ST elevation myocardial infarction case study four

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 case study four 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 case study four
CDC on ST elevation myocardial infarction case study four
ST elevation myocardial infarction case study four in the news
Blogs on ST elevation myocardial infarction case study four
Directions to Hospitals Treating ST elevation myocardial infarction
Risk calculators and risk factors for ST elevation myocardial infarction case study four

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Case 4: Coagulative Necrosis

Clinical Summary

This was a 57-year-old male whose hospital course following abdominal surgery was characterized by progressive deterioration and hypotension.

Four days post-operatively, the patient sustained an anterior myocardial infarction and died the next day.

Autopsy Findings

The patient's heart weighed 410 grams.

Examination of the coronary arteries revealed marked atherosclerotic narrowing of all three vessels with focal occlusion by a thrombus of the left anterior descending artery.

Fresh necrosis of the anterior wall of the left ventricle and anterior portion of the septum was present, extending from the endocardium to the inner half of the ventricular wall.

Histopathological Findings

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

In this gross photograph of the heart from this case, note the area of fresh myocardial infarction (arrows) in the anterior portion of the left ventricle and extending into the anterior portion of the interventricular septum. Note that the walls of the left and right ventricle are slightly thicker than normal.

This is a low-power photomicrograph of the left ventricular free wall extending from the epicardium (1) to the endocardium (2). The area of infarction is the darker red (hypereosinophilic area) along the subendocardium (3).

This higher-power photomicrograph shows endocardium on the right side of this image. Directly beneath the endocardium is a pale area consisting of cardiac myocytes exhibiting vacuolar degeneration (1). The area of infarction is visible as a hypereosinophilic area (2) and there is a second zone of vacuolated myocytes (3) between the infarct and the normal myocardium (4).

This high-power photomicrograph shows the area of infarction on the right (1). There is an area of vacuolated myocytes (2) adjacent to the infarcted myocytes and then normal cardiac muscle to the left (3).

This high-power photomicrograph shows the endocardium (1) and the area of subendocardial vacuolar degeneration (2). The area of infarction (3) contains some red blood cells.

This high-power photomicrograph demonstrates the border between the vacuolated subendocardial myocytes (1) and the infarcted myocytes (2).

This high-power photomicrograph contains normal myocytes (1), vacuolated myocytes (2), and infarcted myocytes (3).