Author + information
- Marzia Rigolli, MBChB, MD,
- Sanjay Sivalokanathan, MBBS, BSc,
- Sacha Bull, MA, DPhil,
- Rohan S. Wijesurendra, MBBChir, MA,
- Rina Ariga, MBBS, BSc,
- Margaret Loudon, MBChB, DPhil,
- Jane M. Francis, DCR(R), DNM,
- Theodoros D. Karamitsos, MD, PhD,
- Stefan Neubauer, MD,
- Masliza Mahmod, MBChB, DPhil and
- Saul G. Myerson, MBChB, MD∗ ()
- ↵∗University of Oxford Centre for Clinical Magnetic Resonance Research, Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, United Kingdom
The right ventricle (RV) has been poorly studied in patients with aortic stenosis (AS) and normal left ventricular (LV) function, due to the belief that it is only affected by pulmonary hypertension (PH) secondary to advanced LV dysfunction. Despite this, increased RV afterload is frequent in AS (1), difficult to assess noninvasively (2), and may be present without detectable PH. The RV is extremely sensitive to afterload changes and may provide an earlier marker of progression than pulmonary pressures. Although RV dysfunction is the typical response to an increase in acute pulmonary pressure, RV adaptation to chronic afterload involves increasing contractility (3,4). Therefore, we hypothesized that in progressive AS with chronic afterload elevation, RV function would increase before detectable PH, which would affect symptoms and normalize after aortic valve replacement (AVR).
Eighty patients with isolated AS (23 with moderate, 24 with severe asymptomatic, 33 with severe symptomatic AS) and 28 control subjects of similar age and sex distribution (18 normotensive; 10 hypertensive) were prospectively recruited. Exclusions were LV ejection fraction (EF) <55%, increased pulmonary pressures, underlying cardiomyopathies, and other severe valvular disease. Cardiovascular magnetic resonance (CMR) was performed at baseline and in 21 patients who underwent surgery 8 ± 2 months post-AVR to assess biventricular function and RV circumferential strain by tissue-tracking, a technique that may overcome limitations in RV myocardial deformation (5). RVEF was similar to that in control subjects in early LV afterload stages (hypertensive control subjects: 61 ± 4%; moderate AS patients: 62 ± 4%; p = 0.89), but increased significantly with AS severity (asymptomatic severe AS patients: 68 ± 7%; symptomatic AS patients: 74 ± 4%; p < 0.001) (Figure 1). The hyperdynamic RV was accompanied by elevated circumferential RV strain (symptomatic AS patients: −17 ± 4% vs. controls subjects: −14 ± 4%; p = 0.02). RVEF was correlated with peak aortic velocity (r = 0.62; p < 0.001) (Figure 1), symptoms of valve obstruction (r = 0.66; p < 0.001), and brain natriuretic peptide values (r = 0.41; p = 0.04). RVEF ≥71% had the best accuracy in detecting symptoms (area under the receiver-operating characteristics curve: 0.89; p < 0.001), whereas an RVEF ≥63% defined all symptomatic AS. Baseline RVEF was also correlated with LV mass regression post-AVR (r = 0.61; p = 0.01), and RV parameters were restored toward normal post-AVR (RVEF: 75 ± 4% → 61 ± 7%; p < 0.001; RV strain: −17 ± 4 → −16 ± 4; p = 0.05 in pre- and post-AVR, respectively).
We thus demonstrated that a hyperdynamic RV is associated with increasing AS severity, clinical decompensation, and LV recovery post-AVR. Right-sided compensation might play an important role in adapting to chronic AS; the hypertrophic, stiff, and subclinically impaired LV might be aided by increased RV systolic function to preserve filling and maintain stroke volume across the valve obstruction. A hyperdynamic RV might be a novel early objective marker of decompensated AS and might be particularly useful to examine patients who had symptoms that are difficult to assess (e.g., those less able to move or those with multiple comorbidities). If confirmed in larger scale studies, a hyperdynamic RV might result in a stimulus for consideration of valve replacement and be a new treatment target in patients with right heart conditions in whom the blunted compensatory response might lead to earlier decompensation.
Please note: †Drs. Mahmod and Myerson contributed equally to this work and are joint senior authors. This study was supported by the National Institute for Health Research, Oxford Biomedical Research Centre, Oxford, United Kingdom and the British Heart Foundation Centre of Research Excellence, Oxford, United Kingdom. The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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