Cargando…

Association of Inadequately Low Left Ventricular Mass with Enhanced Myocardial Contractility in Severe Degenerative Aortic Stenosis

Background: Left ventricular hypertrophy (LVH), traditionally considered an adaptive mechanism that is aimed at the maintenance of LV systolic function, is absent in 10%–35% of patients with severe aortic stenosis (AS). Our aim was to estimate the clinical and hemodynamic characteristics in patients...

Descripción completa

Detalles Bibliográficos
Autores principales: Chyrchel, Bernadeta, Długosz, Dorota, Bolt, Klaudiusz, Kruszelnicka, Olga, Dziewierz, Artur, Świerszcz, Jolanta, Wieczorek-Surdacka, Ewa, Hryniewiecki, Tomasz, Surdacki, Andrzej
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6306843/
https://www.ncbi.nlm.nih.gov/pubmed/30469477
http://dx.doi.org/10.3390/jcm7120464
Descripción
Sumario:Background: Left ventricular hypertrophy (LVH), traditionally considered an adaptive mechanism that is aimed at the maintenance of LV systolic function, is absent in 10%–35% of patients with severe aortic stenosis (AS). Our aim was to estimate the clinical and hemodynamic characteristics in patients with severe AS and absent LVH, or inadequately low LV mass (i-lowLVM) relative to an individual hemodynamic load. Methods: We retrospectively analyzed in-hospital records of 100 patients with pure severe degenerative AS, preserved LV systolic function and without relevant coexistent diseases, except for well-controlled hypertension or diabetes. Results: Clinical characteristics were similar in patients with and without LVH, as well as those with and without i-lowLVM, except for slightly lower GFR at i-lowLVM. When compared to their counterparts, subjects without LVH or with i-lowLVM had smaller LV cavities, decreased LV wall thicknesses and higher EF. There were no significant differences in stenosis severity and indices of afterload (valvulo-arterial impedance and circumferential end-systolic LV wall stress), according to the presence or absence of either LVH or i-lowLVM. However, LV fractional shortening at the midwall level was elevated only in patients with i-lowLVM, but not in those without LVH, compared to the remainder (15.8 ± 3.3 vs. 12.9 ± 3.2%, p < 0.001 for those with and without i-lowLVM, respectively; 13.7 ± 3.7 vs. 13.8 ± 3.6% for LVH presence and absence, p = 0.9). Conclusions: Inadequately low LVM relative to the individual hemodynamic load could potentially reflect a different mode of the LV response to severe AS, associated with enhanced load-independent LV systolic performance, i.e., better LV contractility. If confirmed in a large series of patients, our small preliminary study may add to the possible mechanisms of a previously reported counterintuitive tendency of a lower, not higher, risk of adverse outcome in patients with low LV mass despite severe AS. Prospective studies are warranted, in order to determine a potential utility of LVM inadequacy in the risk stratification of patients with AS.