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Diagnosis of myocardial infarction

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Myocardial infarction diagnosis
PurposeDiagnose myocardial infarct via physical exam and EKG (plus blood test)

A diagnosis of myocardial infarction is created by integrating the history of the presenting illness and physical examination with electrocardiogram findings and cardiac markers (blood tests for heart muscle cell damage).[1][2] A coronary angiogram allows visualization of narrowings or obstructions on the heart vessels, and therapeutic measures can follow immediately. At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings.

A chest radiograph and routine blood tests may indicate complications or precipitating causes and are often performed upon arrival to an emergency department. New regional wall motion abnormalities on an echocardiogram are also suggestive of a myocardial infarction. Echo may be performed in equivocal cases by the on-call cardiologist.[3] In stable patients whose symptoms have resolved by the time of evaluation, Technetium (99mTc) sestamibi (i.e. a "MIBI scan"), thallium-201 chloride or Rubidium-82 Chloride can be used in nuclear medicine to visualize areas of reduced blood flow in conjunction with physiologic or pharmacologic stress.[3][4] Thallium may also be used to determine viability of tissue, distinguishing whether non-functional myocardium is actually dead or merely in a state of hibernation or of being stunned.[5]

Diagnostic criteria

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According to the WHO criteria as revised in 2000,[6] a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI.

Previous WHO criteria[7] formulated in 1979 put less emphasis on cardiac biomarkers; according to these, a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:

  1. Clinical history of ischaemic type chest pain lasting for more than 20 minutes
  2. Changes in serial ECG tracings
  3. Rise and fall of serum cardiac biomarkers such as creatine kinase-MB fraction and troponin

Physical examination

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The general appearance of patients may vary according to the experienced symptoms; the patient may be comfortable, or restless and in severe distress with an increased respiratory rate. A cool and pale skin is common and points to vasoconstriction. Some patients have low-grade fever (38–39 °C). Blood pressure may be elevated or decreased, and the pulse can become irregular.[8][9]: 1444 

If heart failure ensues, elevated jugular venous pressure and hepatojugular reflux, or swelling of the legs due to peripheral edema may be found on inspection. Rarely, a cardiac bulge with a pace different from the pulse rhythm can be felt on precordial examination. Various abnormalities can be found on auscultation, such as a third and fourth heart sound, systolic murmurs, paradoxical splitting of the second heart sound, a pericardial friction rub and rales over the lung.[8][9]: 1450 

Electrocardiogram

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Main article: Electrocardiography in myocardial infarction
12-lead electrocardiogram showing ST-segment elevation (orange) in I, aVL and V1-V5 with reciprocal changes (blue) in the inferior leads, indicative of an anterior wall myocardial infarction.

The primary purpose of the electrocardiogram is to detect ischemia or acute coronary injury in broad, symptomatic emergency department populations. A serial ECG may be used to follow rapid changes in time. The standard 12 lead ECG does not directly examine the right ventricle, and is relatively poor at examining the posterior basal and lateral walls of the left ventricle. In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG.[10] The use of additional ECG leads like right-sided leads V3R and V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction.[citation needed]

The 12 lead ECG is used to classify patients into one of three groups:[11]

  1. those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with thrombolytics or primary PCI),
  2. those with ST segment depression or T wave inversion (suspicious for ischemia), and
  3. those with a so-called non-diagnostic or normal ECG.

A normal ECG does not rule out acute myocardial infarction. Mistakes in interpretation are relatively common, and the failure to identify high risk features has a negative effect on the quality of patient care.[12]

It should be determined if a person is at high risk for myocardial infarction before conducting imaging tests to make a diagnosis.[13] People who have a normal ECG and who are able to exercise, for example, do not merit routine imaging.[13] Imaging tests such as stress radionuclide myocardial perfusion imaging or stress echocardiography can confirm a diagnosis when a person's history, physical exam, ECG and cardiac biomarkers suggest the likelihood of a problem.[13]

Cardiac markers

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Main article: Cardiac marker

Cardiac markers or cardiac enzymes are proteins that leak out of injured myocardial cells through their damaged cell membranes into the bloodstream. Until the 1980s, the enzymes SGOT and LDH were used to assess cardiac injury. Now, the markers most widely used in detection of MI are MB subtype of the enzyme creatine kinase and cardiac troponins T and I as they are more specific for myocardial injury. The cardiac troponins T and I which are released within 4–6 hours of an attack of MI and remain elevated for up to 2 weeks, have nearly complete tissue specificity and are now the preferred markers for assessing myocardial damage.[14] Heart-type fatty acid binding protein is another marker, used in some home test kits. Elevated troponins in the setting of chest pain may accurately predict a high likelihood of a myocardial infarction in the near future.[15] New markers such as glycogen phosphorylase isoenzyme BB are under investigation.[16] Note that only the cardiac troponins are used clinically for myocardial infarction as creatine kinase adds little value in diagnosing MI while adding to system cost.[17][18][19]

The diagnosis of myocardial infarction requires two out of three components (history, ECG, and enzymes). When damage to the heart occurs, levels of cardiac markers rise over time, which is why blood tests for them are taken over a 24-hour period. Because these enzyme levels are not elevated immediately following a heart attack, patients presenting with chest pain are generally treated with the assumption that a myocardial infarction has occurred and then evaluated for a more precise diagnosis.[20]

Angiography

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Angiogram of the coronary arteries.
Main article: Coronary catheterization

In difficult cases or in situations where intervention to restore blood flow is appropriate, coronary angiography can be performed. A catheter is inserted into an artery (typically the radial or femoral artery[21]) and pushed to the vessels supplying the heart. A radio-opaque dye is administered through the catheter and a sequence of x-rays (fluoroscopy) is performed. Obstructed or narrowed arteries can be identified, and angioplasty applied as a therapeutic measure (see below). Angioplasty requires extensive skill, especially in emergency settings. It is performed by a physician trained in interventional cardiology.[citation needed]

Histopathology

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Micrograph of a myocardial infarction (ca. 400x H&E stain ) with prominent contraction band necrosis.

Histopathological examination of the heart may reveal infarction at autopsy. Gross examination may reveal signs of myocardial infarction.[citation needed]

  • A one-week-old myocardial infarction of the posterior left ventricle, with focal rupture, in fresh state (left) and after formalin fixation (right). The infarcted area is pale whereas the rupture is hemorrhagic (dark red).
    A one-week-old myocardial infarction of the posterior left ventricle, with focal rupture, in fresh state (left) and after formalin fixation (right). The infarcted area is pale whereas the rupture is hemorrhagic (dark red).
  • Cross-section of the heart, showing an old myocardial infarction of the posterior wall of the left ventricle (seen as pale areas).
    Cross-section of the heart, showing an old myocardial infarction of the posterior wall of the left ventricle (seen as pale areas).

Under the microscope, myocardial infarction presents as a circumscribed area of ischemic, coagulative necrosis (cell death). On gross examination, the infarct is not identifiable within the first 12 hours.[22]

Although earlier changes can be discerned using electron microscopy, one of the earliest changes under a normal microscope are so-called wavy fibers.[23] Subsequently, the myocyte cytoplasm becomes more eosinophilic (pink) and the cells lose their transversal striations, with typical changes and eventually loss of the cell nucleus.[24] The interstitium at the margin of the infarcted area is initially infiltrated with neutrophils, then with lymphocytes and macrophages, who phagocytose ("eat") the myocyte debris. The necrotic area is surrounded and progressively invaded by granulation tissue, which will replace the infarct with a fibrous (collagenous) scar (which are typical steps in wound healing). The interstitial space (the space between cells outside of blood vessels) may be infiltrated with red blood cells.[22]

These features can be recognized in cases where the perfusion was not restored; reperfused infarcts can have other hallmarks, such as contraction band necrosis.[25]

These tables gives an overview of the histopathology seen in myocardial infarction by time after obstruction.[citation needed]

By individual parameters

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Myocardial histologic parameters (HE staining)[26] Earliest manifestation[26] Full development[26] Decrease/disappearance[26] Image
Stretched/wavy fibres 1–2 h
Coagulative necrosis: cytoplasmic hypereosinophilia 1–3 h 1–3 days; cytoplasmic hypereosinophilia and loss of striations > 3 days: disintegration
Interstitial edema 4–12 h
Coagulative necrosis: 'nuclear changes' 12–24 (pyknosis, karyorrhexis) 1–3 days (loss of nuclei) Depends on size of infarction
Neutrophil infiltration 12–24 h 1–3 days 5–7 days
Karyorrhexis of neutrophils 1.5–2 days 3–5 days
Macrophages and lymphocytes 3–5 days 5–10 days (including 'siderophages') 10 days to 2 months
Vessel/endothelial sprouts* 5–10 days 10 days–4 weeks 4 weeks: disappearance of capillaries; some large dilated vessels persist
Fibroblast and young collagen* 5–10 days 2–4 weeks After 4 weeks; depends on size of infarction;
Dense fibrosis 4 weeks 2–3 months No
  • Some authors summarize the vascular and early fibrotic changes as 'granulation tissue', which is maximal at 2–3 weeks

Differential diagnoses for myocardial fibrosis:

  • Interstitial fibrosis, which is nonspecific, having been described in congestive heart failure, hypertension, and normal aging.[27]
  • Subepicardial fibrosis, which is associated with non-infarction diagnoses such as myocarditis[28] and non-ischemic cardiomyopathy.[29]
  • Healthy myocardium versus interstitial fibrosis in dilated cardiomyopathy. Alcian blue stain.
    Healthy myocardium versus interstitial fibrosis in dilated cardiomyopathy. Alcian blue stain.
  • Subepicardial fibrosis (epicardium at top)
    Subepicardial fibrosis (epicardium at top)

Chronological

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Time Gross examination Histopathology
by light microscopy
0 - 0.5 hours None[note 1] None[note 1]
0.5 – 4 hours None[note 2]
  • Glycogen Depletion, as seen with a PAS Stain
  • Possibly waviness of fibers at border
4 – 12 hours
12 – 24 hours
  • Dark mottling
1 – 3 days
  • Infarct center becomes yellow-tan
  • Continued coagulation necrosis
  • Loss of nuclei and striations
  • Increased infiltration of neutrophils to interstitium
3 – 7 days
  • Hyperemia at border
  • Softening yellow-tan center
  • Beginning of disintegration of dead muscle fibers
  • Apoptosis of neutrophils
  • Beginning of macrophage removal of dead cells at border
7 – 10 days
  • Maximally soft and yellow-tan
  • Red-tan margins
  • Increased phagocytosis of dead cells at border
  • Beginning of granulation tissue formation at margins
10 – 14 days
  • Red-gray and depressed borders
2 – 8 weeks
  • Gray-white granulation tissue
  • Increased collagen deposition
  • Decreased cellularity
More than 2 months Completed scarring[note 3] Dense collagenous scar formed[note 3]
If not else specified in boxes, then reference is nr[31]

See also

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Notes

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  1. ^ a b For the first ~30 minutes no change at all can be seen by gross examination or by light microscopy in histopathology. However, in electron microscopy relaxed myofibrils, as well as glycogen loss and mitochondrial swelling can be observered.
  2. ^ It is often possible, however, to highlight the area of necrosis that first becomes apparent after 2 to 3 hours by immersion of tissue slices in a solution of triphenyltetrazolium chloride. This dye imparts a brick-red color to intact, noninfarcted myocardium where the dehydrogenase activity is preserved. Because dehydrogenases are depleted in the area of ischemic necrosis (i.e., they leak out through the damaged cell membranes), an infarcted area is revealed as an unstained pale zone. Instead of a triphenyltetrazolium chloride dye, a LDH (lactate dehydrogenase) dye can also be used to visualize an area of necrosis.
  3. ^ a b Once scarring is completed, there is yet no common method of discerning the actual age of the infarct, since e.g. a scar that is four months old looks identical to a scar that is ten years old.

References

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  1. ^ Mallinson T (2010). "Myocardial Infarction". Focus on First Aid (15): 15. Archived from the original on 2010-05-21. Retrieved 2010-06-08.
  2. ^ "Myocardial infarction: diagnosis and investigations". GPnotebook. Retrieved 27 November 2006.
  3. ^ a b Fenton DE, Stahmer S, Baumann DM. McNamara RM, Talavera F, Halamka J, Feied C (eds.). "Myocardial infarction]". eMedicine. Archived from the original on 25 December 2006. Retrieved 27 November 2006.
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  14. ^ Eisenman A (July 2006). "Troponin assays for the diagnosis of myocardial infarction and acute coronary syndrome: where do we stand?". Expert Review of Cardiovascular Therapy. 4 (4): 509–514. doi:10.1586/14779072.4.4.509. PMID 16918269. S2CID 38481075.
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  16. ^ Apple FS, Wu AH, Mair J, Ravkilde J, Panteghini M, Tate J, et al. (May 2005). "Future biomarkers for detection of ischemia and risk stratification in acute coronary syndrome". Clinical Chemistry. 51 (5): 810–824. doi:10.1373/clinchem.2004.046292. PMID 15774573.
  17. ^ Mechanic OJ, Gavin M, Grossman SA (2024). "Acute Myocardial Infarction". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 29083808. Retrieved 2024-02-05.
  18. ^ Wiens EJ, Arbour J, Thompson K, Seifer CM (July 2019). "Routine creatine kinase testing does not provide clinical utility in the emergency department for diagnosis of acute coronary syndromes". BMC Emergency Medicine. 19 (1): 37. doi:10.1186/s12873-019-0251-4. PMC 6617848. PMID 31288735.
  19. ^ Taggart C, Wereski R, Mills NL, Chapman AR (May 2021). "Diagnosis, Investigation and Management of Patients with Acute and Chronic Myocardial Injury". Journal of Clinical Medicine. 10 (11): 2331. doi:10.3390/jcm10112331. PMC 8199345. PMID 34073539.
  20. ^ Braunwald E, Antman EM, Beasley JW, Califf RM, Cheitlin MD, Hochman JS, et al. (October 2002). "ACC/AHA 2002 guideline update for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction--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)". Journal of the American College of Cardiology. 40 (7): 1366–1374. doi:10.1016/s0735-1097(02)02336-7. PMID 12383588.
  21. ^ Kolkailah AA, Alreshq RS, Muhammed AM, Zahran ME, Anas El-Wegoud M, Nabhan AF (April 2018). "Transradial versus transfemoral approach for diagnostic coronary angiography and percutaneous coronary intervention in people with coronary artery disease". The Cochrane Database of Systematic Reviews. 2018 (4): CD012318. doi:10.1002/14651858.CD012318.pub2. PMC 6494633. PMID 29665617.
  22. ^ a b Rubin E, Gorstein F, Rubin R, Schwarting R, Strayer D (2001). Rubin's Pathology — Clinicopathological Foundations of Medicine. Maryland: Lippincott Williams & Wilkins. p. 546. ISBN 978-0-7817-4733-2.
  23. ^ Eichbaum FW (1975). "'Wavy' myocardial fibers in spontaneous and experimental adrenergic cardiopathies". Cardiology. 60 (6): 358–365. doi:10.1159/000169735. PMID 782705.
  24. ^ Roy S. "Myocardial infarction". Retrieved 28 November 2006.
  25. ^ Fishbein MC (March 1990). "Reperfusion injury". Clinical Cardiology. 13 (3): 213–217. doi:10.1002/clc.4960130312. PMID 2182247. S2CID 23499085.
  26. ^ a b c d Unless otherwise specified in boxes, reference is: Michaud K, Basso C, d'Amati G, Giordano C, Kholová I, Preston SD, et al. (February 2020). "Diagnosis of myocardial infarction at autopsy: AECVP reappraisal in the light of the current clinical classification". Virchows Archiv. 476 (2): 179–194. doi:10.1007/s00428-019-02662-1. PMC 7028821. PMID 31522288.
  27. ^ Chute M, Aujla P, Jana S, Kassiri Z (September 2019). "The Non-Fibrillar Side of Fibrosis: Contribution of the Basement Membrane, Proteoglycans, and Glycoproteins to Myocardial Fibrosis". Journal of Cardiovascular Development and Disease. 6 (4): 35. doi:10.3390/jcdd6040035. PMC 6956278. PMID 31547598.
  28. ^ Gräni C, Eichhorn C, Bière L, Kaneko K, Murthy VL, Agarwal V, et al. (February 2019). "Comparison of myocardial fibrosis quantification methods by cardiovascular magnetic resonance imaging for risk stratification of patients with suspected myocarditis". Journal of Cardiovascular Magnetic Resonance. 21 (1): 14. doi:10.1186/s12968-019-0520-0. PMC 6393997. PMID 30813942.
  29. ^ Bhaskaran A, Tung R, Stevenson WG, Kumar S (January 2019). "Catheter Ablation of VT in Non-Ischaemic Cardiomyopathies: Endocardial, Epicardial and Intramural Approaches". Heart, Lung & Circulation. 28 (1): 84–101. doi:10.1016/j.hlc.2018.10.007. PMID 30385114. S2CID 54349750.
  30. ^ Bishop JE, Greenbaum R, Gibson DG, Yacoub M, Laurent GJ. Enhanced deposition of predominantly type I collagen in myocardial disease. J Mol Cell Cardiol. 1990;22:1157–1165
  31. ^ Table 11-2 in: Mitchell, Richard Sheppard, Kumar, Vinay, Abbas, Abul K., Fausto, Nelson (1997). Robbins Basic Pathology. Philadelphia: Saunders. ISBN 1-4160-2973-7. 8th edition.
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