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Published Online
on November 7, 2005

Circulation. 2005
Published online before print November 7, 2005, doi: 10.1161/CIRCULATIONAHA.105.555367
A more recent version of this article appeared on November 15, 2005
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Submitted on January 11, 2005
Revised on August 10, 2005
Accepted on August 11, 2005

Continuous Aortic Flow Augmentation. A Pilot Study of Hemodynamic and Renal Responses to a Novel Percutaneous Intervention in Decompensated Heart Failure

Marvin A. Konstam MD*, Barbara Czerska MD, Michael Böhm MD, PhD, Ron M. Oren MD, Jerzy Sadowski MD, PhD, Sanjaya Khanal MD, William T. Abraham MD, Andrae Wasler MD, Johannes B. Dahm MD, Antonello Gavazzi MD, Sinisa Gradinac MD, PhD, Victor Legrand MD, Paul Mohacsi MD, Gerhard Poelzl MD, Branislav Radovancevic MD, Adrian B. Van Bakel MD, Michael R. Zile MD, Barry Cabuay MD, Krzysztof Bartus MD, and Piet Jansen MD

From Tufts-New England Medical Center and Tufts University (M.A.K.), Boston, Mass; Henry Ford Heart & Vascular Institute (B.C., S.K.), Detroit, Mich; University Hospital Saarland (M.B.), Homburg, Germany; University of Iowa (R.M.O., B.C.), Iowa City, Iowa; Jagiellonian University (J.S., K.B.), Krakow, Poland; The Ohio State University (W.T.A.), Columbus, Ohio; University Hospital Graz (A.W.), Graz, Austria; University Hospital (J.B.D.), Greifswald, Germany; Riuniti Hospital (A.G.), Bergamo, Italy; Dedinje Cardiovascular Institute (S.G.), Belgrade, Yugoslavia, Sart Tilman University Hospital (V.L.), Liege, Belgium; University Hospital Bern (P.M.), Bern, Switzerland, University Hospital Innsbruck (G.P.), Innsbruck, Austria; Texas Heart Institute at St. Luke’s Episcopal Hospital (B.R.), Houston, Tex; Medical University of South Carolina (A.B.V.B., M.R.Z.), Charleston, SC; and Orqis Medical (P.J.), Lake Forest, Calif.

* To whom correspondence should be addressed. E-mail: MKonstam{at}tufts-nemc.org.

Background--Diminished aortic flow may induce adverse downstream vascular and renal signals. Investigations in a heart failure animal model have shown that continuous aortic flow augmentation (CAFA) achieves hemodynamic improvement and ventricular unloading, which suggests a novel therapeutic approach to patients with heart failure exacerbation that is inadequately responsive to medical therapy.

Methods and Results--We studied 24 patients (12 in Europe and 12 in the United States) with heart failure exacerbation and persistent hemodynamic derangement despite intravenous diuretic and inotropic and/or vasodilator treatment. CAFA (mean±SD 1.34±0.12 L/min) was achieved through percutaneous (n=19) or surgical (n=5) insertion of the Cancion system, which consists of inflow and outflow cannulas and a magnetically levitated and driven centrifugal pump. Hemodynamic improvement was observed within 1 hour. Systemic vascular resistance decreased from 1413±453 to 1136±381 dyne · s · cm-5 at 72 hours (P=0.0008). Pulmonary capillary wedge pressure decreased from 28.5±4.9 to 19.8±7.0 mm Hg (P<0.0001), and cardiac index (excluding augmented aortic flow) increased from 1.97±0.44 to 2.27±0.43 L · min-1 · m-2 (P=0.0013). Serum creatinine trended downward during treatment (overall P=0.095). There were 8 complications during treatment, 7 of which were self-limited. Hemodynamics remained improved 24 hours after CAFA discontinuation.

Conclusions--In patients with heart failure and persistent hemodynamic derangement despite intravenous inotropic and/or vasodilator therapy, CAFA improved hemodynamics, with a reduction in serum creatinine. CAFA represents a promising, novel mode of treatment for patients who are inadequately responsive to medical therapy. The clinical impact of the observed hemodynamic improvement is currently being explored in a prospective, randomized, controlled trial.


Key words: heart failure • hemodynamics • vasodilation • nitric oxide • heart-assist device


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