ABSTRACT
BACKGROUND: Left ventricular ejection fraction (LVEF) is among the parameters that are usually employed to define surgical timing of severe aortic stenosis (AS). Our hypothesis states that even when their LVEF is preserved, patients with severe symptomatic AS have impaired myocardial structure and function, and such impairment is related to the deleterious progression of left ventricular hypertrophy (LVH) from the compensated to the decompensated stage, as shown by the changes in diastolic function and the increase in left ventricular end-diastolic pressure (LVEDP). METHODS AND RESULTS: A total of 26 patients with severe AS and LVEF > 50% referred for aortic valve replacement underwent catheterization, echocardiography and an intraoperative biopsy. Patients with severe symptomatic AS were classified as: group 1 (G1; compensated LVH, LVEDP < 15 mm Hg without coronary artery disease [CAD], n = 7), group 2a (G2a, decompensated LVH, without CAD, n = 7), and group 2b (G2b, decompensated LVH with CAD, n = 12). Differences were seen in the following: myocyte area [µm2]: G1: 328 ± 66, G2a: 376 ± 22, G2b: 385 ± 13, p < 0.01; collagen volume [%]: G1: 4.77 ± 1.27, G2a: 8.40 ± 1.27, G2b: 11.05 ± 3.08, p < 0.01; LVEDP normalized by diastolic diameter [mm Hg/mm]: G1: 0.27 ± 0.01, G2a: 0.39 ± 0.06, G2b: 0.44 ± 0.11, p < 0.02; +dP/dtmax/LVEDP [mm Hg/s/mm Hg]: G1: 176 ± 45, G2a: 89.6 ± 20, G2b: 113.1 ± 41, p < 0.01; two-dimensional peak systolic longitudinal strain [%]: G1: 17.7 ± 4.75, G2a: 13.4 ± 3.04, G2b: 13.5 ± 3.13, p < 0.05. CONCLUSIONS: Patients with severe symptomatic AS and preserved ejection fraction who develop decompensated LVH characterized by increased LVEDP, exhibit an abnormal myocardial structure and diastolic and systolic impairment.
Subject(s)
Aortic Valve Stenosis/physiopathology , Clinical Decision-Making , Hypertrophy, Left Ventricular/physiopathology , Myocardium/pathology , Stroke Volume/physiology , Ventricular Function, Left/physiology , Aged , Aortic Valve Stenosis/complications , Aortic Valve Stenosis/diagnosis , Biopsy , Cardiac Catheterization , Echocardiography , Female , Follow-Up Studies , Humans , Hypertrophy, Left Ventricular/diagnosis , Hypertrophy, Left Ventricular/etiology , Male , Middle Aged , Prospective Studies , Severity of Illness Index , Systole , Ventricular Pressure/physiologyABSTRACT
Introducción: En la estenosis aórtica sintomática grave (EASG), la alteración del strain global longitudinal sistólico (SGLS) tendría correlación con las modificaciones de la histoarquitectura y podría identificar compromiso contráctil temprano en pacientes con fracción de eyección conservada (FEyC). Objetivo: Analizar el SGLS, el volumen de colágeno (VC), el área miocitaria (ArMi) y el compromiso contráctil en pacientes con EASG y FEyC. Material y métodos: Se incorporaron 26 pacientes con EASG y FEyC (edad 67 ± 11 años, 53% hombres). Se realizaron un estudio hemodinámico preoperatorio y una biopsia endomiocárdica intraoperatoria para determinar el VC y el ArMi. Se identificaron tres grupos de pacientes: G1, hipertrofia ventricular izquierda (HVI) compensada sin enfermedad coronaria (n = 8); G2, HVI descompensada sin enfermedad coronaria (n = 7) y G3, HVI descompensada con enfermedad coronaria (n = 11). El SGLS se normalizó por volumen sistólico, estrés meridional de fin de sístole (δ) y diámetro de fin de diástole (DFD). Resultados: G1, G2 y G3, sin diferencias en volumen sistólico, 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), ArMi (mm²) (G1: 328,7 ± 66,2; G2: 376,7 ± 21,9; G3: 385,0 ± 13,0; p = 0,01), PFDVI (mm Hg) (G1: 13,1 ± 1,5; G2: 19,0 ± 3,8; G3: 23,6 ± 5,8; p < 0,01), +dP/dt máx (mm Hg/seg / PFDVI, mm Hg) (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). El SGLS se correlacionó con VC y PFDVI y hubo tendencia con un índice de contractilidad (+dP/dt máx mm Hg/seg / PFDVI, mm Hg). Conclusiones: Las alteraciones del SGLS en pacientes con EASG y FEyC son expresión de alteraciones estructurales del miocardio relacionadas con incremento del VC, asociado con un aumento de la PFDVI y con probable falla miocárdica contráctil.(AU)
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/dt max (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 GLSS (%) (G1: -17.9 ± 4.2, G2: -13.5 ± 2.5, G3: -13.6 ± 3; p = 0.021). GLSS correlated with CV and LVEDP and it evidenced a trend to correlate with a contractility index (+dP/dt max mm Hg/s / LVEDP, mm Hg). Conclusions: Altered GLSS in patients with SSAS and PEF expresses myocardial structural changes related to increase in C V, which is associated with enhanced LVEDP and probable myocardial contractile failure.(AU)
ABSTRACT
Introducción: En la estenosis aórtica sintomática grave (EASG), la alteración del strain global longitudinal sistólico (SGLS) tendría correlación con las modificaciones de la histoarquitectura y podría identificar compromiso contráctil temprano en pacientes con fracción de eyección conservada (FEyC). Objetivo: Analizar el SGLS, el volumen de colágeno (VC), el área miocitaria (ArMi) y el compromiso contráctil en pacientes con EASG y FEyC. Material y métodos: Se incorporaron 26 pacientes con EASG y FEyC (edad 67 ± 11 años, 53% hombres). Se realizaron un estudio hemodinámico preoperatorio y una biopsia endomiocárdica intraoperatoria para determinar el VC y el ArMi. Se identificaron tres grupos de pacientes: G1, hipertrofia ventricular izquierda (HVI) compensada sin enfermedad coronaria (n = 8); G2, HVI descompensada sin enfermedad coronaria (n = 7) y G3, HVI descompensada con enfermedad coronaria (n = 11). El SGLS se normalizó por volumen sistólico, estrés meridional de fin de sístole (δ) y diámetro de fin de diástole (DFD). Resultados: G1, G2 y G3, sin diferencias en volumen sistólico, 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), ArMi (mm²) (G1: 328,7 ± 66,2; G2: 376,7 ± 21,9; G3: 385,0 ± 13,0; p = 0,01), PFDVI (mm Hg) (G1: 13,1 ± 1,5; G2: 19,0 ± 3,8; G3: 23,6 ± 5,8; p < 0,01), +dP/dt máx (mm Hg/seg / PFDVI, mm Hg) (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). El SGLS se correlacionó con VC y PFDVI y hubo tendencia con un índice de contractilidad (+dP/dt máx mm Hg/seg / PFDVI, mm Hg). Conclusiones: Las alteraciones del SGLS en pacientes con EASG y FEyC son expresión de alteraciones estructurales del miocardio relacionadas con incremento del VC, asociado con un aumento de la PFDVI y con 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/dt max (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 GLSS (%) (G1: -17.9 ± 4.2, G2: -13.5 ± 2.5, G3: -13.6 ± 3; p = 0.021). GLSS correlated with CV and LVEDP and it evidenced a trend to correlate with a contractility index (+dP/dt max mm Hg/s / LVEDP, mm Hg). Conclusions: Altered GLSS in patients with SSAS and PEF expresses myocardial structural changes related to increase in C V, which is associated with enhanced LVEDP and probable myocardial contractile failure.
