European Heart Journal Advance Access originally published online on September 4, 2008
European Heart Journal 2008 29(20):2453-2455; doi:10.1093/eurheartj/ehn393
Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org
Nitric oxide: the missing lusitrope in failing myocardium
1 Department of Cardiology, Institute for Cardiovascular Research, VU University Medical Center (VUMC), Amsterdam, The Netherlands
2 Department of Physiology, Institute for Cardiovascular Research, VU University Medical Center (VUMC), Amsterdam, The Netherlands
* Corresponding author. Tel: +31 20 4448110, Fax: +31 20 4448255, Email: wj.paulus@vumc.nl
This editorial refers to Differential effects of arginine methylation on diastolic dysfunction and disease progression in patients with chronic systolic heart failure
by W.H. Wilson Tang et al., on page 2506
Footnotes
The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.
doi:10.1093/eurheartj/ehn360 ![]()
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During the last decade, the effects of nitric oxide (NO) on contractile function of failing myocardium elicited a lot of interest and research activity. Because of initial reports of NO acutely reducing the extent and velocity of shortening of isolated cardiomyocytes, especially following β-adrenergic stimulation, and because of increased activity of inducible nitric oxide synthase (NOS2) in human cardiomyopathic myocardium, numerous reports and reviews have persistently and erroneously identified NO as deleterious for contractile function of failing myocardium.1 Shortly after these initial reports, a rosier picture of NO's functional myocardial effects emerged, highlighting NO's ability to improve left ventricular (LV) diastolic function. In the normal human heart, intracoronary administration of NO donors instantaneously hastens onset of LV relaxation and
Microvascular inflammation and diastolic LV dysfunction
Lusitropic actions of NO
Treatment of diastolic LV dysfunction
Conclusions
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