
Genetically determined pattern of left ventricular function in normal and hypertensive hearts
Author(s) -
Kovács Attila,
Molnár Andrea Ágnes,
Kolossváry Márton,
Szilveszter Bálint,
Panajotu Alexisz,
Lakatos Bálint Károly,
Littvay Levente,
Tárnoki Ádám Domonkos,
Tárnoki Dávid László,
Voros Szilard,
Jermendy György,
Sengupta Partho P.,
Merkely Béla,
MaurovichHorvat Pál
Publication year - 2018
Publication title -
the journal of clinical hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 67
eISSN - 1751-7176
pISSN - 1524-6175
DOI - 10.1111/jch.13271
Subject(s) - medicine , heritability , ejection fraction , cardiology , speckle tracking echocardiography , diastole , population , hypertensive heart disease , heart failure , blood pressure , genetics , environmental health , biology
We sought to assess the inheritance of left ventricular ( LV ) function using speckle‐tracking echocardiography and the impact of hypertension on modifying the genetically determined pattern of contraction in a population of twins. We recruited 92 Caucasian twin pairs, including 74 hypertensive ( HTN ) siblings. Beyond standard echocardiographic protocol, a speckle‐tracking analysis was performed, including global longitudinal strain ( GLS ). Systolic function, as assessed by ejection fraction, showed moderate heritability (61%); however, GLS showed higher and dominant heritability (75%). Heterogeneity models revealed that there were no differences between the HTN and non‐ HTN subjects regarding the heritability of GLS . However, the heritability estimates of diastolic function parameters, including early diastolic strain rate, were low. LV systolic biomechanics is highly heritable. GLS shows dominant heritability, despite the presence of early‐stage hypertensive heart disease. Early diastolic parameters are rather determined by environmental factors. These findings suggest the presence of a genetic framework that conserves systolic function despite the expression of diastolic dysfunction and may underlie the phenotypic progression towards heart failure with preserved ejection fraction.