ST elevation myocardial infarction histopathology

Jump to: navigation, search

Acute Coronary Syndrome Main Page

ST Elevation Myocardial Infarction Microchapters

Home

Patient Information

Overview

Pathophysiology

Pathophysiology of Vessel Occlusion
Pathophysiology of Reperfusion
Gross Pathology
Histopathology

Causes

Differentiating ST elevation myocardial infarction from other Diseases

Epidemiology and Demographics

Risk Factors

Triggers

Natural History and Complications

Risk Stratification and Prognosis

Pregnancy

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

EKG Examples

Chest X Ray

Cardiac MRI

Echocardiography

Coronary Angiography

Treatment

Pre-Hospital Care

Initial Care

Oxygen
Nitrates
Analgesics
Aspirin
Beta Blockers
Antithrombins
The coronary care unit
The step down unit
STEMI and Out-of-Hospital Cardiac Arrest
Pharmacologic Reperfusion
Reperfusion Therapy (Overview of Fibrinolysis and Primary PCI)
Fibrinolysis
Reperfusion at a Non–PCI-Capable Hospital:Recommendations
Mechanical Reperfusion
The importance of reducing Door-to-Balloon times
Primary PCI
Adjunctive and Rescue PCI
Rescue PCI
Facilitated PCI
Adjunctive PCI
CABG
Management of Patients Who Were Not Reperfused
Assessing Success of Reperfusion
Antithrombin Therapy
Antithrombin therapy
Unfractionated heparin
Low Molecular Weight Heparinoid Therapy
Direct Thrombin Inhibitor Therapy
Factor Xa Inhibition
DVT prophylaxis
Long term anticoagulation
Antiplatelet Agents
Aspirin
Thienopyridine Therapy
Glycoprotein IIbIIIa Inhibition
Other Initial Therapy
Inhibition of the Renin-Angiotensin-Aldosterone System
Magnesium Therapy
Glucose Control
Calcium Channel Blocker Therapy
Lipid Management

Pre-Discharge Care

Recommendations for Perioperative Management–Timing of Elective Noncardiac Surgery in Patients Treated With PCI and DAPT

Post Hospitalization Plan of Care

Long-Term Medical Therapy and Secondary Prevention

Overview
Inhibition of the Renin-Angiotensin-Aldosterone System
Cardiac Rehabilitation
Pacemaker Implantation
Long Term Anticoagulation
Implantable Cardioverter Defibrillator
ICD implantation within 40 days of myocardial infarction
ICD within 90 days of revascularization

Case Studies

Case #1

Case #2

Case #3

Case #4

Case #5

ST elevation myocardial infarction histopathology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on ST elevation myocardial infarction histopathology

CDC on ST elevation myocardial infarction histopathology

ST elevation myocardial infarction histopathology in the news

Blogs on ST elevation myocardial infarction histopathology

Directions to Hospitals Treating ST elevation myocardial infarction

Risk calculators and risk factors for ST elevation myocardial infarction histopathology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

Histopathological examination of the heart may reveal infarction at autopsy. 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.[1]

Histopathology

Wavy fiber phase

Although earlier changes can be discerned using electron microscopy, one of the earliest changes under a normal microscope are so-called wavy fibers.[2]Thin wavy myocytes are (the earliest light microscopic finding of acute myocardial infarction) visible as early as one hour following the onset of infarction. [3]

Eosinophilic phase with loss of cell nucleus

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.[4]

Coagulation necrosis

Coagulation necrosis, characterized by hypereosinophilia and nuclear pyknosis, followed by karyorrhexis, karyolysis, total loss of nuclei and loss of cytoplasmic cross-striations, is generally first visible in the period from 4-12 hours following infarction.[5]. Necrotic myocytes may retain their striations for a long time.[6]

Neutrophilic infiltration (acute inflammation), edema and hemorrhage are also first visible at 4-12 hours but generally closer to 12 hours. 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.[1]

Acute inflammation is generally present in a narrow band of the periphery at 24 hours, in a broad band of the periphery at 48 hours and tends to be maximal around 72 hours, with extensive basophilic debris from degenerating neutrophils.[6]

Infiltration by macrophages, lymphocytes, eosinophils, fibroblasts and capillaries begins around the periphery at 3-10 days. Contraction band necrosis, characterized by hypereosinophilic transverse bands of precipitated myofibrils in dead myocytes is usually seen at the edge of an infarct or with reperfusion (e.g. with thrombolytic therapy).[7]

Reperfusion of an infarct is also associated with more hemorrhage, less acute inflammation, less limitation of the acute inflammation to the periphery in the first few days, reactive stromal cells, more macrophage infiltration earlier and a more patchy distribution of necrosis, especially around the periphery.[8]

These features can be recognized in cases where the perfusion was not restored; reperfused infarcts can have other hallmarks, such as contraction band necrosis.[9]

Summary of time from onset and morphologic findings:

Images

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Acute Myocardial infarction with PMNs
Acute Myocardial infarction, coagulative necrosis
H&E, medium magnification view of healing infarct.
Myocardial infarction, subacute phase.
Myocardial infarction, subacute, granulation tissue.
Myocardial infarction, subendocardial ischemia with swollen myocytes
Myocardial infarction, mural thrombus
Acute myocardial infarction, ischemic fibers demonstrated by aldehyde fuchsin stain


Virtual Microscopic Images

References

  1. 1.0 1.1 Rubin's Pathology - Clinicopathological Foundations of Medicine. Maryland: Lippincott Williams & Wilkins. 2001. pp. p. 546. ISBN 0-7817-4733-3.  Unknown parameter |coauthors= ignored (help)
  2. Eichbaum FW (1975). "'Wavy' myocardial fibers in spontaneous and experimental adrenergic cardiopathies". Cardiology. 60 (6): 358–65. PMID 782705. 
  3. Bouchardy B, Majno G (1974). "Histopathology of early myocardial infarcts. A new approach". Am. J. Pathol. 74 (2): 301–30. PMC 1910768Freely accessible. PMID 4359735.  Unknown parameter |month= ignored (help)
  4. S Roy. Myocardial infarction. Retrieved November 28, 2006.
  5. Schoen FJ. The heart. Chapter 12 in Robbins Pathologic Basis of Disease, fifth edition, 1994, Cotran RS, Kumar V, Schoen FJ, eds., Philadelphia, W.B.Saunders, pp.517-582
  6. 6.0 6.1 Fishbein MC, Maclean D, Maroko PR (1978). "The histopathologic evolution of myocardial infarction". Chest. 73 (6): 843–9. PMID 657859.  Unknown parameter |month= ignored (help)
  7. Reichenbach D, Cowan MJ. Healing of myocardial infarction with and without reperfusion. Chapter 5, in Cardiovascular Pathology, 1991, Virmani R, Atkinson JB, Fenoglio JJ, eds., Philadelphia, W.B.Saunders, pp. 86-98.
  8. Reichenbach D, Cowan MJ. Healing of myocardial infarction with and without reperfusion. Chapter 5, in Cardiovascular Pathology, 1991, Virmani R, Atkinson JB, Fenoglio JJ, eds., Philadelphia, W.B.Saunders, pp. 86-98.
  9. Fishbein MC (1990). "Reperfusion injury". Clin Cardiol. 13 (3): 213–7. PMID 2182247.  Unknown parameter |month= ignored (help)

Linked-in.jpg