《心肺复苏指南》参考资料（英文版）Part 8：Stabilization of the Patient With Acute Coronary Syndromes

Part 8: Stabilization of the Patient With Acute Coronary Syndromes Iv-93 onset of symptoms to a hospital without capability for A direct comparison of the outcome of primary or early PCI primary PCI had better outcome (improved 30-day combined patients with patients who received fibrinolytic therapy only incidence of death, reinfarction, or stroke)when they were was not reported transferred to a skilled PCI center(interventionalist perform- ing >75 procedures per year) rather than receiving fibrino- fer of stable patients for early PCI after successful adminis- lytics at the presenting hospital. In these studies balloon tration of fibrinolytics in community hospitals or the out-of- inflation occurred <93 minutes after decision to treat. 80, 83-85 hospital setting. Patients <75 years of age and selected Thus, interfacility transfer is indicated for patients with patients >75 years of age who develop cardiogenic shock or STEMI presenting >3 hours from onset of symptoms from persistent ischemic symptoms within 36 hours of STEMI of providing primary PCI when the transfer can be accom- ERV if ERV can be pene experienced facilities capable of hospitals that lack primary PCI capability to centers capable should be transferred to med within 18 hours of onset of plished as soon as possible. The ACC/AHa guidelines shock. 12 recommend a treatment delay of no more than 90 minutes. In patients with STEMI presenting <3 hours from onset of ED Evaluation and Risk Stratification ymptoms, the superiority of immediate administration of (Figure 1, Boxes 3 and 4) fibrinolytics in the hospital or transfer for primary PCl is not Focused Assessment and ECG Risk Stratification stablished( Class Indeterminate) ED providers should quickly assess patients with possible In-Hospital Fibrinolytics and Interfacility Transfer for ACS. Ideally within 10 minutes of ED arrival, providers should obtain a targeted history while a monitor is attached to Data from the 1980s to 1990s did not support a strategy of the patient and a 12-lead ECG is obtained (if not done in the fibrinolytic therapy combined with transfer for facilitated PCI prehospital setting).9% The evaluation should focus on ches (LOE 186-88 and meta-analyses89-9D). But all of the studies discomfort, associated signs and symptoms, prior cardiac involved in-hospital administration of fibrinolytics, and most history, risk factors for ACS, and historical features that may were completed before the era of coronary stenting and preclude the use of fibrinolytics or other therapies. This initial without use of contemporary pharmacologic therapies or PCI evaluation must be efficient because if the patient has techniques. Three small randomized trials(LOE 1)92-94 sup- STEMI, the goals of reperfusion are to administer fibrinolyt- ported the strategy of fibrinolytics plus transfer for PCI; ics within 30 minutes of arrival(30-minute interval"door-to- however, the timing of PCI after administration of fibrinolyt drug") or to provide PCI within 90 minutes of arrival ics, the inclusion of patients who required transfer for PCI, ( 90-minute interval"door-to-balloon inflation"in the cathe- the use of coronary stents, and the control group interventions terization suite). differ considerably among these trials. The most recent Potential delay during the in-hospital evaluation period study? was fairly small and showed a benefit of early PCI may occur from door to data, from data(ECG)to decision with 1-year follow-up.94 and from decision to drug (or PCI). These 4 major points of At present there is inadequate evidence to recommend the in-hospital therapy are commonly referred to as the 4 D's"9 routine transfer of patients for early PCI (ie, within 24 hours) All providers must focus on minimizing delays at each of after successful administration of fibrinolytics in a commu- these points. Out-of-hospital transport time constitutes only nity hospital. The use of out-of-hospital administration of 5% of delay to treatment time; in-hospital evaluation consti- fibrinolytics followed by early PCI has not been specifically tutes 25% to 33% of this delay 100,101 The physical examination is performed to aid diagnosis Special Transfer Considerations rule out other causes of the patients symptoms, and eva Special transfer considerations are appropriate for patients the patient for complications related to ACS. Although the use of clinical signs and symptoms may increase suspicion of bpm,and SBP <100 mm Hg). The Second National Registry ACS, evidence does not support the use of any single sign or of Myocardial Infarction found that the mortality rate patients with AMI and shock was lower in those treated with the diagnosis. 102-105 PCI as a primary strategy than in those treated with fibrino- When the patient presents with signs of ACS, the clinician lysis. 5 In the SHOCK (Should We Emergently Revascularize uses ECG findings(Figure I, Box 4)to classify the patient Occluded Coronaries for Cardiogenic Shock) trial, 152 into I of 3 group tients with cardiogenic shock were randomly assigned to an early revascularization (ERV) strategy, 150 patients were 1. ST-segment elevation or presumed new LBBB(Box 5)is assigned to a strategy of initial medical stabilization that characterized by ST-segment elevation >l mm(0.1 mv) in included fibrinolytics, and 25% had delayed revascularize 2 or more contiguous precordial leads or 2 or more adjacent limb leads and is classified as ST-elevation MI(STEMI tion%6 Although there was no difference in the 30-day 2. Ischemic ST-segment depression 20.5 mm(0.05 mV)or mortality rate, the mortality rate at 6 months was significantly ynamic T-wave inversion with pain or discomfort(Box d lower in the ERV group(50.3% versus 63. 1%) In a prespeci 9) is classified as high-risk UA/non-ST-elevation MI fied subgroup analysis for patients <75 years of age, early (NSTEMI). Nonpersistent or transient ST-segment eleva- revascularization was associated with a 15. 4% reduction in tion 20.5 mm for <20 minutes is also included in this 30-day mortality and improvement in l-year survival rates. 9 category

onset of symptoms to a hospital without capability for primary PCI had better outcome (improved 30-day combined incidence of death, reinfarction, or stroke) when they were transferred to a skilled PCI center (interventionalist perform￾ing
75 procedures per year) rather than receiving fibrino￾lytics at the presenting hospital. In these studies balloon inflation occurred
93 minutes after decision to treat.80,83– 85 Thus, interfacility transfer is indicated for patients with STEMI presenting
3 hours from onset of symptoms from hospitals that lack primary PCI capability to centers capable of providing primary PCI when the transfer can be accom￾plished as soon as possible. The ACC/AHA guidelines recommend a treatment delay of no more than 90 minutes.12 In patients with STEMI presenting 3 hours from onset of symptoms, the superiority of immediate administration of fibrinolytics in the hospital or transfer for primary PCI is not established (Class Indeterminate). In-Hospital Fibrinolytics and Interfacility Transfer for PCI Data from the 1980s to 1990s did not support a strategy of fibrinolytic therapy combined with transfer for facilitated PCI (LOE 186 – 88 and meta-analyses89 –91). But all of the studies involved in-hospital administration of fibrinolytics, and most were completed before the era of coronary stenting and without use of contemporary pharmacologic therapies or PCI techniques. Three small randomized trials (LOE 1)92–94 sup￾ported the strategy of fibrinolytics plus transfer for PCI; however, the timing of PCI after administration of fibrinolyt￾ics, the inclusion of patients who required transfer for PCI, the use of coronary stents, and the control group interventions differ considerably among these trials. The most recent study79 was fairly small and showed a benefit of early PCI with 1-year follow-up.94 At present there is inadequate evidence to recommend the routine transfer of patients for early PCI (ie, within 24 hours) after successful administration of fibrinolytics in a commu￾nity hospital. The use of out-of-hospital administration of fibrinolytics followed by early PCI has not been specifically studied. Special Transfer Considerations Special transfer considerations are appropriate for patients with signs of shock (pulmonary congestion, heart rate
100 bpm, and SBP 100 mm Hg). The Second National Registry of Myocardial Infarction found that the mortality rate in patients with AMI and shock was lower in those treated with PCI as a primary strategy than in those treated with fibrino￾lysis.95 In the SHOCK (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock) trial, 152 pa￾tients with cardiogenic shock were randomly assigned to an early revascularization (ERV) strategy, 150 patients were assigned to a strategy of initial medical stabilization that included fibrinolytics, and 25% had delayed revasculariza￾tion.96 Although there was no difference in the 30-day mortality rate, the mortality rate at 6 months was significantly lower in the ERV group (50.3% versus 63.1%). In a prespeci￾fied subgroup analysis for patients 75 years of age, early revascularization was associated with a 15.4% reduction in 30-day mortality and improvement in 1-year survival rates.97 A direct comparison of the outcome of primary or early PCI patients with patients who received fibrinolytic therapy only was not reported. There is inadequate evidence to recommend routine trans￾fer of stable patients for early PCI after successful adminis￾tration of fibrinolytics in community hospitals or the out-of￾hospital setting. Patients 75 years of age and selected patients
75 years of age who develop cardiogenic shock or persistent ischemic symptoms within 36 hours of STEMI should be transferred to experienced facilities capable of ERV if ERV can be performed within 18 hours of onset of shock.12 ED Evaluation and Risk Stratification (Figure 1, Boxes 3 and 4) Focused Assessment and ECG Risk Stratification ED providers should quickly assess patients with possible ACS. Ideally within 10 minutes of ED arrival, providers should obtain a targeted history while a monitor is attached to the patient and a 12-lead ECG is obtained (if not done in the prehospital setting).98 The evaluation should focus on chest discomfort, associated signs and symptoms, prior cardiac history, risk factors for ACS, and historical features that may preclude the use of fibrinolytics or other therapies. This initial evaluation must be efficient because if the patient has STEMI, the goals of reperfusion are to administer fibrinolyt￾ics within 30 minutes of arrival (30-minute interval “door-to￾drug”) or to provide PCI within 90 minutes of arrival (90-minute interval “door-to– balloon inflation” in the cathe￾terization suite). Potential delay during the in-hospital evaluation period may occur from door to data, from data (ECG) to decision, and from decision to drug (or PCI). These 4 major points of in-hospital therapy are commonly referred to as the “4 D’s.”99 All providers must focus on minimizing delays at each of these points. Out-of-hospital transport time constitutes only 5% of delay to treatment time; in-hospital evaluation consti￾tutes 25% to 33% of this delay.100,101 The physical examination is performed to aid diagnosis, rule out other causes of the patient’s symptoms, and evaluate the patient for complications related to ACS. Although the use of clinical signs and symptoms may increase suspicion of ACS, evidence does not support the use of any single sign or combination of clinical signs and symptoms alone to confirm the diagnosis.102–105 When the patient presents with signs of ACS, the clinician uses ECG findings (Figure 1, Box 4) to classify the patient into 1 of 3 groups: 1. ST-segment elevation or presumed new LBBB (Box 5) is characterized by ST-segment elevation
1 mm (0.1 mV) in 2 or more contiguous precordial leads or 2 or more adjacent limb leads and is classified as ST-elevation MI (STEMI). 2. Ischemic ST-segment depression 0.5 mm (0.05 mV) or dynamic T-wave inversion with pain or discomfort (Box 9) is classified as high-risk UA/non–ST-elevation MI (NSTEMI). Nonpersistent or transient ST-segment eleva￾tion 0.5 mm for 20 minutes is also included in this category. Part 8: Stabilization of the Patient With Acute Coronary Syndromes IV-93

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. Physicians

3. 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

Part 8: Stabilization of the Patient With Acute Coronary Syndromes 1-95 Step 1: A 2. ST-Segment Elevation or New or Presumably New LBBB: Evaluation for Reperfusion Assess time and risk since onset of symptoms isk of sTemi Risk of fibrinolysis Time required to transport to skilled PCl catheterization suite Step 2: Select reperfusion(fibrinolysis or invasive) strategy Note: If presentation <3 hours and no delay for PCl, then no preference for either strategy Early presentation(s3 hours from symptom onset) Late presentation (symptom onset >3 hours ago Invasive strategy is not an option (eg, lack of access to skilled Skilled PCl facility available with surgical backup PCi facility or difficult vascular access) or would be delayed -Medical contact-to-balloon or door-balloon >90 min Medical contact-to-balloon or door-balloon <90 min -Door-to-balloon)minus(door-to-needle)is >1 hour .(Door-to-balloon)minus(door-to-needle)is <1hour No contraindications to fibrinolysis e Contraindications to fibrinolysis, including increased risk of bleeding and ICH High risk from STEMI(CHF, Killip class is 23) Diagnosis of STEMI is in doubt Modified from ACC/AHA 2004 Update Recommendations. need to appreciate that other disorders can increase cardiac with MACE. Use of aspirin within the previous 7 days, for troponin, eg, myocarditis, congestive heart failure, and pul- example, would not seem to be an indicator of a bad outcome. out aspirin use was in fact found to be one of the most Risk Stratification powerful predictors. 22 It is possible that aspirin use identified a subgroup of patients at higher risk or on active but failed Braunwald Stratification therapy for CAD. There are many ways to risk-stratify patients with chest pain. The creators of the timi risk score validated it with 3 A well-recognized approach is the one initially proposed and groups of patients, and 4 clinical trials showed a significant later refined by Braunwald and colleagues on the ACC/AHa interaction between the TIMI risk score and outcome. 24-128 Task Force on the Management of Patients With Unstable These findings confirm the value of the tImi risk score as a Angina. 11, 117-120 This approach is based on a combination of guide to therapeutic decisions. A PDA download of this risk historical, clinical, laboratory, and ECG variables assessmentisavailableatwww.TimlOrG Table 3 is a modified version of what has been a work in By classifying patients into I of 3 risk strata, the Braun- progress by Braunwald and colleagues over several publica- wald (Table 3)and TIMI (Table 4)risk scores serve as the tions. 118, 120, 12I Patients are initially risk-stratified according to dominant clinical guides for predicting the risk of MACE in the likelihood that symptoms are due to unstable coronary patients with ACS. Risk stratification is applicable to patients artery disease(CAD). Patients at intermediate or high risk fc at intermediate or high risk of symptoms due to CAD and not CAD are further classified by their risk of MACE. This the larger general population of patients presenting with chest second classification is useful for prospectively identifying pain or symptoms possibly due to anginal equivalents. Risk patients at intermediate or high risk who can benefit from an stratification enables clinicians to direct therapy to those invasive strategy and more aggressive pharmacology with patients at intermediate or high risk of MACE and avoids antiplatelet and antithrombin agents unnecessary therapy and the potential for adverse conse quences in patients who are at lower risk. TIMI Risk score The risk of mace has been further studied and refined The TIMI risk score has become the primary tool for TIMI-IIB and ESSENCE (Efficacy and Safety of Subcuta- gained for patients with higher risk scoresapiey entally Researchers who derived the important Thrombolysis in evaluating therapeutic recommendations. Increm yocardial Ischemia(TIMI) risk score used data from the greater benefit from some of the newer the neous Enoxaparin in Non-Q-Wave Coronary Events) trials One additional product of the TIMI trials is the TIMI for UA/NSTEMi22, 23 and from the In-time trial for grading system of coronary artery blood flow. Investigators from the TIMI study developed and validated a coronary STEMI. 124 The TIMI risk score comprises 7 independent artery perfusion scoring system, characterizing the degree of prognostic variables(Table 4). These 7 variables were sig- reperfusion of a coronary artery on a scale of 0(no flow)to nificantly associated with the occurrence within 14 days of at least one of the primary end points: death, new or recurrent 3(normal, brisk flow). This TIMI grading system is now used MI or need for urgent revascularization The score is derived as an outcome measure in many studies of ACS interventions from complex multivariate logistic regression and includes Indicators for Early Invasive Strategies variables that seem counterintuitive. It is useful to note that Risk stratification(Figure l, Box 12) helps the clinician traditional cardiac risk factors are only weakly associated identify patients with NSTEMI and UA who should be

need to appreciate that other disorders can increase cardiac troponin, eg, myocarditis, congestive heart failure, and pul￾monary embolism. Risk Stratification Braunwald Stratification There are many ways to risk-stratify patients with chest pain. A well-recognized approach is the one initially proposed and later refined by Braunwald and colleagues on the ACC/AHA Task Force on the Management of Patients With Unstable Angina.11,117–120 This approach is based on a combination of historical, clinical, laboratory, and ECG variables. Table 3 is a modified version of what has been a work in progress by Braunwald and colleagues over several publica￾tions.118,120,121 Patients are initially risk-stratified according to the likelihood that symptoms are due to unstable coronary artery disease (CAD). Patients at intermediate or high risk for CAD are further classified by their risk of MACE. This second classification is useful for prospectively identifying patients at intermediate or high risk who can benefit from an invasive strategy and more aggressive pharmacology with antiplatelet and antithrombin agents. TIMI Risk Score The risk of MACE has been further studied and refined. Researchers who derived the important Thrombolysis in Myocardial Ischemia (TIMI) risk score used data from the TIMI-11B and ESSENCE (Efficacy and Safety of Subcuta￾neous Enoxaparin in Non–Q-Wave Coronary Events) trials for UA/NSTEMI122,123 and from the In-TIME trial for STEMI.124 The TIMI risk score comprises 7 independent prognostic variables (Table 4). These 7 variables were sig￾nificantly associated with the occurrence within 14 days of at least one of the primary end points: death, new or recurrent MI, or need for urgent revascularization. The score is derived from complex multivariate logistic regression and includes variables that seem counterintuitive. It is useful to note that traditional cardiac risk factors are only weakly associated with MACE. Use of aspirin within the previous 7 days, for example, would not seem to be an indicator of a bad outcome. But aspirin use was in fact found to be one of the most powerful predictors.122 It is possible that aspirin use identified a subgroup of patients at higher risk or on active but failed therapy for CAD. The creators of the TIMI risk score validated it with 3 groups of patients, and 4 clinical trials showed a significant interaction between the TIMI risk score and outcome.124 –128 These findings confirm the value of the TIMI risk score as a guide to therapeutic decisions. A PDA download of this risk assessment is available at www.TIMI.org. By classifying patients into 1 of 3 risk strata, the Braun￾wald (Table 3) and TIMI (Table 4) risk scores serve as the dominant clinical guides for predicting the risk of MACE in patients with ACS. Risk stratification is applicable to patients at intermediate or high risk of symptoms due to CAD and not the larger general population of patients presenting with chest pain or symptoms possibly due to anginal equivalents. Risk stratification enables clinicians to direct therapy to those patients at intermediate or high risk of MACE and avoids unnecessary therapy and the potential for adverse conse￾quences in patients who are at lower risk. The TIMI risk score has become the primary tool for evaluating therapeutic recommendations. Incrementally greater benefit from some of the newer therapies may be gained for patients with higher risk scores. One additional product of the TIMI trials is the TIMI grading system of coronary artery blood flow. Investigators from the TIMI study developed and validated a coronary artery perfusion scoring system, characterizing the degree of reperfusion of a coronary artery on a scale of 0 (no flow) to 3 (normal, brisk flow). This TIMI grading system is now used as an outcome measure in many studies of ACS interventions. Indicators for Early Invasive Strategies Risk stratification (Figure 1, Box 12) helps the clinician identify patients with NSTEMI and UA who should be TABLE 2. ST-Segment Elevation or New or Presumably New LBBB: Evaluation for Reperfusion Step 1: Assess time and risk Time since onset of symptoms Risk of STEMI Risk of fibrinolysis Time required to transport to skilled PCI catheterization suite Step 2: Select reperfusion (fibrinolysis or invasive) strategy Note: If presentation 3 hours and no delay for PCI, then no preference for either strategy. Fibrinolysis is generally preferred if: An invasive strategy is generally preferred if: ● Early presentation (
3 hours from symptom onset) ● Late presentation (symptom onset
3 hours ago) ● Invasive strategy is not an option (eg, lack of access to skilled PCI facility or difficult vascular access) or would be delayed ● Skilled PCI facility available with surgical backup —Medical contact-to-balloon or door-balloon
90 min ● Medical contact-to-balloon or door-balloon 90 min —(Door-to-balloon) minus (door-to-needle) is
1 hour ● (Door-to-balloon) minus (door-to-needle) is 1 hour ● No contraindications to fibrinolysis ● Contraindications to fibrinolysis, including increased risk of bleeding and ICH ● High risk from STEMI (CHF, Killip class is 3) ● Diagnosis of STEMI is in doubt Modified from ACC/AHA 2004 Update Recommendations.112 Part 8: Stabilization of the Patient With Acute Coronary Syndromes IV-95