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| |  Cinaciguat Safely Improves Cardiopulmonary Haemodynamics in Acute Decompensated Heart Failure: Presented at HF2008 By Chris Berrie MILAN, Italy -- June 17, 2008 -- The soluble guanylate cyclase activator cinaciguat (BAY 58-2667) is well tolerated and induces potent arterial and venous vasodilation in patients with acute decompensated heart failure, according to research presented here at the Heart Failure 2008 (HF2008) Congress. This vasodilation effect of cinaciguat is associated with significant decreases in pulmonary capillary wedge pressure, pulmonary artery pressure (PAP), mean right arterial pressure (RAP), and pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR), and an increase in cardiac output. These results, from a multicentre, nonrandomised, nonblinded, phase 2 study were presented on June 15 by researcher Veselin Mitrovic, MD, Kerckhoff Clinic, Bad Nauheim, Germany. Cinaciguat is a potent activator of nitric oxide-independent and heme-free soluble guanylate cyclase that has been shown to preferentially induce vasodilation in damaged vessels. Dr. Mitrovic and colleagues conducted their study to evaluate the clinical and haemodynamic effects of intravenous cinaciguat in patients with acute decompensated heart failure. The study included patients 18 years or older with New York Heart Association (NYHA) class 3/4 acute decompensated heart failure and a pulmonary capillary wedge pressure of 18 mm Hg or greater. The main exclusion criteria were unstable acute heart failure requiring specific interventions or treatments or severe renal failure. After their screening evaluation, 33 patients (mean age, 64.7 years; male, 94%) received treatment with cinaciguat at a dosage of 100 mcg per hour. The dose was adjusted after 2 hours according to target blood pressure, to complete the 6-hour infusion of cinaciguat 50 (n = 2), 200 (n = 12), and 400 (n = 16) mcg/hour. Compared with baseline haemodynamic measures, during the cinaciguat infusion there were significant decreases that were maximal at 6 hours for (baseline; infusion effect): pulmonary capillary wedge pressure (P < .0001); PAP-mean (P < .0001); RAP (P < .0001); SVR (P < .0001); and PVR (P < .05). Cardiac output instead significantly increased to 6 hours of cinaciguat infusion (4.240; +1.679 L/min, P < .0001). Although these haemodynamic benefits were reduced after stopping treatment, the improved scores for dyspnoea seen in 27%, 73%, and 87% of patients at 2, 4, and 6 hours of cinaciguat infusion, respectively, were maintained up to at least 18 hours postinfusion. A total of 11 adverse events occurred in 6 patients, but few were related to the study drug, and all were resolved, except for 1 patient who died from cardiac decompensation not related to the study drug, according to the researchers. "There is no question that this is a new promising drug, with a new mode of action; and it promotes potent preload and afterload reductions, and it can improve clinical signs and symptoms," Dr. Mitrovic added. Funding for this study was provided by Bayer Healthcare. HF2008 is the annual congress of the European Society of Cardiology.
[Presentation title: The Soluble Guanylate Cyclase Activator Cinaciguat (BAY 58-2667) Has a Favourable Safety Profile and Improves Cardiopulmonary Haemodynamics in Acute Decompensated Heart Failure. Abstract P33]
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