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This article is part of the supplement: Abstracts of the 2011 SCMR/Euro CMR Joint Scientific Sessions

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Relation of microvascular dysfunction to exercise capacity and symptoms in patients with severe aortic stenosis

Christopher D Steadman1*, Michael Jerosch-Herold2, Benjamin Grundy3, Suzanne Rafelt1, Leong L Ng1, Iain B Squire1, Nilesh J Samani1 and Gerry P McCann1

  • * Corresponding author: Christopher D Steadman

Author Affiliations

1 Department of Cardiovascular Sciences, University of Leicester, Leicester, UK

2 Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA

3 NIHR Leicester Cardiovascular Biomedical Research Unit, Leicester, UK

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Journal of Cardiovascular Magnetic Resonance 2011, 13(Suppl 1):O5  doi:10.1186/1532-429X-13-S1-O5

The electronic version of this article is the complete one and can be found online at:

Published:2 February 2011

© 2011 Steadman et al; licensee BioMed Central Ltd.

This is an open access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The aim of this study was to assess the impact of left ventricular hypertrophy, myocardial fibrosis, myocardial perfusion reserve (MPR) and diastolic dysfunction on objectively measured aerobic exercise capacity (peak VO2) in severe aortic stenosis (AS).


The management of asymptomatic patients with severe AS remains controversial and clinical practice varies. Echocardiographic measures of severity do not discriminate between symptomatic status or predict exercise capacity. The purpose of this study was to investigate the mechanisms contributing to symptom generation and exercise intolerance. This needs to be fully understood to optimise the management of asymptomatic AS.


Patients were prospectively enrolled from a single cardiac surgical centre. Inclusion criteria: age 18-85, isolated severe AS referred for valve replacement. Exclusion criteria: syncope; other moderate/severe valve disease, previous valve surgery, obstructive coronary artery disease (>50% luminal stenosis on invasive angiography), chronic obstructive pulmonary disease, atrial fibrillation, estimated glomerular filtration rate <30mL/min. Investigations and primary outcome measures; cardiac magnetic resonance (CMR) - left ventricular mass index (LVMI), MPR (calculated from absolute myocardial blood flow during adenosine hyperaemia and rest determined by model-independent deconvolution of signal intensity curves with an arterial input function), late gadolinium enhancement (LGE); echocardiography - AS severity, tissue Doppler-derived diastolic function; symptom-limited bicycle ergometer cardiopulmonary exercise testing (CPEX) - peak VO2. Linear regression investigated possible predictors of continuous outcome measures. Stepwise selection methods were used to determine the most important predictors of outcome.


Four patients with variable LVMI, LGE and MPR are shown, Figure 1. Univariate analyses and results from the stepwise model selection for peak VO2 are summarised in Table 1. Only MPR was of independent significance in predicting age and sex corrected peak VO2. The relationship between peak VO2 and MPR is shown, Figure 2. Patients with higher NYHA Class had lower MPR (p=0.001). Examining predictors of MPR the best stepwise model contained LVMI and LGE category as independent predictors, Table 2.

thumbnailFigure 1. Patients (A-D). i) Short-axis cine end-diastole; ii) LGE - white arrows; Perfusion imaging mid-LV slice iii) hyperaemia, iv) rest.

Table 1. Predictors of Peak VO2

thumbnailFigure 2. Peak VO2 and MPR

Table 2. Predictors of Perfusion Reserve


MPR is a novel independent predictor of peak VO2 and is inversely related to NYHA functional class in severe AS. Microvascular dysfunction is determined by a combination of factors including AS severity, LVMI, diastolic perfusion time, myocardial fibrosis and LV filling pressure. Further work is required to determine the clinical significance of microvascular dysfunction in AS.