The interplay between renin-angiotensin system activation, abnormal myocardial deformation and neurohumoral activation in hypertensive heart disease: a speckle tracking echocardiography study

Angiotensin converting enzyme (ACE) promotes cardiac fibrosis. LV myocardial deformation and torsion are markers of subclinical myocardial dysfunction. We investigated the association of serum ACE levels with LV deformation markers in untreated hypertensives. In 120 untreated patients (age: 53.5 ± 11.2 years) with essential hypertension and 60 healthy controls, we measured (a) LV longitudinal, circumferential and radial strain (S), peak torsion and the percentage changes between peak twisting and untwisting at the end of early diastolic filling (%dpTw-Utw EDF ) using speckle tracking echocardiography and (b) serum levels of ACE and NTproBNP. Compared to controls, patients had decreased longitudinal strain (−19.1 ± 2.9 vs. −21.7 ± 1.8%), increased peak twisting (19.1 ± 4.6 vs.14.0 ± 3.7 deg) but decreased %dpTw-Utw EDF (78 ± 8 vs. 86 ± 8%) and higher serum ACE levels (27.6 ± 8.0 vs 20.9 ± 7.1 U/ml) (p