Relación entre el strain rate y la estructura miocárdica en la estenosis aórtica grave;
Relationship Between Strain Rate and Myocardial Structure in Severe Aortic Stenosis

Introducción: En la estenosis aortica severa (EASS) la alteración del strain global longitudinal sistólico (SGLS) tendría correlación con las modificaciones de la histoarquitectura y podría identificar compromiso contráctil temprano en pacientes (ptes) con fracción de eyección conservada (FEYC). Objetivo: Analizar SGLS, volumen de colágeno (VC), área miocitaria (ArMy) y compromiso contráctil en ptes con EASS y FEYC. Métodos: ingresaron 26 ptes con EASS y FEYC (edad 67±11 años, 53%  hombres). Se realizó estudio hemodinámico preoperatorio y biopsia endomiocárdica intraoperatoria determinando VC y ArMy. Se identificaron tres grupos (G) de ptes: G1, HVIC compensada sin enfermedad coronaria (n: 8); G2, HVID sin enfermedad coronaria (n: 7) y G3 HVID con enfermedad coronaria (n: 11). El SGLS se normalizó por: volumen sistólico (VS), estrés meridional de fin de sístole (δ) y diámetro de fin de diástole (DFD). Resultados: G1, G2 y G3  sin diferencias en: VS, δ y DFD y con diferencias en: VC (%)  (G1: 4.7±1.2 , G2: 8.4±1.2, G3: 11.0±3.0;  p<0.01), ArMy (µm2) (G1: 328.7±66.2,  G2: 376.7±21.9,  G3: 385.0±13.0;  p=0.01), PFDVI (mmHg) (G1: 13.1±1.5 , G2: 19.0±3.8,  G3: 23.6±5.8;  p<0.01) , +dP/dt máx (mmHg/seg/PFDVI, mmHg)  (G1: 176.4±45.5,  G2: 89.6±20.1,  G3: 113.1± 43.7; p<0.01), SGLS (%) (G1: -17.9±4.2, G2: -13.5±2.5, G3: -13.6±3; p=0.021). SGLS correlacionó con: VC, PFDVI y hubo tendencia con un índice de contractilidad (+dP/dt máx mmHg/seg/ PFDVI, mmHg). Conclusiones: Las alteraciones del SGLS en ptes con EASS y FEY conservada es expresión  de alteraciones estructurales del miocardio relacionado con incremento del VC, asociado a un aumento de la PFDVI y  a probable falla miocárdica contráctil.

Background: In severe symptomatic aortic stenosis (SSAS) altered global longitudinal systolic strain (GLSS) would correlate with changes in myocardial histological architecture and could identify early contractile involvement in patients with preserved ejection fraction (PEF).Objective: The aim of this study was to analyze GLSS, collagen volume (CV), myocyte area (MyAr) and contractile involvement in patients with SSAS and PEF.Methods: Twenty six patients with SSAS and PEF (67±11 years old, 53% male) were included in the study. A preoperative hemodynamic study and an intraoperative endomyocardial biopsy were performed to determine CV and MyAr. Three groups of patients were identified: G1: compensated left ventricular hypertrophy (LVH) without coronary disease (n=8); G2: decompensated LVH without coronary disease (n=7) and G3: decompensated LVH with coronary disease (n=11). GLSS was normalized by stroke volume, meridional end-systolic wall stress (δ) and end-diastolic diameter (EDD).Results: No significant differences in stroke volume, δ and EDD were observed between groups G1, G2 and G3. Differences between groups were observed in: CV (%) (G1: 4.7 ± 1.2, G2: 8.4 ± 1.2, G3: 11.0 ± 3.0; p < 0.01), MyAr (mm2) (G1: 328.7 ± 66.2, G2: 376.7 ± 21.9, G3: 385.0 ± 13.0; p = 0.01), LVEDP (mm Hg) (G1: 13.1 ± 1.5, G2: 19.0 ± 3.8, G3: 23.6 ± 5.8; p < 0.01), +dP/dtmax (mm Hg/sec / LVEDP, mm Hg) (G1: 176.4 ± 45.5, G2: 89.6 ± 20.1, G3: 113.1 ± 43.7; p < 0.01), and SGLS (%) (G1: -17.9 ± 4.2, G2: -13.5 ± 2.5, G3: -13.6 ± 3; p = 0.021). SGLS correlated with CV and LVEDP and it evidenced a trend to correlate with a contractility index (+dP/dtmax mm Hg/s / LVEDP, mm Hg).Conclusions: Altered GLSS in patients with SSAS and PEF expresses myocardial structural changes related to increase in CV, which is associated with enhanced LVEDP and probable myocardial contractile failure.