Acute coronary syndrome

Last updated: June 7, 2022

Summarytoggle arrow icon

Acute coronary syndrome (ACS) is the clinical manifestation of myocardial infarct and commonly the default working diagnosis in patients with new-onset chest pain suspected to be of cardiac ischemic origin. Clinical findings (e.g., onset and characteristics of pain, patient history) in combination with ECG and troponin are the mainstays of diagnosis. Based on ECG findings, patients are categorized into those with ST-elevation (STE-ACS) or non-ST-elevation ACS (NSTE-ACS). Depending on serum levels of cardiac troponin (cTn), NSTE-ACS can be categorized as NSTEMI or unstable angina (UA). STE-ACS patients require immediate revascularization therapy. The timing and necessity of revascularization therapy in NSTE-ACS is determined based on multiple risk factors. All ACS patients receive dual antiplatelet therapy and initially anticoagulation. Adjunctive therapy (e.g., beta blockers, oxygen) helps reduce symptoms and can have a positive impact on mortality.

This article concerns the initial management of ACS patients. See “Myocardial infarction” for more details regarding, e.g., histopathology and long-term management.

Overview of acute coronary syndrome (ACS) [1][2]
Unstable angina (UA) Non-ST-segment elevation myocardial infarction (NSTEMI) ST-segment elevation myocardial infarction (STEMI)
Clinical presentation
  • Symptoms are not reproducible/predictable.
  • Angina at rest/with minimal exertion and is usually not relieved by rest or nitroglycerin [3]
  • New-onset angina
  • Severe, persistent, and/or worsening angina (crescendo angina)
  • Autonomic symptoms may be present: diaphoresis, syncope, palpitations, nausea, and/or vomiting
  • Partial occlusion of coronary vessel decreased blood supply → ischemic symptoms (also at rest)
Cardiac troponin
  • Not elevated
  • Elevated
  • Usually elevated
ECG findings

Subtypes of ACS cannot be differentiated based on clinical presentation alone.

Classically, it has been taught that STEMI manifests with more severe symptoms than NSTEMI, but this is not always the case.

Approach [1][2][6][7]

Patients suspected of having STE-ACS should be evaluated immediately for revascularization therapy.

12-lead ECG [1][2]

  • Indicated for every patient with suspected ACS (best initial test) within 10 minutes of presentation [2]
  • Findings: should always be interpreted in the context of clinical findings and patient history
  • Repeat every 15–30 minutes in the first hour (especially if the first ECG is inconclusive or symptoms recur or change in quality)
  • Compare with previous ECGs (if available).

ECG findings can change within minutes and ST elevations can appear or disappear.

Cardiac troponin [2][7]

  • Indication: obtain troponin T/I in every patient with suspected ACS [2][8]
  • Timing
    • At arrival and after 1–6 hours
    • Repeat if symptoms or ECG changes occur.
    • Consider repeat after 72 hours as a marker of infarct size.
  • Findings: should always be interpreted in combination with clinical findings.

Transthoracic echocardiography (TTE) [1][2][7][8]

TTE is generally not necessary and should not delay reperfusion therapy. However, it may be a helpful study in patients with atypical symptoms or if the diagnosis is unclear.

Imaging should not delay treatment of ACS.

  • Several scoring systems are available to help identify low-risk patients, facilitate disposition (e.g., necessity of ICU admission), and guide timing of PCI in patients with chest pain.
  • Risk stratification tools are not a substitute for clinical judgment.
  • Should not be used for patients suspected of having STEMI

Risk stratification tools are not appropriate in the setting of STEMI; patients suspected of having STEMI should be evaluated immediately for revascularization.

GRACE score for risk of mortality in ACS [2][9][10]

  • Based on the Global Registry of Acute Coronary Events (GRACE)
  • May be used to inform management and disposition (e.g., ICU admission, timing of intervention in NSTE-ACS).
  • Incorporates different criteria to estimate risk of mortality in patients with ACS, including:

HEART score [11]

  • The HEART score is an acronym of its components: history, ECG, age, risk factors, and troponin values.
  • Risk assessment for major adverse cardiovascular events (MACE) in patients with chest pain presenting to the emergency department
    • Can be integrated into decision pathways for early discharge
    • Potentially reduces hospital admissions of low-risk patients
    • Should not be used in patients with STEMI or those who are hemodynamically unstable
HEART score for the risk of MACE [11]
Component Characteristic Points
History Slightly suspicious 0
Moderately suspicious 1
Highly suspicious 2
ECG Normal 0
Nonspecific repolarization changes 1
Significant ST depression 2
Age < 45 years 0
45–65 years 1
≥ 65 years 2
Risk factors None 0
1–2 1
≥ 3 or history of atherosclerotic disease 2
Troponin (initial) [12][13] normal 0
1–2 x upper limit 1
> 2 x upper limit 2


  • Score ≤ 3 (low risk): consider early discharge
  • Score 4–6 (intermediate risk): hospital admission
  • Score ≥ 7 (high risk): consider early invasive strategy
  • Any positive troponin level: usually considered non-low risk and requires further evaluation [14]

TIMI score for NSTE-ACS [2][15][16]

TIMI score for NSTE-ACS [16]
Characteristics Points
Age ≥ 65 years 1

≥ 3 CAD risk factors (e.g., family history of CAD, DM, smoking, HTN, hypercholesterolemia)

Known CAD (stenosis > 50%) 1
≥ 2 episodes of severe angina in the last 24 hours 1
ASA use in the past 7 days 1
ST deviation (≥ 0.5 mm) 1
Elevated cardiac biomarkers 1


  • Score of 0–1 (low-risk): favors an ischemia-guided strategy [15]
  • Score ≥ 2 (non-low-risk): favors an invasive strategy

Patients with STEMI require immediate revascularization and should be identified as soon as possible. ECG findings can change over time and with fluctuations in symptoms, which is why the diagnosis of STEMI should not be excluded based on a single ECG. Percutaneous coronary intervention (PCI) within 90 minutes of first medical contact (FMC) is the treatment of choice. Intravenous fibrinolytics are an alternative if PCI can not be performed within 120 minutes and no contraindications are present.

ECG changes in STEMI [1][6][8][17]

Any patient with ST elevations on ECG requires immediate evaluation for urgent revascularization. The administration of other therapies should not delay care.

Classical timeline of ECG changes in STEMI

The sequence of ECG changes over several hours to days: hyperacute T waveST elevation → pathological Q waveT-wave inversionST normalizationT-wave normalization

STEMI-equivalent ECG findings [1][6][17]

Presence of any of the following findings requires immediate evaluation for revascularization therapy (i.e., management is the same as that for STEMI).

Modified Sgarbossa criteria for suspected STEMI in patients with LBBB [6][21][22]

Assessment of ST elevations in the presence of left bundle branch block (LBBB) can be difficult. If clinical suspicion for myocardial ischemia is high, patients with this constellation should be managed like patients with STEMI.

The following recommendations are generally consistent with the 2013 AHA/ACC guidelines for the management of STE-ACS. [1]

"Time is muscle": Revascularization should occur as soon as possible in patients with STEMI! All other interventions can wait!

Approach [1]

Immediate revascularization [1]

Emergency coronary angiography with PCI [1]

Fibrinolytic therapy in STEMI [1]

PCI should be performed even if lysis is successful.

Common contraindications for fibrinolysis in STEMI and STEMI-equivalents [1][6][23]
Absolute contraindications
Relative contraindications

Streptokinase is nonfibrin-specific and highly antigenic. It is contraindicated within 6 months of previous exposure to streptokinase.


  • Coronary artery bypass grafting: Not routinely recommended for acute STEMI [1]
    • Consider in the following cases:
      • Coronary anatomy poorly suited to PCI
      • After unsuccessful PCI
      • STEMI occurring at the time of surgical repair of a mechanical defect

Antiplatelet therapy and anticoagulation in STEMI [1]

Dual antiplatelet therapy (DAPT) and anticoagulation in STEMI [1]
Class Regimen if undergoing PCI Regimen if undergoing fibrinolysis
Dual antiplatelet therapy (DAPT) [1]
Anticoagulation [1]

Glycoprotein IIb/IIIa inhibitor (GPI) [1]

  • Not routinely recommended

For patients < 120 min away from a PCI-capable facility

For patients > 120 min away from a PCI-capable facility and symptom onset < 12 hours

For all patients with STEMI

Patients with NSTE-ACS are classified based on the presence (NSTEMI) or absence (UA) of significantly elevated cardiac troponin (cTn) levels. A key element of management is to assess the necessity for and timing of PCI (fibrinolytics are not indicated in NSTE-ACS). Hemodynamically unstable patients and those with intractable angina require immediate PCI (i.e., they are managed like STEMI patients). Multiple risk scores (e.g., HEART, TIMI, GRACE) can help to determine an adequate strategy but are no substitute for individual clinical judgment. Dual antiplatelet therapy and anticoagulation is indicated initially and the preferred regimens vary based on patient risk factors and timing of revascularization. Some low-risk NSTE-ACS patients can be managed conservatively.

To identify STEMI or STEMI-equivalent ECG findings, repeat ECGs if the initial one is inconclusive or any changes in symptoms occur.

The following recommendations are generally consistent with the 2014 AHA/ACC guidelines for the management of NSTE-ACS. [2]

Risk-dependent timing of revascularization [2][7]

Risk-dependent timing of revascularization in NSTE-ACS [2][7]
Revascularization strategy Risk group Criteria
Urgent revascularization (< 2 hours)
  • Very high
Early invasive strategy (< 24 hours)
  • High
Delayed invasive (24–72 hours)
  • Intermediate
  • Low
  • None of the criteria above
  • GRACE score < 109
  • TIMI score 0 or 1
  • Individual decision based on patient and physician preferences

Patients with NSTEMI who have unstable hemodynamics, intractable angina, suspected posterior infarction, and/or left main-vessel occlusion require urgent PCI (< 2 hours), even if no ST elevations are present. [1][2][6]

Fibrinolytic therapy is not indicated in patients with unstable angina or NSTEMI.

Antiplatelet therapy and anticoagulation in NSTE-ACS [2]

Dual antiplatelet therapy (DAPT) and anticoagulation in NSTEMI [2]
Class Regimen
Dual antiplatelet therapy (DAPT) [2]

Anticoagulation [2]

Glycoprotein IIb/IIIa inhibitor (GPI) [2]

  • Timing [2]
    • Start DAPT as soon as possible; duration depends on whether PCI is performed or not.
    • Start anticoagulation as soon as possible; continue for the duration of hospitalization or until PCI is performed.
    • GPI should only be started in high-risk patients undergoing PCI and in consultation with a cardiologist.


  • Continuous cardiac monitoring
  • Serial 12-lead ECG every 15–30 minutes for the first hour
  • Serial serum troponin measurement (every 1–6 hours)

Adjunct medical therapy in ACS [1][2]

Adjunct medical therapy in ACS [1][2][6][7]
Class Drug Indications Contraindications and additional considerations


Beta blockers


ACE inhibitors/ARB

Aldosterone antagonists [1][2][6]

High-intensity statin

Options for initial MI treatment include “MONA-BASH”: Morphine, Oxygen, Nitroglycerin, Antiplatelet drugs (aspirin + ADP receptor inhibitor), Beta blockers, ACE inhibitors, Statins, and Heparin. The scope of interventions depends on the patient's risk profile (see “Indications”).

Supportive measures

Subsequent measures

See “Differential diagnoses of chest pain.”

Differential diagnoses of increased troponin [7]

Differential diagnoses of ST elevations on ECG [1]

The differential diagnoses listed here are not exhaustive.

Interested in the newest medical research, distilled down to just one minute? Sign up for the One-Minute Telegram in “Tips and links” below.

  1. Roffi M, Patrono C, Collet J-P, et al. 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J. 2015; 37 (3): p.267-315. doi: 10.1093/eurheartj/ehv320 . | Open in Read by QxMD
  2. O’Gara PT, Kushner FG, et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction. Circulation. 2013; 127 (4). doi: 10.1161/cir.0b013e3182742cf6 . | Open in Read by QxMD
  3. Amsterdam EA, Wenger NK, Brindis RG, et al.. 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes. J Am Coll Cardiol. 2014 . doi: 10.1016/j.jacc.2014.09.017 . | Open in Read by QxMD
  4. Fox KAA, Dabbous OH, Goldberg RJ, et al. Prediction of risk of death and myocardial infarction in the six months after presentation with acute coronary syndrome: prospective multinational observational study (GRACE). BMJ. 2006; 333 (7578): p.1091. doi: 10.1136/bmj.38985.646481.55 . | Open in Read by QxMD
  5. Fox KAA, FitzGerald G, Puymirat E, et al. Should patients with acute coronary disease be stratified for management according to their risk? Derivation, external validation and outcomes using the updated GRACE risk score. BMJ Open. 2014; 4 (2): p.e004425. doi: 10.1136/bmjopen-2013-004425 . | Open in Read by QxMD
  6. Six AJ, Backus BE, Kelder JC. Chest pain in the emergency room: value of the HEART score. Netherlands Heart Journal. 2008; 16 (6): p.191-196. doi: 10.1007/bf03086144 . | Open in Read by QxMD
  7. McCord J, Cabrera R, Lindahl B, et al. Prognostic Utility of a Modified HEART Score in Chest Pain Patients in the Emergency Department. Circ Cardiovasc Qual Outcomes. 2017; 10 (2). doi: 10.1161/circoutcomes.116.003101 . | Open in Read by QxMD
  8. Mahler SA, Stopyra JP, Apple FS, et al. Use of the HEART Pathway with high sensitivity cardiac troponins: A secondary analysis. Clin Biochem. 2017; 50 (7-8): p.401-407. doi: 10.1016/j.clinbiochem.2017.01.003 . | Open in Read by QxMD
  9. Mahler SA, Riley RF, Hiestand BC, et al. The HEART Pathway Randomized Trial. Circ Cardiovasc Qual Outcomes. 2015; 8 (2): p.195-203. doi: 10.1161/circoutcomes.114.001384 . | Open in Read by QxMD
  10. Ramjane Khalill, MD, Lei Han, MD, Chang Jing, PhD, and He Quan, PhD. The use of risk scores for stratification of non-ST elevation acute coronary syndrome patients. Experimental & Clinical Cardiology. 2009 .
  11. Antman EM, Cohen M, Bernink PJLM, et al. The TIMI Risk Score for Unstable Angina/Non–ST Elevation MI. JAMA. 2000; 284 (7): p.835. doi: 10.1001/jama.284.7.835 . | Open in Read by QxMD
  12. Braunwald E. Unstable angina and non–ST elevation myocardial infarction. Am J Respir Crit Care Med. 2012; 185 (9): p.924-932. doi: 10.1164/rccm.201109-1745ci . | Open in Read by QxMD
  13. Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2). McGraw-Hill Education / Medical ; 2018
  14. Walls R, Hockberger R, Gausche-Hill M. Rosen's Emergency Medicine. Elsevier Health Sciences ; 2018
  15. Ibanez B, James S, Agewall S, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2017; 39 (2): p.119-177. doi: 10.1093/eurheartj/ehx393 . | Open in Read by QxMD
  16. Thygesen K, Alpert JS, Jaffe AS, et al. Fourth Universal Definition of Myocardial Infarction (2018). J Am Coll Cardiol. 2018; 72 (18): p.2231-2264. doi: 10.1016/j.jacc.2018.08.1038 . | Open in Read by QxMD
  17. Montalescot G, Pitt B, Lopez de Sa E, et al. Early eplerenone treatment in patients with acute ST-elevation myocardial infarction without heart failure: The Randomized Double-Blind Reminder Study. Eur Heart J. 2014; 35 (34): p.2295-2302. doi: 10.1093/eurheartj/ehu164 . | Open in Read by QxMD
  18. Kjell Nikus, Yochai Birnbaum, Markku Eskola, Samuel Sclarovsky, Zhan Zhong-qun, and Olle Pahlm. Updated Electrocardiographic Classification of Acute Coronary Syndromes. Current Cardiology Reviews. 2014 .
  19. Jain S, Ting HT, Bell M, et al. Utility of Left Bundle Branch Block as a Diagnostic Criterion for Acute Myocardial Infarction. Am J Cardiol. 2011; 107 (8): p.1111-1116. doi: 10.1016/j.amjcard.2010.12.007 . | Open in Read by QxMD
  20. Chang AM, Shofer FS, Tabas JA, Magid DJ, McCusker CM, Hollander JE. Lack of association between left bundle-branch block and acute myocardial infarction in symptomatic ED patients. Am J Emerg Med. 2009; 27 (8): p.916-921. doi: 10.1016/j.ajem.2008.07.007 . | Open in Read by QxMD
  21. Widimsky P, Rohac F, Stasek J, et al. Primary angioplasty in acute myocardial infarction with right bundle branch block: should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy?. Eur Heart J. 2011; 33 (1): p.86-95. doi: 10.1093/eurheartj/ehr291 . | Open in Read by QxMD
  22. Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic Diagnosis of Evolving Acute Myocardial Infarction in the Presence of Left Bundle-Branch Block. N Engl J Med. 1996; 334 (8): p.481-487. doi: 10.1056/nejm199602223340801 . | Open in Read by QxMD
  23. Smith SW, Dodd KW, Henry TD, Dvorak DM, Pearce LA. Diagnosis of ST-Elevation Myocardial Infarction in the Presence of Left Bundle Branch Block With the ST-Elevation to S-Wave Ratio in a Modified Sgarbossa Rule. Ann Emerg Med. 2012; 60 (6): p.766-776. doi: 10.1016/j.annemergmed.2012.07.119 . | Open in Read by QxMD
  24. Nikus K, Pahlm O, Wagner G, et al. Electrocardiographic classification of acute coronary syndromes: a review by a committee of the International Society for Holter and Non-Invasive Electrocardiology. J Electrocardiol. 2010; 43 (2): p.91-103. doi: 10.1016/j.jelectrocard.2009.07.009 . | Open in Read by QxMD
  25. Switaj TL, et al. Acute Coronary Syndrome: Current Treatment.. Am Fam Physician. 2017; 95 (4): p.232-240.
  26. Squire IB, et al. Humoral and cellular immune responses up to 7·5 years after administration of streptokinase for acute myocardial infarction. Eur Heart J. 1999; 20 (17): p.1245-1252. doi: 10.1053/euhj.1999.1528 . | Open in Read by QxMD
  27. Kasper DL, Fauci AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison's Principles of Internal Medicine. McGraw-Hill Education ; 2015
  28. Le T, Bhushan V, Chen V, King M. First Aid for the USMLE Step 2 CK. McGraw-Hill Education ; 2015
  29. Marx JA, Hockberger RS, Walls RM et al. Rosen's Emergency Medicine - Concepts and Clinical Practice. Saunders ; 2013
  30. Reeder GS, Awtry E, Mahler SA. Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate.§ionRank=1&anchor=H14#H14.Last updated: October 3, 2016. Accessed: February 22, 2017.
  31. Goljan EF. Rapid Review Pathology. Elsevier Saunders ; 2018
  32. Le T, Bhushan V,‎ Sochat M, Chavda Y, Zureick A. First Aid for the USMLE Step 1 2018. McGraw-Hill Medical ; 2017
  33. European Association for the Study of the Liver (EASL). EASL Clinical Practice Guidelines on the prevention, diagnosis and treatment of gallstones.. J Hepatol. 2016; 65 (1): p.146-181. doi: 10.1016/j.jhep.2016.03.005 . | Open in Read by QxMD
  34. Tao Le, Vikas Bhushan, Deol M, Reyes G. First Aid for the USMLE Step 2 CK, Tenth Edition. McGraw-Hill Education ; 2018
  35. Wu S-D. Effects of narcotic analgesic drugs on human Oddi’s sphincter motility. World Journal of Gastroenterology. 2004; 10 (19): p.2901. doi: 10.3748/wjg.v10.i19.2901 . | Open in Read by QxMD
  36. Thune A, Baker RA, Saccone GTP, Owen H, Toouli J. Differing effects of pethidine and morphine on human sphincter of Oddi motility. Br J Surg. 1990; 77 (9): p.992-995. doi: 10.1002/bjs.1800770911 . | Open in Read by QxMD
  37. Masudi T, Capitelli-McMahon H, Anwar S. Acute pain management in symptomatic cholelithiasis. World Journal of Gastrointestinal Surgery. 2016; 8 (10): p.713. doi: 10.4240/wjgs.v8.i10.713 . | Open in Read by QxMD
  38. Barr J, Fraser GL, Puntillo K, et al. Clinical Practice Guidelines for the Management of Pain, Agitation, and Delirium in Adult Patients in the Intensive Care Unit. Crit Care Med. 2013; 41 (1): p.263-306. doi: 10.1097/ccm.0b013e3182783b72 . | Open in Read by QxMD
  39. Schrör K, Nitschmann S. Kardiovaskuläre Sicherheit von Celecoxib. Internist (Berl). 2017; 58 (8): p.863-865. doi: 10.1007/s00108-017-0260-x . | Open in Read by QxMD
  40. Blondell RD, Azadfard M et al.. Pharmacologic therapy for acute pain.. Am Fam Physician. 2013; 87 (11): p.766-72.
  41. McCarberg BH, Argoff CE. Topical diclofenac epolamine patch 1.3% for treatment of acute pain caused by soft tissue injury. Int J Clin Pract. 2010; 64 (11): p.1546-1553. doi: 10.1111/j.1742-1241.2010.02474.x . | Open in Read by QxMD
  42. Blondell R, Azadfard M, Wisniewski A. Pharmacologic Therapy for Acute Pain. Am Fam Physician.. 2013 .
  43. Rushfeldt CF, Sveinbjørnsson B, Søreide K, Vonen B. Risk of anastomotic leakage with use of NSAIDs after gastrointestinal surgery. Int J Colorectal Dis. 2011; 26 (12): p.1501-1509. doi: 10.1007/s00384-011-1285-6 . | Open in Read by QxMD
  44. Khanna IK, Pillarisetti S. Buprenorphine - an attractive opioid with underutilized potential in treatment of chronic pain.. Journal of pain research. 2015; 8 : p.859-70. doi: 10.2147/JPR.S85951 . | Open in Read by QxMD

3 free articles remaining

You have 3 free member-only articles left this month. Sign up and get unlimited access.
 Evidence-based content, created and peer-reviewed by physicians. Read the disclaimer