LAUSR

Introduction Recent progress has been focused on severe aortic stenosis (AS), while its antecedent, moderate AS, still poses a clinical challenge. Notably, in moderate AS, depressed LV performance, like symptomatic status, may be due to non-valvular causes, e.g. CAD, primary myocardial dysfunction, hypertension or noncardiac diseases, all of which require different management. LV hypertrophy (LVH), traditionally perceived as an adaptive mechanism to preserve LV systolic function, frequently develops already in moderate AS. However, inappropriately high LV mass, i.e. disproportionate to LV afterload, predicts adverse outcome in AS and hypertension. Additionally, in concentric LVH, indices based on LV midwall mechanics reflect LV systolic function more accurately than EF which overestimates LV performance. Aim To assess whether renal function is related to LV systolic performance and the appropriateness of LVH in real-world patients with moderate AS. Methods We reviewed hospital records of 150 subjects with moderate degenerative AS, out of whom 70 with pure AS in sinus rhythm, with EF>40% and stable in-hospital creatinine entered the final analysis. The patients were compared according to GFR [ml/min per 1.73 m 2 ] estimated by the CKD-EPI equation from averaged serum creatinine: group A (GFR>85), B (GFR = 60−85) and C (GFR = 15−59). From routine echocardiographic records and blood pressure, we calculated valvulo-arterial impedance (Zva), an index of global LV afterload, and excess of LV mass (ELVM). ELVM is the deviation from the LVM predicted individually from hemodynamic load, expressed as a proportion of the predicted LVM. LV midwall fractional shortening (mwFS) was also derived from standard records, assuming a constant LV wall volume during the cardiac cycle. Results The 3 groups did not differ in aortic valve area, EF, Zva, LV mass, prevalence of symptoms, CAD or diabetes. ELVM increased gradually across decreasing GFR categories (p = 0.01 for trend). Compared to group A, group B subjects had lower mwFS (p Conclusions Progressive GFR deterioration seems associated with excessive LVH and LV dysfunction at the midwall level in moderate AS, irrespective of global LV afterload and EF. Excessive LVH can be triggered by slightly reduced LV contractility already in mild renal impairment as a compensatory, yet ineffective, mechanism aimed at restoring LV performance by lowering LV wall stress. Whether prevention of early GFR decline may attenuate LVH and improve prognosis in AS, remains to be studied.