Influence of Aging on Level and Layer-Specific Left Ventricular Longitudinal Strain in Subjects Without Structural Heart Disease

Abstract

Values for level- (apical, mid, and basal) and layer-based (endocardial, mid-myocardial, and epicardial) left ventricular (LV) longitudinal strain across age are scarce. The present study evaluates the effect of aging on level- and layer-specific LV longitudinal strain in subjects without structural heart disease. A total of 408 subjects (mean age 58 years [range 16 to 91]; 49% men) were evaluated retrospectively. Subjects were divided into equal groups based on age and gender. Subjects with evidence of structural heart disease or arrhythmias were excluded. Mean LV ejection fraction was 62 ± 6.2%. A gradual increase in magnitude of level LV longitudinal strain was observed from basal to mid and apical levels (-16.7 ± 2.1%, -18.8 ± 2.0%, -22.6 ± 3.8%; p <0.001, respectively). Across age groups, there was a borderline significant decrease in magnitude of basal longitudinal strain in older subjects, whereas the magnitude in the apical level significantly increased. On layer-based analysis, the magnitude of longitudinal strain increased from epicardium to endocardium across all age groups. On multivariable analysis, only diabetes mellitus was associated with more impaired longitudinal strain in the endocardium, and male gender was associated with more impaired longitudinal strain at the epicardium layer. In conclusion, with increasing age, the magnitude of LV longitudinal strain at the basal level declines while the apical LV longitudinal strain increases. In contrast, layer-specific LV longitudinal strain remains unchanged with aging. The presence of diabetes mellitus modulated the effect of age on the LV endocardial layer, and male gender was associated with more impaired longitudinal strain at the epicardial layer.

Long-term athletic training does not alter age-associated reductions of left-ventricular mid-diastolic lengthening or expansion at rest

“…Without additional level-specific (base-apex gradient) analysis of longitudinal strain, it is difficult to ascertain whether the lower longitudinal lengthening in older age is uniform along with the LV or specific to the apical and/or basal regions. Indeed, a region-specific pattern of diastolic deformation is plausible, since longitudinal systolic strain has demonstrated subtle increases and decreases in apical and basal strain, respectively with advancing age (Abou et al 2017 ). Thus, regional dissemination of strain during diastole warrants further work that specifically examines whether altered diastolic strain profiles with ageing are localized or uniform along with the LV.…”

“…Similarly, circumferential strain may be maintained (Zghal et al 2011 ; Nagata et al 2017 ) or even increase with ageing (Sun et al 2013 ; Hung et al 2017 ). Strain is not homogenous across the LV wall, however, but is highest in the endocardium and lowest in the epicardium (Abou et al 2017 ). The most recent versions of STE software enable the identification of strain within three myocardial layers to ascertain mechanical (dys) function (Sharif et al 2018 ), through layer-specific analysis.…”

Prevalence of left ventricular systolic dysfunction in pre‐dialysis and dialysis patients with preserved left ventricular ejection fraction

“…Left ventricular GLS was measured with speckle tracking echocardiography. Left ventricular systolic dysfunction despite preserved LVEF was defined by a value of LV GLS lower than two standard deviations below the mean value of LV GLS derived from individuals without structural heart disease . Patients were followed up for the occurrence of HF hospitalization and all‐cause mortality at the Leiden University Medical Centre.…”

“…Normally, LV GLS is reported as a negative value since it indicates the shortening of the myocardium relative to the original length; however, the magnitude (absolute value) of LV GLS is presented in this analysis . Patients were divided into two groups according to LV GLS >15.2% (more preserved) and LV GLS ≤15.2% (more impaired), a cut‐off value obtained from 2 standard deviations below the mean value of LV GLS derived from healthy controls …”

Characterizing Sphingosine Kinases and Sphingosine 1-Phosphate Receptors in the Mammalian Eye and Retina

“…S1PR2 is important for cell migration [29] and S1PR2 mutations induce hearing loss by disrupting endocochlear potential gradients [30]. S1PR3 has demonstrated an important role in a bacterial infection response [31], nociception and itching sensation [32]. S1PR4 and S1PR5 expression is more restricted and they are mostly found on the cells of the immune and nervous systems, respectively [33,34].…”