The 13th Annual Scientific Meeting
HFSA
S21
Collaborative of NT-proBNP (ICON) study were evaluated. WRF was defined as a 0.3 mg/dL rise in serum creatinine during index hospitalization. Results: WRF occcured in 247 of 623 patients (40%) with acute HF. Compared to patients without WRF, patients with WRF were less likely to have a prior diagnosis of coronary artery disease (46% vs. 60%; P ! .001) or myocardial infarction (28% vs. 39%; P 5 .006), and had higher body-mass index (27.3 6 5.9 vs. 26.3 6 5.9 kg/m2; P 5 .08), lower hemoglobin (12.2 6 2.0 vs. 12.8 6 2.1 g/dL; P ! .001), lower baseline estimated glomerular filtration rate (eGFR: 54 6 24 vs. 61 6 27 ml/min/1.73 m2; P 5 .002), and higher NT-pro-BNP level (median 10312 vs. 9195 pg/mL; P 5 0.01). In logistic regression, the only predictor of WRF was baseline eGFR ! 60 mL/min/ 1.73m2 (OR 1.02, 95% CI 1.01-1.05; P ! .001). There was a trend toward improved 60 day post-discharge mortality in patients without WRF as compared to those with WRF (15% vs. 11%, P 5 .08), but no difference in one year post-discharge mortality. At each quartile of eGFR, patients with WRF did not experience a statistically significant difference in 60 day and one year post-discharge mortality when compared to patients without WRF. Conclusion: Although differences exist in patient characteristics as a function of future WRF, only impaired baseline renal function independently predicted WRF in acute HF. This indicates a need for better ways to identify impending WRF in this setting. As currently defined, WRF did not increase the risk of adverse outcome and suggests the current definition for cardiorenal syndrome may require reconsideration.
therapy, blood pressure at baseline and after 3 and 6 months did not differ between study groups (see table below).
055
057
What Predicts Troponin Release in Acutely Decompensated Heart Failure? Ravi V. Shah1, A. Mark Richards2, Antoni Bayes-Genis3, Yigal Pinto4, John Lainchbury2, Jordi Ordonez3, Roland van Kimmenade5, James L. Januzzi1; 1 Medicine, Massachusetts General Hospital, Boston, MA; 2Cardioendocrine Research Group, Department of Medicine, University of Otago, Christchurch, Christchurch, New Zealand; 3Medicina, Hospital de la Santa Creu i Sant Pau & Universitat Auto`noma, Barcelona, Spain; 4Heart Failure Research Center, University of Amsterdam, Amsterdam, Netherlands; 5Department of Cardiology, University Hospital Maastricht, Maastricht, Netherlands
Intramural Dyssynchrony and Response to CRT in Heart Failure Patients with and without Previous Right Ventricular Pacing Alan J. Bank1, Christopher L. Kaufman1, Kevin V. Burns1, Joshua Parah1, Lauren Johnson2, Daniel R. Kaiser2; 1Cardiovascular Research, St. Paul Heart Clinic, St. Paul, MN; 2Medtronic Inc
Introduction: Detectable concentrations of cardiac troponin (cTn) are prognostic in patients with acute decompensated heart failure (ADHF), but the predictors of a positive cTn and the etiology of a positive cTn in ADHF remain elusive. Methods: cTnT concentrations in 670 patients with acute HF from the International Collaborative of NT-proBNP (ICON) study were evaluated. Bootstrapped multivariate logistic and linear regression models were constructed with covariates from history, physical examination and laboratory testing. Results: 542 (80.8%) subjects had a detectable cTnT; reflecting inclusion criteria for the ICON study, only 7% of the subjects had an acute coronary syndrome. Independent predictors of detectable cTn concentrations were age (t 5 3.36; P 5 .001), presence of diabetes mellitus (t 5 2.91; P 5 .004), severity of dyspnea (t 5 -3.69; P ! .001), left ventricular ejection fraction (t 5 -3.55; P ! .001), serum creatinine (t 5 5.15; P ! .001), and NT-proBNP level (t 5 4.48; P ! .001). In a bootstrapped multivariate linear regression model for independent predictors of absolute cTnT concentrations (including those unmeasurable at presentation), severity of dyspnea (t 5 -6.97; P ! .001), glucose level (t 5 3.11, P 5 .002) and NTproBNP level (t 5 3.71, P ! .001) independently predicted cTnT levels. Conclusions: cTn elevation in ADHF is common, and is independent of a diagnosis of acute coronary syndrome. The predictive variables in our analysis point toward subendocardial ischemia due to wall stress and/or occult coronary artery disease as the most likely explanation for cTn release in ADHF. Our results have considerable implication with the growing use of ‘‘higher sensitivity’’ cTnT methods, assays which will likely universally detect cTn elevation in these subjects.
056 Administration of Erythropoietin Alfa in Patients with Heart Failure with a Preserved Ejection Fraction (HFPEF) without Elevating Blood Pressure Joseph A. Shatzkes, Sergio L. Teruya, Helen R. Gil, Stephen Helmke, Mathew S. Maurer; Division of Cardiology, Columbia University, New York, NY Background: Chronic hypertension is a known etiological factor of Heart Failure with a Preserved Ejection Fraction (HFPEF) and acute elevations in systemic blood pressure have been shown to lead to clinical decompensation. Anemia is common in patients with HFPEF and is one possible modifiable factor in improving overall health in these patients. A common known side effect of recombinant erythropoietin is hypertension. In this analysis of the data from an ongoing randomized control trial we evaluated whether erythropoietin can be administered to patients with HFPEF and anemia without raising blood pressure. Methods: As part of an ongoing single blind, randomized control trial, (NCT00286182) 22 patients with clinical heart failure with ejection fractions O40% and anemia defined as Hb !12 g/dl were randomized to receive either weekly injections of erythropoietin alfa or placebo. Patients had weekly monitoring of their blood pressure during the duration of the trial (24 weeks) and differences in blood pressure between the study arms were evaluated. Baseline medications at randomization and weekly medication changes were documented. Blood pressure was measured during principal visits at baseline, 3 and 6 months as well as weekly during home visits with the subject in a seated position after 5 minutes of rest using an automated oscillometric blood pressure monitor (Omron, Bannockburn, Illinois). Results: Despite an increase in Hb of w1.5 g/dl during active
Placebo
SBP DBP MAP
Erythropoietin
Baseline
3Mo.
6Mo.
Baseline
3Mo.
6Mo.
136 6 6 69 6 9 91 6 6
141 6 16 70 6 10 93 6 11
135 6 17 67 6 9 90 6 8
147 6 9 68 6 5 94 6 5
146 6 16 63 6 5 91 6 8
146 6 16 65 6 8 92 6 8
Similar lack of differences was observed in weekly blood pressure monitoring which averaged 143 6 2.1/71 6 1.2 mmHg (n5238 measurements) in subjects on placebo and 146 6 1.5/64 6 1.0 mmHg (n5209 measurements) in subjects on active therapy. Baseline medications, weekly dose adjustments, and addition or discontinuation of medications did not differ between the groups and therefore did not account for the lack of differences observed. Conclusions: Preliminary data suggests that in patients with Heart Failure with a Preserved Ejection Fraction and anemia, who often have underlying hypertension, erythropoietin can be administered on a weekly basis to correct anemia, without significantly elevating blood pressure.
Background: We have previously demonstrated that acute RV pacing (RVp) in patients with normal left ventricular (LV) function produces a novel type of longitudinal mechanical dyssynchrony (intramural dyssynchrony, IMD) within the septal and lateral walls of the LV. This study was performed to determine if intramural dyssynchrony: 1) was present in patients with RVp and chronic heart failure (HF), 2) could help differentiate these patients from those with HF and wide QRS but not RVp (nRVp), and 3) improves with cardiac resynchronization therapy (CRT). Methods: Echocardiograms (ECHO) with tissue Doppler imaging (TDI) were performed before and after (153 6 63 days) CRT in RVp (n531) and nRVp (n549) HF patients meeting standard criteria for CRT. Standard ECHO/TDI measurements were obtained to assess LV size, function and dyssynchrony. IMD was measured using tissue-tracking TDI to determine longitudinal dyssynchrony within the septal and lateral walls rather than between the 2 walls. IMD was quantified using a proprietary cross-correlation synchrony index (CCSI) which involves a pair-wise correlation analysis of 5 myocardial segment displacement waveforms during systole. An additional IMD score was also determined as # segments with abnormal longitudinal motion toward the base during systole. Results: RVp patients had baseline characteristics similar to nRVP patients except for age (75.2 6 11.2 vs 68.0 6 13.0 years, p!0.05) and QRS duration (163 6 30 vs 141 6 19 ms, p!0.001). Despite similar EF’s at baseline (27.8 6 7.2 vs 27.2 6 6.3%), RVp patients had smaller LVEDV (143 6 54 vs 183 6 62 ml, p!0.005) and LVESV (105 6 44 vs 133 6 51 ml, p!0.01). Septal IMD score was greater in RVp (3.1 6 1.8 vs 1.3 6 1.7, p!0.001) but CCSI septal was not significantly lower (0.73 6 0.34 vs 0.80 6 0.33, p50.17). With CRT, RVp patients had greater improvement in EF (12.8 6 9.2 vs 7.4 6 7.6%,p!0.01), septal IMD score (-1.5 6 2.5 vs -0.4 6 2.3, p!0.001) and CCSI septal (0.16 6 0.32 vs 0.05 6 0.28 ,p!0.05) but not CCSI lateral (0.12 6 0.36 vs 0.03 6 0.22,p50.12) as compared to nRVp patients. Conclusion: RVp HF patients have smaller LV volumes and more septal IMD as compared with nRVp patients with similar EF. Both LV IMD and EF improve to a greater extent in RVp vs nRVp HF patients. IMD may help differentiate pacing-induced dyssynchrony from other causes of wide-QRS HF and may be a marker for improved response to CRT.
058 Ascites Is Not Invariably Present in Heart Failure Patients with Elevated IntraAbdominal Pressure Poh Shuan Daniel Yeo, Julio A. Barcena, Carmel M. Halley, W.H. Wilson Tang; Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH Background: Intra-abdominal pressure (IAP) is elevated in the setting of significant ascites. This contributes to renal dysfunction probably by decreasing renal perfusion pressure. In heart failure (HF) patients with acute decompensation, it has been observed that despite having elevated IAP, a substantial number do not have demonstrable ascites clinically and on imaging. We hypothesized that elevated IAP in this sub-group of patients is due to visceral edema rather than free intra-peritoneal fluid. We sought to support this by studying the association of IAP elevation with the presence or absence of ascites. Methods: We performed a retrospective records review of patients admitted to the Heart Failure Intensive Care Unit who also had a Foley catheter and contemporaneous abdominal imaging to determine the presence and degree of ascites (ultrasound or CT). IAP was measured via the Foley catheter as previously described in the published literature. Elevated IAP was defined as $8mmHg. The patients received standard HF pharmacotherapy including diuretics and vasodilators.