Impact of pulse pressure on left ventricular global longitudinal strain in normotensive and newly diagnosed, untreated hypertensive patients. Academic Article uri icon

Overview

abstract

  • OBJECTIVES: Little is known about the impact of pulse pressure on left ventricular systolic function. The aim of our study was to evaluate whether high pulse pressure is associated with subclinical left ventricular systolic dysfunction. METHODS: The study population included 143 participants (68 newly diagnosed, never-treated hypertensive, and 75 normotensive individuals) evaluated by echo-Doppler, including determination of global longitudinal strain (GLS) by speckle tracking. According to pulse pressure tertiles, participants were divided in two groups: the first group merging the first and second pulse pressure tertiles (n = 93, pulse pressure <55 mmHg) and the second group including the highest pulse pressure tertile (HPPT; n = 50, pulse pressure ≥55 mmHg). RESULTS: The two groups were comparable for sex, BMI, and heart rate, whereas age was higher in individuals with the HPPT (P < 0.0001). Left ventricular mass index was significantly higher in individuals with the HPPT (P < 0.01), with no significant difference in relative wall thickness. Among several indices of left ventricular systolic function, only GLS was lower in individuals with the HPPT (P < 0.001). Transmitral E/A ratio (P = 0.006) was lower and E/e' ratio higher (P < 0.001) in the HPPT group. By a multilinear regression analysis, HPPT (P < 0.020) and overweight (P = 0.025) were independent correlates of low GLS. Replacing HPPT with the highest systolic blood pressure tertile, GLS was independently associated with BMI (P = 0.040), but not with the highest systolic blood pressure tertile (P = 0.069). CONCLUSION: Elevated pulse pressure negatively influences left ventricular longitudinal mechanics in a mixed population of normotensive and untreated hypertensive individuals.

publication date

  • June 1, 2016

Research

keywords

  • Blood Pressure
  • Hypertension
  • Ventricular Dysfunction, Left

Identity

Scopus Document Identifier

  • 84961391111

Digital Object Identifier (DOI)

  • 10.1097/HJH.0000000000000906

PubMed ID

  • 27008173

Additional Document Info

volume

  • 34

issue

  • 6