This Article Full Text Full Text (PDF) All Versions of this Article: 112/20/3107    most recent CIRCULATIONAHA.105.555367v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Konstam, M. A. Articles by Jansen, P. Search for Related Content PubMed PubMed Citation Articles by Konstam, M. A. Articles by Jansen, P. Related Collections Health policy and outcome research Other Treatment Related Article

(Circulation. 2005;112:3107-3114.)
© 2005 American Heart Association, Inc.

Heart Failure

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; 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.

Correspondence to Marvin A. Konstam, MD, Tufts-New England Medical Center, 750 Washington St, Boston, MA 02111. E-mail MKonstam{at}tufts-nemc.org

Received January 11, 2005; de novo received April 12, 2005; revision received August 10, 2005; accepted August 11, 2005.

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

Related Article:

Issue Highlights
Circulation 2005 112: 3025. [Full Text]