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Vasopeptidase inhibition with omapatrilat in chronic heart failure: acute and long-term hemodynamic and neurohumoral effects

Dougal R. McClean, MD^*, Hamid Ikram, MD, PhD^*,*, Sukh Mehta, MD, J. Thomas Heywood, MD, Michel F. Rousseau, MD, Alan L. Niederman, MD^||, Rafael F. Sequeira, MD^¶, Eckart Fleck, MD^#, Steven N. Singh, MD^**, Benoit Coutu, MD, Peter Hanrath, MD, Michel Komajda, MD, Catherine C. Bryson^||||, Chunlin Qian, PhD^||||, James J. Hanyok, PharmD^|||| Omapatrilat Hemodynamic Study Group

^* Christchurch Hospital, Christchurch, New Zealand
San Bernadino, California, USA
Jerry L. Pettis Veterans Administration Medical Center, Loma Linda, California, USA
Cliniques Universitaires Saint-Luc, Brussels, Belgium
^|| Greater Fort Lauderdale Heart Group Research, Fort Lauderdale, Florida, USA
^¶ University of Miami/Jackson Memorial Medical Center, Miami, Florida, USA
^# Deutsches Herzzentrum Berlin, Berlin, Germany
^** Veterans Administration Medical Center, Washington, DC, USA
Pavillon Hopital Notre-Dame, Montreal, Canada
Medizinische Fakultat der RWTH, Aachen, Germany
Hôpital Pitiê-Salpetrire, Paris, France
^|||| Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey, USA

View larger version (21K): [in a new window]   Figure 1 Change from pretreatment day 1 baseline levels in pulmonary capillary wedge pressure (PCWP) (a) and systolic blood pressure (SBP) (b) after the final dose of omapatrilat at 12 weeks. Panel I: open diamond = 2.5 mg; star = 5 mg; open triangle = 10 mg. Panel II: + = 2.5 mg; open square = 20 mg; open circle = 40 mg. Shaded symbols indicate a significant difference (p < 0.05) in the 0-h to 12-h average change from predose day 1 for omapatrilat dose compared with the respective 2.5 mg group.