Aims Myocardial deformation assessed by strain analysis represents a significant advancement
in our assessment of cardiac mechanics. However, whether this variable is genetically
heritable or whether all/most of its variability is related to environmental factors
is currently unknown. We sought to determine the heritability of echocardiographically
determined cardiac mechanics indices in a population setting. Methods and results
A total of 1357 initially healthy subjects (women 51.6%; 48.2 & PLUSMN; 14.1 years)
were included in this study from 20-year follow-up after the fourth visit of the longitudinal
familial STANISLAS cohort (Lorraine, France). Data were acquired using state-of-the-art
cardiac ultrasound equipment, using acquisition and measurement protocols recommended
by the EACVI (European Association of Cardiovascular Imaging)/ASE (American Society
of Echocardiography)/Industry Task Force. Layer-specific global longitudinal strain
(GLS) and global circumferential strain (full-wall, subendocardial, and subepicardial)
and conventional structural and functional cardiac parameters and their potential
heritability were assessed using restricted maximum likelihood analysis, with genetic
relatedness matrix calculated from genome-wide association data. Indices of longitudinal/circumferential
myocardial function and left ventricular (LV) ejection fraction had low heritability
(ranging from 10% to 20%). Diastolic and standard LV function parameters had moderate
heritability (ranging from 20% to 30%) except for end-systolic and end-diastolic volumes
(30% and 45%, respectively). In contrast, global longitudinal subendocardial strain
(GLSEndo)/global longitudinal subepicardial strain (GLSEpi) ratio had a high level
of heritability (65%). Except for GLSEndo/GLSEpi ratio, a large percentage of variance
remained unexplained (>50%). Conclusions In our population cohort, GLSEndo/GLSEpi
ratio had a high level of heritability, whereas other classical and mechanical LV
function parameters did not. Given the increasing recognition of GLSEndo/GLSEpi ratio
as an early/sensitive imaging biomarker of systolic dysfunction, our results suggest
the possible existence of individual genetic predispositions to myocardial decline.
