Recombinant Human Neuregulin-1 (rhNRG-1) Improves Cardiac Output in Patients with Stable Chronic Heart Failure

2007 ◽  
Vol 16 ◽  
pp. S13
Author(s):  
A. Jabbour ◽  
C. Hayward ◽  
A. Keogh ◽  
E. Kotlyar ◽  
X. Liu ◽  
...  
2016 ◽  
Vol 64 (S 01) ◽  
Author(s):  
A. Beiras-Fernandez ◽  
J. Rothkopf ◽  
S. Kreth ◽  
A. Kornberger ◽  
U. Stock ◽  
...  

1999 ◽  
Vol 83 (11) ◽  
pp. 1573-1576 ◽  
Author(s):  
Akihiro Matsumoto ◽  
Haruki Itoh ◽  
Ikuo Yokoyama ◽  
Teruhiko Aoyagi ◽  
Seiryo Sugiura ◽  
...  

2018 ◽  
Vol 107 (5) ◽  
pp. 395-404 ◽  
Author(s):  
Sebastian Roth ◽  
Henrik Fox ◽  
Uwe Fuchs ◽  
Uwe Schulz ◽  
Angelika Costard-Jäckle ◽  
...  

1988 ◽  
Vol 254 (4) ◽  
pp. H727-H733 ◽  
Author(s):  
J. R. Wilson ◽  
W. Matthai ◽  
V. Lanoce ◽  
M. Frey ◽  
N. Ferraro

To investigate whether heart failure impairs peripheral sympathetic vasoconstriction, hindlimb vascular responses to lumbar chain stimulation (0.5-20 Hz) were studied in normal dogs and in dogs with chronic heart failure produced by rapid ventricular pacing. At lumbar chain stimulation rates of 0.5-3 Hz, hindlimb vascular responses were comparable in both groups. However, at stimulation rates of 5-20 Hz, vascular responses were significantly attenuated in the dogs with heart failure. Vascular responses to norepinephrine (0.1, 1, and 10 micrograms/min) were not altered. These findings suggest that chronic heart failure results in impaired sympathetic vasoconstriction, probably because of reduced neurotransmitter release. This abnormality may interfere with the capacity of the failing circulation to compensate for a low cardiac output and thereby intensify the severity of heart failure.


Author(s):  
Gaia Cattadori ◽  
Piergiuseppe Agostoni ◽  
Anna Apostolo ◽  
Giancarlo Marenzi

2009 ◽  
Vol 18 ◽  
pp. S192
Author(s):  
A. Jabbour ◽  
C.S. Hayward ◽  
A.M. Keogh ◽  
E. Kotlyar ◽  
J. McCrohon ◽  
...  

2004 ◽  
Vol 9 (5) ◽  
pp. 277-280 ◽  
Author(s):  
Stephen J. Leslie ◽  
Sin??ad McKee ◽  
David E. Newby ◽  
David J. Webb ◽  
Martin A. Denvir

Author(s):  
Kazem Rahimi

Heart failure is a clinical syndrome characterized by an inadequate cardiac output for the needs of the body in the absence of low filling pressures, and reflects abnormal cardiac structure or function. Although various definitions for acute heart failure (AHF) exist, here AHF is defined as new-onset heart failure or an acute exacerbation of chronic heart failure, requiring urgent therapy. Patients with AHF typically have clinical features of organ hypoperfusion, with or without pulmonary and peripheral oedema.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Audrey Borghi-Silva ◽  
Luiz Eduardo Nery ◽  
Dirceu R de Almeida ◽  
Jose Alberto Neder

Introduction: Progressive chronic heart failure slows the recovery of microvascular oxygen delivery and utilization, which produce deleterious implications to exercise capacity. Respiratory muscle unloading can enhance the responses to exercise thereby allowing a closer matching between skeletal muscle oxygen delivery and utilization in patients with chronic heart failure (CHF). Hypothesis: We reasoned that noninvasive ventilation administered by proportional assisted ventilation (PAV) could accelerate skeletal muscle reoxygenation after high intensity exercise in CHF humans. To test this hypothesis, we conducted a study with 12 patients with stable CHF who were randomized to receive PAV or sham ventilation during high-intensity constant work exercise and compared the effects of these interventions on oxygen pulmonary (O2p), cardiac output and [[Unable to Display Character: &#8710;]][deoxi-Hb+Mb] off kinetics. Methods: Twelve patients with CHF (NYHA class II and III and left ventricle ejection fraction= 26±9%) underwent two high-intensity, constant-work rate (80% peak) cycle ergometer tests receiving PAV or sham ventilation. Off-exercise kinetics of the primary component of oxygen uptake, an index of fractional oxygen extraction by near infrared spectroscopy (~[[Unable to Display Character: &#8710;]][deoxy-Hb+Mb]) in the vastus lateralis) and cardiac output (QT) by impedance cardiography were assessed. Results: PAV significantly accelerated the recovery of O2p when compared with sham τ = 56±22 vs. 77±42s, respectively, p<0.05). Interestingly, PAV was associated with faster fractional O2 extraction (~[[Unable to Display Character: &#8710;]][deoxy-Hb+Mb] by near-infrared spectroscopy) (τ= 31±19 vs. 42±22s, respectively, p<0.05) . In addition, kinetics of QT were significantly faster with PAV than sham (τ = 39±22 vs. 78±46s, respectively, p<0.05). Conclusions: These data indicate that PAV has beneficial effects on recovery of muscle metabolism and central hemodynamics after high-intensity exercise in CHF patients. Financial Support: FAPESP 2009-01842-0


1991 ◽  
Vol 71 (3) ◽  
pp. 1070-1075 ◽  
Author(s):  
M. J. Sullivan ◽  
F. R. Cobb

We examined the central hemodynamic (n = 5) and leg blood flow (n = 9) responses to one- and two-leg bicycle exercise in nine ambulatory patients with chronic heart failure due to left ventricular systolic dysfunction (ejection fraction 17 +/- 9%). During peak one- vs. two-leg exercise, leg blood flow (thermodilution) tended to be higher (1.99 +/- 0.91 vs. 1.67 +/- 0.91 l/min, P = 0.07), whereas femoral arteriovenous oxygen difference was lower (13.6 +/- 3.1 vs. 15.0 +/- 2.9 ml/dl, P less than 0.01). Comparison of data from exercise stages matched for single-leg work rate during one- vs. two-leg exercise demonstrated that cardiac output was similar while both oxygen consumption and central arteriovenous oxygen differences were lower, indicating relative improvement in the cardiac output response at a given single-leg work rate during one-leg exercise. This was accompanied by higher leg blood flow (1.56 +/- 0.76 vs. 1.83 +/- 0.72 l/min, P = 0.02) and a tendency for leg vascular resistance to be lower (92 +/- 54 vs. 80 +/- 48 Torr.l-1.min, P = 0.08) without any change in blood lactate. These data indicate that, in patients with chronic heart failure, leg vasomotor tone is dynamically regulated, independent of skeletal muscle metabolism, and is not determined solely by intrinsic abnormalities in skeletal muscle vasodilator capacity. Our results suggest that relative improvements in central cardiac function may lead to a reflex release of skeletal muscle vasoconstrictor tone in this disorder.


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