The 18th Annual Scientific Meeting � HFSA S41

furosemide infusion, impaired natriuretic response to furosemide is associated withgreater likelihood of worsening renal function and future adverse long-term outcomesthat is independent and incremental to intrinsic glomerular filtration.

Table. Baseline and changes in hemodynamics, stratified by PVR # or O 5Wood units on follow up

PVR # 5 WU(n 5 49)

PVR O 5 WU(n 517) P value*

BaselinePVR (WU) 5.1 [3.6, 5.9] 6.0 [5.1, 8.4] 0.008TPG (mmHg) 16 [13, 20] 22 [20, 23] 0.012DPG (mmHg) 4 [1, 7] 9.5 [5, 12] 0.017CI (L/min/m2) 1.62 [1.39, 1.81] 1.47 [1.33, 1.64] 0.108

ChangesD in PVR (WU) -1.7 [-3.3, -0.5] 0.3 [-1.8, 1.0] 0.004D in mean PA -9 [-15, -1] 2 [-1, 3] !0.0001

099Treating Rapid Atrial Fibrillation in Acute Decompensated Heart Failure:Metoprolol and Diltiazem are Equally Safe, yet Metoprolol IncreasesConversion to Sinus RhythmFarhan Katchi, Shashikanth Nagabandi, Jerrica Shuster, Eric Novak, Susan Joseph;Washington University School of Medicine, Saint Louis, MO

Objective: We sought to determine the difference in efficacy and safety between betaand calcium channel blockade for the acute treatment of atrial fibrillation with rapidventricular response (AF-RVR) in the setting of decompensated congestive heart fail-ure (HF). Background: Rate control is an acceptable treatment strategy for AF-RVR,yet common rate controlling agents such as metoprolol and diltiazem are cautioned indecompensated HF for fear of exacerbating HF symptoms. Studies directlycomparing these two agents in this setting are lacking and treatment recommenda-tions are primarily derived from subgroup analysis from larger HF or AF trials.Methods: We performed a retrospective analysis of patients admitted with decom-pensated HF and AF-RVR who received either IV metoprolol or IV diltiazem from3/2009 to 3/2013. The primary endpoint was a composite of achievement of rate con-trol (!110 bpm) or conversion to sinus rhythm by 24 hours after start of drug. Sec-ondary endpoints included incidence of hypotension (MAP !65mmHg), bradycardia(!60 bpm), DC cardioversion, or worsening heart failure (defined as increasing ox-ygen requirement, worsening pulmonary edema, inotropic support, and weight gain)within the 24 hour study period. Results: There were no baseline differences betweenthe metoprolol (n583) and diltiazem (n590) cohorts. While there was no differencein the composite primary endpoint (87% vs. 84%, p50.83), the metoprolol grouphad a higher rate of conversion to sinus rhythm (41% vs. 23%, p50.014, see figure)by 24 hours. There were no differences in hypotension (18% vs. 10%, p50.19),bradycardia (16%, p51), DC cardioversion (4% vs. 2%, p50.67), increasing O2 re-quirements (14% vs. 10%, p50.49), pulmonary edema (2% vs. 4%, p50.68),inotropic support (2% vs. 1%, p50.61), or weight gain (7% vs. 9%, p50.78). Con-clusions: In patients with AF-RVR in the setting of decompensated HF, metoprololand diltiazem have similar efficacy for rate control, but metoprolol is associatedwith higher conversion to sinus rhythm. Further, despite their negative inotropic ef-fects, both agents were equally safe without a significant rate of adverse effects orworsening heart failure.

Figure.

pressure (mmHg:n 5 65)

D in TPG (mmHg) -4 [-8, 0] 2 [-1, 7] !0.0001D in DPG (mmHg) -3 [-6, 1] 3 [-2. 7] !0.0001D in CI (L/min/m2) 0.40 [0.12, 0.59] 0.20 [0.04, 0.50] 0.137

*Comparison between PVR groups.

100Hemodynamic Response to Continuous Outpatient Milrinone Infusion inAdvanced Heart Failure Patients with Mixed Pulmonary HypertensionArun Krishnamoorthy1,2, Sneha Vakamudi1, Mara H. Watson3, Jennifer S. Byrns3,Sudarshan Rajagopal1, G. Michael Felker1,2, Joseph G. Rogers1,2, Chetan B.Patel1,2; 1Duke University School of Medicine, Durham, NC; 2Duke ClinicalResearch Institute, Durham, NC; 3Duke University Hospital, Durham, NC

Background: Advanced heart failure (HF) patients can develop mixed pulmonaryhypertension (PH) with pre- and post-capillary components. The hemodynamicresponse to continuous outpatient milrinone infusion and outcomes in these patientsare not well described.Methods: Between 2004 and 2012, 206 advanced HF patientstreated with continuous outpatient inotropes were identified. Patients included foranalysis had mixed PH before milrinone initiation and follow up hemodynamicassessment. Mixed PH was defined as either 1) mean pulmonary artery pressure(mPAP) $ 25 mmHg, pulmonary capillary wedge pressure (PCWP) O 15 mmHg,

and transpulmonary gradient (TPG) O 15 mmHg; or 2) PVR O 3 Wood units(WU). Patients were stratified by a PVR # or O 5 WU at follow up (thresholdfor a relative contraindication to orthotopic heart transplantation [OHT]). Hemody-namics at baseline and changes between the PVR groups were compared. We alsoreport progression to advanced HF therapies and outcomes after OHT. Results: In66 patients, baseline hemodynamics demonstrated a low cardiac index and confirmedmixed PH: PVR (5.3 [4.0, 6.5] WU); mPAP (44 [39, 48] mmHg); PCWP (27 [22, 30]mmHg); TPG (18 [12, 22] mmHg). Median time between hemodynamic assessmentswas 27 [7, 71] days with median treatment with milrinone for 23 [5, 62] days. Atfollow up, patients had reductions in PVR (-1.3 [-2.8, -0.1] WU), mPAP (-4 [-13,1] mmHg), and PCWP (-4 [-11, 2] mmHg), and an increase in CI by 0.35 [0.09,0.58] L/min/m2. After milrinone, 49 patients had a PVR # 5 WU and 17 patientshad a PVR O 5 WU (Table). In patients with a PVR # 5 WU, TPG and diastolicpressure gradient (DPG) were significantly lower at baseline, accompanied by signif-icant reductions in mean PAP, TPG, and DPG on follow up. There were no significantdifferences in CI between groups. In patients with a PVR # 5 WU, 26 underwentOHT (2 after durable mechanical circulatory support [MCS] bridge), and 3 hadpost-operative right HF. In patients with a PVR O 5 WU, 7 patients eventually pro-ceeded to OHT (5 after durable MCS bridge), and none had right HF post OHT.Conclusion: In a majority of advanced HF patients with mixed PH, continuous mil-rinone infusion lowered PVR. A PVR # 5 at follow up was associated with a lowerTPG and DPG at baseline and a greater reduction in mPAP, suggesting directimprovement in PH from pulmonary vasodilation with milrinone over time. In theoverall cohort, the incidence of right HF post OHT was low.

101Effect of Mineralocorticoid Receptor Antagonists on Cardiac Structure andFunction in Patients with Diastolic Impairment and Preserved EjectionFraction: A Meta-AnalysisAmbarish Pandey1, Sushil Garg2, Susan Matulevicius1, Amil Shah3, Jalaj Garg4,Kazeen Abdullah1, Mark Drazner1, Alpesh Amin1, Jarett Berry1, Thomas H.Marwick5, James de Lemos1, Dharam Kumbhani1; 1University of TexasSouthwestern Medical Center, Dallas, TX; 2University of Minnesota, Minneapolis,MN; 3Brigham and Womens Hospital, Boston, MA; 4New York Medical Center,Valhalla, NY; 5Menzies Research Institute, University of Tasmania, Hobart, Australia

Background: Impact of aldosterone antagonists (AA) on left ventricular (LV) struc-ture and function in patients with diastolic dysfunction (DD) and heart failure withpreserved ejection fraction (HFpEF) is not well understood. Methods: We performeda systematic review of randomized controlled trials that evaluated the efficacy of AAin patients with DD or HFpEF. Primary outcomes included changes in echocardio-graphic measures of diastolic function and LV end diastolic diameter (LVEDD). Sec-ondary outcomes included changes in blood pressure (BP), exercise tolerance andquality of life (QoL) in these subjects. A stratified analysis (HFPEF vs. DD) wasalso performed to assess the differential effects of AA in these subgroups. Results:Ten trials with 894 patients (276 with DD and 618 with HFPEF; mean age 63 years;48% female) were included, in which 446 received AA (86% spironolactone).Weighted mean duration of follow-up was 9.2 months. Significant reductions in sys-tolic (weighted mean difference [WMD]:-2.89 mm Hg, 95% CI -5.10 to -0.68,p50.01) and diastolic (WMD: -1.54 mm Hg, 95% CI -3.04 to -0.05; p50.04) BPwere noted with AA use compared with placebo. The use of AA was associatedwith a significant improvement in E/E’ ratio (WMD: -1.28; 95% CI -2.03 to -0.53,p50.0008) and interventricular relaxation time (IVRT) (WMD: -7.21; 95% CI:-12.33 to -2.08, p50.006), but not in E/A ratio (WMD: 0.08, 95% CI -0.06 to0.23, p50.27) from baseline (Figure). Stratified analysis showed that the favorableeffects on BP and diastolic function were limited to HFpEF patients, and were notobserved in the DD subset. Also, LVEDD was significantly reduced in patientswith HFpEF who received AA compared with placebo (WMD: -1.33; 95%CI:

S42 Journal of Cardiac Failure Vol. 20 No. 8S August 2014

-2.44 to -0.19, p50.02). No significant improvements were observed on 6-minutewalk test performance (WMD: -14.4; 95% CI: -38.2 to 9.51, p50.24) or QoL mea-sures (WMD: -1.25; 95% CI: -5.24 to 2.74, p50.54) with AA use. Conclusion: Theuse of AA in patients with diastolic dysfunction or HFpEF is associated with im-provements in BP and some measures of LV diastolic function and structure, withouta significant change in exercise tolerance or quality of life. Future studies are neces-sary to better define the role of AA in this patient subset.

Figure. Forest Plot showing effect of Aldosterone antagonist (AA) therapy on mea-sures of Left ventricular diastolic function.