Abstract
Purpose
In patients with acute decompensated heart failure (ADHF) and left ventricular systolic dysfunction (LVSD), the role of initial vasodilator therapy remains uncertain. The present study aimed to evaluate the acute efficacy of initial carperitide therapy and to predict its response in ADHF patients with LVSD.
Methods
Twenty-four consecutive patients with ADHF and LVSD were enrolled. Inclusion criteria were a left ventricular ejection fraction < 40%, systolic blood pressure (BP) > 90 mm Hg, and pulmonary capillary wedge pressure ≥18 mm Hg at baseline. Hemodynamic parameters were evaluated by right heart catheterization before and after carperitide infusion. Responders were defined as a ≥30% reduction of pulmonary capillary wedge pressure (PCWP) or a decrease to < 16 mm Hg within 6 h after carperitide infusion.
Results
Seventeen (71%) of the 24 patients were responders for initial carperitide therapy. The responders had significantly higher systolic BP and cardiac index at baseline compared with nonresponders. The area under the curve (AUC) for systolic BP was 0.93 and a cut-off value of 120 mm Hg had a sensitivity of 94% and specificity of 86% for predicting the efficacy of carperitide. The AUC for the cardiac index was 0.88 and a cut-off value of 2.30 L/min/m2 had a sensitivity of 65% and a specificity of 100% for predicting the response to carperitide.
Conclusions
The initial use of carperitide therapy safely reduces PCWP in ADHF patients with LVSD and baseline systolic BP may be useful for predicting the response to initial carperitide therapy for ADHF with LVSD.
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Acknowledgement
We express our appreciation to Katsunori Shimada, PhD (STATZ Institute, Inc., Tokyo, Japan) for expert statistical assistance.
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There were no funding sources and no conflicts of interest.
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Kajimoto, K., Sashida, Y., Minami, Y. et al. Systolic Blood Pressure at Admission as a Predictor of the Response to Initial Carperitide Therapy in Patients Hospitalized for Acute Decompensated Heart Failure with Left Ventricular Systolic Dysfunction. Cardiovasc Drugs Ther 23, 481–488 (2009). https://doi.org/10.1007/s10557-009-6207-2
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DOI: https://doi.org/10.1007/s10557-009-6207-2