© 2007 European Society of Cardiology
Differences in arterial compliance, microvascular function and venous capacitance between patients with heart failure and either preserved or reduced left ventricular systolic function
a British Heart Foundation Cardiovascular Research Centre, University of Glasgow Glasgow G12 8TA, Scotland, UK
b Division of Infection, Immunology and Inflammation, University of Glasgow, Scotland, UK
* Corresponding author. Tel./fax: +44 141 211 1838, +44 7811113015 (mobile). E-mail address: seanbalmain{at}hotmail.com
 |
Abstract |
|---|
Background: Up to 50% of patients with the clinical syndrome of heart failure have preserved left ventricular systolic function (HF-PSF). These patients may have abnormalities of ventriculo-vascular coupling, due to increased vascular and ventricular stiffness.
Methods: We compared arterial compliance, microvascular vasodilator function and venous capacitance (VC) in 3 groups of patients (n<=12 each) matched for the presence of coronary heart disease: 1) HF and preserved systolic function (HF-PSF), 2) HF and reduced systolic function (HF-RSF) and 3) controls (no HF, PSF). Arterial compliance was assessed by measuring aortic pulse wave velocity (PWV) with applanation tonometry. Cutaneous microvascular function was assessed using Laser Doppler imaging (LDI) coupled with iontophoresis of endothelium-dependent (acetylcholine) and -independent (sodium nitroprusside) vasodilators. VC was measured using venous occlusion plethysmography.
Results: PWV was significantly higher in HF-PSF subjects than in both HF-RSF and control groups (10.7 [1.1], 8.9 [1.7] and 8.6 [2.1] m/s respectively, p<0.05). Acetylcholine and nitroprusside induced vasodilatation were equally impaired in HF-PSF and HF-RSF, as compared to controls (p<0.01). VC was higher in HF-RSF subjects compared with HF-PSF subjects (1.75 [0.41], 1.34 [0.34] ml/100 ml forearm vol. respectively, p<0.05).
Conclusions: These findings are consistent with a more marked increase in vascular stiffness in HF-PSF than in HF-RSF and suggest that arterial stiffness, dynamic vasodilator function and venous abnormalities may be implicated in the complex pathophysiology of HF-PSF.
Key Words: Heart failure • Diastole • Arteries • Veins • Endothelium
Received October 12, 2006; Revised March 9, 2007; Accepted June 7, 2007
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  E. R. Rabelo, K. Ruschel, H. Moreno Jr., M. Rubira, F. M. Consolim-Colombo, M. C. Irigoyen, and L. E. Rohde Venous endothelial function in heart failure: Comparison with healthy controls and effect of clinical compensation Eur J Heart Fail, August 1, 2008; 10(8): 758 - 764. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Cotter, M. Metra, O. Milo-Cotter, H. C. Dittrich, and M. Gheorghiade Fluid overload in acute heart failure -- Re-distribution and other mechanisms beyond fluid accumulation Eur J Heart Fail, February 1, 2008; 10(2): 165 - 169. [Abstract] [Full Text] [PDF]
|
|