BackgroundThe development of left ventricular systolic dysfunction (LVSD) after liver transplant (LT) can result in increased morbidity and mortality in the immediate period following liver transplant. The aim of this study was to evaluate low muscle mass due to chronic liver disease, as a potential risk factor for LVSD after LT.Material/MethodsA retrospective chart review was completed for all adult patients who received a liver transplant between January 2002 and January 2015 at a single academic LT center. Collected data included patient demographics, medical history, laboratory data, radiology results, and pathology. Echocardiograms were reviewed for patients identified as having LVSD diagnosed within 1 year after LT (left ventricular ejection fraction <55%). The total psoas area (TPA), a marker of low muscle mass, was determined by measuring the average cross-sectional area of the psoas muscle on MRI or CT scans before transplant at the level of L4 vertebra.ResultsOf the 503 post-LT patients reviewed, 144 (28.6%) had pre-and post-LT echocardiograms. Of these 144 patients, 17 developed LVSD, of which 15 (88.2%) occurred within 1 year after LT. The average age at transplant of those with LVSD was 58.9±6 years, with a mean MELD score of 30.7±6. The mean TPA normalized for height for patients with LVSD was 297.68±86.99 mm2/m2 compared to 382.1±104.2 mm2/m2 for those with normal EF (p= 0.002). BMI, MELD score, and etiology of cirrhosis were not significant risk factors for post-LT LVSD in our study population. During the study period, 35.2% (n=6) of LVSD patients died within 1 year after LT.ConclusionsAlthough LVSD is thought to be a rare complication after LT, those with muscle loss as predicted by mean TPA measurements normalized for height may be at highest risk.

BackgroundWall stress is a useful concept to understand the progression of ventricular remodeling. We measured cumulative LV wall stress throughout the cardiac cycle over unit time and tested whether this “integrated wall stress (IWS)” would provide a reliable marker of total ventricular workload.Methods and resultsWe applied IWS to mice after experimental myocardial infarction (MI) and sham-operated mice, both at rest and under dobutamine stimulation. Small infarcts were created so as not to cause subsequent overt hemodynamic decompensation. IWS was calculated over one minute through simultaneous measurement of LV internal diameter and wall thickness by echocardiography and LV pressure by LV catheterization. At rest, the MI group showed concentric LV hypertrophy pattern with preserved LV cavity size, LV systolic function, and IWS comparable with the sham group. Dobutamine stimulation induced a dose-dependent increase in IWS in MI mice, but not in sham mice; MI mice mainly increased heart rate, whereas sham mice increased LV systolic and diastolic function. IWS showed good correlation with a product of peak-systolic wall stress and heart rate. We postulate that this increase in IWS in post-MI mice represents limited myocardial contractile reserve.ConclusionWe hereby propose that IWS provides a useful estimate of total ventricular workload in the mouse model and that increased IWS indicates limited LV myocardial contractile reserve.

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