increased thrombus burden and microvascular embolization. Cardiac biomarkers should be obtained during the initial evaluation of the patient, but therapeutic decisions and reperfusion therapy for patients with STEMI should not be delayed pending the results of these tests. Important limita￾tions to these tests exist because they are insensitive during the first 4 to 6 hours of presentation unless continuous persistent pain has been present for 6 to 8 hours. For this reason cardiac biomarkers are not useful in the prehospital setting.107–112 Serial marker testing (CK-MB and cardiac troponin) over time improves sensitivity for detection of myocardial infarc￾tion but remains insensitive in the first 4 to 6 hours.113,114 ST-Segment Elevation MI (Figure 1, Boxes 5 Through 8) Patients with STEMI usually have complete occlusion of an epicardial coronary vessel. The mainstay of treatment is reperfusion therapy through administration of fibrinolytics (pharmacologic reperfusion) or primary PCI (mechanical reperfusion). Providers should rapidly identify patients with STEMI and quickly screen them for indications and contra￾indications to fibrinolytic therapy and PCI. The first physician who encounters a patient with AMI should be able to determine the need for reperfusion therapy and direct its administration (see Tables 1 and 2). If the patient meets the criteria for fibrinolytic therapy, a door-to￾needle time (needle time is the beginning of infusion of a fibrinolytic agent)
30 minutes is desired. Results of cardiac biomarkers do not delay the administration of fibrinolytic therapy or referral for PCI. They are normal in a significant percentage of patients who present early with STEMI. Con￾sultation with a cardiologist or the patient’s personal physi￾cian delays therapy, is associated with increased hospital mortality rates, and is recommended only in equivocal or uncertain cases.115 Hospitals with capabilities for angiogra￾phy and PCI should have a clear protocol directing ED triage and initial management. Confusion about the method of reperfusion, eg, fibrinolysis or PCI, delays definitive therapy. UA and NSTEMI (Figure 1, Boxes 9 Through 17) In the absence of ST-segment elevation, patients with ische￾mic-type chest pain can present with ST-segment depression or nondiagnostic or normal ECGs. ST-segment depression identifies a population at increased risk for MACE. Patients with ischemic-type pain and ECGs consistent with NSTEMI or normal or nondiagnostic ECGs do not benefit from fibrinolytic therapy, and fibrinolysis may be harmful.116 Although many patients will not have ACS (ie, the ECG change is due to an alternative diagnosis, such as LV hypertrophy), initial triage and therapy appropriately includes antiplatelet, antithrombin, and antianginal therapy. These patients usually have a partially or intermittently occluding thrombus. Clinical features can correlate with the dynamic nature of clot formation and degradation, eg, waxing and waning clinical symptoms. Serial cardiac markers are often obtained during evalua￾tion, including CK-MB and cardiac troponins. At any point during evaluation, elevation of cardiac troponin places a patient at increased risk for MACE. Studies have shown that patients with increased troponin are best managed with a strategy of small-molecule glycoprotein (GP) IIb/IIIa inhibi￾tor therapy and an early invasive strategy (cardiac catheter￾ization with possible revascularization). Troponin serves as an additional and incremental adjunct to the ECG. Physicians TABLE 1. Fibrinolytic Therapy: Contraindications and Cautions for Fibrinolytic Use in STEMI From ACC/AHA 2004 Guideline Update* Absolute Contraindications • Any prior intracranial hemorrhage • Known structural cerebral vascular lesion (eg, AVM) • Known malignant intracranial neoplasm (primary or metastatic) • Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours • Suspected aortic dissection • Active bleeding or bleeding diathesis (excluding menses) • Significant closed head trauma or facial trauma within 3 months Relative Contraindications • History of chronic, severe, poorly controlled hypertension • Severe uncontrolled hypertension on presentation (SBP
180 mm Hg or DBP
110 mm Hg)† • History of prior ischemic stroke
3 months, dementia, or known intracranial pathology not covered in contraindications • Traumatic or prolonged (
10 minutes) CPR or major surgery (3 weeks) • Recent (within 2 to 4 weeks) internal bleeding • Noncompressible vascular punctures • For streptokinase/anistreplase: prior exposure (
5 days ago) or prior allergic reaction to these agents • Pregnancy • Active peptic ulcer • Current use of anticoagulants: the higher the INR, the higher the risk of bleeding AVM indicates arteriovenous malformation; SBP, systolic blood pressure; DBP, diastolic blood pressure; and INR, International Normalized Ratio. *Viewed as advisory for clinical decision making and may not be all-inclusive or definitive. †Could be an absolute contraindication in low-risk patients with myocardial infarction. IV-94 Circulation December 13, 2005