7:30 PM, Monday, March 24
Delaware, Suite A
Attack of the Killer T Cells
(Inflammation in Cardiovascular Disease)
Gayle L. Winters
Brigham and Women's Hospital
Click on each slide thumbnail image for an enlarged view
Allen P. Burke
Armed Forces Institute of Pathology
A 60 year old white male, 5'11", 180 lbs., complained of chest pain one day prior to being found
unresponsive on the ground in front of his home. He had a history of thyroid problems, asthma, and recent
sinus infection. He was taking anti-allergy medicines [Advair Discus (fluticasone/salmeterol), Allegra-D
(fexofenadine & pseudoephedrine), Atrovent (ipratropium bromide), Nasonex (mometasone furoate), and
Singulair (montelukast)], an antibiotic [Cefzil (cefprozil)], and Synthroid (levothyroxine). At autopsy,
his heart weighed 400 grams; the foramen ovale was probe patent; left ventricular chamber dimensions were
normal; there was mild right ventricular hypertrophy (6 mm thick at posterior wall); and there were focal
myocardial scarring and hyperemia in the posteroseptal left ventricle and posterior right ventricle. A
section of the proximal right coronary artery is available for review.
Bruce M. McManus
University of British Columbia
Vancouver, British Columbia
A 54-year-old female dentist had a 5-day history of 'flu-like' symptoms (including cough, fatigue,
shortness of breath chills and malaise). On admission to hospital for shortness of breath and an
inability to sleep, she was found to have left ventricular failure, cardiogenic shock and marked
hypoxemia. She then developed uncontrollable cardiac arrhythmias, became profoundly hypotensive,
terminating in ventricular tachycardia and death on the same day.
A 27-year-old female was admitted to hospital with a 5 day history of exertional chest pain and dyspnea.
Her initial ECG demonstrated ST elevation in the anteroseptal leads, ST depression laterally, complete
atrioventricular block and frequent premature ventricular complexes. She deteriorated clinically during
the first 48 hours, with worsening of hypotension and heart failure requiring inotropic support and
intubation. Novel therapies resulted in improvement of the patient's condition by 6 days after initial
Henry D. Tazelaar
A 79 year-old woman with reactive airways disease and systemic hypertension presented with increasing
dyspnea, fever and cough. A chest radiograph showed bilateral apical infiltrates and a dilated aorta.
Sputum cultures grew H. influenzae. Subsequent transesophageal echo showed a 5.3 cm diameter ascending
aortic aneurysm and marked aortic insufficiency. She underwent surgery at which time a large aortic
aneurysm involving the aortic root and ascending aorta was identified. The aorta was normal distally.
The wall was not obviously thickened, the aneurysm was resected and a graft placed. The specimen
received in pathology was an opened portion of aorta measuring 9.4 x 5.1 x 0.1 cm. The endothelial
surface was unremarkable.
Richard N. Mitchell
Brigham and Women's Hospital
The patient was a 34 year old male with a history of congenital heart disease (D-transposition of the
great arteries); a Mustard repair procedure at age 4 was complicated by right phrenic nerve damage and
right diaphragmatic paralysis. He subsequently developed progressive failure of his systemic ventricle,
and underwent cardiac transplantation in 1990 (at the age of 22); his post-transplant immunosuppression
consisted of cyclosporine A, azothioprine, and corticosteroids. His course was notable for two episodes
of acute rejection in the first year following transplantation, treated with solumedrol boluses. In
addition, within 4 months of transplant, he developed a post-transplant lymphoma in a left submandibular
node. This was resected, and he experienced no further recurrence after his immunosuppressive therapy
was slightly tapered. Other complications included obesity (eventually developing Pickwickian
symptomatology), hypertension, osteoporosis, and hyperlipidemia.
The patient had annual angiographic evaluation of his coronaries; beginning approximately 10 years after
transplant, diffuse coronary artery disease was first seen, most apparent in the smaller coronary
arteries. Intravascular ultrasound also documented moderate-severe diffuse epicardial vessel disease
with up to 85% chronic stenoses. Beginning 11 years after transplant, the patient developed progressive,
severe exertional dyspnea and biventricular failure (R>L), although ejection fractions were largely
maintained; moderate pulmonary hypertension was documented. PFT's documented profound restrictive and
obstructive lung disease; although he was found to be a carrier for cystic fibrosis, his findings were
felt overall to be most consistent with central neurogenic hypoventilation.
The patient presented terminally with right lower abdomenal discomfort; CT evaluation showed only mild
thickening of the distal ileum and he was discharged to be worked up electively. He subsequently
suffered a cardiac arrest at home, and could not be resuscitated. Slides available for review are a
representative coronary artery and myocardium from the failed allograft.