Cardiology I Flashcards
Remote thrombosis with recanalization
2 small, narrow channels
Atherosclerosis of coronary artery
Severe narrowing
Blue area = calcification
Pink to red recent thrombosis in narrowed coronary artery
Lumen occluded
Cholesterol clefts (narrow white spaces)
High magnification of atheroma shows many foam cells & occasional cholesterol cleft
Some dark blue inflammatory cells
Aortic atherosclerosis (mild-bottom to severe-top)
Top has extensive ulcerations
Abdominal aortic aneurysm
Bulge just above aortic bifurcation
Prone to rupture
Pulsatile mass on PE
Microscopic cross section of aorta
Large atheroma on left (contains cholesterol clefts)
Far left - hemorrhage
Foam cells + cholesterol clefts
Severe aortic atherosclerosis
Atheromatous plaques have ulcerations + formation of mural thrombus
Cholesterol clefts
Cholesterol emboli rare
Left coronary artery from aortic root on left
Extending across middle of picture to right is anterior descending branch
Severe atherosclerosis w/ extensive calcification + significant narrowing (far right)
Coronary atherosclerosis complicated by hemorrhage into atheromatous plaque
May acutely narrow arterial lumen
Shows large LV and small RV
Pale region surrounded by hyperemia = MI from anterior to septum
Neovascularization around MI area
Transmural because extends thru full thickness of ventricular wall
Earliest change seen in MI (day 1) - CONTRACTION BAND NECROSIS
Myocardial fibers lose cross striation, lose nuclei, irregular dark pink wavy contraction bands extend across fibers
Infarction (1-2 days)
Dark red contraction bands on myocardial fibers
Almost all myocardial cell nuclei disappeared
Beginning of acute inflammation
Extensive hemorrhage + myocardial fiber necrosis w/ contraction bands & loss of nuclei
NOT FROM LECTURE
3-4 days old
Extensive acute inflam. cell infiltrate; myocardial fibers so necrotic, that outlines barely visible
Intermediate MI 1-2 weeks old
Normal remaining myocardial fibers at top
Below are many macrophages with many capillaries & little collagenization
LV free wall in R, septum in center
MI in anterior LV free wall & septum
White appearance of endocardial surface -> extensive scarring
Complication of MI = rupture myocardium
Most likely to occur in 3-5 days following initial event (myocardium softest)
White arrow = point of rupture (anterior-inferior MI of LV free wall & spetum)
Dark red blood clot in hemopericardium, risk for tamponade
Arrow = point of rupture
MI 3 weeks before & another MI occurred, rupturing through already thin ventricular wall 3 days later
Previous extensive transmural MI involving free wall of LV
Normal thickness of wall at top, but inferiorly, only THIN FIBROUS WALL. Infarction was so bad that after healing, ventricular wall was replaced by thin band of collagen -> ANEURYSM -> noncontractile -> decreased SV -> strain remaining myocardium.
Stasis of blood also predisposes aneurysm to mural thrombosis.
Ventricular aneurysm with thin wall
Increased risk for mural thrombus (present in pic)
Aortic dissection may lead to hemipericardium when blood dissects thru media proximally –> can lead to cardiac tamponade
Longitudinally opened aorta revealing limited dissection
Red-brown thrombus extends around aorta
Creates double lumen to aorta
Aorta dissection went into muscular wall
Blood can dissect up (close off carotids) or down (shut off coronaries) aorta