Table 1. Echocardiography parameters and relative blood volume change(%) before, two hours after hemodialysis started and at the end of

hemodialysis.

Variables Pre-HD Hour 2 Post-HD p-valuea

Blood volumechange (%)

- -6.8 (3.9-7.5) -9.3 (6.0-11.8) 0.004

Mitral E velocity(cm/s)

102 (88-136) 83 (78-94)b 98 (78-111) 0.097

Septal e’ velocity(cm/s)

6.5 (6-7) 6 (6-8) 6 (5-7) 0.22

E/septal e’velocity (cm/s)

14.9 (11.0-22.7) 13.8 (9.8-17.2) 16.4 (12.3-22.2) 0.12

LVEDV (mL) 123 (80-143) 88 (69-101 )b 115 (72-130) 0.03LVESV (mL) 44 (35-62) 38 (29-43) � 42 (25-49)b 0.003LVEF (%) 58 (50-61) 61 (52-62) 63 (61-65)b 0.03GLS (%) -11.9 (9.6-13.0) -11.7 (10.2-13.6) -11.2 (8.8-12.8) 0.72

Data were expressed as median (interquartile range).Abbreviations: HD, hemodialysis; LVEDV, left ventricular end diastolic volume; leftventricular end systolic volume; left ventricular ejection fraction; GLS, globallongitudinal strain.a p-value for the overall change,b p!0.05 and c p!0.01 when compared to pre-dialysis values.

Figure 1. Percent change in blood volume, left ventricular volume, left ventricularejection fraction and global longitudinal strain (A) and diastolic parameters (B)when compared to pre-dialysis values. Data was expressed as median.Abbreviations:as Table.

S18 Journal of Cardiac Failure Vol. 20 No. 8S August 2014

subcutaneously every 14 days over the course of 1 month. Cardiac function was as-sessed by echocardiography. Neurohormones were measured by RIA. Fibrosis wasdetermined by picrosirius red staining. Results: Chronic treatment of ISP in diabeticrats had a significant effect on blood glucose and plasma insulin levels. ISP improvedrenal function and structure as measured by reductions in plasma creatinine and pro-teinuria with decreased renal medullary fibrosis. However, it did not affect LVfibrosis or hypertrophy. Table 1.Conclusion: This novel peptide stimulates insulinsecretion and lowers blood glucose with improved renal function and structure inthis rodent model of experimental diabetes.

045Congruity between Mental Stress-Induced and Adenosine-Induced MyocardialIschemia Assessed Using SPECT in Heart Failure PatientsStephen S. Gottlieb1, Vasken Dilsizian1, Andrew J. Wawrzyniak2, Mark Smith1,Kristie M. Harris2, Kerry Whittaker2, David Krantz2; 1University of Maryland,Baltimore, MD; 2Uniformed Services University of the Health Sciences, Bethesda,MD

Background: Mental stress can trigger myocardial ischemia in a substantial percent-age of patients with coronary artery disease, but the prevalence of mental stressinduced ischemia is unknown in patients with heart failure. Increased neuroendocrineactivation in these patients could significantly impact the effects of mental stress oncoronary blood flow and myocardial perfusion.Objective: The purpose of the currentstudy was to characterize mental stress-induced versus adenosine-induced changes inmyocardial ischemia in heart failure patients with reduced LV function using single-photon emission computed tomography (SPECT) to objectively and precisely quan-tify segment-level myocardial perfusion. Methods: Entry criteria included a historyof heart failureO 3 months, ejection fraction! 40%, and clinically proven coronaryartery disease. Subjects were administered a standard 6-minute adenosine stresstest. Mental stress consisted of anger recall (4-minute speech about a recent anger-provoking incident) followed by mental arithmetic (verbally subtracting serial 7swhile being urged to improve performance). Ischemia was quantified using sepa-rate-acquisition dual-isotope myocardial perfusion SPECT, with 17 segments classi-fied as normal, ischemic, or scar tissue. Results: There were 31 men and 3 women(age: 62 6 10 years). Although all subjects had known coronary disease, only onereported ongoing angina. 68% had at least one ischemic segment during mentalstress; 81% had at least one ischemic segment during adenosine. On a segment-by-segment analysis, perfusion in each type of stress was highly correlated (rho range:0.436 - 0.915, p ! .013, see figure). No significant differences were found betweenany two time points for BNP, TNF-alpha, IL-1b, troponin, VEGF, IL-17a, MMP-9, orCRP. ET-1 and IL-6 significantly increased between the stressor and 30 minutes post-stress, p 5 0.028, and p 5 0.046, respectively; IL-10 significantly decreased betweenthe same time points, p 5 0.035). Conclusion: There was a high concordance be-tween ischemic perfusion defects induced by adenosine and mental stress. This sug-gests that in heart failure patients, mental stress is equivalent to pharmacologic stresstesting in eliciting clinically significant defects in myocardial perfusion. Psychosocialstressors during daily life may contribute to the ischemic burden of heart failure pa-tients who have coronary artery disease.

Figure.

046Global Longitudinal Strain of Left Ventricle and Tissue Doppler Velocity atMitral Annulus are Not Significantly Affected by Changes in Blood VolumeDuring Hemodialysis SessionSrisakul Chirakarnjanakorn, Lily Tranchito, Timothy Engelman, Zoran B. Popovi�c,Martin E. Lascano, Allen G. Borowski, W.H. Wilson Tang; Cleveland Clinic,Cleveland, OH

Introduction: Effects of hemodialysis (HD) on several echocardiographic parame-ters have been demonstrated. Decrease in preload may affect these changes.

However, the evolution of these parameters during HD session at each time pointcompared to blood volume (BV) change has not been well studied. Hypothesis:We sought to study that 1) whether echocardiographic parameters change alongHD session and 2) whether there is correlation between changes of those parametersand BV changes. Methods: We prospectively studied 8 patients (age 5869 years,87% female) who have been receiving maintenance HD for $ 3 months at ClevelandClinic between February and March 2014. Comprehensive echocardiography wasperformed before, at 2 hours after HD started and at the end of HD. Global longitu-dinal strain (GLS) was derived from the average of 18 segments in the 3 apical viewsof left ventricle (LV) by 2D speckle tracking. Relative BV change was calculated bychanges in hematocrit derived from the Crit-Line monitoring. Results: At 2 hours af-ter HD started, LV volume in both of diastole and systole as well as mitral inflow Evelocity significantly decreased (p50.021, 0.008 and 0.038, respectively). At the endof HD, despite BV was continuingly decreasing, there were no significant changes ofall echocardiographic parameters compared to those at 2 hours after HD started. OnlyLVend systolic volume and LVejection fraction significantly changed at post-dialysiswhen compared to pre-dialysis values. Although LV ejection fraction and mitralinflow E velocity significantly changed, GLS as well as septal e’ velocity did notchange significantly (Table 1). There was no significant correlation between neitherBV changes or ultrafiltration rate and change in echocardiographic parameters(Figure 1). Conclusions: Global longitudinal strain of LVand tissue Doppler velocityof mitral annulus are less affected by preload reduction from HD than volumetricechocardiographic methods. Nevertheless, there are no correlations between changesof relative blood volumes and echocardiographic parameters. Further larger studiesare needed to seek the plausible mechanisms of these changes.

047Cirrhotic Cardiomyopathy; Does It Really Exist?Ahmed Ibrahim1, Andres Schuster1, Abraham Sonny2, Jacek B. Cywinski2, Wael A.Jaber1; 1Cleveland Clinic Foundation, Cleveland, OH; 2Cleveland Clinic Foundation,Cleveland, OH

Background: For the last two decades, cirrhotic cardiomyopathy (CCM) has beensuggested as a major cause of cardiovascular decompensation in end stage liver

The 18th Annual Scientific Meeting � HFSA S19

disease (ESLD) patients after liver transplantation (LT) and Transjugular intrahepaticportosystemic shunt placement, independently of ESLD cause.The classic CCM diagnostic criteria include diastolic dysfunction (DD), decreasedchronotropic response leading to non-diagnostic stress test (NDST) and prolongedQTc interval. There is no data available in a large series of patients to support theexistence of this cardiovascular entity. The aim of this study is to assess theprevalence of CCM criteria in a large group of ESLD and compared it to matchednon-ESLD controls. Methods: We retrospectively assessed 204 patients from theCleveland Clinic LT database between the years 2012 to 2013. Clinical characteris-tics obtained from the electronic records, echocardiograms, stress tests and EKG,swere analyzed by 2 independent observers in the standard manner: NDST if heartrate was !85% maximum predicted, prolonged QTc defined by O 440 msec inmen and O460 msec in women, and DD defined by diastology stage 1 or higherby American Society of Echocardiography guidelines definition. These patientswere compared to 74 matched controls with no history of liver disease. Results:The mean age was 5668 years and 68% were male. The causes of ESLD wereHCV in 30%, non-alcoholic steatetohepatitis or cryptogenic 18%, biliary 17%, andalcohol 16%. The mean Model for ESLD (MELD) score was 156 6, 81% of patientswere Child B or C, 43% were hypertensive, 48% diabetic, 14% had CKD and 14%had history of CAD. All patients had normal LVEF (O50%), and there were no sig-nificant valvular disease.Compared to controls, patients with ESLD had a higher CO (5.662 vs. 4.461.2 L/min; p50.001), left atrial (LA) volume index (34610 vs. 2467 ml/m2; p!0.001),LV end diastolic volume index (57617 vs. 49.5612 ml/m2; p50.001, mitral valveE inflow velocity (86 6 25 vs. 75620 cm/sec; p!0.001), and septal andlateral E’ velocities (8.562 vs. 762 cm/sec; p!0.001 and 1163 vs. 8.863 cm/sec; p!0.001, respectively).There was no difference in E/E’ ratio, relative wall thickness and LV mass index be-tween ESLD and controls. From the CCM criteria, prolonged QTc interval had a sig-nificant difference between groups (52.5% in ESLD vs. 19% in controls; p50.0001),while there was no difference in prevalence of DD (58 vs. 59%; p50.9) or NDST (25vs. 22%; p50.7) after adjusting for Beta Blockers use, cause of ESLD or MELDscore. Conclusions: The existence of the CCM as an entity is not supported byour study, where only a prolonged QTc was more prevalent in the ESLDpatients but not DD nor NDST. The patients with ESLD presented with a hyperdy-namic state manifested by increased CO, LA, LV volumes and mitral valve inflowvelocities.

048Natriuretic Response to Diuretic Therapy in Decompensated Heart Failure withReduced Ejection Fraction and Volume OverloadFrederik H. Verbrugge1, Matthias Dupont1, Philippe B. Bertrand1, Petra Nijst1, JorisPenders1, Joseph Dens1, David Verhaert1, Pieter Vandervoort1, W.H. Wilson Tang2,Wilfried Mullens1; 1Ziekenhuis Oost-Limburg, Genk, Belgium; 2Cleveland Clinic,Cleveland, OH

Background: The natriuretic response to diuretics, the mainstay treatment in acutedecompensated heart failure (ADHF), is insufficiently elucidated. Methods: Consec-utive ADHF patients (n554) with left ventricular ejection fraction #45% andplanned treatment with intravenous loop diuretics were included. Patients receivedprotocol-driven diuretic therapy until complete disappearance of congestion signs.Urine was collected during three consecutive 24h intervals. Results: Per mg

Figure 2.

Figure 1.

bumetanide administered, natriuresis was 146 mmol (76-206 mmol), 74 mmol (37-167 mmol) and 74 mmol (53-134 mmol) during the first, second and third 24h-inter-val, respectively. Diastolic blood pressure (b523.048610.788; P-value50.036),plasma aldosterone (b525.722611.560; P-value50.029), and combination therapywith acetazolamide (b5103.241640.962; P-value50.014) were independent predic-tors of natriuresis (Table). Patients with a stronger natriuretic response demonstratedmore pronounced decreases in plasma NT-proBNP levels (P-value50.025; Figure2A), while a weaker response was associated with higher peak plasma aldosteronelevels (P-value50.013; Figure 2B) and plasma renin activity (P-value50.033; Figure2C). Natriuresis per loop diuretic dose predicted freedom from all cause mortality or