atherosclerosis Flashcards
what is a vulnerable plaque
characterized by a THIN, FIBROUS CAP with a large soft lipid cholesterol pool underneath it
these characteristics + normal stress on artery walls due to contraction and relaxation of vessels contribute to a high mechanical stress zone on the fibrous cap
prone to rupture
what is the usual cause for sudden onset MI symptoms
embolism secondary to plaque rupture and thrombus formation
what % of infarcts are caused by coronary artery atherosclerotic plaque erosion/thrombosis
90%
what is the lethal cellular even in MI
cell membrane ion pumps fail
which layer of the heart is most susceptible, comparatively, to infarction
subendocardium
infarction spreads from subendocardium to subepicardium in a WAVEFRONT phenomenon
changes seen in cardiac tissue in early MI/ischemic injury phase of MI
microscopic–>
- EM changes in myocytes and their membranes within first 15-20 min
- wary fibers–> intracellular edema
- coagulation necrosis–> hypereisonophilic myocytes
- contraction band necrosis–> compaction of Z lines of sarcomeres
macroscopic–>
- if no reperfusion of infarcted area, then pallor due to extrusion of erythrocytes from capillary bed
- if reperfused then hemorrhagic from blood vessel bursting
changes seen in cardiac tissue during the inflammatory stage of an MI
occurs from about 12 hours-5 days post MI
microscopic–>
- influx of PMNs (if there is no reperfusion then they collect at the borders of the infarct, and if there is reperfusion then they are distributed throughout the infarct)
- macrophages are seen after about 5 days
- myocyte nuclei start to disappear and myocytes become attenuated and separated as phagocytosis of myocytes occurs
macroscopic–>
1. yellow center with hyperemic border (not reperfused) or prominent hemorrhage (reperfused)
changes seen in cardiac tissue during the granulation tissue formation phase of an MI
occurs from about 1-3 weeks post MI
microscopic–>
- residual macrophages
- revascularization
- fibroblasts and early collagen formation
macroscopic–>
infarct turns from yellow to grey
changes seen in cardiac tissue during scar formation stage of MI
occurs from about 2-8 weeks post MI
microscopic–>
1. decrease in inflammatory cells with increasing collagen deposition and prominent capillary vessels
macroscopic–>
1. infarct changing from gray to white as collagenization becomes complete
what are some complications from infarctions
- death
- arrhythmias
- ventricular dysfunction
- cardiogenic shock
- recurrent infarction
- infarct expansion
- myocardial rupture
- RV infarction
- pericarditis
- mural thrombus
- ventricular aneurysm
what usually causes death from MI
ventricular arrhythmia (vent tachy or vent fib)
50% of people die from their MI
how do MIs lead to arrhythmias
arises from ischemic but non-infarcted tissue at the MI border zone
major determinant of post discharge mortality
when does cardiogenic shock occur as a result of MI
when infarction of over 40% of myocardium occurs
causes low CO and BP which exacerbates the ischemia
what is a transmural infarct
death of myocardium that extends from the endocardium to the epicardium as a result of MI