Myocardial infarction

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Part of the heart muscle is deprived of oxygen. If this continues it will die. The patient may, even before then. Nowadays, we have the technology to reverse the former.

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Acute coronary syndrome describes the spectrum of ischaemic heart disease presentations from ST elevation myocardial infarction (STEMI or simply MI) covered further in this article to non ST Elevation Myocardial Infarction (NSTEMI). These conditions are well covered by high quality up to date open access guidelines such as those from European Society of Cardiology (ESC) and National Institute for Health and Clinical Excellence(NICE) and the reader should refer to these for a detailed review and understanding of the subject. Myocardial infarction with survival was described between 1878 and 1918 - see timeline below.


Almost invariably the cause is occlusion of part of the coronary arterial circulation as a result of a clot forming from, on and downstream of an atherosclerotic lesion in the wall of the artery, a plaque. Much information about the initial process of atheromatous lesion formation exists, but lacks a wholly convincing narrative to tie it together. Plaques may persist for long periods, they may regress, at least in young generally healthy people whose coronary arteries have been imaged incidentally and they may, for reasons which are unclear, suddenly progress to activating platelets on their surface, triggering a coagulation cascade and occlusion consequent upon that.

Lipids - cholesterol - appear to be involved in the plaque-forming process.


The classic presentation is with severe pain of a gripping, squeezing or pressing nature in the centre of the chest, which commonly radiates to the left upper arm, not uncommonly to the jaw and sometimes to the epigastrium. The patient is ill, is obliged to cease activities, appears pale and sweats. There has often been some prodromal episode of pain which was not so bad, nor so long.

LogoWarningBox4.png A normal ECG does not exclude MI

Presentations other than classic are common, and modern medical thought favours a high degree of suspicion, rapid admission, monitoring and biochemical testing, and rapid discharge if MI or angina is excluded. Management of typical presentations should in general be based on consensus guidelines, which can be local, national or international[1]

LogoWarningBox4.png An absence of risk factors does not reduce the likelihood of an MI in a patient with signs and symptoms suggestive of the diagnosis.[2]


  • Old WHO criteria: 2/3 (history, ECG and cardiac enzymes) becoming increasing problematical by [3]
  • Universal definition based on troponin as biomarker[4][5].
    • This increased diagnosis by 25% but provided criteria that proved to be an independent predictor of long term mortality[6]
  • As of third universal definition[7]
Info bulb.png In sudden unobserved death in patients with previously known Ischemic Heart Disease, myocardial infarction is not the most likely cause, a sudden acute cardiac failure following reduction of coronary perfusion pressure below a critical value or a dysrhthymia is. In the absence of more clear indication of an actual MI, it is desirable to give a cause of death as IHD rather than assume an MI occurred.


  • Characteristic ECG changes if present interpreted in patient context

Blood tests

  • Troponin serial levels interpreted in patient context


  • CXR
  • Angiography (increasingly incidental result of primary PCI in ST elevation MI)


Prompt access to defibrillation after myocardial infarction is more important than thrombolysis or PCA



  • Defibrillation - this is actually the most effective technology after the event and tends to be overlooked as an established technology and most early fatalities occur before hospitalisation. Improving access times to thrombolysis actually benefits more patients by giving them prompter access to a defibrillator.
  • In ST elevation myocardial infarction (STEMI) primary PCI is superior to thrombolysis in the first 2 hours after presentation[8]
  • Thrombolysis provided certain criteria are met. Thrombolysis can be combined with late PCI in the window 1 to 3 hours for superior outcome[9].
  • Immediate revascularisation may be superior, but is more complicated and expensive and has some of its own problems and complications.

Treatment after infarction

ACE inhibitors such as Ramipril, platelet aggregation suppressors such as Clopidogrel and of course Aspirin and a beta-adrenergic -blocker such as typically Bisoprolol for varying periods and a statin such as Simvastatin for ever variously improve the remodelling of an injured ventricle; avoid further occlusions; resist a misbalance between oxygen supply and demand at the myocardium and make people less likely to have heart failure and subsequent infarctions. Treatment may be a balance between the ideal according to theory and what the patient can tolerate.




The condition was not recognised in life for years because:

  • It had no specific clinical signs
  • Dogma had it that myocardial damage was uniformally fatal
  • Clinicians had no diagnostic test so tended to say so what (still a tendency today with any condition without objective criteria !)

External Links

  • Braunwald E. Evolution of the management of acute myocardial infarction: a 20th century saga. Lancet 1998; 352:1771-1774[41]
  • Fye WB. The delayed diagnosis of myocardial infarction: it took half a century! Circulation. 1985;72(2):262-71.[42]
60px-Flag of EU.png

The Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology. Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation. European Heart Journal, doi:10.1093/eurheartj/ehn416 free full text pdf [43]


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  4. Thygesen K, Alpert JS, White HD, Jaffe AS, Apple FS, Galvani M, Katus HA, Newby LK, Ravkilde J, Chaitman B, Clemmensen PM, Dellborg M, Hod H, Porela P, Underwood R, Bax JJ, Beller GA, Bonow R, Van der Wall EE, Bassand JP, Wijns W, Ferguson TB, Steg PG, Uretsky BF, Williams DO, Armstrong PW, Antman EM, Fox KA, Hamm CW, Ohman EM, Simoons ML, Poole-Wilson PA, Gurfinkel EP, Lopez-Sendon JL, Pais P, Mendis S, Zhu JR, Wallentin LC, Fernández-Avilés F, Fox KM, Parkhomenko AN, Priori SG, Tendera M, Voipio-Pulkki LM, Vahanian A, Camm AJ, De Caterina R, Dean V, Dickstein K, Filippatos G, Funck-Brentano C, Hellemans I, Kristensen SD, McGregor K, Sechtem U, Silber S, Tendera M, Widimsky P, Zamorano JL, Morais J, Brener S, Harrington R, Morrow D, Lim M, Martinez-Rios MA, Steinhubl S, Levine GN, Gibler WB, Goff D, Tubaro M, Dudek D, Al-Attar N. Universal definition of myocardial infarction. Circulation. Nov 27; 116(22):2634-53.(Link to article – subscription may be required.)
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  8. Bhatt DL. Timely PCI for STEMI - Still the Treatment of Choice. The New England journal of medicine. Mar 10.(Link to article – subscription may be required.)
  9. Armstrong PW, Gershlick AH, Goldstein P, Wilcox R, Danays T, Lambert Y, Sulimov V, Ortiz FR, Ostojic M, Welsh RC, Carvalho AC, Nanas J, Arntz HR, Halvorsen S, Huber K, Grajek S, Fresco C, Bluhmki E, Regelin A, Vandenberghe K, Bogaerts K, Van de Werf F. Fibrinolysis or Primary PCI in ST-Segment Elevation Myocardial Infarction. The New England journal of medicine. Mar 10.(Link to article – subscription may be required.)
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  41. Braunwald E. Evolution of the management of acute myocardial infarction: a 20th century saga. Lancet 1998; 352:1771-1774
  42. Fye WB. The delayed diagnosis of myocardial infarction: it took half a century! Circulation. 1985;72(2):262-71.
  43. The Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology. Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation. European Heart Journal, doi:10.1093/eurheartj/ehn416