• ecocardiografia
• preipertensione
• strain bidimensionale
• tissue Doppler imaging
• ventricolo destro

Purpose: To analyze the relationship between increasing systemic blood pressure and right ventricular function by means of Tissue-Doppler Imaging (TDI) and Two-dimesional Strain echocardiographic techniques.
Subjects and methods: Ninety-eight never-treated, nonobese patients with blood pressure values varying from the optimal to the mild hypertensive range were recruited. Peak early (Em) and late (Am) diastolic and systolic (Sm) velocities were recorded at the tricuspid and mitral annuli by TDI. Longitudinal peak strain and strain rate (SR) were sampled by speckle-tracking methodology at the right ventricle (RV) free wall and interventricular septum (IVS) and RV and left ventricular (LV) structure and function were evaluated by conventional echo-Doppler sonography. Insulin sensitivity was tested by homeostasis model assessment (HOMA) index. Data were analyzed by 24-h systolic BP (SBP) (cut-offs 117 and 130 mmHg), thus partitioning an optimal BP from an intermediate high-normal and an upper mildly increased BP stratum.
Results: Em decreased in the mid-third and decelerated further in association with reduced Sm in the upper BP tertile; both correlated negatively to septal thickness and positively to homologous TDI-derived LV indices. RV peak systolic strain and early diastolic SR decreased in the mid-BP third without further changes in the upper tertile. IVS thickened gradedly by increasing systemic 24-h SBP; posterior wall remodelled to a lesser extent and poorly related to BP load and LV mass index did not change. RV and IVS systolic and diastolic strain indices associated inversely with increasing septal thickness. RV and LV indices of global ventricular function, estimated pulmonary pressure, HOMA did not differ by systemic BP.
Conclusion: TDI and 2D-strain echocardiography showed a RV diastolic and systolic function impairment in response to slightly increased systemic BP. The process paralleled homologous changes at the LV side and was driven by interventricular septum remodeling, perhaps as a reflection of its role in RV function and biventricular interdependence. Insulin sensitivity seemed to play no relevant role.