CV WebPath Flashcards
1
Q
This is the left ventricular wall. What is going on?
A
- This is the left ventricular wall which has been sectioned lengthwise to reveal a large recent myocardial infarction
- The center of the infarct contains necrotic muscle that appears yellow-tan
- Surrounding this is a zone of red hyperemia
- Remaining viable myocardium is reddish- brown.
2
Q
What is going on here?
A
- This cross section through the heart shows the larger left ventricular chamber and the small right ventricle
- Extending from the anterior portion and into the septum is a large recent pale myocardial infarction. The center is tan with surrounding hyperemia
- This infarction is “transmural” because it extends through the full thickness of the ventricular wall
3
Q
What do you see?
A
- Earliest change histologically seen with acute myocardial infarction in the first day is contraction band necrosis
- Myocardial fibers are beginning to lose cross striations and the nuclei are not clearly visible in most of the cells seen here
- Note the many irregular darker pink wavy contraction bands extending across the fibers
4
Q
What do you see?
A
- High power microscopic view of the myocardium demonstrates an infarction of about 1 to 2 days in duration
- Myocardial fibers have dark red contraction bands extending across them. The myocardial cell nuclei have almost all disappeared
- Beginning acute inflammation
- Clinically, such an acute myocardial infarction is marked by changes in the electrocardiogram and by a rise in the MB fraction of creatine kinase
5
Q
What do you see?
A
- In this microscopic view of a recent myocardial infarction, there is extensive hemorrhage along with myocardial fiber necrosis with contraction bands and loss of nuclei
6
Q
What do you see?
A
- This myocardial infarction is about 3 to 4 days old. There is an extensive acute inflammatory cell infiltrate and the myocardial fibers are so necrotic that the outlines of them are only barely visible
7
Q
What do you see?
A
- This is an intermediate myocardial infarction of 1 to 2 weeks in age
- Note that there are remaining normal myocardial fibers at the top
- Below these fibers are many macrophages along with numerous capillaries and little collagenization
8
Q
What do you see?
A
- At 3 to 4 weeks of age the intermediate myocardial infarction shown involving a papillary muscle at low power above and medium power below have decreasing cellularity along with more prominence of collagen
- Note the remaining normal red myocardial fibers. Cardiac biomarkers are not positive at this stage and myocardial rupture is unlikely. The degree of cardiac failure depends upon the extent of myocardial loss
9
Q
What do you see?
A
- Myocardium shown demonstrates pale fibrosis with collagenization following healing of a myocardial infarction. There is minimal cellularity; a few remaining viable red myocardial fibers are present
- This stage is reached about 2 months following the initial ischemic event. This collagenous scar is nonfunctional for contraction and will diminish the ejection fraction
- Such a scar will not rupture
10
Q
What do you see?
A
- Heart is opened to reveal the left ventricular free wall on the right and the septum in the center. There has been a remote myocardial infarction that extensively involved the anterior left ventricular free wall and septum
- The white appearance of the endocardial surface indicates the extensive scarring
11
Q
What do you see?
A
- One complication of a transmural MI is rupture of the myocardium. This is most likely to occur in the first week between 3 to 5 days following the initial event, when the myocardium is the softest
- White arrow marks the point of rupture in this anterior-inferior myocardial infarction of the left ventricular free wall and septum
- Note dark red blood clot forming hemopericardium. The hemopericardium can lead to tamponade
12
Q
What do you see?
A
- Previous extensive transmural MI involving the free wall of the left ventricle. Note that the thickness of the myocardial wall is normal superiorly, but inferiorly is only a thin fibrous wall
- Infarction was so extensive that, after healing, the ventricular wall replaced by thin band of collagen, forming an aneurysm. Such an aneurysm represents non-contractile tissue that reduces stroke volume and strains the remaining myocardium. Stasis of blood in aneurysm predisposes to mural thrombosis.
13
Q
What do you see?
A
- A cross section through the heart reveals a ventricular aneurysm with a very thin wall at the arrow
- Note how the aneurysm bulges out
- The stasis in this aneurysm allows mural thrombus, which is present here, to form within the aneurysm
14
Q
What do you see?
A
- There is a tear (arrow) located 7 cm above the aortic valve and proximal to the great vessels in this aorta with marked atherosclerosis. This is an aortic dissection
15
Q
What do you see?
A
- Microscopically, the tear (arrow) in this aorta extends through the media, but blood also dissects along the media (asterisk)
16
Q
What do you see?
A
- This aorta has been opened longitudinally to reveal an area of fairly limited dissection that is organizing. The red-brown thrombus can be seen in on both sides of the section as it extends around the aorta. The intimal tear would have been at the left. This creates a “double lumen” to the aorta
- This aorta shows severe atherosclerosis which, along with cystic medial necrosis and hypertension, is a risk factor for dissection
17
Q
What do you see?
A
- Here, the dissection went into the muscular wall. In any case, an aortic dissection is an extreme emergency and can lead to death in a matter of minutes. The blood can dissect up or down the aorta
- Blood dissecting up around the great vessels can close off the carotids. Blood can dissect down to the coronaries and shut them off
18
Q
What do you see?
A
- Right carotid artery compressed by blood dissecting upward from a tear with aortic dissection. Blood may also dissect to coronary arteries
- Patients with aortic dissection may have symptoms of severe chest pain (for distal dissection) or may present with findings that suggest a stroke (with carotid dissection) or myocardial ischemia (with coronary dissection)
19
Q
What do you see?
A
- This aortic dissection occurred just above the aortic root in a patient with Marfan’s syndrome
- The tear extends across the aorta
- Hemopericardium with tamponade occurred within minutes of this event
20
Q
What do you see?
A
- Mitral valve is shown in the same patient with Marfan syndrome. The leaftlets of the mitral valve are redundant, and the one on the far left is ballooned upward
- Characteristic of floppy mitral valve with mitral valve prolapse. The chordae tendineae that hold the leaflets become long and thin
21
Q
What do you see?
A
- Miitral valve in a patient with Marfan’s syndrome depicts a floppy mitral valve
- The leaflet on the lower left has ballooned upward and the prolapse has resulted in contusion of the top of the leaflet, with a red black area of discoloration
22
Q
This is a mucin stain of the wall of the aorta. What do you see?
A
- Demonstrates cystic medial necrosis, typical for Marfan’s syndrome and causes the connective tissue weakness that explains the aortic dissection
- Pink elastic fibers, instead of running in parallel arrays, are disrupted by pools of blue mucinous ground substance
23
Q
What do you see?
A
- Infective endocarditis
- Aortic valve demonstrates a large, irregular, reddish tan vegetation. Virulent organisms, such as Staphylococcus aureus, produce an “acute” bacterial endocarditis, while some organisms such as Streptococcus viridans group produce a “subacute” bacterial endocarditis
24
Q
What do you see?
A
- The small pink vegetation on the rightmost cusp margin represents the typical finding with non-bacterial thrombotic endocarditis (or so-called “marantic endocarditis”). This is non-infective
- It tends to occur in persons with a hypercoagulable state (Trousseau’s syndrome, a paraneoplastic syndrome associated with malignancies) and in very ill persons.
25
Q
What do you see?
A
- Marantic vegetation (non-bacterial thrombotic endocarditis) on the leftmost cusp
- These vegetations are rarely over 0.5 cm in size
- Friable and very prone to embolize
26
Q
What do you see?
A
- Flat, pale tan, spreading vegetations over mitral valve surface and on chordae tendineae
- This pt has systemic lupus erythematosus, so these vegetations are consistent with Libman-Sacks endocarditis
- Appear in about 4% of SLE pts and rarely cause problems bc they are not large and rarely embolize
- Thickened, shortened, fused chordae tendineae that represent remote rheumatic heart disease
27
Q
What do you see?
A
- Small verrucous vegetations seen along the closure line of this mitral valve are associated with acute rheumatic fever
- These warty vegetations average only a few millimeters and form along the line of valve closure over areas of endocardial inflammation
- Such verrucae are too small to cause serious cardiac problems
28
Q
What do you see?
A
- This two year old child died suddenly. At autopsy, a large firm, white tumor mass was found filling much of the left ventricle
- This is a cardiac rhabdomyoma. Such primary tumors of the heart are rare, and are seen mainly in children.
29
Q
What do you see?
A
- Primary tumors of the heart are uncommon.
- Metastases to the heart are more common, but rare overall (only about 5 to 10% of all malignancies have cardiac metastases). Seen over the surface of the epicardium are pale white-tan nodules of metastatic tumor
- Metastases may lead to a hemorrhagic pericarditis.
30
Q
What do you see?
A
- The neoplasm with the greatest propensity to metastasize to heart is melanoma. The metastatic melanoma is seen here to be infiltrating into the myocardium
- At the arrow can be seen some brown-black pigment characteristic of melanoma.
