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Acute Coronary Syndrome

  • Author: David L Coven, MD, PhD; Chief Editor: Eric H Yang, MD  more...
 
Updated: Sep 09, 2015
 

Practice Essentials

Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations ranging from those for ST-segment elevation myocardial infarction (STEMI) to presentations found in non–ST-segment elevation myocardial infarction (NSTEMI) or in unstable angina. It is almost always associated with rupture of an atherosclerotic plaque and partial or complete thrombosis of the infarct-related artery.

The image below illustrates an algorithm for triaging patients with chest pain.

Suggested algorithm for triaging patients with che Suggested algorithm for triaging patients with chest pain. ACS = ACS; ASA = aspirin; EKG = ECG; MI = myocardial infarction; Rx = treat; STEMI = ST-elevation myocardial infarction. Courtesy of Wu et al (1999).

See Are You Missing Subtle MI Clues on ECGs? Test Your Skills, a Critical Images slideshow, to help identify a variety of electrocardiographic abnormalities.

Essential update: ACP releases guidelines on screening for coronary heart disease

In 2015, the American College of Physicians (ACP) released guidelines on screening for coronary heart disease, including the following[1] :

  • There is no evidence that cardiac screening improves patient outcomes in asymptomatic, low-risk adults.
  • Potential harms of cardiac screening include false-positive results causing patients to undergo potentially unnecessary tests and procedures.
  • Among adults at low risk, prevalence of coronary heart disease is low, and cardiac screening is of low predictive value. Therefore, cardiac screening is of low yield, and the probability that positive findings will influence therapeutic decision making is low.
  • Clinicians should therefore emphasize strategies to reduce cardiovascular risk even further among low-risk adults by treating modifiable risk factors (smoking, diabetes, blood pressure, hyperlipidemia, overweight, and exercise).
  • Clinicians should not screen asymptomatic, low-risk adults for cardiac disease using resting or stress electrocardiography, stress echocardiography, or stress myocardial perfusion imaging.
  • Clinicians should conduct cardiovascular risk assessment with a global risk score combining individual risk factor measurements into a single quantitative estimate of risk.
  • The ACP recommendations do not apply to symptomatic patients or to screening athletes before participation in various events.

Signs and symptoms

Atherosclerosis is the primary cause of ACS, with most cases occurring from the disruption of a previously nonsevere lesion. Complaints reported by patients with ACS include the following:

  • Palpitations
  • Pain, which is usually described as pressure, squeezing, or a burning sensation across the precordium and may radiate to the neck, shoulder, jaw, back, upper abdomen, or either arm
  • Exertional dyspnea that resolves with pain or rest
  • Diaphoresis from sympathetic discharge
  • Nausea from vagal stimulation
  • Decreased exercise tolerance

Physical findings can range from normal to any of the following:

  • Hypotension: Indicates ventricular dysfunction due to myocardial ischemia, myocardial infarction (MI), or acute valvular dysfunction
  • Hypertension: May precipitate angina or reflect elevated catecholamine levels due to anxiety or to exogenous sympathomimetic stimulation
  • Diaphoresis
  • Pulmonary edema and other signs of left heart failure
  • Extracardiac vascular disease
  • Jugular venous distention
  • Cool, clammy skin and diaphoresis in patients with cardiogenic shock
  • A third heart sound (S 3) and, frequently, a fourth heart sound (S 4)
  • A systolic murmur related to dynamic obstruction of the left ventricular outflow tract
  • Rales on pulmonary examination (suggestive of left ventricular dysfunction or mitral regurgitation)

Potential complications include the following:

  • Ischemia: Pulmonary edema
  • Myocardial infarction: Rupture of the papillary muscle, left ventricular free wall, and ventricular septum

See Clinical Presentation for more detail.

Diagnosis

Guidelines for the management of non-ST-segment elevation ACS were released in 2011 by the European Society of Cardiology (ESC).[2] The guidelines include the use of the CRUSADE risk score (Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA guidelines).

In the emergency setting, electrocardiography (ECG) is the most important diagnostic test for angina. ECG changes that may be seen during anginal episodes include the following:

  • Transient ST-segment elevations
  • Dynamic T-wave changes: Inversions, normalizations, or hyperacute changes
  • ST depressions: These may be junctional, downsloping, or horizontal

Laboratory studies that may be helpful include the following:

  • Creatine kinase isoenzyme MB (CK-MB) levels
  • Cardiac troponin levels
  • Myoglobin levels
  • Complete blood count
  • Basic metabolic panel

Diagnostic imaging modalities that may be useful include the following:

  • Chest radiography
  • Echocardiography
  • Myocardial perfusion imaging
  • Cardiac angiography
  • Computed tomography, including CT coronary angiography and CT coronary artery calcium scoring

See Workup for more detail.

Management

Initial therapy focuses on the following:

  • Stabilizing the patient’s condition
  • Relieving ischemic pain
  • Providing antithrombotic therapy

Pharmacologic anti-ischemic therapy includes the following:

  • Nitrates (for symptomatic relief)
  • Beta blockers (eg, metoprolol): These are indicated in all patients unless contraindicated

Pharmacologic antithrombotic therapy includes the following:

  • Aspirin
  • Clopidogrel
  • Prasugrel
  • Ticagrelor
  • Glycoprotein IIb/IIIa receptor antagonists (abciximab, eptifibatide, tirofiban)

Pharmacologic anticoagulant therapy includes the following:

  • Unfractionated heparin (UFH)
  • Low-molecular-weight heparin (LMWH; dalteparin, nadroparin, enoxaparin)
  • Factor Xa inhibitors (rivaroxaban, fondaparinux)

Additional therapeutic measures that may be indicated include the following:

  • Thrombolysis
  • Percutaneous coronary intervention (preferred treatment for ST-elevation MI)

Current guidelines for patients with moderate- or high-risk ACS include the following:

  • Early invasive approach
  • Concomitant antithrombotic therapy, including aspirin and clopidogrel, as well as UFH or LMWH

See Treatment and Medication for more detail.

The image below depicts a 62-year-old woman with a history of chronic stable angina and a "valve problem."

A 62-year-old woman with a history of chronic stab A 62-year-old woman with a history of chronic stable angina and a "valve problem" presents with new chest pain. She is symptomatic on arrival, complaining of shortness of breath and precordial chest tightness. Her initial vital signs are blood pressure = 140/90 mm Hg and heart rate = 98. Her electrocardiogram (ECG) is as shown. She is given nitroglycerin sublingually, and her pressure decreases to 80/palpation. Right ventricular ischemia should be considered in this patient.
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Background

Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations ranging from those for ST-segment elevation myocardial infarction (STEMI) to presentations found in non–ST-segment elevation myocardial infarction (NSTEMI) or in unstable angina. In terms of pathology, ACS is almost always associated with rupture of an atherosclerotic plaque and partial or complete thrombosis of the infarct-related artery. (See Etiology.)

In some instances, however, stable coronary artery disease (CAD) may result in ACS in the absence of plaque rupture and thrombosis, when physiologic stress (eg, trauma, blood loss, anemia, infection, tachyarrhythmia) increases demands on the heart. The diagnosis of acute myocardial infarction in this setting requires a finding of the typical rise and fall of biochemical markers of myocardial necrosis in addition to at least 1 of the following[3] (See Workup.):

  • Ischemic symptoms
  • Development of pathologic Q waves
  • Ischemic ST-segment changes on electrocardiogram (ECG) or in the setting of a coronary intervention

The terms transmural and nontransmural (subendocardial) myocardial infarction are no longer used because ECG findings in patients with this condition are not closely correlated with pathologic changes in the myocardium. Therefore, a transmural infarct may occur in the absence of Q waves on ECGs, and many Q-wave myocardial infarctions may be subendocardial, as noted on pathologic examination. Because elevation of the ST segment during ACS is correlated with coronary occlusion and because it affects the choice of therapy (urgent reperfusion therapy), ACS-related myocardial infarction should be designated STEMI or NSTEMI. (See Workup.)

Attention to the underlying mechanisms of ischemia is important when managing ACS. A simple predictor of demand is rate-pressure product, which can be lowered by beta blockers (eg, metoprolol or atenolol) and pain/stress relievers (eg, morphine), while supply may be improved by oxygen, adequate hematocrit, blood thinners (eg, heparin, IIb/IIIa agents such as abciximab, eptifibatide, tirofiban, or thrombolytics), and/or vasodilators (eg, nitrates, amlodipine). (See Medications.)

In 2010, the American Heart Association (AHA) published new guideline recommendations for the diagnosis and treatment of ACS.[4]

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Etiology

Acute coronary syndrome (ACS) is caused primarily by atherosclerosis. Most cases of ACS occur from disruption of a previously nonsevere lesion (an atherosclerotic lesion that was previously hemodynamically insignificant yet vulnerable to rupture). The vulnerable plaque is typified by a large lipid pool, numerous inflammatory cells, and a thin, fibrous cap.

Elevated demand can produce ACS in the presence of a high-grade fixed coronary obstruction, due to increased myocardial oxygen and nutrition requirements, such as those resulting from exertion, emotional stress, or physiologic stress (eg, from dehydration, blood loss, hypotension, infection, thyrotoxicosis, or surgery).

ACS without elevation in demand requires a new impairment in supply, typically due to thrombosis and/or plaque hemorrhage.

The major trigger for coronary thrombosis is considered to be plaque rupture caused by the dissolution of the fibrous cap, the dissolution itself being the result of the release of metalloproteinases (collagenases) from activated inflammatory cells. This event is followed by platelet activation and aggregation, activation of the coagulation pathway, and vasoconstriction. This process culminates in coronary intraluminal thrombosis and variable degrees of vascular occlusion. Distal embolization may occur. The severity and duration of coronary arterial obstruction, the volume of myocardium affected, the level of demand on the heart, and the ability of the rest of the heart to compensate are major determinants of a patient's clinical presentation and outcome. (Anemia and hypoxemia can precipitate myocardial ischemia in the absence of severe reduction in coronary artery blood flow.)

A syndrome consisting of chest pain, ischemic ST-segment and T-wave changes, elevated levels of biomarkers of myocyte injury, and transient left ventricular apical ballooning (takotsubo syndrome) has been shown to occur in the absence of clinical CAD, after emotional or physical stress. The etiology of this syndrome is not well understood but is thought to relate to a surge of catechol stress hormones and/or high sensitivity to those hormones.

Baseline blood glucose levels appear to be an independent risk factor for a major adverse cardiac event (MACE) in emergency department (ED) patients with suspected ACS.[5, 6] In an analysis of data from 1708 Australian and New Zealand patients in a prospective observational study, investigators noted a MACE occurred within 30 days of presentation in 15.3% of patients whose ED admission blood glucose levels were below 7 mmol/L (about 126 mg/dL); however, in the same time period, a MACE occurred in twice as many patients (30.9%) whose blood glucose levels were above 7 mmol/L.[6] After controlling for various factors, patients who had admission blood glucose levels of 7 mmol/L or higher were at 51% higher risk of experiencing a MACE compared with patients who had lower baseline blood glucose levels.[6] Other significant predictors of MACE included male sex, older age, family history, hypertension, dyslipidemia, ischemic findings on ECG, and positive troponintests.[5, 6]

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Prognosis

Six-month mortality rates in the Global Registry of Acute Coronary Events (GRACE) were 13% for patients with NSTEMI ACS and 8% for those with unstable angina.

An elevated level of troponin (a type of regulatory protein found in skeletal and cardiac muscle) permits risk stratification of patients with ACS and identifies patients at high risk for adverse cardiac events (ie, myocardial infarction, death) up to 6 months after the index event.[7, 8] (See Workup.)

The PROVE IT-TIMI trial found that after ACS, a J-shaped or U-shaped curve association is observed between BP and the risk of future cardiovascular events.[9]

LeLeiko et al determined that serum choline and free F(2)-isoprostane are also predictors of cardiac events in ACS. The authors evaluated the prognostic value of vascular inflammation and oxidative stress biomarkers in patients with ACS to determine their role in predicting 30-day clinical outcomes. Serum F(2)-isoprostane had an optimal cutoff level of 124.5 pg/mL, and serum choline had a cutoff level of 30.5 µmol/L. Choline and F(2)-isoprostane had a positive predictive value of 44% and 57% and a negative predictive value of 89% and 90%, respectively.[10]

Testosterone deficiency is common in patients with coronary disease and has a significant negative impact on mortality. Further study is needed to assess the effect of treatment on survival.[11]

A study by Sanchis et al suggests renal dysfunction, dementia, peripheral artery disease, previous heart failure, and previous myocardial infarction are the comorbid conditions that predict mortality in NSTEMI ACS.[12] In patients with comorbid conditions, the highest risk period was in the first weeks after NSTEMI ACS. In-hospital management of patients with comorbid conditions merits further investigation.

Patients with end-stage renal disease often develop ACS, and little is known about the natural history of ACS in patients receiving dialysis. Gurm et al examined the presentation, management, and outcomes of patients with ACS who received dialysis before presentation for an ACS. These patients were enrolled in the Global Registry of Acute Coronary Events (GRACE) at 123 hospitals in 14 countries from 1999-2007.

NSTEMI ACS was the most common in patients receiving dialysis, occurring in 50% of patients (290 of 579) versus 33% (17,955 of 54,610) of those not receiving dialysis The in-hospital mortality rates were higher among patients receiving dialysis (12% vs 4.8%; p < 0.0001). Higher 6-month mortality rates (13% vs 4.2%; p < 0.0001), recurrent myocardial infarction incidence (7.6% vs 2.9%; p < 0.0001), and unplanned rehospitalizations (31% vs 18%; p < 0.0001) were found among those who survived to discharge. Outcomes in patients who received dialysis was worse than was predicted by the calculated GRACE risk score for in-hospital mortality (7.8% predicted vs 12% observed; p < 0.05). This suggests that the GRACE risk score underestimated the risk of major events in these patients.[13]

In a study that assessed the impact of prehospital time on STEMI outcome, Chughatai et al suggest that "total time to treatment" should be used as a core measure instead of "door-to-balloon time."[14] This is because on-scene time was the biggest fraction of "pre-hospital time." The study compared groups with total time to treatment of more than 120 minutes compared with 120 minutes or less and found mortalities were 4 compared with 0 and transfers to a tertiary care facility were 3 compared with 1, respectively.

STEMI mechanisms and stenting outcome similar in women and men

Despite their smaller coronary vessels and higher risk profile, women with STEMI appear to respond just as well as men to primary PCI and stenting, according to the Optical Coherence Tomography Assessment of Gender Diversity in Primary Angioplasty (OCTAVIA) study.[15] OCTAVIA, which was designed to examine gender differences at the time of primary PCI, included 140 STEMI patients at 14 Italian centers, matched by age and risk factors, who received an everolimus-eluting stent.[15]

On initial OCT, no differences by gender were found in the proportion of ruptured or eroded plaques, thus suggesting that the pathophysiology of STEMI is nearly identical in men and women.[15] On repeat OCT at nine months, intended to assess stent healing, more than 90% of both men and women had fully covered stent struts. Although OCTAVIA was not powered for clinical end points, no significant differences in death, reinfarction, stroke, stent thrombosis, or target vessel reintervention were evident at one year.[15]

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Patient Education

Patient education of risk factors is important, but more attention is needed regarding delays in door-to-balloon time, and one major barrier to improving this delay is patient education regarding his or her symptoms. Lack of recognition of symptoms may cause tremendous delays in seeking medical attention.

Educate patients about the dangers of cigarette smoking, a major risk factor for coronary artery disease (CAD). The risk of recurrent coronary events decreases 50% at 1 year after smoking cessation. Provide all patients who smoke with guidance, education, and support to avoid smoking. Smoking-cessation classes should be offered to help patients avoid smoking after a myocardial infarction. Bupropion increases the likelihood of successful smoking cessation.

Diet plays an important role in the development of CAD. Therefore, prior to hospital discharge, a patient who has had a myocardial infarction should be evaluated by a dietitian. Patients should be informed about the benefits of a low-cholesterol, low-salt diet. In addition, educate patients about AHA dietary guidelines regarding a low-fat, low-cholesterol diet.

A cardiac rehabilitation program after discharge may reinforce education and enhance compliance.

The following mnemonic may useful in educating patients with CAD regarding treatments and lifestyle changes necessitated by their condition:

  • A = Aspirin and antianginals
  • B = Beta blockers and blood pressure (BP)
  • C = Cholesterol and cigarettes
  • D = Diet and diabetes
  • E = Exercise and education

For patients being discharged home, emphasize the following:

  • Timely follow-up with primary care provider
  • Compliance with discharge medications, specifically aspirin and other medications used to control symptoms
  • Need to return to the ED for any change in frequency or severity of symptoms

For patient education resources, see the Heart Health Center and Cholesterol Center, as well as High Cholesterol, Cholesterol Charts (What the Numbers Mean), Lifestyle Cholesterol Management, Chest Pain, Coronary Heart Disease, Heart Attack, Angina Pectoris, Cholesterol-Lowering Medications, and Statins for Cholesterol.

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Contributor Information and Disclosures
Author

David L Coven, MD, PhD Assistant Professor of Clinical Medicine, Columbia University College of Physicians and Surgeons; Director, Cardiology Outpatient Clinic, St Luke’s Site, Attending Physician, Department of Medicine, Division of Cardiology, St Luke’s-Roosevelt Hospital Center

David L Coven, MD, PhD is a member of the following medical societies: American College of Physicians, American Medical Association, Massachusetts Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Jamshid Shirani, MD Director of Cardiology Fellowship Program, Director of Echocardiography Laboratory, Director of Hypertrophic Cardiomyopathy Clinic, St Luke's University Health Network

Jamshid Shirani, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society of Echocardiography, Association of Subspecialty Professors, American College of Cardiology, American College of Physicians, American Heart Association

Disclosure: Nothing to disclose.

Arun Kalyanasundaram, MD, MPH Interventional Cardiology Fellow, Department of Cardiology, Cleveland Clinic

Arun Kalyanasundaram, MD, MPH is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, Society for Cardiovascular Angiography and Interventions, Society of General Internal Medicine, Southern Medical Association, Society of Hospital Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD Associate Professor of Medicine, Director of Cardiac Catherization Laboratory and Interventional Cardiology, Mayo Clinic Arizona

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Acknowledgements

Craig T Basson, MD, PhD Gladys and Roland Harriman Professor of Medicine, Director of the Center for Molecular Cardiology, Director of Cardiovascular Research, Division of Cardiology, Department of Medicine, Weill Cornell Medical College; Attending Physician, New York Presbyterian Hospital

Craig T Basson, MD, PhD is a member of the following medical societies: American College of Cardiology and American Heart Association

Disclosure: Nothing to disclose.

Edward Bessman, MD, MBA Chairman and Clinical Director, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Steven J Compton, MD, FACC, FACP Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Chou R, for the High Value Care Task Force of the American College of Physicians. Cardiac screening with electrocardiography, stress echocardiography, or myocardial perfusion imaging: advice for high-value care from the American College of Physicians. Ann Intern Med. 2015 Mar 17. 162(6):438-47. [Medline].

  2. Hamm CW, Bassand JP, Agewall S, et al. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: The Task Force for the management of acute coronary syndromes (ACS) in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J. 2011 Sep 21. [Medline].

  3. Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol. 2000 Sep. 36(3):959-69. [Medline].

  4. O'Connor RE, Bossaert L, Arntz HR, Brooks SC, Diercks D, Feitosa-Filho G, et al. Part 9: acute coronary syndromes: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation. 2010 Oct 19. 122(16 Suppl 2):S422-65. [Medline].

  5. Gardner LS, Nguyen-Pham S, Greenslade JH, et al. Admission glycaemia and its association with acute coronary syndrome in Emergency Department patients with chest pain. Emerg Med J. 2014 Oct 24. [Medline].

  6. Boggs W. Blood glucose predicts outcomes of patients with chest pain. Reuters Health Information. November 11, 2014. [Full Text].

  7. Antman EM, Tanasijevic MJ, Thompson B, Schactman M, McCabe CH, Cannon CP, et al. Cardiac-specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes. N Engl J Med. 1996 Oct 31. 335(18):1342-9. [Medline].

  8. Heidenreich PA, Alloggiamento T, Melsop K, McDonald KM, Go AS, Hlatky MA. The prognostic value of troponin in patients with non-ST elevation acute coronary syndromes: a meta-analysis. J Am Coll Cardiol. 2001 Aug. 38(2):478-85. [Medline].

  9. Bangalore S, Qin J, Sloan S, Murphy SA, Cannon CP. What is the optimal blood pressure in patients after acute coronary syndromes?: Relationship of blood pressure and cardiovascular events in the PRavastatin OR atorVastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction (PROVE IT-TIMI) 22 trial. Circulation. 2010 Nov 23. 122(21):2142-51. [Medline].

  10. LeLeiko RM, Vaccari CS, Sola S, Merchant N, Nagamia SH, Thoenes M, et al. Usefulness of elevations in serum choline and free F2)-isoprostane to predict 30-day cardiovascular outcomes in patients with acute coronary syndrome. Am J Cardiol. 2009 Sep 1. 104(5):638-43. [Medline].

  11. Ma RC, Tong PC. Testosterone levels and cardiovascular disease. Heart. 2010 Nov. 96(22):1787-8. [Medline].

  12. Sanchis J, Nunez J, Bodi V, et al. Influence of comorbid conditions on one-year outcomes in non-ST-segment elevation acute coronary syndrome. Mayo Clin Proc. 2011 Apr. 86(4):291-6. [Medline]. [Full Text].

  13. Gurm HS, Gore JM, Anderson FA Jr, et al. Comparison of Acute Coronary Syndrome in Patients Receiving Versus Not Receiving Chronic Dialysis (from the Global Registry of Acute Coronary Events [GRACE] Registry). Am J Cardiol. 2012 Jan 1. 109(1):19-25. [Medline].

  14. Chughtai H, Ratner D, Pozo M, et al. Prehospital delay and its impact on time to treatment in ST-elevation myocardial infarction. Am J Emerg Med. 2011 May. 29(4):396-400. [Medline].

  15. Wood S. STEMI in Women: Same Plaques, Same Stent Outcomes: OCTAVIA. Medscape Medical News. Available at http://www.medscape.com/viewarticle/825391. Accessed: May 27, 2014.

  16. Than M, Cullen L, Reid CM, Lim SH, Aldous S, Ardagh MW, et al. A 2-h diagnostic protocol to assess patients with chest pain symptoms in the Asia-Pacific region (ASPECT): a prospective observational validation study. Lancet. 2011 Mar 26. 377(9771):1077-84. [Medline].

  17. Scheuermeyer FX, Innes G, Grafstein E, et al. Safety and Efficiency of a Chest Pain Diagnostic Algorithm With Selective Outpatient Stress Testing for Emergency Department Patients With Potential Ischemic Chest Pain. Ann Emerg Med. 2012 Jan 4. [Medline].

  18. Amsterdam EA, Wenger NK. The 2014 American College of Cardiology ACC/American Heart Association guideline for the management of patients with non-ST-elevation acute coronary syndromes: ten contemporary recommendations to aid clinicians in optimizing patient outcomes. Clin Cardiol. 2015 Feb. 38(2):121-3. [Medline].

  19. Keller T, Zeller T, Ojeda F, et al. Serial changes in highly sensitive troponin I assay and early diagnosis of myocardial infarction. JAMA. 2011 Dec 28. 306(24):2684-93. [Medline].

  20. O'Neil BJ, Hoekstra J, Pride YB, Lefebvre C, Diercks D, Frank Peacock W, et al. Incremental benefit of 80-lead electrocardiogram body surface mapping over the 12-lead electrocardiogram in the detection of acute coronary syndromes in patients without ST-elevation myocardial infarction: Results from the Optimal Cardiovascular Diagnostic Evaluation Enabling Faster Treatment of Myocardial Infarction (OCCULT MI) trial. Acad Emerg Med. 2010 Sep. 17(9):932-9. [Medline].

  21. Damman P, Holmvang L, Tijssen JG, et al. Usefulness of the Admission Electrocardiogram to Predict Long-Term Outcomes After Non-ST-Elevation Acute Coronary Syndrome (from the FRISC II, ICTUS, and RITA-3 [FIR] Trials). Am J Cardiol. 2012 Jan 1. 109(1):6-12. [Medline].

  22. Damman P, Wallentin L, Fox KA, et al. Long-Term Cardiovascular Mortality After Procedure-Related or Spontaneous Myocardial Infarction in Patients With Non-ST-Segment Elevation Acute Coronary Syndrome: A Collaborative Analysis of Individual Patient Data From the FRISC II, ICTUS, and RITA-3 Trials (FIR). Circulation. 2012 Jan 31. 125(4):568-76. [Medline].

  23. Iliou MC, Fumeron C, Benoit MO, Tuppin P, Calonge VM, Moatti N, et al. Prognostic value of cardiac markers in ESRD: Chronic Hemodialysis and New Cardiac Markers Evaluation (CHANCE) study. Am J Kidney Dis. 2003 Sep. 42(3):513-23. [Medline].

  24. Ohman EM, Armstrong PW, Christenson RH, Granger CB, Katus HA, Hamm CW, et al. Cardiac troponin T levels for risk stratification in acute myocardial ischemia. GUSTO IIA Investigators. N Engl J Med. 1996 Oct 31. 335(18):1333-41. [Medline].

  25. Lindahl B, Toss H, Siegbahn A, Venge P, Wallentin L. Markers of myocardial damage and inflammation in relation to long-term mortality in unstable coronary artery disease. FRISC Study Group. Fragmin during Instability in Coronary Artery Disease. N Engl J Med. 2000 Oct 19. 343(16):1139-47. [Medline].

  26. Newby LK, Christenson RH, Ohman EM, Armstrong PW, Thompson TD, Lee KL, et al. Value of serial troponin T measures for early and late risk stratification in patients with acute coronary syndromes. The GUSTO-IIa Investigators. Circulation. 1998 Nov 3. 98(18):1853-9. [Medline].

  27. Lindahl B, Venge P, Wallentin L. Relation between troponin T and the risk of subsequent cardiac events in unstable coronary artery disease. The FRISC study group. Circulation. 1996 May 1. 93(9):1651-7. [Medline].

  28. Stubbs P, Collinson P, Moseley D, Greenwood T, Noble M. Prognostic significance of admission troponin T concentrations in patients with myocardial infarction. Circulation. 1996 Sep 15. 94(6):1291-7. [Medline].

  29. Apple FS, Parvin CA, Buechler KF, Christenson RH, Wu AH, Jaffe AS. Validation of the 99th percentile cutoff independent of assay imprecision (CV) for cardiac troponin monitoring for ruling out myocardial infarction. Clin Chem. 2005 Nov. 51(11):2198-200. [Medline].

  30. Eggers KM, Oldgren J, Nordenskjöld A, Lindahl B. Diagnostic value of serial measurement of cardiac markers in patients with chest pain: limited value of adding myoglobin to troponin I for exclusion of myocardial infarction. Am Heart J. 2004 Oct. 148(4):574-81. [Medline].

  31. Macrae AR, Kavsak PA, Lustig V, Bhargava R, Vandersluis R, Palomaki GE, et al. Assessing the requirement for the 6-hour interval between specimens in the American Heart Association Classification of Myocardial Infarction in Epidemiology and Clinical Research Studies. Clin Chem. 2006 May. 52(5):812-8. [Medline].

  32. Kavsak PA, MacRae AR, Newman AM, Lustig V, Palomaki GE, Ko DT, et al. Effects of contemporary troponin assay sensitivity on the utility of the early markers myoglobin and CKMB isoforms in evaluating patients with possible acute myocardial infarction. Clin Chim Acta. 2007 May 1. 380(1-2):213-6. [Medline].

  33. Meune C, Balmelli C, Twerenbold R, et al. Patients with Acute Coronary Syndrome and Normal High-sensitivity Troponin. Am J Med. 2011 Dec. 124(12):1151-7. [Medline].

  34. Saenger AK, Jaffe AS. Requiem for a heavyweight: the demise of creatine kinase-MB. Circulation. 2008 Nov 18. 118(21):2200-6. [Medline].

  35. Sorensen JT, Terkelsen CJ, Steengaard C, et al. Prehospital troponin T testing in the diagnosis and triage of patients with suspected acute myocardial infarction. Am J Cardiol. 2011 May 15. 107(10):1436-40. [Medline].

  36. Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE Jr, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-Elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction) developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interve... J Am Coll Cardiol. 2007 Aug 14. 50(7):e1-e157. [Medline].

  37. Venge P, Ohberg C, Flodin M, Lindahl B. Early and late outcome prediction of death in the emergency room setting by point-of-care and laboratory assays of cardiac troponin I. Am Heart J. 2010 Nov. 160(5):835-41. [Medline].

  38. O'Riordan M. Negative Troponin and Copeptin Tests Rule Out Acute Coronary Syndrome. Medscape Medical News. Sep 3 2013. [Full Text].

  39. Misra D, Leibowitz K, Gowda RM, Shapiro M, Khan IA. Role of N-acetylcysteine in prevention of contrast-induced nephropathy after cardiovascular procedures: a meta-analysis. Clin Cardiol. 2004 Nov. 27(11):607-10. [Medline].

  40. Charpentier S, Cournot M, Lauque D, et al. Usefulness of initial glucose level to improve acute coronary syndrome diagnosis in the emergency department. Emerg Med J. 2011 Jul. 28(7):564-8. [Medline].

  41. de Lemos JA, Morrow DA, Bentley JH, Omland T, Sabatine MS, McCabe CH, et al. The prognostic value of B-type natriuretic peptide in patients with acute coronary syndromes. N Engl J Med. 2001 Oct 4. 345(14):1014-21. [Medline].

  42. James SK, Lindahl B, Siegbahn A, Stridsberg M, Venge P, Armstrong P, et al. N-terminal pro-brain natriuretic peptide and other risk markers for the separate prediction of mortality and subsequent myocardial infarction in patients with unstable coronary artery disease: a Global Utilization of Strategies To Open occluded arteries (GUSTO)-IV substudy. Circulation. 2003 Jul 22. 108(3):275-81. [Medline].

  43. Hubbard BL, Newton CR, Carter PM, Fowler JJ, Schaldenbrand J, Singal B, et al. The inability of B-type natriuretic protein to predict short-term risk of death or myocardial infarction in non-heart-failure patients with marginally increased troponin levels. Ann Emerg Med. 2010 Nov. 56(5):472-80. [Medline].

  44. Cavusoglu E, Marmur JD, Hojjati MR, et al. Plasma interleukin-10 levels and adverse outcomes in acute coronary syndrome. Am J Med. 2011 Aug. 124(8):724-30. [Medline].

  45. Giugliano RP, Braunwald E. The year in non-ST-segment elevation acute coronary syndrome. J Am Coll Cardiol. 2008 Sep 23. 52(13):1095-103. [Medline].

  46. Jaffe AS, Babuin L, Apple FS. Biomarkers in acute cardiac disease: the present and the future. J Am Coll Cardiol. 2006 Jul 4. 48(1):1-11. [Medline].

  47. Hjortshoj S, Kristensen SR, Ravkilde J. Diagnostic value of ischemia-modified albumin in patients with suspected acute coronary syndrome. Am J Emerg Med. 2010 Feb. 28(2):170-6. [Medline].

  48. Katritsis DG, Siontis GC, Kastrati A, van't Hof AW, Neumann FJ, Siontis KC, et al. Optimal timing of coronary angiography and potential intervention in non-ST-elevation acute coronary syndromes. Eur Heart J. 2011 Jan. 32(1):32-40. [Medline].

  49. Antman EM, Cohen M, Bernink PJ, McCabe CH, Horacek T, Papuchis G, et al. The TIMI risk score for unstable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making. JAMA. 2000 Aug 16. 284(7):835-42. [Medline].

  50. Nabi F, Chang SM, Pratt CM, Paranilam J, Peterson LE, Frias ME, et al. Coronary artery calcium scoring in the emergency department: identifying which patients with chest pain can be safely discharged home. Ann Emerg Med. 2010 Sep. 56(3):220-9. [Medline].

  51. Rogers IS, Banerji D, Siegel EL, Truong QA, Ghoshhajra BB, Irlbeck T, et al. Usefulness of comprehensive cardiothoracic computed tomography in the evaluation of acute undifferentiated chest discomfort in the emergency department (CAPTURE). Am J Cardiol. 2011 Mar 1. 107(5):643-50. [Medline].

  52. Litt HI, Gatsonis C, Snyder B, Singh H, Miller CD, Entrikin DW, et al. CT angiography for safe discharge of patients with possible acute coronary syndromes. N Engl J Med. 2012 Apr 12. 366(15):1393-403. [Medline].

  53. Rosenberg S, Elashoff MR, Beineke P, Daniels SE, Wingrove JA, Tingley WG. Multicenter validation of the diagnostic accuracy of a blood-based gene expression test for assessing obstructive coronary artery disease in nondiabetic patients. Ann Intern Med. 2010 Oct 5. 153(7):425-34. [Medline].

  54. Miller CD, Hwang W, Hoekstra JW, Case D, Lefebvre C, Blumstein H, et al. Stress cardiac magnetic resonance imaging with observation unit care reduces cost for patients with emergent chest pain: a randomized trial. Ann Emerg Med. 2010 Sep. 56(3):209-219.e2. [Medline].

  55. Rogers IS, Banerji D, Siegel EL, et al. Usefulness of comprehensive cardiothoracic computed tomography in the evaluation of acute undifferentiated chest discomfort in the emergency department (CAPTURE). Am J Cardiol. 2011 Mar 1. 107(5):643-50. [Medline].

  56. Mehta SR, Yusuf S. The Clopidogrel in Unstable angina to prevent Recurrent Events (CURE) trial programme; rationale, design and baseline characteristics including a meta-analysis of the effects of thienopyridines in vascular disease. Eur Heart J. 2000 Dec. 21(24):2033-41. [Medline].

  57. Stone GW, Maehara A, Lansky AJ, de Bruyne B, Cristea E, Mintz GS, et al. A prospective natural-history study of coronary atherosclerosis. N Engl J Med. 2011 Jan 20. 364(3):226-35. [Medline].

  58. Rosner GF, Kirtane AJ, Genereux P, Lansky AJ, Cristea E, Gersh BJ, et al. Impact of the Presence and Extent of Incomplete Angiographic Revascularization After Percutaneous Coronary Intervention in Acute Coronary Syndromes: The Acute Catheterization and Urgent Intervention Triage Strategy (ACUITY) Trial. Circulation. 2012 May 29. 125(21):2613-20. [Medline].

  59. Yan TD, Padang R, Poh C, et al. Drug-eluting stents versus coronary artery bypass grafting for the treatment of coronary artery disease: a meta-analysis of randomized and nonrandomized studies. J Thorac Cardiovasc Surg. 2011 May. 141(5):1134-44. [Medline].

  60. Ribichini F, Tomai F, De Luca G, et al. Immunosuppressive Therapy with Oral Prednisone to Prevent Restenosis after PCI. A Multicenter Randomized Trial. Am J Med. 2011 May. 124(5):434-43. [Medline].

  61. Stone GW, Witzenbichler B, Guagliumi G, et al. Heparin plus a glycoprotein IIb/IIIa inhibitor versus bivalirudin monotherapy and paclitaxel-eluting stents versus bare-metal stents in acute myocardial infarction (HORIZONS-AMI): final 3-year results from a multicentre, randomised controlled trial. Lancet. 2011 Jun 25. 377(9784):2193-204. [Medline].

  62. Mehta SR, Granger CB, Boden WE, Steg PG, Bassand JP, Faxon DP, et al. Early versus delayed invasive intervention in acute coronary syndromes. N Engl J Med. 2009 May 21. 360(21):2165-75. [Medline].

  63. Jernberg T, Johanson P, Held C, et al. Association between adoption of evidence-based treatment and survival for patients with ST-elevation myocardial infarction. JAMA. 2011 Apr 27. 305(16):1677-84. [Medline].

  64. Thadani U, Opie LH. Nitrates for unstable angina. Cardiovasc Drugs Ther. 1994 Oct. 8(5):719-26. [Medline].

  65. Collaborative overview of randomised trials of antiplatelet therapy--I: Prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. Antiplatelet Trialists' Collaboration. BMJ. 1994 Jan 8. 308(6921):81-106. [Medline]. [Full Text].

  66. [Guideline] Wright RS, Anderson JL, Adams CD, Bridges CR, Casey DE Jr, Ettinger SM, et al. 2011 ACCF/AHA Focused Update of the Guidelines for the Management of Patients With Unstable Angina/ Non-ST-Elevation Myocardial Infarction (Updating the 2007 Guideline): A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2011 May 10. 123(18):2022-60. [Medline]. [Full Text].

  67. Nijjer SS, Watson G, Athanasiou T, Malik IS. Safety of clopidogrel being continued until the time of coronary artery bypass grafting in patients with acute coronary syndrome: a meta-analysis of 34 studies. Eur Heart J. 2011 Dec. 32(23):2970-88. [Medline].

  68. Morel O, El Ghannudi S, Jesel L, Radulescu B, Meyer N, Wiesel ML, et al. Cardiovascular mortality in chronic kidney disease patients undergoing percutaneous coronary intervention is mainly related to impaired P2Y12 inhibition by clopidogrel. J Am Coll Cardiol. 2011 Jan 25. 57(4):399-408. [Medline].

  69. [Guideline] Abraham NS, Hlatky, MA, Antman EM, Bhatt DL, Bjorkman DJ, et al. ACCF/ACG/AHA 2010 expert consensus document on the concomitant use of proton pump inhibitors and thienopyridines: a focused update of the ACCF/ACG/AHA 2008 expert consensus document on reducing the gastrointestinal risks of antiplatelet therapy and NSAID use. J Am Coll Cardiol. Published online November 8, 2010:[Full Text].

  70. Dexilant (dexlansoprazole). Prescribing information revised October 28, 2011. Takeda Pharmaceutical Company LTD. Available at http://www.accessdata.fda.gov/drugsatfda_docs/label/2011/022287s011lbl.pdf.

  71. Prevacid (lansoprazole). Prescribing information revised October 28, 2011. Takeda Pharmaceutical Company LTD. Available at http://www.accessdata.fda.gov/drugsatfda_docs/label/2011/020406s076,021428s023lbl.pdf.

  72. Squizzato A, Keller T, Romualdi E, Middeldorp S. Clopidogrel plus aspirin versus aspirin alone for preventing cardiovascular disease. Cochrane Database Syst Rev. 2011 Jan 19. CD005158. [Medline].

  73. Simon T, Steg PG, Gilard M, Blanchard D, Bonello L, Hanssen M, et al. Clinical Events as a Function of Proton Pump Inhibitor Use, Clopidogrel Use, and Cytochrome P450 2C19 Genotype in a Large Nationwide Cohort of Acute Myocardial Infarction: Results From the French Registry of Acute ST-Elevation and Non-ST-Elevation Myocardial Infarction (FAST-MI) Registry. Circulation. 2011 Feb 8. 123(5):474-82. [Medline].

  74. Morrow DA, Wiviott SD, White HD, Nicolau JC, Bramucci E, Murphy SA, et al. Effect of the novel thienopyridine prasugrel compared with clopidogrel on spontaneous and procedural myocardial infarction in the Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel-Thrombolysis in Myocardial Infarction 38: an application of the classification system from the universal definition of myocardial infarction. Circulation. 2009 Jun 2. 119(21):2758-64. [Medline].

  75. Montalescot G, Collet JP, Ecollan P, et al. Effect of Prasugrel Pre-Treatment Strategy in Patients Undergoing Percutaneous Coronary Intervention for NSTEMI: The ACCOAST-PCI Study. J Am Coll Cardiol. 2014 Dec 23. 64(24):2563-71. [Medline].

  76. Boggs W. Hold Prasugrel Until Revascularization Decision Is Made, Researchers Say. Medscape. Dec 18 2014. [Full Text].

  77. Wiviott SD, Braunwald E, McCabe CH, Montalescot G, Ruzyllo W, Gottlieb S, et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2007 Nov 15. 357(20):2001-15. [Medline].

  78. Roe MT, Armstrong PW, Fox KA, White HD, Prabhakaran D, Goodman SG, et al. Prasugrel versus Clopidogrel for Acute Coronary Syndromes without Revascularization. N Engl J Med. 2012 Aug 25. [Medline].

  79. Scirica BM, Bonaca MP, Braunwald E, De Ferrari GM, Isaza D, Lewis BS, et al. Vorapaxar for secondary prevention of thrombotic events for patients with previous myocardial infarction: a prespecified subgroup analysis of the TRA 2°P-TIMI 50 trial. Lancet. 2012 Oct 13. 380(9850):1317-24. [Medline].

  80. James S, Akerblom A, Cannon CP, Emanuelsson H, Husted S, Katus H, et al. Comparison of ticagrelor, the first reversible oral P2Y(12) receptor antagonist, with clopidogrel in patients with acute coronary syndromes: Rationale, design, and baseline characteristics of the PLATelet inhibition and patient Outcomes (PLATO) trial. Am Heart J. 2009 Apr. 157(4):599-605. [Medline].

  81. Douglas D. Ticagrelor more cardioprotective than clopidogrel. Medscape Medical News. Jan 11, 2013. Available at http://www.medscape.com/viewarticle/777535. Accessed: January 23, 2013.

  82. Kohli P, Wallentin L, Reyes E, Horrow J, Husted S, Angiolillo DJ, et al. Reduction in First and Recurrent Cardiovascular Events with Ticagrelor Compared with Clopidogrel in the PLATO Study. Circulation. 2012 Dec 31. [Medline].

  83. US FDA approves expanded indication for BRILINTA to include long-term use in patients with a history of heart attack [press release]. AstraZeneca. Available at http://www.astrazeneca.com/Media/Press-releases/Article/20150903. September 3, 2015; Accessed: September 9, 2015.

  84. Bonaca MP, Bhatt DL, Cohen M, et al, for the PEGASUS-TIMI 54 Steering Committee and Investigators. Long-term use of ticagrelor in patients with prior myocardial infarction. N Engl J Med. 2015 May 7. 372 (19):1791-800. [Medline].

  85. O'Riordan M. Ticagrelor bests clopidogrel for reducing stent-thrombosis risk: PLATO. Medscape Medical News. August 2, 2013. [Full Text].

  86. Steg PG, Harrington RA, Emanuelsson H, Katus HA, Mahaffey KW, Meier B, et al. Stent Thrombosis with Ticagrelor versus Clopidogrel in Patients with Acute Coronary Syndromes: An Analysis from the Prospective Randomized PLATO Trial. Circulation. 2013 Jul 30. [Medline].

  87. Kastrati A, Mehilli J, Neumann FJ, Dotzer F, ten Berg J, Bollwein H, et al. Abciximab in patients with acute coronary syndromes undergoing percutaneous coronary intervention after clopidogrel pretreatment: the ISAR-REACT 2 randomized trial. JAMA. 2006 Apr 5. 295(13):1531-8. [Medline].

  88. Roffi M, Moliterno DJ, Meier B, Powers ER, Grines CL, DiBattiste PM, et al. Impact of different platelet glycoprotein IIb/IIIa receptor inhibitors among diabetic patients undergoing percutaneous coronary intervention: : Do Tirofiban and ReoPro Give Similar Efficacy Outcomes Trial (TARGET) 1-year follow-up. Circulation. 2002 Jun 11. 105(23):2730-6. [Medline].

  89. Roe MT, Harrington RA, Prosper DM, Pieper KS, Bhatt DL, Lincoff AM, et al. Clinical and therapeutic profile of patients presenting with acute coronary syndromes who do not have significant coronary artery disease.The Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) Trial Investigators. Circulation. 2000 Sep 5. 102(10):1101-6. [Medline].

  90. Theroux P, Alexander J Jr, Pharand C, et al. Glycoprotein IIb/IIIa receptor blockade improves outcomes in diabetic patients presenting with unstable angina/non-ST-elevation myocardial infarction: results from the Platelet Receptor Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms (PRISM-PLUS) study. Circulation. 2000 Nov 14. 102(20):2466-72. [Medline].

  91. Giugliano RP, White JA, Bode C, Armstrong PW, Montalescot G, Lewis BS, et al. Early versus delayed, provisional eptifibatide in acute coronary syndromes. N Engl J Med. 2009 May 21. 360(21):2176-90. [Medline].

  92. Chadow HL, Hauptman RE, VanAuker M, Rafii SE, Gunsburg MY, Giarraffa L, et al. Drip and ship: a new strategy for the treatment of acute coronary syndromes. J Thromb Thrombolysis. 2000 Aug. 10(1):77-82. [Medline].

  93. Januzzi JL, Chae CU, Sabatine MS, Jang IK. Elevation in serum troponin I predicts the benefit of tirofiban. J Thromb Thrombolysis. 2001 May. 11(3):211-5. [Medline].

  94. Oler A, Whooley MA, Oler J, Grady D. Adding heparin to aspirin reduces the incidence of myocardial infarction and death in patients with unstable angina. A meta-analysis. JAMA. 1996 Sep 11. 276(10):811-5. [Medline].

  95. Steg PG, Jolly SS, Mehta SR, Afzal R, Xavier D, Rupprecht HJ, et al. Low-dose vs standard-dose unfractionated heparin for percutaneous coronary intervention in acute coronary syndromes treated with fondaparinux: the FUTURA/OASIS-8 randomized trial. JAMA. 2010 Sep 22. 304(12):1339-49. [Medline].

  96. Fox KA, Antman EM, Cohen M, Bigonzi F. Comparison of enoxaparin versus unfractionated heparin in patients with unstable angina pectoris/non-ST-segment elevation acute myocardial infarction having subsequent percutaneous coronary intervention. Am J Cardiol. 2002 Sep 1. 90(5):477-82. [Medline].

  97. Mahaffey KW, Ferguson JJ. Exploring the role of enoxaparin in the management of high-risk patients with non-ST-elevation acute coronary syndromes: the SYNERGY trial. Am Heart J. 2005 Apr. 149(4 Suppl):S81-90. [Medline].

  98. Lev EI, Hasdai D, Scapa E, Tobar A, Assali A, Lahav J, et al. Administration of eptifibatide to acute coronary syndrome patients receiving enoxaparin or unfractionated heparin: effect on platelet function and thrombus formation. J Am Coll Cardiol. 2004 Mar 17. 43(6):966-71. [Medline].

  99. Alexander JH, Lopes RD, James S, et al. Apixaban with antiplatelet therapy after acute coronary syndrome. N Engl J Med. 2011 Aug 25. 365(8):699-708. [Medline].

  100. Boggs W. Lower rivaroxaban dose better in acute coronary syndrome. Medscape Medical News. May 30, 2013. [Full Text].

  101. Mega JL, Braunwald E, Wiviott SD, Murphy SA, Plotnikov A, Gotcheva N, et al. Comparison of the Efficacy and Safety of Two Rivaroxaban Doses in Acute Coronary Syndrome (from ATLAS ACS 2-TIMI 51). Am J Cardiol. 2013 May 24. [Medline].

  102. van Rees Vellinga TE, Peters RJ, et al. Efficacy and safety of fondaparinux in patients with ST-segment elevation myocardial infarction across the age spectrum. Results from the Organization for the Assessment of Strategies for Ischemic Syndromes 6 (OASIS-6) trial. Am Heart J. 2010 Dec. 160(6):1049-55. [Medline].

  103. Jolly SS, Faxon DP, Fox KA, et al. Efficacy and safety of fondaparinux versus enoxaparin in patients with acute coronary syndromes treated with glycoprotein IIb/IIIa inhibitors or thienopyridines: results from the OASIS 5 (Fifth Organization to Assess Strategies in Ischemic Syndromes) trial. J Am Coll Cardiol. 2009 Jul 28. 54(5):468-76. [Medline].

  104. Najjar SS, Rao SV, Melloni C, et al. Intravenous erythropoietin in patients with ST-segment elevation myocardial infarction: REVEAL: a randomized controlled trial. JAMA. 2011 May 11. 305(18):1863-72. [Medline].

  105. Sorensen JT, Terkelsen CJ, Norgaard BL, et al. Urban and rural implementation of pre-hospital diagnosis and direct referral for primary percutaneous coronary intervention in patients with acute ST-elevation myocardial infarction. Eur Heart J. 2011 Feb. 32(4):430-6. [Medline].

  106. Damman P, Hirsch A, Windhausen F, Tijssen JG, de Winter RJ. 5-year clinical outcomes in the ICTUS (Invasive versus Conservative Treatment in Unstable coronary Syndromes) trial a randomized comparison of an early invasive versus selective invasive management in patients with non-ST-segment elevation acute coronary syndrome. J Am Coll Cardiol. 2010 Mar 2. 55(9):858-64. [Medline].

  107. Stone GW, McLaurin BT, Cox DA, Bertrand ME, Lincoff AM, Moses JW, et al. Bivalirudin for patients with acute coronary syndromes. N Engl J Med. 2006 Nov 23. 355(21):2203-16. [Medline].

  108. Kastrati A, Neumann FJ, Schulz S, et al. Abciximab and heparin versus bivalirudin for non-ST-elevation myocardial infarction. N Engl J Med. 2011 Nov 24. 365(21):1980-9. [Medline].

  109. Braunwald E, Antman EM, Beasley JW, Califf RM, Cheitlin MD, Hochman JS, et al. ACC/AHA guideline update for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction--2002: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina). Circulation. 2002 Oct 1. 106(14):1893-900. [Medline].

  110. Bueno H, Betriu A, Heras M, et al. Primary angioplasty vs. fibrinolysis in very old patients with acute myocardial infarction: TRIANA (TRatamiento del Infarto Agudo de miocardio eN Ancianos) randomized trial and pooled analysis with previous studies. Eur Heart J. 2011 Jan. 32(1):51-60. [Medline]. [Full Text].

  111. Chang AM, Walsh KM, Shofer FS, McCusker CM, Litt HI, Hollander JE. Relationship Between Cocaine Use and Coronary Artery Disease in Patients With Symptoms Consistent With an Acute Coronary Syndrome. Acad Emerg Med. 2010 Dec 23. [Medline].

  112. James S, Angiolillo DJ, Cornel JH, Erlinge D, Husted S, Kontny F, et al. Ticagrelor vs. clopidogrel in patients with acute coronary syndromes and diabetes: a substudy from the PLATelet inhibition and patient Outcomes (PLATO) trial. Eur Heart J. 2010 Dec. 31(24):3006-16. [Medline]. [Full Text].

  113. [Guideline] Kushner FG, Hand M, Smith SC Jr, King SB 3rd, Anderson JL, Antman EM, et al. 2009 Focused Updates: ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction (updating the 2004 Guideline and 2007 Focused Update) and ACC/AHA/SCAI Guidelines on Percutaneous Coronary Intervention (updating the 2005 Guideline and 2007 Focused Update): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2009 Dec 1. 120(22):2271-306. [Medline]. [Full Text].

  114. Lopes RD, Alexander KP, Manoukian SV, Bertrand ME, Feit F, White HD, et al. Advanced age, antithrombotic strategy, and bleeding in non-ST-segment elevation acute coronary syndromes: results from the ACUITY (Acute Catheterization and Urgent Intervention Triage Strategy) trial. J Am Coll Cardiol. 2009 Mar 24. 53(12):1021-30. [Medline].

  115. Malkin CJ, Pugh PJ, Morris PD, Asif S, Jones TH, Channer KS. Low serum testosterone and increased mortality in men with coronary heart disease. Heart. 2010 Nov. 96(22):1821-5. [Medline].

  116. Mehta SR, Tanguay JF, Eikelboom JW, Jolly SS, Joyner CD, Granger CB, et al. Double-dose versus standard-dose clopidogrel and high-dose versus low-dose aspirin in individuals undergoing percutaneous coronary intervention for acute coronary syndromes (CURRENT-OASIS 7): a randomised factorial trial. Lancet. 2010 Oct 9. 376(9748):1233-43. [Medline].

  117. Morrow DA, Scirica BM, Karwatowska-Prokopczuk E, Murphy SA, Budaj A, Varshavsky S, et al. Effects of ranolazine on recurrent cardiovascular events in patients with non-ST-elevation acute coronary syndromes: the MERLIN-TIMI 36 randomized trial. JAMA. 2007 Apr 25. 297(16):1775-83. [Medline].

  118. Pare G, Mehta SR, Yusuf S, et al. Effects of CYP2C19 genotype on outcomes of clopidogrel treatment. N Engl J Med. 2010 Oct 28. 363(18):1704-14. [Medline].

  119. Rao SV, Sherwood MW. Isn't it about time we learned how to use blood transfusion in patients with ischemic heart disease?. J Am Coll Cardiol. 2013 Dec 6. [Medline].

  120. Silvain J, Abtan J, Kerneis M, Martin R, Finzi J, Vignalou JB, et al. Impact of Red Blood Cell Transfusion on Platelet Aggregation and Inflammatory Response in Anemic Coronary and Non-Coronary Patients The TRANSFUSION-2 study. J Am Coll Cardiol. 2013 Dec 6. [Medline].

  121. Stiles S. More Evidence That Blood Transfusions Raise Thrombosis Risk in ACS Patients. Medscape [serial online]. Available at http://www.medscape.com/viewarticle/818076. Accessed: December 30, 2013.

 
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A 50-year-old man with type 1 diabetes mellitus and hypertension presents after experiencing 1 hour of midsternal chest pain that began after eating a large meal. Pain is now present but is minimal. Aspirin is the single drug that will have the greatest potential impact on subsequent morbidity. In the setting of ongoing symptoms and electrocardiogram (ECG) changes, nitrates titrated to 10% reduction in blood pressure and symptoms, beta blockers, and heparin are all indicated. If the patient continues to have persistent signs and/or symptoms of ischemia, addition of a glycoprotein IIb/IIIa inhibitor should be considered.
A 62-year-old woman with a history of chronic stable angina and a "valve problem" presents with new chest pain. She is symptomatic on arrival, complaining of shortness of breath and precordial chest tightness. Her initial vital signs are blood pressure = 140/90 mm Hg and heart rate = 98. Her electrocardiogram (ECG) is as shown. She is given nitroglycerin sublingually, and her pressure decreases to 80/palpation. Right ventricular ischemia should be considered in this patient.
This plot shows changes in cardiac markers over time after the onset of symptoms. Peak A is the early release of myoglobin or creatine kinase isoenzyme MB (CK-MB) after acute myocardial infarction (AMI). Peak B is the cardiac troponin level after infarction. Peak C is the CK-MB level after infarction. Peak D is the cardiac troponin level after unstable angina. Data are plotted on a relative scale, where 1.0 is set at the myocardial-infarction cutoff concentration. Courtesy of Wu et al (1999). ROC = receiver operating characteristic.
Suggested algorithm for triaging patients with chest pain. ACS = ACS; ASA = aspirin; EKG = ECG; MI = myocardial infarction; Rx = treat; STEMI = ST-elevation myocardial infarction. Courtesy of Wu et al (1999).
Use of cardiac markers in the ED. Studies on troponins in ACS.
Use of cardiac markers in the ED. Troponin I levels and cardiac mortality in ACS.
Use of cardiac markers in the ED. Cardiac event rates in the platelet receptor inhibition for ischemic syndrome (PRISM) study based on troponin I results.
Use of cardiac markers in the ED. Effect of time to treatment in patients with acute coronary syndrome (ACS) who are treated with the GIIb/IIIa inhibitor eptifibatide.
Table. TIMI Risk Score for Unstable Angina and NSTEMI [49]
Characteristic Risk Score
History
Age ≥65 years 1
At least 3 risk factors for coronary heart disease 1
Previous coronary stenosis ≥50% 1
Use of aspirin in previous 7 days 1
Presentation
At least 2 anginal episodes in the previous 24 hours 1
ST-segment elevation on admission ECG 1
Elevated levels of serum biomarkers 1
Total Score 0-7
Note: Event rates significantly increased as the TIMI risk score increased in the test cohort in the TIMI IIB study. Rates were 4.7% for a score of 0/1, 8.3% for 2, 13.2% for 3, 19.9% for 4, 26.2% for 5, and 40.9% for 6/7 (P < .001, χ2 test for the trend). The pattern of increasing event rates with increasing TIMI risk score was confirmed in all 3 validation groups (P < .001).
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