MI Pathology Flashcards
Ischemia
Injury resulting from hypoxia induced by reduced blood flow
Effects of impaired inflow of blood
Reduced oxygen, reduced nutrients
Effects of impaired outflow of blood
Insufficient removal of metabolites
Ischemic heart disease
A group of syndromes that result from inadequate blood supply to meet the oxygen demands of the heart resulting from ischemia.
90% caused by coronary artery disease
Principal presentations of ischemic heart disease
Angina
MI
Chronic IHD w/HF
Sudden Cardiac Death - regional ischemia causes fatal ventricular arrhythmia
MI
Irreversible myocardial muscle damage caused by prolonged cardiac ischemia.
Discrete focus of ischemic muscle necrosis.
Circumflex artery supplies
Lateral edge of left ventricle
LAD supplies
Front and bottom of left ventricle. Anterior edge of IVSeptum
RCA supplies
Blood to the right atrium, ventricle, and bottom of left ventricle, and posterior edge of septum. Also, PAPILLARY MUSCLE
Progression of MI
Starts in the subendocardium and in the central portion of the area at risk. Progresses as a wavefront of necrosis moves from subendo to subepicardium
Transmural infarct
Ischemic necrosis involves full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery.
What causes transmural infarcts
Acute plaque change and superimposed thrombus with sustained obstruction.
Common complications of transmural infarcts
Pericarditis or ventricular rupture
Subendocardial infarct
ischemic necrosis limited to the inner 1/3 or 1/2 of the ventricular wall. Subendocardial zone is the least perfused and most vulnerable to any reduction in flow.
Regional subendocardial infarct
transient obstruction of a coronary artery which is relieved before the necrosis extends across the full thickness of the myocardium.
Circumferential subendocardial infarct
Due to prolonged severe hypotension.
Multifocal microinfarction
Due to pathology only involving smaller intramural vessels.
Can be from microemboli, vasculitis, vascular spasm (cocaine/adrenaline)
Outcome of multifocal microinfarcts
Sudden cardiac death due to fatal arrhythmia, ischemic dilated cardiomyopathy.
What do the cellular consequences of myocardial ischemia depend on?
Severity and duration of the blood flow deprivation
Characteristics of early ischemia
Switch from aerobic to anaerobic metabolism, decreased ATP and accumulation of lactate. Glycogen depletion. ATP deficiency leads to failure of NA K pump, so water rushes in. Mild cellular and mitochondrial swelling.
This is potentially reversible
Characteristics of late ischemia
This occurs after 20-30 minutes of ischemia. Disruptions in the sarcolemma occur and intracellular molecules leak out (biomarkers).
Amorphous densities in the mitochondria.
This is non-reversible
Effect of ischemia on mitochondria
Creation of amorphous densities
Curve of ATP concentration vs minutes
Decreasing exponentially
Curve of lactate concentration vs minutes
Increasing sigmoidally
When is myocardial injury reversible
20-30 minutes after onset of severe ischemia. After that, dead myocardium starts to accumulate.
When is myocardial loss of viability after MI complete?
6-12 hours after onset of severe ischemia
Cellular consequences of myocardial ischemia over the course of: Seconds Minutes 20-30 Minutes 1 hour
Seconds: Onset of ATP depletion (cessation of aerobic metabolism
Minutes: Decrease in contractility due to depletion of atp
20-30 Minutes: irreversible cell injury
1 Hour is microvascular injury
Is MI apparent on gross exam?
Yes, but only after 12 hours or so
Gross features 12-24 hours post MI
Dark Mottling due to coagulative necrosis. Reddish blue discoloration. Looks like red jello.
Gross features3-7 days
Hyperemic border due to granulation tissue, central yellow-tan softening due to inflammatory infiltrates.
Gross features >2 months
Complete scarring (grey-white)
Microscopic features 12-24 hours post MI
Coagulative necrosis with wavy fibers
Microscopic features 3-7 d
Neutrophils, macrophages and removal of necrotic tissue. Some granulation tissue (very congested vessels)
Microscopic features >2 months
Fibrous tissue and collagenous scar stained blue with trichrome.
Can you see histologic changes very early after infarction?
Not on H and E, but if you stain for complement you can!
Features of coagulative necrosis
Loss of nuclei
When are neutrophils most common?
1-3 days post MI
When are macrophages most common?
3-7 days post MI
Granulation tissue
Very congested vasculature, las lymphoid cells, fibroblasts, lots of capillaries even wtihout blood cells
Does >2 months look like 10 years after MI?
Yes.
Old MI Scar
Dense collagen fibrous tissue, no inflammatory infiltrates.
Myocardial rupture
Due to softening and weakening of necrotic and inflamed myocardium.
Rupture of free wall (most common) causes hemopericardium and cardiac tamponade. Happens in the first 2 weeks post MI
Rupture of the Ventricular septum (L->R shunt can cause death)
Papillary muscle rupture
True aneurysms
Occur weeks->months post MI. Can cause incompetent mitral valve or mural thrombi.
MI induced pericarditis
Happens with transmural thrombi only. Can cause fibrinous or fibrinohemorrhagic pericarditis.
Dressler Syndrome
Autoimmune mediated pericarditis months after MI
Proposed mechanisms of reperfusion injury
- Oxidative stress from reoxygenation (ROS cause injuries)
- Intracellular calcium overload (causes bands)
- Inflammation (brings neutrophils)
- Complement activation
Common pathologic findings in reperfusion injury
Hemorrhage (due to leakage from weakened ischemic vessels)
Contraction bands in lethally injured cells (exaggerated contraction of sarcomeres due to flooding of new plasma calcium)
