Objective: The renin-angiotensin system and endothelial function have been both associated with hypertension, but there are very few data in resistant hypertension. The aim of the present study was to assess the relationship between insertion/ deletion polymorphism in the gene encoding the angiotensin-converting enzyme (ACE I/D) and estimation of cardiovascular and metabolic complications in resistant hypertensive patients. Design and method: In the present study we analyzed and genotyped data from 150 patients with resistant hypertension. We have evaluated arterial stiffness (AS) indices, carotid intima-media thickness (cIMT), HOMA index and clinical data. Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved. Abstracts e257 Results: D allele was more prevalent, and 74 patients presented DD homozygosis. Sixty-eight patients had metabolic syndrome (MetS), without signifi cant differences between DD and I allele carriers. DD genotype appeared strongly associated with higher HOMA values (p < 0.001), and also with both AIx (p = 0.003) and PWV (p = 0.023). A signifi cant association was found between DD genotype and cIMT (p < 0.005), and the presence of carotid plaques (p < 0.001). HOMA was correlated with AS (PWV: p < 0.001; AIx: p < 0.01). Conclusions: Our results are in agreement with experimental evidences suggesting that DD genotype appeared to be associated with AS, increased cIMT, HOMA index, and the presence of carotid plaques, and confi rming that D allele plays an important risk role on development of cardiovascular and metabolic complications in patients with resistant hypertension, independently from the presence of other risk factors.

CLINICAL IMPACT OF ANGIOTENSIN CONVERTING ENZYME (ACE) POLYMORPHISM ON DEVELOPMENT OF CARDIOVASCULAR AND METABOLIC COMPLICATIONS IN SUBJECTS WITH RESISTANT HYPERTENSION

DI STEFANO, ROSSELLA;FELICE, FRANCESCA;
2016-01-01

Abstract

Objective: The renin-angiotensin system and endothelial function have been both associated with hypertension, but there are very few data in resistant hypertension. The aim of the present study was to assess the relationship between insertion/ deletion polymorphism in the gene encoding the angiotensin-converting enzyme (ACE I/D) and estimation of cardiovascular and metabolic complications in resistant hypertensive patients. Design and method: In the present study we analyzed and genotyped data from 150 patients with resistant hypertension. We have evaluated arterial stiffness (AS) indices, carotid intima-media thickness (cIMT), HOMA index and clinical data. Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved. Abstracts e257 Results: D allele was more prevalent, and 74 patients presented DD homozygosis. Sixty-eight patients had metabolic syndrome (MetS), without signifi cant differences between DD and I allele carriers. DD genotype appeared strongly associated with higher HOMA values (p < 0.001), and also with both AIx (p = 0.003) and PWV (p = 0.023). A signifi cant association was found between DD genotype and cIMT (p < 0.005), and the presence of carotid plaques (p < 0.001). HOMA was correlated with AS (PWV: p < 0.001; AIx: p < 0.01). Conclusions: Our results are in agreement with experimental evidences suggesting that DD genotype appeared to be associated with AS, increased cIMT, HOMA index, and the presence of carotid plaques, and confi rming that D allele plays an important risk role on development of cardiovascular and metabolic complications in patients with resistant hypertension, independently from the presence of other risk factors.
2016
https://journals.lww.com/jhypertension/Abstract/2016/09002/_PP_23_10__CLINICAL_IMPACT_OF_ANGIOTENSIN.756.aspx
File in questo prodotto:
File Dimensione Formato  
_PP_23_10__CLINICAL_IMPACT_OF_ANGIOTENSIN.756.pdf

accesso aperto

Tipologia: Versione finale editoriale
Licenza: Creative commons
Dimensione 81.33 kB
Formato Adobe PDF
81.33 kB Adobe PDF Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11568/842697
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus ND
  • ???jsp.display-item.citation.isi??? 0
social impact