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The endogenous NOS inhibitor asymmetric dimethylarginine (ADMA) predicts LV mass independent of afterload
Citation
Sverdlov, AL and Ngo, DTM and Nightingale, AK and Rajendran, S and Mishra, K and Heresztyn, T and Ritchie, RH and Marwick, TH and Frenneaux, MP and Horowitz, JD, The endogenous NOS inhibitor asymmetric dimethylarginine (ADMA) predicts LV mass independent of afterload, Nitric Oxide, 25, (1) pp. 41-46. ISSN 1089-8603 (2011) [Refereed Article]
Copyright Statement
Copyright 2011 Published by Elsevier Inc
DOI: doi:10.1016/j.niox.2011.04.009
Abstract
Background
Nitric oxide (NO) is a modulator of left ventricular hypertrophy (LVH) and myocardial relaxation. The impact of NO availability on development of LVH has never been demonstrated in humans. We tested the hypotheses that elevation of asymmetric dimethylarginine (ADMA) concentrations (biochemical marker of decreased NO generation), and impairment of vascular responsiveness to NO donor GTN, would each predict the presence of LVH and associated LV diastolic dysfunction in a normal aging population.
Methods and results In 74 subjects aged 68 ± 6 years, LV volumes and mass indexed to height2.7 (LVMI) were calculated from cardiac MRI. Despite the absence of clinically-defined LVH, there was a relationship (r = 0.29; p = 0.01) between systolic BP and LVMI. Both elevation of ADMA levels to the highest quartile or impairment of GTN responsiveness (determined by applanation tonometry) to the lowest quartile were determinants of LVMI independent of systolic BP (p = 0.01 and p = 0.03, respectively). Filling pressure (E/E′ ratio from echocardiography) was increased in patients with impaired vascular NO responsiveness (p < 0.05) irrespective of LVMI. ADMA remained a significant determinant of LVMI on multivariate analysis.
Conclusions These data imply that NO bioavailability within the myocardium modulates earliest stages of LVH development and facilitates development of diastolic dysfunction at a given LV mass.
Methods and results In 74 subjects aged 68 ± 6 years, LV volumes and mass indexed to height2.7 (LVMI) were calculated from cardiac MRI. Despite the absence of clinically-defined LVH, there was a relationship (r = 0.29; p = 0.01) between systolic BP and LVMI. Both elevation of ADMA levels to the highest quartile or impairment of GTN responsiveness (determined by applanation tonometry) to the lowest quartile were determinants of LVMI independent of systolic BP (p = 0.01 and p = 0.03, respectively). Filling pressure (E/E′ ratio from echocardiography) was increased in patients with impaired vascular NO responsiveness (p < 0.05) irrespective of LVMI. ADMA remained a significant determinant of LVMI on multivariate analysis.
Conclusions These data imply that NO bioavailability within the myocardium modulates earliest stages of LVH development and facilitates development of diastolic dysfunction at a given LV mass.
Item Details
| Item Type: | Refereed Article |
|---|---|
| Keywords: | left ventricular mass, nitric oxide, vascular function, diastolic function, asymmetric dimethylarginine |
| Research Division: | Biomedical and Clinical Sciences |
| Research Group: | Cardiovascular medicine and haematology |
| Research Field: | Cardiology (incl. cardiovascular diseases) |
| Objective Division: | Health |
| Objective Group: | Clinical health |
| Objective Field: | Clinical health not elsewhere classified |
| UTAS Author: | Marwick, TH (Professor Tom Marwick) |
| ID Code: | 90927 |
| Year Published: | 2011 |
| Web of Science® Times Cited: | 11 |
| Deposited By: | Menzies Institute for Medical Research |
| Deposited On: | 2014-05-01 |
| Last Modified: | 2014-06-05 |
| Downloads: | 0 |
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