questions 6

Myocardial Infarction

Topic updated on 11/22/17 3:15pm

  • 65-year-old male has been in the CCU for the last three days following an anteroseptal myocardial infarction. On Day #4 of this admission, his chest pain returns. On exam, he is found to have a third heart sound (S3) and bibasilar rales. Labs demonstrate an elevated CK-MB and a LDH1/LDH2 flip.
  • An occlusion or spasm causing myocardial ischemia and subsequent myocardial tissue death.
  • Most commonly caused by acute thrombus formation on a ruptured atherosclerotic plaque
    • other causes include
      • cocaine
      • embolus
      • vasculitis (polyarteritis nodosa, Kawasaki disease)
  • Types
    • subendocardial (involves inner 1/3 of heart wall)
    • transmural (involves full thickness of heart wall)
  • Risk factors are the same as in Ischemic Heart Disease
    • see topic 
  • Vessels involved
    • right ventricle + posterior 1/3 of septum = RCA
    • anterior left ventricle + anterior 2/3 of septum = LAD
Evolution of MI
  • 0-24 hours post-ischemia
    • ischemic injury to cardiomyocytes is irreversible (30 minutes)
    • No visible changes in first 4 hours
    • contraction bands visible (12-24 hours)
    • coagulation necrosis (4-24 hours) 
      • myocytes release contents around 4 hours
      • neutrophils beginning to emigrate around 24 hours
    • infarcted region of heart appears mottled and stains pale with tetrazolium 
    • risk for arrhythmia
      • can cause sudden death
  • 24-72 hours post-ischemia 
    • acute inflammation
    • hyperemia 
    • neutrophils destroying dead tissue, extensive neutrophilic infiltration and continued coagulation necrosis on histology
    • infarcted region of heart appears pale
    • risk of fibrinous pericarditis 
      • due to an extensive neutrophilic infiltrate
  • 3-7 days post-ischemia 
    • early granulation tissue encircles area of infarction 
    • macrophages remove debris via phagocytosis as well as structural components resulting in weakness in the infarcted area
    • highest risk of free wall rupture (tamponade), septal rupture (ventricular-septal defect), papillary muscle rupture (mitral regurgation)
  • 7-10 days post-ischemia 
    • necrotic area is yellow
    • continued macrophage infiltration with formation of granulation tissue
  • 10-14 days post ischemia 
    • extensive granulation tissue present 
    • revascularization of infarcted territory begins
  • 2 weeks - 2 months post ischemia
    • fibroblasts deposit type I collagen, resulting in notably decreased cellularity of tissue 
    • ongoing contraction of scar through myofibroblast action
  • > 2 months post-ischemia
    • dense collagen scar is formed 
    • risk for ventricular aneurysm
  • Symptoms
    • acute-onset chest pain that may radiate to the left arm, jaw, neck, epigastrium and shoulder
      • lasting > 30 minutes
      • not relieved by nitroglycerin
    • diaphoresis
    • shortness of breath
    • nausea/vomiting
    • lightheadedness/dizziness
    • be aware of silent MIs
      • biggest concern in the elderly, post-menopausal women, and diabetics
  • Physical exam 
    • tachycardia
    • new mitral regurgitation
      • via ruptured papillary muscle 
    • S4
    • hypotension
      • secondary to cardiogenic shock from decreased cardiac output
    • crackles
      • from pulmonary edema
      • caused by backflow secondary to decreased cardiac output
  • Diagnosis made by demonstrating at least 2 out of 3 of the following
    1. ECG changes
      • ST-elevation or ST-depression 
        • reflects transmural ischemia or subendothelial ischemia, respectively
        • occurs within minutes and resolves after 24-48 hours
      • T-wave inversion 
        • reflects transmural infarction
        • occurs within hours, returns to upright after weeks
      • Q-waves 
        • reflect transmural infarction
        • occur within hours
    2. Positive cardiac enzymes 
      • troponin is standard in first 8 hours
        • most specific
        • disappears between 7-10 days
      • CK-MB standard in the first 24 hours
        • disappears around 3-4 days
        • diagnosis of re-infarction if CK-MB rises four days after initial presentation
      • LDH1 is best for 2-7 days after symptoms
        • LDH2 found in skeletal muscle and is normally higher
        • LDH1 > LDH2 is termed an LDH flip
  • Acute management
    • morphine
    • oxygen
    • nitroglycerin
    • ACEI
    • aspirin
    • beta-blockers (if no hypotension, bradycardia, or pulmonary edema)
    • heparin
  • In the first 6-hours
    • can use thrombolytics (TPA)
    • heparin (give 48 hrs post-infarct if TPA has been used to lyse the clot)
    • streptokinase
  • Long term therapy (post-MI)
    • aspirin
    • beta-blockers
    • lipid-lowering drugs
      • HMG-CoA reductase inhibitors decrease mortality post-MI
    • ACEIs
    • reduction of social habit risk factors
      • smoking cessation
    • potentially schedule for CABG or stenting procedures if needed
Prognosis, Prevention, and Complications
  • Cardiac arrhythmias (90%) are the most common cause of death
  • LV failure and pulmonary edema (60%)
  • Mural thrombus
    • danger of embolization
  • Cardiogenic shock
    • via decreased cardiac output due to decreased contractile tissue and/or ventricular aneurysm
      • ventricular aneurysm rupture is uncommon but may facilitate embolus formation
        • presents as precordial bulge during systole
  • Fibrinous pericarditis
    • results in friction rub 3-5 days post MI
    • pain relieved by leaning forward
  • Dressler's Syndrome
    • autoimmune disease
    • leads to fibrinous pericarditis several weeks post-MI


Qbank (5 Questions)

(M1.CV.34) An autopsy is being performed on an elderly man who died from a myocardial infarction. Biopsy of the heart is likely to reveal necrosis most similar to necrosis seen in which of the following scenarios? Topic Review Topic

1. The central nervous system following a stroke
2. The lung following a tuberculosis infection
3. Acute pancreatitis resulting from release of enzymatically active enzymes into the pancreas
4. A region of kidney where blood flow is obstructed
5. An abscess

(M1.CV.35) A 64-year-old male with a past medical history of obesity, diabetes, hypertension, and hyperlipidemia presents with an acute onset of nausea, vomiting, diaphoresis, and crushing substernal chest pain. Vital signs are temperature 37° C, HR 110, BP 149/87, and RR of 22 with an oxygen saturation of 99% on room air. Physical exam reveals a fourth heart sound (S4), and labs are remarkable for an elevated troponin. EKG is shown below. The pathogenesis of the condition resulting in this patient’s presentation involves:
Topic Review Topic
FIGURES: A          

1. Genetic inheritance of a mutation in ß-myosin or troponin expressed in cardiac myocytes
2. A fully obstructive thrombus at the site of a ruptured, ulcerated atherosclerotic plaque
3. A partially occlusive thrombus at the site of a ruptured, ulcerated atherosclerotic plaque
4. Destruction of the vasa vasorum caused by vasculitic phenomena
5. A stable atheromatous lesion without overlying thrombus

(M1.CV.75) A 68-year-old male with a history of type 2 diabetes, hypertension, and COPD presents to the emergency department with severe substernal chest pain. On exam, he is diaphoretic and in obvious distress. An EKG is obtained which is demonstrated in Figure F. He immediately receives treatment for his condition and is subsequently admitted to the cardiac intensive care unit (CICU). In the CICU, he does well until day 5 of hospitalization when he begins to complain of severe shortness of breath and chest pain. Vitals are noted to be T: 36 deg C, HR: 130 bpm, BP: 65/40 mmHg, RR: 12, SaO2: 98%. He is clearly in distress and has elevated JVP. Which of the following histologic images would you expect to see if a biopsy of the myocardium was performed on this patient? Topic Review Topic
FIGURES: A   B   C   D   E   F

1. Figure A
2. Figure B
3. Figure C
4. Figure D
5. Figure E

(M1.CV.102) A 60-year-old woman with history of type I diabetes currently on hormone replacement therapy is seen in your ED complaining of "bad indigestion", dizziness and nausea for the past several hours. Vitals are T98.9, HR 102, BP 130/100, RR 25 and she is mildly diaphoretic. An EKG is shown in Figure A. At what time point does the injury to her affected cells become irreversible? Topic Review Topic
FIGURES: A          

1. 5 seconds
2. 60 seconds
3. 10 minutes
4. 30 minutes
5. 1 hour

(M1.CV.138) A 62-year-old male collapses while mowing the lawn, and it is determined that he experienced sudden cardiac death. The patient's medical history is significant for a preceding myocardial infarction that was managed conservatively. Posthumous histologic evaluation of the patient's heart reveals extensive granulation tissue replacing dead myocardium as well as early evidence of neovascularization, which is shown in Figure A. How long prior to death did this patient most likely experience his myocardial infarction? Topic Review Topic
FIGURES: A          

1. 16 hours
2. 3 days
3. 8 days
4. 2 weeks
5. 2 months

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Pfeffer MA, Braunwald E, Moyé LA, Basta L, Brown EJ, Cuddy TE, Davis BR, Geltman EM, Goldman S, Flaker GC
N. Engl. J. Med.. 1992 Sep;327(10):669-77. PMID: 1386652 (Link to Pubmed)
0 responses
Pfeffer MA, Braunwald E, Moyé LA, Basta L, Brown EJ, Cuddy TE, Davis BR, Geltman EM, Goldman S, Flaker GC
N. Engl. J. Med.. 1992 Sep;327(10):669-77. PMID: 1386652 (Link to Pubmed)
0 responses

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