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Aortic stenosis and mitral regurgitation cause respectively left ventricular pressure and volume overload and induce ultrastructural changes of the myocardial extracellular matrix with fibrosis formation.
Myocardial fibrosis leads to increased left ventricular stiffness, diastolic dysfunction and subclinical systolic dysfunction in the early stages of aortic stenosis and mitral regurgitation preceeding reduction in left ventricular ejection fraction and left ventricular remodeling.
Advances in non-invasive imaging techniques (echocardiography, magnetic resonance and nuclear imaging) have permitted direct and indirect assessment of left ventricular fibrosis and early detection of structural and functional left ventricular abnormalities in aortic stenosis and mitral regurgitation.
Curriculum topic: Valvular heart disease
Currently, the most encountered valve diseases include aortic stenosis (AS) and mitral regurgitation (MR); data from population based studies have shown that approximately 9% of individuals aged 65 years or more have either MR or AS.1 w1 While indications for surgery are well defined in symptomatic patients, the optimal timing of surgery in asymptomatic severe AS or MR remains controversial. Currently, surgical intervention is considered in the presence of reduced left ventricular ejection fraction (LVEF), left ventricular (LV) dilatation, pulmonary hypertension, reduced exercise capacity, increased plasma concentrations of biomarkers (eg, N-terminal pro-brain natriuretic peptide (NT-proBNP)), and arrhythmias (eg, atrial fibrillation), since all these variables are associated with worse prognosis if treated medically.w2 w3 However, most of these variables are encountered only when AS or MR have progressed significantly, leading to suboptimal clinical outcomes after surgery.w2 w3
Accordingly, markers that could identify early structural and functional abnormalities of the LV are needed to potentially facilitate the decision for timing of surgery, thereby improving clinical outcomes. In both AS and MR, ultrastructural changes of the LV with expansion of the extracellular matrix and fibrosis formation may occur due to pressure and volume overload, respectively.w4 w5 Fibrosis causes increased LV stiffness, leading to …
Contributors All authors contributed to this paper.
Competing interests In compliance with EBAC/EACCME guidelines, all authors participating in Education in Heart have disclosed potential conflicts of interest that might cause a bias in the article. PD was partially supported by a Sadra Medical Research Grant (Boston Scientific) and with a European Association of Cardiovascular Imaging (EACVI) Research Grant, and receives speaker fees from Abbott Vascular (MitraClip Crossroads Faculty) and Philips Healthcare. VD received consulting fees from St Jude Medical and Medtronic. The Department of Cardiology of Leiden University Medical Centre received research grants from Biotronik, Medtronic, Boston Scientific, Lantheus Medical Imaging, Edwards Lifesciences, St Jude Medical, GE Healthcare. No specific financial support for this work is involved.
Provenance and peer review Commissioned; externally peer reviewed.
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