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Cardiovascular Pathology
Wednesday, March 28, 2007, 7:30 PM
Convention Center 4
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Moderator:
ALLEN B. BURKE
University of Maryland School of Medicine
Baltimore, MD
Disclosure: The speakers have indicated they have nothing to disclose.
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for Text and References
Submitted by: Elena Ladich - CVPath Institute, Inc., Gathersburg, MD
34 year old white woman, 5'4", 128 lbs, with prior history of myocardial infarction and stent placement two years ago; complained of chest pain en route to hospital where she had an acute myocardial infarction.
Case 1 - Slide 1
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Case 1 - Figure 1 - Platelet-rich thrombus around stent strut with persistent peri-strut fibrin (Movat x 10)
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Case 1 - Figure 2 - Lumen with occlusive platelet-rich thrombus (Movat x 2)
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for Text and References
Submitted by: William D. Edwards - Mayo Clinic, Rochester, MN
A 51-year-old man had a history of carotid endarterectomy for stenosis due to atherosclerosis. He had recently undergone cardiac catheterization for coronary angiography.
Two weeks later, he developed a swollen, tender, reddened lesion on his right wrist. The pre-operative diagnosis was an infectious process with a possible pseudoaneurysm of his right radial artery.
Soft tissue cultures, taken from the right wrist at the time of operation, were negative for bacteria, fungi, and mycobacteria. In addition, GMS and AFB stains were negative in slides from the surgically resected tissue.
Case 2 - Slide 1
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for Text and References
Submitted by: Jagdish Butany - Toronto General Hospital, Toronto, ON, Canada
Mr. MC, a 61-year-old male from Newfoundland, had ischemic heart disease. (1st M.I.in 1987). He did not have any revascularization, or other interventions. He had an AID implanted in 2002 and had one episode of "shock"(upgraded to a biventricular Guidant H190 device, in 2004). Medications included - Lisinopril, Digoxin, Coreg, Lasix, Aspirin, Gabapentin, Allopurinol and Triazolam. His functional cardiac status was severely limited and he was a NYHA class 3. In 2002, he was considered, but rejected for heart and heart/lung transplantation, because of severe fixed pulmonary hypertension associated with hemoptysis.
In 2006, he had repeated admissions for exacerbation of heart failure, requiring intravenous diuretic therapy. He did not need inotropic therapy on any of these occasions.
He was considered for mechanical support and then in July 2006 was once again evaluated for destination mechanical support. For destination (VAD) therapy, the HeartMate 2 was the only one available as part of a clinical trial and , he was randomized into the HeartMate trial. On 2nd November he had insertion of the HeartMate LVAD, and a single CABG to the RCA.
Post-operatively he developed fever, leukocytosis, thrombocytopenia and a persistent watery diarrhea (history of ulcerative colitis and repeated prednisone therapy) felt to be an exacerbation of is ulcerative colitis. No source of infection was identified, though a chest x-ray suggested the possibility of pneumonia. He began to deteriorate on post-operative day 9 -10 and on the 12th of November, he had an episode of atrial fibrillation and later ventricular tachycardia that was converted to atrial fibrillation by his ACID.
His urine output was decreasing, blood pressure falling, potassium rising and oxygen requirements increasing. On Nov.13, he was started on hemodialysis. Soon after he became increasingly hypotensive and his blood pressure could not be restored despite manipulation of the VAD,. He died on day 11 postoperative day 11.
Case 3 - Slide 1
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Case 3 - Figure 1
The left side of the heart has been opened and shows the atrium , mitral valve and the left ventricle. The LV apex shows the inflow cannula (A) of the LVAD in place . The LVAD pump has been disconnected. The outflow cannula (B) is also seen. The LV endomyocardium close to the cannula, shows an interesting lesion, which was sectioned. -
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Case 3 - Figure 2
A low power section from the H&E stained slide shows the interventricular septum. (Stain H&E, Original Magnification x2.5) -
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Case 3 - Figure 3
A higher magnification of the upper boxed area , from the slide #1. (Stain H&E, Original Magnification x 10.0, ) -
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Case 3 - Figure 4
A higher magnification of the upper boxed area from slide # 2. (Stain H&E, Original Magnification x 20.0) -
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Case 3 - Figure 5
A higher power image from the lower box from slide #2,showing the Right ventricular aspect of the IV septum. (Stain H&E, Original Magnification x2.5) -
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for Text and References
Submitted by: Michael C. Fishbein - David Geffen School of Medicine at UCLA, Los Angeles, CA
Fourteen year old male born with restrictive VSD and RVOT obstruction. At age 5 months, the VSD was closed and RVOT tissue excised. Over the years, the patient developed progressive aortic regurgitation requiring valve repair at age 11. The patient did well initially, but then developed recurrent aortic regurgitation. At age 14, the patient underwent aortic replacement. Tissue on slide represents the excised aortic valve.
Case 4 - Slide 1
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Case 4 - Figure 1 - Diagram showing aortic view of bicuspid aortic valve after repair with pericardial extension.
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Case 4 - Figure 2 - Diagram showing side view of bicuspid aortic valve after repair with pericardial extension.
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Case 4 - Figure 3 - Kaplan-Meier curve showing freedom from reoperation after pericardial extension of aortic valve leaflets in children.
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Case 4 - Figure 4 - Kaplan-Meier curve showing freedom from reoperation after pericardial extension of aortic valve leaflets in adults.
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Case 4 - Figure 5 - Histologic sections showing junction of native valve (NV) and pericardial tissue valve (PV) after pericardial extension of aortic valve leaflets (2 left panels, H&E and trichrome x40). Third panel shows higher magnification of native valve tissue (x100) and 4th panel shows suture site (S) with pericardial tissue (P) covered by fibrosis (F)(x200).
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Case 4 - Figure 6 - Gross photograph of inflow and outflow surfaces of aortic valve after pericardial extension. Note white fibrous tissue and focal calcification (yellow) of leaflets.
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Case 4 - Figure 7 - Another gross example of inflow and outflow surfaces of aortic valve after pericardial extension.
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Case 4 - Figure 8 - Histologic section showing junction of native tissue (NT) and pericardial tissue (PT) with overlying fibrosis (F). Von Kossa stain confirms the presence of calcification (left x40, center x100, right x200).
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Case 4 - Figure 9 - Histologic sections of junction of native tissue (NT) and pericardial tissue (PT) with suture present (arrow) (H&E x100). Note connective tissue proliferation with myxoid change present.
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