Myocardial infarction

Last updated: September 13, 2023

Summarytoggle arrow icon

Myocardial infarction (MI) refers to ischemic necrosis of myocardial tissue. The most common underlying cause is coronary artery disease. Type 1 myocardial infarction occurs when an unstable plaque ruptures, leading to occlusion of a coronary artery. Type 2 myocardial infarction occurs when there is a mismatch between oxygen supply and demand (due to, e.g., systemic hypotension, vasospasm). MI manifests clinically with acute coronary syndrome (ACS), a potentially lethal condition. Diagnosis is based on typical clinical features, ECG findings, and elevation of cardiac biomarkers. Definitive diagnosis requires cardiac catheterization, which serves both diagnostic and therapeutic purposes. All patients suspected of having ACS should be considered for emergency revascularization; additional aspects of treatment include anticoagulation, antiplatelet therapy, statin therapy, and other adjunctive measures. Prevention of MI recurrence and complications consists of dual antiplatelet therapy, the initiation of beta blocker and/or ACE inhibitors, statin therapy, and addressing any modifiable risk factors.

The acute management of ACS, including diagnosis and treatment, is described in “Acute coronary syndrome.”

Definitiontoggle arrow icon

Myocardial infarction (MI) [1]

Defined as acute myocardial injury with clinical and diagnostic evidence of acute ischemia. MI is classified into 5 subtypes.

Acute coronary syndrome

Myocardial injury

Epidemiologytoggle arrow icon

Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon

Any condition that causes occlusion of the coronary arteries, reduces myocardial oxygen supply, or increases oxygen demand can potentially lead to myocardial ischemia and infarction.

Pathophysiologytoggle arrow icon

Coronary artery occlusion [1][6][7]

Atherosclerotic plaque disruption (type 1 MI) [1][6][7]

Oxygen supply and demand mismatch (type 2 MI) [1][2]

Nonischemic myocardial injury [1][2]

Clinical featurestoggle arrow icon

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

Diagnosticstoggle arrow icon

Follow ACS protocols if acute myocardial ischemia is suspected (see “Acute coronary syndrome”). Diagnosis is based on typical clinical features, ECG findings, and elevation of cardiac biomarkers.

ECG [1]

Localization of myocardial infarct on ECG [9][13][14]

ECG leads affected Infarct location Vessel involved [12][14]
  • Extensive anterior MI (leads aVL and I may also be affected.)
  • (Antero)septal MI
  • (Antero)apical MI
I, aVL
  • Lateral MI
  • Inferior MI
  • Posterior/posterolateral MI

Infarction of the anterior wall is caused by obstruction of the LAD or its branches. Depending on the extent of anterior wall infarction, it results in ECG changes in the anterior wall leads (V1–6) and/or I and aVL. Infarction of the inferior wall is caused by obstruction of the LCX or RCA or their branches, and ECG changes are seen in leads II, III, and aVF.

To remember the ECG leads with maximal ST elevation in anterior MI, think “SAL”: “Septal (V1–2), Apical (V3–4), Lateral (V5–6).

In severe transmural posterior wall infarction, there may not be any ST elevation on a standard 12-lead ECG.

Cardiac biomarkers [10][15]

Overview of cardiac biomarkers
Biomarker/enzyme Rise Maximum Normalization Characteristics
Troponin T/I
  • Regular assays: 6–8 hours
  • High-sensitive assays: 1–3 hours [10][15][16][17]
  • 12–24 hours
  • 7–10 days
  • ∼ 4–9 hours
  • 12–24 hours
  • 2–3 days
  • No longer commonly used clinically; has been replaced by cardiac troponin in the diagnosis of ACS [10]
  • CK-MB is more specific to cardiac tissue than total CK (but may also be due to skeletal muscle injury).
  • Can be helpful for evaluating reinfarction because of its short half-life but is no longer commonly used
  • The degree of elevation often correlates with the size of the infarct.
  • ∼ 1 hour
  • 4–12 hours
  • 24 hours
  • Nonspecific marker that is no longer commonly used

Serum troponin T and I are the most important cardiac-specific markers.

The timing of a detectable rise in cardiac troponin levels depends (among other factors) on the assay used by the laboratory.

Additional laboratory studies [19][20]

Coronary angiography

The most commonly occluded coronary arteries (in descending order): left anterior descending artery, right coronary artery, circumflex artery.

Transthoracic echocardiography [1][10]

Pathologytoggle arrow icon

Histopathological findings of MI [21]

Time interval post-infarction Histopathological findings
Microscopic Macroscopic

0–24 hrs

  • 0–12 hours: no gross changes
  • 12–24 hours: dark mottling

1–3 days

3–14 days

  • Hyperemic border
  • Center: yellow-brown, soft

2 weeks to several months

Obstruction of a coronary artery branch due to > 90% stenosis or embolization results in coagulation necrosis of the post-stenotic zone.

Cellular changes


Differential diagnosestoggle arrow icon

The differential diagnoses listed here are not exhaustive.

Treatmenttoggle arrow icon

This section provides an overview of the most important treatment aspects of myocardial infarction. See “Acute coronary syndrome” for more detailed management.

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

Critical management [10][12]

Adjunctive therapy [10][12]

See “Adjunct medical therapy in ACS” for details.

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.

Further management

Further management includes treatment of underlying ischemia (PTCA or CABG) and management of risk factors to prevent recurrence; see also “Prevention of coronary heart disease.”

Prevention of recurrent myocardial infarction [10][12]

Complicationstoggle arrow icon

Overview of MI complications [24]
Time Gross changes Microscopic changes Complications
0–4 hours
  • None
  • Wavy fibers
4–24 hours
  • Dark mottling or discoloration
1–3 days
3–14 days
  • Hyperemic or red-tan margins surrounding the yellow-tan pallor → gray-white scar, progresses from the border toward the core of the infarct
2 weeks–months
  • Dense collagenous scar

0–24 hours post-infarction [6][25]

1–3 days post-infarction [6][25]

3–14 days post-infarction [6][25]

2 weeks to months post-infarction [6][25]

We list the most important complications. The selection is not exhaustive.

Preventiontoggle arrow icon

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Referencestoggle arrow icon

  1. 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
  2. Alpert JS, Thygesen KA, White HD, Jaffe AS. Diagnostic and Therapeutic Implications of Type 2 Myocardial Infarction: Review and Commentary. Am J Med. 2014; 127 (2): p.105-108.doi: 10.1016/j.amjmed.2013.09.031 . | Open in Read by QxMD
  3. Kristian Thygesen , Joseph S. Alpert , Allan S. Jaffe , Maarten L. Simoons , Bernard R. Chaitman , and Harvey D. White. Third Universal Definition of Myocardial Infarction. Circulation. 2012.
  4. $Distinguishing myocardial infarction type 1 and type 2.
  5. Benjamin EJ, Muntner P, Alonso A, et al. Heart Disease and Stroke Statistics—2019 Update: A Report From the American Heart Association. Circulation. 2019; 139 (10).doi: 10.1161/cir.0000000000000659 . | Open in Read by QxMD
  6. Kasper DL, Fauci AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison's Principles of Internal Medicine. McGraw-Hill Education ; 2015
  7. Kumar V, Abbas AK, Aster JC. Robbins & Cotran Pathologic Basis of Disease. Elsevier Saunders ; 2014
  8. 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
  9. Walls R, Hockberger R, Gausche-Hill M. Rosen's Emergency Medicine. Elsevier Health Sciences ; 2018
  10. 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
  11. 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
  12. 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
  13. 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.
  14. Adriana DM Villa, Eva Sammut, Arjun Nair, Ronak Rajani, Rodolfo Bonamini, and Amedeo Chiribiri. Coronary artery anomalies overview: The normal and the abnormal. World Journal of Radiology. 2016.
  15. Thygesen K, Mair J, Giannitsis E, et al. How to use high-sensitivity cardiac troponins in acute cardiac care. Eur Heart J. 2012; 33 (18): p.2252-2257.doi: 10.1093/eurheartj/ehs154 . | Open in Read by QxMD
  16. Sherwood MW, Kristin Newby L. High‐Sensitivity Troponin Assays: Evidence, Indications, and Reasonable Use. Journal of the American Heart Association. 2014; 3 (1).doi: 10.1161/jaha.113.000403 . | Open in Read by QxMD
  17. 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
  18. Giannitsis E, Steen H, Kurz K, et al. Cardiac Magnetic Resonance Imaging Study for Quantification of Infarct Size Comparing Directly Serial Versus Single Time-Point Measurements of Cardiac Troponin T. J Am Coll Cardiol. 2008; 51 (3): p.307-314.doi: 10.1016/j.jacc.2007.09.041 . | Open in Read by QxMD
  19. Connie E Byrne, Anthony Fitzgerald, Christopher P Cannon, Desmond J Fitzgerald and Denis C Shields. Elevated white cell count in acute coronary syndromes: relationship to variants in inflammatory and thrombotic genes. BMC Medical Genetics. 2004.
  20. Palazzuoli Alberto, Iovine Francesca, Scali Chiara, and Nuti Ranuccio. Acute Coronary Syndromes: From The Laboratory Markers To The Coronary Vessels. Biomarker Insights. 2007.
  21. M Pasotti, F Prati, E Arbustini. Heart. 2006.
  22. Goljan EF. Rapid Review Pathology. Elsevier Saunders ; 2013
  23. Malik AH, Yandrapalli S, Shetty SS, Aronow WS, Cooper HA, Panza JA. Meta-analysis of Dual Antiplatelet Therapy Versus Monotherapy With P2Y12 Inhibitors in Patients After Percutaneous Coronary Intervention.. Am J Cardiol. 2020; 127: p.25-29.doi: 10.1016/j.amjcard.2020.04.027 . | Open in Read by QxMD
  24. Kumar V, Abbas AK, Aster JC. Robbins & Cotran Pathologic Basis of Disease. Elsevier Saunders ; 2015
  25. Mann DL, Zipes DP, Libby P, Bonow RO. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. Saunders ; 2014
  26. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: Executive Summary. Circulation. 2018; 138 (13): p.e210–e271.doi: 10.1161/cir.0000000000000548 . | Open in Read by QxMD
  27. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. J Am Coll Cardiol. 2018; 72 (14): p.e91-e220.doi: 10.1016/j.jacc.2017.10.054 . | Open in Read by QxMD
  28. Jazayeri M-A, Emert MP. Sudden Cardiac Death. Med Clin North Am. 2019; 103 (5): p.913-930.doi: 10.1016/j.mcna.2019.04.006 . | Open in Read by QxMD
  29. Hayashi M, Shimizu W, Albert CM. The Spectrum of Epidemiology Underlying Sudden Cardiac Death. Circ Res. 2015; 116 (12): p.1887-1906.doi: 10.1161/circresaha.116.304521 . | Open in Read by QxMD
  30. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease. Updated: March 17, 2019. Accessed: May 20, 2019.
  31. Strutz J, Mann W, Schumacher K. Praxis der HNO-Heilkunde, Kopf- und Halschirurgie. Thieme Verlag (2009) ; 2009
  32. Wadud A. Updated: January 12, 2017. Accessed: February 22, 2017.
  33. G. N. Levine, E. R. Bates, J. A. Bittl, R. G. Brindis, S. D. Fihn, L. A. Fleisher, C. B. Granger, R. A. Lange, M. J. Mack, L. Mauri, R. Mehran, D. Mukherjee, L. K. Newby, P. T. O’Gara, M. S. Sabatine, P. K. Smith, S. C. Smith Jr.. 2016 ACC/AHA Guideline Focused Update on Duration of Dual Antiplatelet Therapy in Patients With Coronary Artery Disease. Journal of the American College of Cardiology. 2016.
  34. P. Scanlon, D. Faxon, A. Audet, B. Carabello, G. Dehmer, K. Eagle, R. Legako, D. Leon, J. Murray, S. Nissen, C. Pepine, R. Watson, J. Ritchie, R. Gibbons, M. Cheitlin, K. Eagle, T. Gardner, A. Garson Jr, R. Russell Jr, T. Ryan, S. Smith Jr. ACC/AHA guidelines for coronary angiography. Journal of the American College of Cardiology. 1999.
  35. Jarosław Wasilewski, Jacek Niedziela, Tadeusz Osadnik, Agata Duszańska, Wojciech Sraga, Piotr Desperak, Jolanta Myga-Porosiło, Zuzanna Jackowska, Andrzej Nowakowski, and Jan Głowacki. Predominant location of coronary artery atherosclerosis in the left anterior descending artery. The impact of septal perforators and the myocardial bridging effect. Polish Journal of Cardio-Thoracic Surgery. 2015.
  36. Gregory YH Lip, MD, Freek Verheugt, MD, Christopher P Cannon, MD. Chronic anticoagulation after acute coronary syndromes. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. Last updated: December 11, 2017. Accessed: May 20, 2019.
  37. 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
  38. 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
  39. 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
  40. 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
  41. 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
  42. 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
  43. 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
  44. 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
  45. Than M, Cullen L, Aldous S, et al. 2-Hour Accelerated Diagnostic Protocol to Assess Patients With Chest Pain Symptoms Using Contemporary Troponins as the Only Biomarker. J Am Coll Cardiol. 2012; 59 (23): p.2091-2098.doi: 10.1016/j.jacc.2012.02.035 . | Open in Read by QxMD
  46. 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
  47. 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
  48. 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
  49. Switaj TL, et al. Acute Coronary Syndrome: Current Treatment.. Am Fam Physician. 2017; 95 (4): p.232-240.

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