Baylor University Medical Center Proceedings April 2014, Volume 27, Number 2 | Page 106

Results: Three of these 5 patients had a history of progressive dyspnea,
and the anomalous cord, which was intact at operation, appeared to
cause chronic AR by preventing proper coaptation of the 2 aortic valve
cusps. The other 2 patients heard a “pop” during physical exertion and
immediately became dyspneic, and at operation, the anomalous cord
was found to have ruptured. Prolapse of the conjoined aortic valve cusp
toward the left ventricular cavity resulted in severe acute AR.
Conclusions: This variant of the purely regurgitant BAV may cause
either chronic AR (when the anomalous cord does not rupture) or
acute severe AR (when the cord ruptures).

JOURNAL OF HEPATOLOGY
Role of magnetic resonance elastography in compensated and
decompensated liver disease
Asrani SK, Talwalkar JA, Kamath PS, Shah VH, Saracino G, Jennings
L, Gross JB, Venkatesh S, Ehman RL
J Hepatol 2013 Dec 19 [Epub ahead of print]. Reprinted with permission from Elsevier.
Background and aims: Non-invasive predictors identifying subjects
with compensated liver disease at highest risk for transitioning to a
decompensated state are lacking. We hypothesized that liver shear stiffness as measured by magnetic resonance elastography is an important
non-invasive predictor of hepatic decompensation.
Methods: Among patients with advanced fibrosis undergoing magnetic
resonance elastography (2007–11), a baseline cohort and follow up
cohort (compensated liver disease) were established. Cause specific
Cox proportional hazards analysis adjusting for competing risks was
utilized to determine the association between elevated liver shear stiffness and development of decompensation (hepatic encephalopathy,
ascites, f&