Methods and Procedures:
The patient had a complicated hospital course. Determining the etiology
for cardiac arrest was a challenge for the multidisciplinary team. A
CT-pulmonary angiogram ruled out pulmonary embolism. A transthoracic
echocardiogram showed no intracardiac thrombus or valve vegetation and a
48% ejection fraction. A 72-hour holter was normal.
A family history of cardiomyopathy, CAD, sudden cardiac death, or any
inborn errors of metabolism was negative. There was no history of
smoking, alcohol intake, illicit drug use, over-the-counter pills,
supplements, or herbal medications.
Traditional risk factors of CAD, including dyslipidemia, diabetes,
hypertension, or hypercoagulability, were absent. The hypercoagulability
workup revealed no abnormality in PT, aPTT, fibrinogen, protein C,
protein S, Antithrombin III deficiency, factor V Leiden and homocysteine
levels.
An extensive workup for any cause of immunocompromise was unrevealing
except for the ANA panel. HIV antibodies and serology for hepatitis A,
B, and C were all negative. ANA titer was 1:160, and repeated titer was
1:40. The patient had no other clinical or laboratory features
suggestive of auto-immune diseases. Anticardiolipin, Lupus
anticoagulant, ANCA, anti-double stranded-DNA, anti-Jo, anti-Ro,
anti-LA, anti-RNP, anti-Scl-70, anti-Smith, C3, and C4 were
unremarkable.
The CMV IgG and IgM were elevated along with high serum CMV-PCR titers.
The histopathological examination of the colon showed active CMV
colitis. Also, of note are the patient’s liver enzymes found elevated on
a regular health screen before the cardiac arrest. The liver enzymes
started to improve with ganciclovir treatment. Coronary angiography
showed a complete LAD plaque with small thrombus leading to occlusion.