Cardiol Clin 24 (2006) ix

                                                    Foreword
           Emergency Cardiac Care:...
Cardiol Clin 24 (2006) xi–xii

                                                      Preface
           Emergency Cardiac ...
xii                                                PREFACE


    Congestive heart failure (CHF) is common in          Howe...
Cardiol Clin 24 (2006) 1–17




   Initial Approach to the Patient who has Chest Pain
                 Luis H. Haro, MDa,b...
2                                                 HARO   et al

                                                          ...
INITIAL EVALUATION OF CHEST PAIN                                          3

to a facility that has only intravenous fibrin...
4                                                   HARO   et al

Placement on a monitor, intravenous access,             ...
INITIAL EVALUATION OF CHEST PAIN                                     5

of hepatic congestion and abdominal aortic        ...
6                                                    HARO   et al

    This flow allows a 30-minute response time for      ...
INITIAL EVALUATION OF CHEST PAIN                                      7

23%) [39]. When combined with IFT, the absolute  ...
8                                                 HARO   et al

classification will change to a class IIB (useful-         ...
INITIAL EVALUATION OF CHEST PAIN                                     9

a mental exercise; others use an algorithmic      ...
10                                                  HARO   et al

who described it in isolation without any symp-         ...
INITIAL EVALUATION OF CHEST PAIN                                     11

ECG findings suggesting ST-segment elevation      ...
12                                                  HARO   et al

consultation. An exception might be isolated arch       ...
INITIAL EVALUATION OF CHEST PAIN                                    13

                                                  ...
14                                                     HARO   et al

alternative diagnoses when PE is not found [84]. CT  ...
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
2006, Vol.24, Issues 1, Emergency Cardiac Care   From Ed To Ccu
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2006, Vol.24, Issues 1, Emergency Cardiac Care From Ed To Ccu

  1. 1. Cardiol Clin 24 (2006) ix Foreword Emergency Cardiac Care: From ED to CCU Michael H. Crawford, MD Consulting Editor Each year I spend considerable time on the in- heart failure specialists and electrophysiologists patient cardiology service and on cardiology con- are increasingly interacting with patients in the sultations. During these activities, my team emergency department first. This issue features interacts daily with the emergency department articles that are dedicated to these emerging physicians. I am also involved administratively interface areas in addition to several articles on in putting together plans of care for various acute acute coronary syndromes, which represent the cardiac diseases that often arrive by way of the majority of cardiac emergency department visits. emergency department. I am sure that many of Finally, this issue will be an excellent companion you share all these activities and more with your to the November 2005 issue on chest pain units, emergency department colleagues. Thus, I was de- which explores this aspect of emergent cardiac lighted when Drs. Amal Mattu and Mark Kele- care. men of the University of Maryland agreed to edit this issue of the Cardiology Clinics. Repre- Michael H. Crawford, MD senting emergency medicine and cardiology, re- Division of Cardiology spectively, they have assembled a group of Department of Medicine outstanding experts from both disciplines for this University of California issue, which is dedicated to the interface between San Francisco Medical Center the two fields. 505 Parnassus Avenue, Box 0124 Today, physician interactions concerning car- San Francisco, CA 94143-0124, USA diac patients are becoming more complex, with E-mail address: new cardiac imaging techniques being installed in michael.crawford@ucsfmedctr.org many emergency departments. Furthermore, 0733-8651/06/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.ccl.2005.10.002 cardiology.theclinics.com
  2. 2. Cardiol Clin 24 (2006) xi–xii Preface Emergency Cardiac Care: From ED to CCU Amal Mattu, MD Mark D. Kelemen, MD Guest Editors Cardiac disease is the leading cause of death in both emergency medicine and cardiology and the United States. Tremendous resources in health therefore are able to provide a coordinated ap- care are devoted toward preventing and treating proach to the evaluation and initial management chronic cardiac disease. Despite this resource allo- of these patients in the ED. The subsequent article cation, emergency department (ED) visits and hos- discusses some of the new concepts in atherogen- pital admissions for emergency cardiac conditions esis. An understanding of the pathophysiology of continue to rise. Two specialties clearly bear the atherosclerotic coronary artery disease is impor- greatest burden of dealing with this rising health tant if physicians are to understand the newer care problem: emergency medicine and cardiology. treatment of patients with acute coronary syn- These two specialties, though functionally and phil- drome (ACS). This article and the following osophically different in many ways, have discovered articles then discuss the evidence-based work-up the importance of working together and coordinat- and therapies for patients who have ACS. With ing efforts in their shared battle against the rising the understanding that optimal management of epidemic of cardiac disease. In this issue of the Car- patients who have ACS requires a multidisciplin- diology Clinics, we have attempted to bridge the gap ary health care team that includes prehospital between emergency medicine and cardiology in providers, ED providers, and in-hospital pro- terms of their respective approaches to treatment viders, this issue also features an article that of various emergency cardiac conditions. focuses on methods of improving community Emergency physicians are usually the first systems of care to optimize treatment of patients physicians to care for patients who have emer- with ACS. gency cardiac conditions. They must initiate The use of cocaine has increased in recent evidence-based therapies in a timely manner, but years, both in inner-city and suburban areas. they must be certain to plan their initial care in Consequently, ED visits for cocaine-related chest conjunction with the cardiologists who continue pain are on the rise. The recent literature has the appropriate therapies and often provide the demonstrated that rapid rule-out protocols are final definitive care. When there is poor coordi- safe and effective for these patients. This issue nation between the treatments provided by the features an article that discusses some of the two separate specialties, patient care suffers. pathophysiology of cocaine-related chest pain The first article in this issue provides an and ACAD. The authors also describe protocols appropriate lead-in to the following articles on for the evaluation and management of these acute coronary syndrome. The authors represent patients. 0733-8651/06/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.ccl.2005.10.001 cardiology.theclinics.com
  3. 3. xii PREFACE Congestive heart failure (CHF) is common in However, there is no doubt that both specialties the United States, and the prevalence of CHF is must overcome that gap if they are to optimize expected to rise as the population ages. ED visits the management of these patients. We hope that for decompensated CHF are on the rise as well. this issue helps to bridge the gap. The use of traditional medications that had been We would like to thank the dedicated authors used for many years is now being questioned, and of this issue of the Cardiology Clinics, all of whom some of the newer therapies are equally contro- contributed significant time researching and writ- versial. A chapter addresses these controversies ing the articles. We would also like to thank Ka- and provides suggestions for reasonable emer- ren Sorensen and Elsevier for their support of gency management of patients who have decom- this issue. Finally, we thank our families for their pensated CHF. patience, support, and encouragement throughout The final two articles address the emergency this process. management of cardiac arrhythmias and severe hypertension, respectively. Many advances in phar- Amal Mattu, MD macology have resulted in improvements in our Division of Emergency Medicine ability to treat acute arrhythmias and hyperten- Department of Surgery sion. The authors of these two articles address some University of Maryland School of Medicine of the new medications available for treatment, and 110 S. Paca Street, Sixth Floor, Suite 200 they suggest optimal management strategies. Baltimore, MD 21201, USA In overseeing the development of this issue of E-mail address: amattu@smail.umaryland.edu Cardiology Clinics, we have tried to maintain both an emergency medicine as well as a cardiology Mark D. Kelemen, MD perspective on the content of the articles. We be- Division of Cardiology lieve that physicians from both specialties will University of Maryland School of Medicine benefit from the topics and the content. Tradition- 22 South Greene Street ally there has been a gap between the specialties of Baltimore, MD 21202, USA emergency medicine and cardiology with regard to their respective approaches to caring for pa- E-mail address: tients who have emergency cardiac conditions. mkelemen@medicine.umaryland.edu
  4. 4. Cardiol Clin 24 (2006) 1–17 Initial Approach to the Patient who has Chest Pain Luis H. Haro, MDa,b,*, Wyatt W. Decker, MDa,b, Eric T. Boie, MDa,b, R. Scott Wright, MDa,c a Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA b Department of Emergency Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA c Division of Cardiology and Cardiac Coronary Unit, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA Scope of the problem tamponade physiology, penetrating ulcer, and tension pneumothorax (Box 1). Once these entities According to Center for Disease Control 2001– are excluded, other benign causes of chest pain are 2002 National Hospital Ambulatory Medical considered. Most of the cases presenting with Care Survey, an estimated 107 to 110 million acute chest pain are of benign origin. visits were made to hospital emergency depart- This article focuses on assessment; diagnosis, ments. Of these, approximately 3.5 to 5.4 million and management within the first 2 to 3 hours of visits (3.4% to 5.3%) were patients who presented emergency department presentation of patients with chest pain as their chief complaint [1]. In who have a chief complain of chest pain and 2001, first-listed and secondary hospital discharge whose clinical status or diagnosis merits admis- data from the National Registry of Myocardial sion to the coronary care unit or medical ICU. Infarction-4 (NRMI-4) indicate there were 1,680,000 unique discharges for acute coronary Prehospital evaluation and interventions syndrome (ACS) [2]. In evaluating acute chest pain, the immediate A patient complaining of chest pain who is at goal is to determine the accurate diagnosis and to risk for ACS should be transported from home or initiate the appropriate life-saving therapies as the outpatient clinic to the emergency department quickly as possible. It is particularly important to by an ambulance with advanced life-support identify as quickly as possible those patients (ALS) capabilities. Only ALS ambulance person- presenting with ST-segment elevation myocardial nel can obtain intravenous access, provide sub- infarction (STEMI) so that the appropriate re- lingual nitroglycerin and morphine, and provide perfusion therapies can be initiated with as little advanced cardiac life support if the patient’s delay as possible. Recent work estimates that at condition deteriorates in route. least 500,000 patients each year qualify for acute Advanced emergency medical services (EMS) reperfusion therapy for STEMI [3]. can also perform and transmit prehospital ECGs The particular challenge facing today’s practi- (PH-ECGs), stabilize a compromised airway in- tioners of emergency medicine is to evaluate every cluding endotracheal intubation and initiation of patient who presents with acute chest pain for mechanical ventilation, and initiate pharmacologic a variety of life-threatening causes of chest pain, support in situations of hemodynamic compromise such as ACS, acute aortic dissection (AD), pul- before arrival at the emergency department. monary embolism (PE), pericardial disease with Many patients who have acute myocardial infarction (AMI) suffer cardiac arrest in the first few hours of the event. Many of these patients die * Corresponding author. Department of Emergency at home suddenly. The use of an ALS-based EMS Medicine, Mayo Clinic, 200 First Street SW, Rochester, offers the best option for early, rapid management MN 55905. of cardiac arrhythmias and sudden cardiac death. E-mail address: haro.luis@mayo.edu (L.H. Haro). Lives are saved by having excellent prehospital 0733-8651/06/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.ccl.2005.09.007 cardiology.theclinics.com
  5. 5. 2 HARO et al obtaining treatment for patients who had STEMI Box 1. Differential diagnosis of chest were 4.7 and 2.3 hours, respectively, from the 14- pain country Global Registry of Acute Coronary Events project [11]. Life-threatening causes The reasons given by patients in the United Acute coronary syndrome States for delay in seeking care have been studied Aortic dissection in the REACT project. The investigators con- Pulmonary embolus ducted focus groups (N ¼ 34,207 participants) in Tension pneumothorax major regions of the United States. Target groups included adults who had had previous heart at- Other cardiovascular and nonischemic tacks, those at higher risk for heart attack, and causes bystanders to heart attacks. Reasons given by Pericarditis the target groups for delaying seeking help were Atypical angina (1) they expected heart attack symptoms to be Hypertrophic cardiomyopathy more dramatic; (2) they unrealistically judged Vasospastic angina their personal risk as low; (3) they understood lit- tle about the benefits of rapid interventions; (4) Other noncardiac causes they were unaware of the benefits of using EMS Boerhaave’s syndrome (esophageal instead of alternative transport; and (5) they rupture with mediastinitis) seemed to need the ‘‘permission’’ or advice of Gastroesophageal reflux and spasm health care providers or family to act [9,12,13]. Chest-wall pain Pleurisy Prehospital ECGs Peptic ulcer disease Panic attack PH-ECGs are an underused component in Biliary or pancreatic pain modern ACS care. In most places in the United Cervical disc or neuropathic pain States they can be obtained easily by advanced Somatization and psychogenic pain EMS personnel and transmitted en route to an disorder emergency department control center. If trans- mission is a problem, delays in the emergency department can be avoided, because the computer readout is highly accurate and can be called in to care for patients who are in ventricular fibrillation the receiving emergency department. Doing so arrest, for whom survival rates to hospital dis- allows emergency department personnel to alert charge with acceptable neurologic function can the coronary care unit and be ready for fibrino- reach 40% [4]. lysis or primary percutaneous intervention Unfortunately, ambulance services are not (PPCI). The use of PH-ECGs reduces door-to- always requested. Despite many national educa- needle time for in-hospital fibrinolysis by a mean tion campaigns, patients continue to bypass the of 10 minutes; NRMI-2 found the use of PH- EMS systems and arrive by other means. In ECGs reduced the door-to-balloon- time for NRMI-2, 53% of patients who had STEMI primary PCI by a mean of 23 minutes [5]. arrived by private means [5]. In other studies, the average percentage of patients who had a con- Prehospital triage firmed coronary event and used EMS was 23%, with a range of 10% to 48%. It is a matter of con- The use of PH-ECGs can also help EMS triage cern that 16% drove themselves to the emergency more efficiently. In general, patients who have department [6], especially considering that ap- STEMI should be transported to the nearest proximately 1 in every 300 patients transported facility that best handles the situation. For exam- to the emergency department by private vehicle ple, a patient who has an uncomplicated STEMI goes into cardiac arrest in route [7]. When they can be transported to the nearest facility that do call an ambulance, the average patient who offers acute reperfusion therapy. The patient who has STEMI does not seek medical care for ap- has STEMI and who is also in cardiogenic shock proximately 2 hours after symptom onset, and should be transported preferentially to a facility this pattern seems to be unchanged during the capable of performing PPCI or coronary artery last decade [8–10]. Average and median delays in bypass graft surgery rather than being transported
  6. 6. INITIAL EVALUATION OF CHEST PAIN 3 to a facility that has only intravenous fibrinolysis reperfusion therapies has been provided by the available, if the transport times are not signifi- ´ French nationwide Unite de Soins Intensifs cantly different. The Should We Emergently Coronaires 2000 registry [18]. In November 2000 Revascularize Occluded Arteries in Cardiogenic in France use of PHF was used for 9% of the pa- Shock (SHOCK) trial demonstrated that emer- tients who had STEMI (range, 7%–26%; N ¼ gency revascularization improved 1-year survival, 180). This therapy seemed to offer the best survival achieving an absolute 12.8% reduction in 6- benefit (Fig. 2). One-year survival was 94% for pa- month mortality in patients treated with early tients treated with PHF, 89% for patients treated revascularization (P ¼ .027) [14]. Because much of with in-hospital fibrinolysis or PPCI, and 79% for the mortality in patients in cardiogenic shock oc- patients who did not receive reperfusion therapy. curs early in the time course, it is prudent to trans- The American College of Cardiology (ACC) port patients rapidly to the nearest center of and the American Heart Association (AHA) excellence that is best equipped to provide the op- recommend establishment of a PHF protocol in timal cardiovascular care. systems where the prehospital transport times are more than 20 minutes and ALS-EMS units have Initiation of prehospital fibrinolysis high volume (O25,000) runs per year [3]. It also Recent work has suggested that time to reper- recommended that the PHF team include full- fusion remains one of the most important deter- time paramedics, have available PH-ECG tech- minants of the degree of salvaged myocardium nology with physician support, and be overseen [15,16]. Fig. 1 suggests that the earlier reperfusion by a medical director committed to developing is initiated, the more myocardium one can sal- and maintaining a quality PHF program. Unfor- vage. Fig. 1 also reveals that a strategy that signif- tunately, no single study in the United States icantly delays primary reperfusion therapy may has demonstrated a reduction in short-term mor- result in little myocardial salvage. Such data tality risks compared with hospital-based fibrino- have inspired clinical trails to perform prehospital lysis. (An in-depth discussion of options for fibrinolysis (PHF). A meta-analysis of PHF trials reperfusion is given elsewhere in this issue.) showed time to treatment was reduced by a mean of 58 minutes, with a range of 33 minutes (Seattle, WA) to 130 minutes (rural Scotland). The pooled Emergency department evaluation data demonstrated a 17% relative risk (RR) re- Once a patient arrives at the emergency de- duction in early mortality [17]. A more real-world partment, the initial nursing triage of patients who contemporary analysis of PHF versus other have chest pain and are at risk for ACS must be to a telemetry bed staffed with nurses and physicians 100 capable of performing an immediate assessment Mortality Reduction, % 80 D Shifts in Potential Outcornes and delivering advanced cardiac life support. With Different Treatment Strategies A to B No Benefit 60 A to C Benefit C B to C Benefit 40 D to B Harm D to C Harm 20 B A Extent of Myocardial Salvage 0 0 4 8 12 16 20 24 Time From Symptom Onset to Reperfusion Therapy, h Critical Time-Dependent Period Time-Independent Period Goal: Myocardial Salvage Goal: Open Infarct-Related Artery Fig. 1. Hypothetical construct of the relationship among the duration of symptoms of acute myocardial infarction before reperfusion therapy, mortality reduc- Fig. 2. Age-adjusted Kaplan-Meier 1-year survival ac- tion and extent of myocardial salvage. (From Gersh cording to reperfusion strategy. PCI, percutaneous pri- JB, Stone WG, White DH, et al. Pharmacological mary intervention. (From Danchin N, Blanchard D, facilitation of primary percutaneous coronary inter- Steg GP, et al. Impact of prehospital thrombolysis for vention for acute myocardial infarction. JAMA acute myocardial infarction on 1-yr outcome. Circula- 2005;293(8):980; with permission.) tion 2004;110:1913; with permission.)
  7. 7. 4 HARO et al Placement on a monitor, intravenous access, focused and is done to identify best those who oxygen administration, and administration of have life-threatening cardiac and noncardiac aspirin (ASA) or clopidogrel (if the patient is situations. allergic to ASA) should be done within 5 minutes The pain characteristics in ACS are frequently of patient arrival. These actions should be driven substernal and are characterized as crushing, by nursing care to minimize the time to initiation aching, vise-like, or pressure. The pain commonly of therapy. In the critically ill patient whose vitals radiates to the neck, jaw, and left arm. Associated signs are compromised (ie, cardiac arrest, tachyar- symptoms include dyspnea, nausea, vomiting, di- rhythmias, severe bradycardia, shock, or hypo- aphoresis, and presyncope. Pain often begins tension), the advanced cardiac life support abruptly, lasting 15 minutes or longer and taking guidelines developed by the AHA should be several minutes to reach maximal intensity. The followed. (Detailed management of particular pain is worse with activity and improves with rest. arrhythmias is discussed elsewhere in this issue.) Although sharp, stabbing, or fleeting pain is If the patient is stable, and if no PH-ECG is regarded as atypical for ischemic pain, such pain available, an ECG should be obtained within 10 is seen in 5% of patients who have AMI [20]. minutes of arrival at the emergency department, Elderly patients who have ACS can present with according to the ACC/AHA guidelines [3]. No a range of complaints including generalized weak- study to date has shown that this can be done con- ness, altered mental status, syncope, atypical chest sistently, however. Barriers to optimizing early pain, and dyspnea. Dyspnea is the single most com- care for patients who have chest pain are relatively mon presenting symptom of angina in patients who trivial but are common in busy emergency depart- are more than 85 years old [21]. Women presenting ments. Such barriers include large or demanding with ACS tend to be older on average than their clinical volumes and time spent undressing the pa- male counterparts, to have more comorbid dis- tient (especially the elderly), in monitor place- ease (eg, diabetes and hypertension), and to ment, in obtaining intravenous access, and in have a longer delay from symptom onset to pre- administering ASA and oxygen. These are impor- sentation in the emergency department [22]. tant and necessary tasks, but they should not de- Assessment of cardiac risk factors is tradition- lay the acquisition of an ECG. The authors ally considered a routine element of the patient encourage all emergency department personnel history, but its value in the emergency department to create a systems-based approach that intention- has been disputed. Patient age, sex, body habitus, ally works to minimize door-to-ECG-acquisition family history of coronary artery disease, and time in a way that facilitates clinical decision mak- comorbid illness including diabetes mellitus, hy- ing and improves patient outcomes. To evaluate pertension, hypercholesterolemia, and tobacco better the patient presenting with chest pain, abuse are all classic coronary risk factors. Aside they advocate using a standard 12-lead ECG from age, sex, and family history of premature and additional ECG techniques including right- coronary artery disease, the actual role of risk sided leads (V3R through V6R), posterior leads factors in predicting ACS or AMI in patients (V7, V8, and V9), and continuous ST-segment presenting to the emergency department with monitoring in selected patients who have ongoing chest pain seems minimal [23]. Risk factors are chest pain and high pretest probability of ACS. based on population studies and thus are more Approximately 20% of patients who present to predictive of development of coronary artery dis- the emergency department with chest pain have ease over a lifetime, not of whether a patient expe- a completely normal 12-lead ECG. The use of riencing chest pain in the emergency department is these additional techniques helps uncover a signif- likely to have ACS [21]. One should not dwell on icant number of patients who have AMI but this component of the history. whose 12-lead ECG is not diagnostic. The rate The initial physical examination should focus of AMI in patients who have chest pain and a to- on the cardiovascular system. The clinician should tally normal ECG remains around 1% to 4% [19]. evaluate the jugular venous pressure, looking for elevation, the presence of a Kussmaul’s sign, and the presence of hepato-jugular reflux. The lung Patient history and examination fields should be examined for signs of congestion The initial history and physical examination and wheezing. The heart and peripheral vascula- optimally should be performed within 10 minutes ture should be examined for abnormalities. The of patient arrival. The initial encounter should be abdomen should also be examined for signs
  8. 8. INITIAL EVALUATION OF CHEST PAIN 5 of hepatic congestion and abdominal aortic the most expeditious reperfusion management. pathology. The authors recommend the use of intravenous fibrinolytic therapy (IFT) in hospitals without on- Cardiac biomarker and laboratory assessment site and experienced catheterization laboratories. The use of IFT should be restricted to patients The use of cardiac biomarkers is well estab- who present within 6 hours of symptom onset and lished in patients who have ACS. These bio- have clear-cut ST segment elevation or new left markers provide the most accurate diagnosis of bundle branch block. IFT should not be used in acute myocardial injury and are considered the asymptomatic patients whose symptoms began reference standard for the diagnosis of AMI more than 24 hours previously [3]. This therapy [3,24,25]. In addition to diagnostic accuracy, the is most useful in the first 3 hours after symptom troponins provide prognostic data [26]. onset and restores coronary flow completely in Additional cardiac biomarkers that provide about half the patients treated with it. The success prognostic data in STEMI and non-STEMI rate, defined as Thrombolysis in Myocardial In- patients include B-type natriuretic peptide (BNP) farction (TIMI)-3 flow at 90 minutes after the and C-reactive protein [27] Patients who had ele- start of treatment, varies between 32% and vations of several of these biomarkers faced the 55%. The great risk of IFT is hemorrhage, includ- greatest risks. In the Orbofiban in Patients with ing a 0.5% to 1.2% risk of intracranial hemor- Unstable Coronary Syndromes Trial 16 study, rhage and a 3% to 6% risk of other major baseline measurements of troponin I, C-reactive bleeding complications (gastrointestinal bleeding, protein, and BNP were performed in 450 patients. retroperitoneal bleeding, a R 4-g drop in hemo- Elevations in troponin I, C-reactive protein, and globin) [29]. PPCI can be performed in nearly all BNP were independent predictors of the composite patients who have STEMI and is more successful of death, myocardial infarction (MI), or congestive than IFT at restoring TIMI-3 flow [30,31]. PPCI heart failure. When patients were categorized on has a lower risk of intracranial hemorrhage and the basis of the number of elevated biomarkers at reinfarction compared with IFT [3,18]. PPCI presentation, there was a near doubling of the mor- must be done promptly. Several groups have tality risk for each additional biomarker that was reported increased mortality with increased elevated (P ¼ .01) [28]. door-to-balloon time [32,33,34]. De Luca and col- Recent work suggests a prognostic role for leagues [35,36], in a study population of 1791 pa- soluble CD-40 ligand and myeloperoxidase in tients who had STEMI treated with emergent patients who have AMI, but additional work is PCI, demonstrated that for every 30-minute delay needed to confirm the long-term prognostic role in reperfusion therapy with PPCI, there was an in- of these newer markers and what value they add creased 1-year mortality of 7.5%. ACC/AHA when combined with troponin, BNP, and C- guidelines stipulate, that after adjusting for base- reactive protein in patients who have AMI. line characteristics, time from symptom onset to The authors recommend additional laboratory balloon inflation is significantly correlated with testing in patients presenting with chest pain. 1-year mortality (RR, 1.08 for each 30-minute de- Glucose, creatinine, and electrolyte levels and lay; P ¼ .04). The ACC recommends a door-to- a complete blood cell count should be obtained. balloon time of 60 to 120 minutes [3]. This goal In patients in whom acute pulmonary embolism is can be achieved only if specific intradepartmental suspected, a D-dimer should be obtained. All time goals are reached for the critical emergency these laboratory measures should be obtained as department actions: soon as possible. 1. The diagnosis: door-to-ECG (preferably less Reperfusion strategies in ST-segment elevation than 10 minutes) myocardial infarction 2. The decision to treat: door-to-catheterization A detailed discussion of reperfusion strategies in team activation (preferably within 15–25 mi- STEMI is given elsewhere in this issue. Following is nutes and preferably performed by the emer- a brief discussion of initial considerations. gency physician on call to minimize delays When faced with a patient whose ECG dem- in consultation) onstrates STEMI or new left bundle branch block, 3. The transition in care: door-to-emergency de- it is important to have pre-established multidisci- partment departure (preferably within 45–60 plinary guidelines in place to indicate the best and minutes)
  9. 9. 6 HARO et al This flow allows a 30-minute response time for Delayed primary percutaneous coronary the catheterization team members to respond after revascularization hours. Most invasive cardiologists are able to In the United States the balance of risk–benefit perform the first balloon inflation within 45 between the expedited transfer of patients for minutes after the patient’s arrival at the catheter- PPCI and more immediate treatment with IFT ization laboratory. This flow would allow a door- remains an uncertain science. The decision re- to-balloon time of 90 to 120 minutes. Although it garding transfer must be based on multiple is impossible to achieve this flow for 100% of factors, and transfer should be made only when patients, maintaining these goals and making there is a clear-cut benefit for the patient. Al- efforts to achieve such timelines are essential steps though there is little consensus in the United in achieving consistency in care and making States regarding a role for delayed PPCI in health care more reliable. Future quality-assur- patients presenting to community hospitals with- ance efforts in emergency medicine and cardiology out PPCI capability, the data from Danish Acute will be to study, publish, and advise on best Myocardial Infarction-2 trial are provocative. The practice models that can serve as blueprints to investigators demonstrated that patients trans- achieve such goals. ferred for PPCI within 2 hours of presentation had a better composite outcome (death, stoke, High-risk ST-segment elevation myocardial and recurrent nonfatal MI) than if treated with infarction fibrinolysis at the local hospital [33,35,38]. No In certain situations, slightly delayed PPCI is consensus has emerged in the United States re- preferable to immediate IFT. Patients who pres- garding this issue, and ongoing randomized clini- ent in cardiogenic shock have a high mortality cal trials are testing this strategy along with risk, and the data from the SHOCK trial sug- a strategy of facilitated PPCI using upstream ad- gested that immediate revascularization is superi- ministration of IFT before PPCI. or to delayed revascularization [14]. In practice, From the current literature, it is not possible to for such patients it is preferable to initiate reperfu- state that a particular reperfusion strategy is sion therapy with PPCI, even delayed PPCI, rather applicable to all STEMI, in all clinical settings, than immediate IFT if one can activate a team for and in all hours of the day. It is most important to PPCI reasonably quickly. Additionally, obser- choose the appropriate reperfusion strategy based vational data from the NRMI registry have sug- on the patient’s clinical presentation and symp- gested that patients who have more advanced tom onset and to provide the therapy in a timely CHF (Killip class R II) have better outcomes fashion. with PPCI than with IFT [5]. Early therapy for acute cardiac syndromes Risk of bleeding Oxygen A rare but important clinical conundrum is the Supplemental oxygen administration has be- patient who does not have a high risk of STEMI come routine for all patients presenting with chest and who has a perceived high risk for bleeding pain. Experimental results indicate that breathing from IFT. What should one do? Delay treatment oxygen might limit ischemic myocardial injury, with IFT and transfer the patient to a facility with and there is evidence that it reduces ST-segment PPCI, accept the risk and administer IFT anyway, elevation. Therefore, the use of oxygen is recom- or withhold all reperfusion therapies? One poten- mended for all AMI patients during in the first 6 tial decision is to withhold IFT in any patient who hours and longer if the AMI is complicated by has a greater than 4% risk for life-threatening congestive heart failure, PE, or other significant bleeding and to transfer the patient to another underlying disease causing hypoxemia. facility for PPCI. To assess risk of bleeding, the Aspirin ACC/AHA has defined contraindications and Aspirin (162–325 mg) should be chewed imme- cautions for fibrinolysis use [3]. Risk scores (based diately at arrival if no ASA allergy exists. ASA on points for bleeding risks) are better predictors, produces a rapid antithrombotic effect by near- and among these the best are those derived from total inhibition of thromboxane A2. The second observational studies [37]. In centers where imme- International Study of Infarct Survival Co- diate PPCI is not available, the use of such risk llaborative (ISIS-2) demonstrated an absolute scores is highly recommended. risk difference in 35-day mortality of 2.4% (RR,
  10. 10. INITIAL EVALUATION OF CHEST PAIN 7 23%) [39]. When combined with IFT, the absolute inhibitor-5 for erectile dysfunction within the difference in mortality was 5.2% (RR, 25%) [40]. last 24 hours. In patients who are allergic to ASA, clopidogrel should be substituted. Morphine sulfate Pain increases sympathetic activity, and surges Unfractionated heparin in catecholamine levels have been implicated as The authors recommend the routine use of having a role in plaque fissuring and thrombus unfractionated heparin (UFH) in all patients who propagation in AMI, as well as reducing the have AMI, and it is essential for those undergoing threshold for ventricular fibrillation. Morphine is IFT. UFH administration should precede IFT useful in controlling the pain of AMI but should in all circumstances. The authors recommend be used judiciously. When necessary, morphine weight-adjusted UFH administration including sulfate should be given in 2 to 4 mg doses a bolus of 60 U/kg (maximum of 4000 U) intravenously with increments 2 to 8 mg at 5- to followed by a 12-U/kg/hour infusion (maximum 15-minute intervals. Recent data from Can Rapid of 1000 U/hour) adjusted to a partial thrombo- Risk Stratification Of Unstable Angina Patients plastin time at 1.5 to 2.0 times control. If a nonse- Suppress Adverse Outcomes With Early Imple- lective fibrinolytic (streptokinase, urokinase, or mentation Of The ACC/AHA Guidelines study anistreplase) is used, UFH can be given only to [41] suggest that the use of morphine, alone or patients who have a high risk of systemic emboli, in combination with nitroglycerin for patients pre- such as large or anterior MI, atrial fibrillation, or senting with non-STEMI, is associated with ad- known left ventricular thrombus. For patients verse outcomes. The rate of AMI increased from who will receive PPCI, the authors recommend 3.0% in the group of patients not receiving mor- a weight-adjusted bolus dose of UFH of 50 to phine (n ¼ 40,036) to 3.8% in the group of pa- 70 U/kg accompanied by a 12-U/kg/hour infusion tients receiving morphine (n ¼ 17,003). Death (maximum of 1000 U/hour). increased from 4.7% to 5.5%, respectively, and the composite endpoint of death and AMI in- Low molecular weight heparin creased from 7.1% to 8.5%, respectively. There Low molecular weight heparin is an acceptable might be a selection bias, because the morphine alterative to UFH for patients younger than 75 group had higher incidence of ST-segment depres- years, provided that serum creatinine is not sion, transient ST-segment elevation, and positive greater than 2.5 mg/dL in men or 2.0 mg/dL in cardiac markers and was more likely to receive an women. ECG within 10 minutes of arrival and to be cared The authors recommend the use of enoxaparin for by a cardiologist. The authors address this po- as a 30-mg intravenous bolus followed by 1.0 mg/ tential by providing a risk adjustment and a pro- kg injected subcutaneously every 12 hours for 48 pensity score matched-pair analysis for 33,972 of to 72 hours. In the United States, the Food and the patients. They conclude that the use of mor- Drug Administration has not yet approved enox- phine is associated with a higher mortality and aparin for treatment of IFT, but ongoing studies raise concerns regarding the safety of using mor- are testing the efficacy of this combination. phine for this selected population. They hypothe- size that common side effects such as hypotension, Nitroglycerin bradycardia, and respiratory depression result in Patients who have ongoing chest discomfort decreased myocardial oxygen delivery, increased should receive sublingual nitroglycerin (0.4 mg) arterial carbon dioxide, and perhaps even de- every 5 minutes for a total of three doses, after creased cerebral perfusion. Unfortunately, these which the need for intravenous infusion is as- parameters were not evaluated in this observa- sessed. Nitrates reduce preload and afterload tional study. The authors’ observation and con- through peripheral arterial and venous dilatation, clusions are interesting and deserve future study. relax the epicardial coronary arteries to improve To date the ACC/AHA recommendations sup- coronary flow, and dilate collateral vessels, poten- port the use of morphine as a class I indication tially creating a favorable subendocardial-to- (conditions for which there is evidence or general epicardial flow ratio. Nitrates are harmful in agreement that a given procedure or treatment is patients who have hypotension, bradycardia, or beneficial, useful, and effective), level of evidence a suspected right ventricular infarction and in C (only consensus opinion of experts, case studies, those who have taken a phosphodiesterase or standard of care exists). It is possible that this
  11. 11. 8 HARO et al classification will change to a class IIB (useful- and Assessment of the Safety and Efficacy of ness/efficacy less well established by evidence/ a New Thrombolytic-3), which tested the efficacy opinion). of combined therapy. It is reasonable to start an intravenous Gp IIB/IIIA antagonist before initi- Beta-blockers ation of PPCI in selected patients. In STEMI, the Intravenous or oral beta-blockers should be evidence favors abciximab for patients receiving given promptly to patients who have AMI and immediate PPCI, but there are no direct compar- who do not have a contraindication. Immediate isons of abciximab and eptifibatide. Decisions beta-blocker therapy seems to reduce the magni- regarding upstream use of a Gp IIb/IIIa agent tude of infarction and the incidence of associated should be made in consultation with the consul- complications in patients not receiving fibrinoly- ting interventional cardiologist. sis, to reduce the rate of reinfarction in those The use of Gp IIb/IIIa inhibitors in unstable receiving fibrinolysis, and to reduce the frequency angina and non-STEMI was best evaluated by of life-threatening arrhythmias. During the first Boersma and colleagues [45] who published a com- few hours of STEMI, beta-blockers diminish prehensive meta-analysis that included six investi- myocardial oxygen demand by reducing heart gations (PARAGON A, Platelet Receptor rate, systemic arterial pressure, and myocardial Inhibition in Ischemic Syndrome Management, contractility. In addition, prolongation of diastole Platelet Receptor Inhibition in Ischemic Syn- may augment perfusion to ischemic myocardium, drome Management in Patients Limited By Un- particularly the subendocardium. In the ISIS-1 stable Signs And Symptoms, GUSTO IV-ACS, trial, immediate oral atenolol, 5 to 10 mg, Platelet IIb/IIIa Antagonist for the Reduction of followed by atenolol, 100 mg daily, reduced 7- Acute Coronary Syndrome Events in a Global day mortality from 4.3% to 3.7% (P ! .02; 6 lives Organization Network B (PARAGON B), and saved per 1000 treated). In the Metoprolol in Platelet Glycoprotein IIb/IIIa in Unstable An- Acute Myocardial Infarction trial [42], metopro- gina: Receptor Suppression Using Integrilin Ther- lol, 15 mg administered intravenously in three di- apy (PURSUIT) The primary endpoint was death vided doses followed by 50 mg orally every 6 or nonfatal MI. The meta-analysis included hours for 48 hours and then 100 mg daily, reduced 31,402 patients. Patients who received the Gp in- 15-day mortality from 4.9% to 4.3% as compared hibitor had a 1.2% risk reduction in the odds of with placebo. The benefits of routine early intra- death or MI after randomization (5.7% versus venous use of beta-blockers in the fibrinolytic 6.9%; P ¼ .0003). Recently, the Treat Angina era have been challenged by two later randomized with Aggrastat and Determine Cost of Therapy trials and by a post hoc analysis of the use of ate- with an Invasive or Conservative Strategy-TIMI 18 nolol in the Global Utilization of Streptokinase trial combined early PCI with a Gp IIb/IIIa antag- and TPA (alteplase) for Occluded Coronary Ar- onist and demonstrated a benefit from the use of the teries (GUSTO-1) trial [43,45]. combination [46]. The authors believe that initia- Beta-blocker therapy is contraindicated in tion of these agents in the emergency department patients who have STEMI and moderate left is reasonable and may facilitate successful early ventricular failure until compensated and in PCI. (A detailed discussion of early management patients who have bradycardia, hypotension, of non-ST-segment elevation ACS appears later shock, a PR interval greater than 0.24 second, in this issue). second- or third-degree atrioventricular block, active asthma, or reactive airway disease. Beta- Undifferentiated chest pain: the threats to life blockers are also contraindicated in cocaine-in- duced chest pain because of the risk of inducing If the ECG obtained has no significant ST- coronary spasm. segment abnormalities, the evaluation of acute chest pain continues with an in-depth clinical Glycoprotein IIb/IIIa inhibitors history taking that focuses on the characteristics Antagonism of glycoprotein (Gp) IIb/IIIa re- of pain, the time of onset, and the duration of ceptor blocks the final common pathway of symptoms, associated symptoms, risk assessment platelet aggregation. Three such agents are avail- for ACS, PE, AD, and pericardial disease with able in the United States: abciximab, tirofiban, tamponade physiology, and an examination that and eptifibatide. The use of these agents with IFT emphasizes vital signs and cardiovascular, pulmo- is not proven despite two large trials (GUSTO-V nary, and neurologic status. Most physicians do
  12. 12. INITIAL EVALUATION OF CHEST PAIN 9 a mental exercise; others use an algorithmic advances in understanding the clinical presenta- approach; but the focus of the evaluation is not tion of AD, based on these and other studies. on determining the most likely cause of chest pain. Instead, the question is: What life threaten- Clinical manifestations of aortic dissection ing entity could cause this patients chest pain Traditionally, AD occurs in patients in the (even if the possibility is less than 5%), and how later decades of life: 95% of these patients are will I make sure that I exclude it? As with missed older than 40 years, and the mean age at pre- AMI, the medical community, patients, and cer- sentation is 65 years [51,53,55]. Risk factors for tainly the judicial system have no tolerance for AD include hypertension, male sex, non-white missed life-threatening entities. The discussion race, connective tissue disease (ie, Ehlers-Danlos that follows is based on the two most important syndrome or Marfan’s syndrome), bicuspid aortic threats to life, AD and PE. valve, coarctation of the aorta, and drug use in- cluding methamphetamine and cocaine. Januzzi and colleagues [56] evaluated patients younger Acute aortic dissection than 40 years who had AD. Of 1078 patients in Epidemiology IRAD who had AD, 69 (6.4%) were younger AD is the most common and most lethal aortic than 40 years old. In these 69 patients, traditional emergency [45,47,48]. The true incidence has been risk factors such as hypertension and atheroscle- difficult to determine, because many incorrectly rosis were significantly lower than in the overall diagnosed cases escape notice. The occurrence of population of patients who had AD. The inci- AD was reported to be between 5 and 20 per mil- dence of Marfan’s syndrome, bicuspid aortic lion population [49]. The incidence of hospital ad- valve, and prior aortic valve surgery was signifi- mission for AD ranged between 1 in 5335 to 1 in cantly higher in these patients (P ! .0001). 16,550 [50]. Among the life-threatening causes of Clinical manifestations of AD are often dom- chest pain, AD has the highest mortalitydan esti- inated by the pathoanatomic characteristics of mated 1% to 2% per hour for the first 48 hours a malperfusion syndrome from a dissection-re- [44]. Unfortunately, when initially evaluating pa- lated side branch obstruction [57]. Severe pain is tients who have AD, physicians correctly suspect the most common presenting symptom; 74% to the diagnosis in as few as 15% to 43% of cases 84% of the patients recall an abrupt onset [51–53]. Diagnostic delays of more than 24 hours [51,53,55]. This symptom alone should trigger sus- after hospitalization are common and occur in up picion of an AD. Anterior chest pain is more fre- to 39% of the cases (31% for proximal AD and quent in patients who have AD involving the 53% for distal AD) [54]. Finally, when the diagno- aortic arch, whereas patients who have AD distal sis is made, it is often an incidental discovery to the left subclavian more often experience back made during an advanced imaging procedures re- pain and abdominal pain (29% of all patients quested to assess for other diagnoses. Several fac- who have AD; 42% of the patients who have dis- tors drive this poor performance. The most tal AD) [55]. Contrary to common belief, pain is frustrating combination for a physician to face described as sharp more often than tearing or rip- when evaluating a patient is a chief complaint ping. Pain that migrates throughout the chest is (ie, chest pain) that has no typical presentation present in only 28% of the patients, with no differ- and is life threatening. Unfortunately, that combi- ence between type A or type B. nation is the rule in AD: classic findings such as Less frequent presentations of AD are stroke ripping interscapular back pain, diastolic mur- (carotid occlusion), heart failure (aortic valve mur, and a wide mediastinum are present less insufficiency), syncope (tamponade, central ner- than one third of the cases [51,53,55]. vous system ischemia), buttock and leg pain with During the last decade a substantial number of or without lower extremity weakness (femoral studies have evaluated the predictive value of artery occlusion), back and flank pain (renal several historical clues and physical examination artery occlusion), abdominal pain (mesenteric findings in AD. Particularly useful is Klompas’ ischemia or celiac trunk involvement), and of [53] comprehensive review of the literature and the course the infamous painless AD. International Registry of Aortic Dissection (the Of particular importance is the presence of IRAD database) whose inception and structure syncope as a symptom of AD. In 2001, IRAD had is based on 18 large referral centers in six coun- identified 728 patients who had AD. Syncope was tries [55]. Following are some of the most recent found in 96 patients (13%), including 24 (3%)
  13. 13. 10 HARO et al who described it in isolation without any symp- this goal. Investigators have looked at soluble toms of chest or back pain [56]. Syncope is more elastic compounds, D-dimer, and smooth muscle frequent in proximal AD than in distal AD myosin heavy chain (SMMHC). (19% versus 3%; P O .001). Those who had syn- SMMHC is a major component of smooth cope were more likely to have cardiac tamponade muscle. Katoh and Suzuki [59] first described the (28% versus 8%; P O .001), stroke (18% versus use of SMMHC in AD in Japan in 1995. 4%; P O .001), and other neurologic deficits SMMHC was tested in serum of healthy subjects such as decreased level of consciousness, coma, with levels of 0.9 G 0.9 ng/mL and in four pa- and spinal cord ischemia (25% versus 14%; P O tients who had AD confirmed by surgery, all .005). In 46% of patients, a cause was not found. four of whom demonstrated elevated levels at pre- Other symptoms that require particular atten- sentation (O 7 ng/mL) that dropped to normal tion are transient ischemic attack and other focal values after 24 hours. The immunoassay showed neurologic complaints. These findings are docu- a sensitivity of 90% in the first 12 hours after on- mented in 4.7% to 17% of the cases [51,53,55]. A set of symptoms with a specificity of 97%. Most complaint of focal deficits paired with chest pain recently, Suzuki and colleagues [60] documented has one of the highest likelihood ratios of being 25 patients enrolled in the IRAD whose measured AD (positive likelihood ratio, 6.6–33) [53]. SMMHC showed elevated levels of 19.6 G 56.6 ng/mL (normal ! 2.5 ng/mL) with a presentation time of 6.1 hours G 4.5 hours. This study showed Findings on physical examination superior diagnostic performance in the early Physical examination findings associated with hours after onset (O 90% sensitivity in the first AD are typically present in less than half the cases 3 hours after onset). The sensitivity decreased to [53]. Among the most useful signs able to predict 44% after 3 hours, however, and decreased most AD is a pulse deficit. A pulse deficit between the significantly after 6 hours [60]. carotid, radial, or femoral arteries is relatively in- Elastin is one of the major components of the frequent (25%–30%) but when present is strongly arterial wall. An ELISA to measure soluble elastin suggestive of AD in the setting of chest or back fragments, a product of human aortic elastin, was pain (positive likelihood ratio, 5.7; 95% CI, 1.4– developed by Shinohara and colleagues [61]. They 23.0) [53]. This finding can predict in-hospital reported that 16 of 25 patients who had AD had complications and mortality. Bossone and col- elevated soluble elastin fragments; unfortunately, leagues [58] noted that in-hospital mortality is all patients who did not have a patent false lumen higher when pulses absent (41% versus 25%). had normal levels. Although the authors conclude The more absent pulses the higher mortality. that the test might be helpful in the diagnosis and Blood pressure on presentation does not seem to screening of AD, one patient who had AMI had be helpful in predicting who might have AD. Al- elevated levels, the study was retrospective, and though approximately half the patients present the negative predictive value was poor and there- with elevated blood pressure, an equal proportion fore not useful to exclude AD. are either hypertensive or normotensive [52,53,55]. D-dimer is frequently used to exclude throm- A history of chronic hypertension as a risk factor is boembolic disease in low-risk patients. It is helpful, however, because it is the most frequent a cross-linked fiber degradation product formed risk factor. Other physical findings are murmur by plasmin, which serves as a marker of clot lysis. of aortic insufficiency (detected in one third of Weber and colleagues [62] prospectively tested D- the cases) and muffled heart tones and jugular ve- dimer levels in 10 patients suspected of having nous distention that point toward cardiac AD. In addition, they retrospectively reviewed tamponade. 14 patients who had proven AD; 35 patients served as a control group. D-dimer was elevated Biomarkers in the workup of aortic dissection in all patients who had AD. No patients who The lack of symptoms or signs that have a good did not have AD had elevated D-dimer. The au- negative predictive value has forced investigators thors concluded that the presence of AD is unlikely to look at serologic means to diagnose AD. This in the setting of a negative D-dimer [62]. This concept is particularly attractive because a serum conclusion is thought provoking and currently test with a good negative predictive value would is being evaluated in a multicenter study along obviate the need for imaging. In the last decade with soluble elastin fragments and SMMHC several efforts have been made toward achieving (L.H. Haro, personal communication, 2004).
  14. 14. INITIAL EVALUATION OF CHEST PAIN 11 ECG findings suggesting ST-segment elevation is the best option. Heparin can be withheld. In myocardial infarction a patient who demonstrates ST-segment elevation Emergency physicians and cardiologists are in the ECG, an anterior distribution, and more frequently challenged by a patient who presents than 3 hours of pain with no findings highly with chest pain that radiates to the back and an suggestive of AD (severe abrupt pain, focal deficit, ECG with ST-segment elevation suggestive of an pulse deficit), and a completely normal chest AMI. In these cases, therapy is frequently de- radiograph, the likelihood of AD is low (likeli- layed, because patients often go to CT or transfer hood ratio, 0.07%; 95% CI, 0.03–0.17) [18], and without fibrinolytic therapy to rule out dissection. the morbidity and mortality of STEMI are high. The frequency of ST-segment elevation and Q The authors recommend fibrinolysis while await- waves suggestive of an AMI in AD are well ing transfer or further imaging such as CT or documented in the literature. In the initial TEE. IRAD publication, the finding was documented in 4.6% of type A and in 0.7% of type B [55]. In Imaging Komplas’ review [53], new MI on ECG was pres- The choice of imaging modality is usually ent in 7% of the cases (95% CI, 4–14). Coronary based on availability and the patient’s stability. artery involvement (CAI) in AD and ST abnor- CT and TEE are frequent choices [55]. CT is the malities in the ECG do not go hand-in-hand, how- most readily available, widely used, noninvasive ever. Bossone and colleagues [63] evaluated the technique for the diagnosis of AD. The sensitivity clinical characteristics and outcomes of 475 pa- and specificity of CT approaches 100% for the di- tients who had AD, of whom 64 (13.5%) had agnosis of AD [64]. Aortography was the tradi- CAI. When they reviewed the ECGs, patients tional method for making the diagnosis of AD, who had CAI were more likely to show new Q with an accuracy of 95% to 99% [65]. Aortogra- wave or ST-segment elevation (16.7% versus phy, however, is highly invasive, requires the pa- 4.3%; P ¼ .000l). Thus, these ECG findings tient be out of the emergency department for an were present in only one of six patients who had extended period of time, and exposes the patient CAI. Therefore, ST-segment elevation in AD to a significant contrast load [47]. TEE is being seems to be uncommon, and the ECG often is used with increasing frequency and has been not diagnostic even when AD with CAI is present. shown to be safe, even in critically ill patients The low frequency of AD with ST-segment eleva- [58,66,67]. The sensitivity of TEE for detecting tion compared with actual STEMI would argue both proximal and distal dissections is 100% for selected and infrequent need for imaging. [59]. The main limitations to the use of the TEE (The US Census Bureau projected a 296,042,501 is a lack of widespread, 24-hour availability. Fi- population for May 2005. The best estimate of nally, MRI is the newest imaging method for the the occurrence of AD is between 5 and 20 per mil- diagnosis of AD. It is highly sensitive and specific lion population, or approximately 1400 to 6000 and does not require exposing the patient to con- new dissections per year, 62% of which would trast material. It is not ideal in ventilated or mon- be type A. Five percent to 7% of those type A dis- itored patients and is not widely available. sections would have ST-segment abnormalities suggestive of a STEMI, representing less than Treatment of aortic dissection 300 cases in the United States each year. Approx- Treatment of AD is aimed at eliminating the imately 500,000 patients in the United States have forces that favor progression of the dissection. STEMI each year.) Prompt production of blood pressures can be In general, when a patient presents with chest accomplished through use of sodium nitroprus- pain and ST-segment elevation in the ECG, one side with a rate adjusted to achieve a systolic should assume STEMI and treat accordingly. The blood pressure between 100 and 120 mm Hg authors believe that reperfusion therapy with [44,47,57]. Concomitant use of a beta-blocker to PPCI is the safest way to proceed. If no culprit avoid reflex tachycardia secondary to the nitro- artery is found, arteriography or intraoperative prusside use is desirable to decrease further the transesophageal echocardiography (TEE) can be shear forces that promote propagation. A target performed. If PPCI is not available, and symptom heart rate of 60 to 80 beats per minute is desirable onset occurred more than 3 hours previously, the [44,57]. benefit of fibrinolysis is low. Obtaining a CT Patients who have acute dissection involving emergently or transferring the patient for PPCI the ascending aorta should receive rapid surgical
  15. 15. 12 HARO et al consultation. An exception might be isolated arch obstructive lung disease, pneumonia, or underly- dissection; most physicians consider this a surgical ing congestive heart failure. In such cases, PE entity. Richartz and colleagues [68] published the can present with the symptoms of any of these international experience with isolated arch dissec- entities [75]. tions. Of 989 patients, 92 (9%) had isolated arch The clinical likelihood of a patient’s having PE dissection. Of these, 39 (42%) were treated surgi- has long been estimated by implicit means. cally, and 53 (58%) were treated medically. Thir- Physician judgment is based on the patient’s ty-day mortality was 17% (23% with surgery and clinical presentation, history and physical evalua- 13% with medical management) and therefore tion, and risk factor assessment. Studies, however, was much lower than typical for type A dissec- have shown poor agreement among physicians tions (35% with surgery and 65% with medical in estimating pretest probability of disease [76]. management). Complications were the same. The Physician experience affects pretest probability as- conclusion was that isolated arch dissections are sessment, with less experienced clinicians demon- best managed conservatively. Distal ADs are in strating less ability to assign pretest probability general traditionally treated medically. Surgery is accurately [77]. Implicit assessment results in indicated in distal dissections when there is evi- a large group of patients being placed in the mod- dence of lower extremity or visceral ischemia, re- erate-risk category. Thus, clinical judgment has nal failure, or paraplegia [47]. yielded disappointing results in accurately deter- mining the pretest probability of disease. Percutaneous management of aortic dissection Therefore, clinical scoring systems have been Complicated type B dissections have been developed. Wells and colleagues [78] and Ander- subject to novel percutaneous therapies such as son and others [79] have created a seven-feature percutaneous fenestration (restoring flow to the bedside assessment tool to categorize patients as true lumen by creating a tear in the dissection flap having low, moderate, or high pretest probability between the true and false lumen) and percutane- of PE. Even with Wells’ criteria, studies have ous stent–graft placement. With these techniques shown poor agreement among physicians on the compromised flow can be restored in 90% of the assignment of pretest probability and poor accu- cases (range, 70%–100%). If a patient survives the racy for the same [80]. Until a reliable, validated intervention, postoperative average 30-day mor- clinical scoring system can be developed, the as- tality is 10% (range, 0%–25%), and additional signment of pretest probability of PE will remain surgical intervention is rarely needed [69]. a challenge. Pulmonary embolism Missed PE is a major source of malpractice History and physical examination litigation in emergency medicine [70]. It is esti- As in the entities previously described, history mated that the diagnosis of PE is missed 400,000 taking in a patient presenting with chest pain times annually, leading to 100,000 preventable suspicious for PE should focus on features of the deaths [71]. Other studies have estimated that only pain and associated symptoms. Particularly im- 30% of PE is diagnosed ante mortem [72]. The mor- portant in patients suspected of having PE is risk tality rate for untreated PE is 18.4%dseven times factor assessment. Box 2 lists the many of risk fac- greater than that of appropriately treated PE tors that need to be considered in a patient who [73]. Certainly, failure to be diagnosed is the great- has possible PE [74]. The physical examination est threat to the patient who has PE [74]. The chal- in a patient suspected of having PE should focus lenges faced in the diagnosis of PE are similar to on vital signs and pulmonary findings. Tachycar- those discussed for ACS and AD. dia and tachypnea are classically described, but In general, the presentation of PE is non- the former is often absent in younger patients, specific. Young patients who have excellent car- and the later is absent in up to 13% of patients diac reserve tend to have mild, transient, or no who have documented PE [74]. The physical ex- symptoms at all [74]. Patients may complain of amination may show pleural rub, rales, or findings chest pain which is typically sudden in onset and consistent with pulmonary consolidation. In sum- pleuritic in nature. Dyspnea, palpitations, presyn- mary, no physical finding is sensitive or specific cope, or syncope may also be presenting com- for the diagnosis of PE. Physical examination of- plaints. Accurate diagnosis is clouded when fers no clues to the diagnosis in 28% to 58% of clinical presentations coexist with underlying cases [74].
  16. 16. INITIAL EVALUATION OF CHEST PAIN 13 D-dimer assays Box 2. Risk factors for pulmonary The advent of quantitative ELISA has improved embolism the sensitivity of D-dimer assays tremendously [81]. D-dimer assays as a whole have poor specificity, Inherited disorders (thrombophilias) with numerous conditions resulting in false-positive Elevated individual clotting factor levels results. They are most useful when combined with (VIII, IX, XI) other noninvasive imaging or clinical probability Factor VLeiden mutation assessment scoring systems. In this way, a negative Hyperhomocystinemia D-dimer can be incorporated into diagnostic algo- Protein C, protein S, or antithrombin III rithms to withhold anticoagulation safely in pa- deficiency tients who have a low pretest probability for PE Prothrombin G20210A mutation [81]. Recent studies report the negative likelihood ratios for a negative result on a quantitative rapid Acquireddpersistent ELISA D-dimer make them as predictive as a nor- Age mal V/Q scan or negative duplex ultrasound [82]. Antiphospholipid antibodies (lupus Eleven prospective clinical studies have evalu- anticoagulant, anticardiolipin ated the role of D-dimer in excluding venous antibody) thromboembolic disease. In patients who have History of pulmonary embolism/deep a high clinical pretest probability of PE but venous thrombosis a negative D-dimer, there is not enough evidence History of superficial thrombophlebitis to support stopping an investigation for PE [73]. Hyperviscosity syndrome (polycythemia In contrast, it has become increasingly accepted vera, malignant melanoma) that the diagnosis of PE is effectively ruled out Immobilization (bedridden, paresis, or in patients who have a low clinical pretest proba- paralysis) bility of disease and a negative quantitative rapid Malignancy ELISA D-dimer [82]. Controversy still exists over Medical conditions the extent of workup necessary in patients who have a moderate pretest clinical probability and Congestive heart failure a negative D-dimer assay. Obesity One significant limitation affecting widespread Nephrotic syndrome use of D-dimer is the numerous commercially available assays that are not interchangeable, Tobacco abuse differing significantly in sensitivity and negative Acute myocardial infarction likelihood ratios [81]. Latex glutination assays and Varicose veins whole-blood qualitative assays do not demon- strate the same negative predictive value as quan- Acquireddtransient titative ELISA assays and should not be Central venous catheter/pacemaker incorporated in diagnostic algorithms similarly. placement Hormone replacement therapy V/Q scanning Immobilizationdisolated extremity The Prospective Investigation of Pulmonary Long distance travel/air travel Embolism Diagnosis investigators employed V/Q Oral contraceptive pills scanning as the primary advanced imaging di- Pregnancy and puerperium agnostic modality for patients suspected of having Surgery PE [83]. Ventilation/perfusion scans are most Trauma helpful when they are read as either normal or high probability. Results of V/Q scans, however, From Sadosty AT, Boie ET, Stead LG. Pul- fail to provide definitive indications for withhold- monary embolism. Emerg Med Clin North ing or administering anticoagulation in up to 70% Am 2003;21(2):363–84; with permission. of patients on whom the test is performed [74]. CT scanning CT is widely available, noninvasive, increasingly sensitive, and has the advantage of revealing
  17. 17. 14 HARO et al alternative diagnoses when PE is not found [84]. CT Heart Association Task Force on Practice Guide- can miss subsegmental PE. Some authors have ar- lines (Committee to Revise the 1999 Guidelines for gued that this finding is insignificant and that out- the Management of Patients with Acute Myocardial come studies of rate of subsequent or recurrent Infarction). J Am Coll Cardiol 2004;44(3):671–719. [4] Bunch TJ, White RD, Gersh BJ, et al. Outcomes and PE and death would be more a appropriate refer- in-hospital treatment of out-of-hospital cardiac ar- ence standard than comparisons to the standard rest patients resuscitated from ventricular fibrilla- of angiographic subsegmental PE detection rates tion by early defibrillation. Mayo Clin Proc 2004; [85]. Eleven such studies exist, both prospective 79(5):613–9. and retrospective, which demonstrate patient out- [5] Canto JG, Zalenski RJ, Ornato JP, et al, for the Na- come is not adversely affected when anticoagula- tional Registry of Myocardial Infarction 2 Investiga- tion is withheld based on a negative spiral CT [86]. tors. Use of emergency medical services in acute myocardial infarction and subsequent quality of Diagnostic evaluation summary care: observations from the National Registry of A review by Fedullo and Tapson [87] provides Myocardial Infarction 2. Circulation 2002;106: rational guidance to the approach to the patient 3018–23. suspected of having PE, using a combination of [6] Brown AL, Mann NC, Daya M, et al. Demographic, pretest probability assessment, D-dimer assays, belief, and situational factors influencing the deci- sion to utilize emergency medical services among and advanced imaging modalities to rule in or chest pain patients: Rapid Early Action for Coro- rule out effectively the diagnosis of PE. nary Treatment (REACT) study. Circulation 2000; Patients who have a low pretest probability of 102:173–8. PE account for 25% to 65% of all patients [7] Becker L, Larsen MP, Eisenberg MS. Incidence of evaluated for PE, with subsequent diagnosis of cardiac arrest during self-transport for chest pain. PE in 5% to 10% of cases [78,88–90]. For these Ann Emerg Med 1996;28:612–6. patients at low clinical probability, a negative [8] Rogers WJ, Canto JG, Lambrew CT, et al. Tempo- quantitative ELISA D-dimer effectively rules out ral trends in the treatment of over 1.5 million the diagnosis of PE. patients with myocardial infarction in the US from Patients who have a high pretest probability 1990 through 1999: the National Registry of Myo- cardial Infarction 1, 2 and 3. J Am Coll Cardiol for PE comprise 10% to 30% of all patients 2000;36:2056–63. evaluated for PE, with subsequent diagnosis of PE [9] Goff DC, Feldman HA, McGovern PG, et al, for the in 70% to 90% [78,88–90]. D-dimer has no signif- Rapid Early Action for Coronary Treatment (RE- icant role in this patient population, because a neg- ACT) Study Group. Prehospital delay in patients ative result does not rule out the presence of PE. hospitalized with heart attack symptoms in the Spiral CT should be performed in these patients. United States: the REACT trial. Am Heart J 1999; If CT is negative, duplex ultrasound or CT venog- 138:1046–57. raphy of the lower extremities may be indicated. If [10] Welsh RC, Ornato J, Armstrong PW. Prehospital lower extremity studies are also negative in this management of acute ST-elevation myocardial in- high-risk patient population, pulmonary angio- farction: a time for reappraisal in North America. Am Heart J 2003;145:1–8. gram is indicated to rule out the presence of PE. [11] Steg PG, Goldberg RJ. Baseline characteristics, Intermediate-risk patients comprise 25% to management practices and in-hospital outcomes 65% of all patients examined for PE, with sub- of patients hospitalized with acute coronary syn- sequent diagnosis of PE in 25% to 45% [78,88–90]. dromes in the Global Registry of Acute Coronary Events (GRACE). Am J Cardiol 2002;90(4): 358–63. References [12] Finnegan JR Jr, Hendrika Meischke H, Zapka JG, [1] McCaig LF, Burt CW. National hospital ambula- et al. Patient delay in seeking care for heart attack tory medical care survey: 2002 emergency depart- symptoms: findings from focus groups conducted ment summary. Adv Data 2004;(340):1–34. in five US regions. Prev Med 2000;31:205–13. [2] American Heart Association. Heart disease and [13] Goff DC Jr, Mitchell P, Finnegan J, et al, for the RE- stroke statisticsd2004 update. Available at: http:// ACT Study Group. Knowledge of heart attack www.americanheart.org/presenter.jhtml?identifier¼ symptoms in 20 US communities. Results from the 3000090. Accessed November 15, 2003. Rapid Early Action for Coronary Treatment Com- [3] Antman EM, Anbe DT, Armstrong PW, et al. ACC/ munity Trial. Prev Med 2004;38(1):85–93. AHA guidelines for the management of patients [14] Hochman JS, Sleeper LA, White HD, et al, for the with ST-elevation myocardial infarction; a report Should We Emergently Revascularize Occluded of the American College of Cardiology/American Coronaries for Cardiogenic Shock (SHOCK)

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