Ischemic heart disease pathology Flashcards Preview

CVPR II > Ischemic heart disease pathology > Flashcards

Flashcards in Ischemic heart disease pathology Deck (15)
Loading flashcards...

List the (2) processes that can lead to total occlusion of a coronary artery with critical atherosclerotic disease and result in downstream ischemia

Thrombosis (cocaine or hypercoagulable state) and plaque rupture/hemorrhage can lead to occlusion


Note the window in which myocardial cells might tolerate ischemia

Beyond 20-30 Min. Irreversible injury. Myocytes are affected the most, followed by endothelial cells, then fibroblasts.


What can be done immediately if MI is suspected to prevent/delay necrosis

aspirin or TPA (tissue plasminogen activator)


complications of ischemia

myoctye death, arrhythmia (can result in sudden death)


Name a drug of abuse that can lead to coronary artery spasm / constriction … on a "normal" or diseased (atherosclerotically compromised) coronary artery



List enzymes / proteins present in cardiac muscle that can be evaluated with respect to proving / disproving the clinical hypothesis of "myocardial infarct

Troponin is most useful (rises in2-4hrs and returns to normal in 7-10days), Creatinine Kinase-MB used in the past; less used today (rises in 2-4 hrs, returns to normal in 3days), Myoglobin rises fastest but (a) falls fast too, (b) is non-specific


Distinguish underlying pathophysiology of (1) typical / stable Angina and (2) unstable / crescendo angina

1. stable: A fixed stenotic lesion limits volume of blood available to myocardium during high demand. Better after rest. 2. Prinzmetal (uncommon): Due to spasm of coronary artery on fixed stenotic lesion or minimal lesion that is seen at rest. 3. Unstable: Occurs with activity or at rest. Lesion is unstable with plaque disruption and associated thrombosis, +/- embolization of thrombus/plaque causing partial occlusion and ischemia, +/- vasospasm with plaque disruption.


Major findings in Initial myocardial injury

Vessel dilation/congestion (red and hot), vessel permeability is increased (swollen), loss of nuclei


Major findings in Acute inflammatory cell response to injury

Polymorphonuclear cell infiltrate


Major findings in Chronic inflammatory cell response to injury

Lymphocytes, macrophages infiltrate


Major findings in Repair process with (1) granulation tissue formation, (2) mature scar formation

granulation tissue: Fibroblasts deposit new collagen/elastin and new vessels develop. Scar: scant mononuclear cells


Area of myocardium affected and pathophys of subendocardial infarct

limited damage. Subendocardial area is more vulnerable to ischemia than subpericardial region due to blood flow patterns (outer to inner circulation). Occurs in the setting of partial occlusion or resolution of complete thrombotic occlusion. Regional subendocardial infarct is due to transient/partial occlusion, circumferential subendocardial infarct is due to global hypertension, diabetic microinfarcts are due to occlusions of small intramural vessels


Area of myocardium affected and pathophys of transmural infarct

Infarct extends from subendocardial to subpericardial. Occurs in the setting of persistent occlusion of coronary artery


List key negative outcomes of myocardial infarct

(1) Electrical activity of myocardium > arrhythmia (possible sudden death). (2) Myocardial defects and deficits > area lacking contractility, aneurysmal dilation. (3) Pericardial reactive or autoimmune process > fibrinous pericarditis (Dressler syndrome)


List complications of: Ventricular aneurysm, ventricular wall rupture, papillary muscle infarction, pericarditis

(1) Ventricular aneurysm: lack of contraction; thrombus formation (2) Ventricular wall rupture : hemopericardium and tamponade. greatest risk of rupture is 3-7 days after infarct
(3) Papillary muscle infarction: mitral valve dysfunction
(4) Pericarditis: fibrosis and in some cases constrictive pericarditis