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Endothelial cell damage and angiotensin-converting enzyme insertion/deletion genotype in elderly hypertensive patients.
J Am Coll Cardiol. 1998 Aug; 32(2):444-50.JACC

Abstract

OBJECTIVES

The purpose of this study was to investigate the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) genotype and endothelial cell dysfunction or hypercoagulable state in elderly hypertensive patients.

BACKGROUND

Angiotensin-converting enzyme (ACE) insertion/ deletion (I/D) polymorphism was recently reported to be associated with various cardiovascular diseases. However, the precise mechanism of this association remains unknown, and some confounding factors might also affect the association. Endothelial cell dysfunction and coagulation activation play important roles in both the atherosclerotic process and the onset of cardiovascular events.

METHODS

We identified the ACE I/D genotype and measured the plasma levels of markers of endothelial cell damage (von Willebrand factor [vWF] and thrombomodulin) and of coagulation activation (prothrombin fragment F1 + 2 [F1 + 2]) in 318 asymptomatic elderly patients with hypertension, aged 59-93 years.

RESULTS

The vWF level was significantly higher in those with the DD genotype (n = 54) than in those with the II genotype (n = 131, p < 0.0001) or with the ID genotype (n = 133, p < 0.0001). The TM levels were also higher in patients with the ID genotype (p < 0.005) and the DD genotype (p < 0.01) than in those with the II genotype. There were no differences in F1 + 2 level among the groups. Positive correlations of systolic blood pressure with levels of both vWF and thrombomodulin were found predominantly in patients with the II genotype (both p < 0.001), but no correlation was noted in those with the DD genotype.

CONCLUSIONS

Considering the increased plasma levels of both endothelial cell-derived markers in the hypertensive patients with ACE DD genotype, we speculate that the ACE D allele is a risk factor for the development of hypertensive cardiovascular disease associated with endothelial cell damage.

Authors+Show Affiliations

Department of Cardiology, Jichi Medical School, Tochigi, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

9708474

Citation

Kario, K, et al. "Endothelial Cell Damage and Angiotensin-converting Enzyme Insertion/deletion Genotype in Elderly Hypertensive Patients." Journal of the American College of Cardiology, vol. 32, no. 2, 1998, pp. 444-50.
Kario K, Matsuo T, Kobayashi H, et al. Endothelial cell damage and angiotensin-converting enzyme insertion/deletion genotype in elderly hypertensive patients. J Am Coll Cardiol. 1998;32(2):444-50.
Kario, K., Matsuo, T., Kobayashi, H., Kanai, N., Hoshide, S., Mitsuhashi, T., Ikeda, U., Nishiuma, S., Matsuo, M., & Shimada, K. (1998). Endothelial cell damage and angiotensin-converting enzyme insertion/deletion genotype in elderly hypertensive patients. Journal of the American College of Cardiology, 32(2), 444-50.
Kario K, et al. Endothelial Cell Damage and Angiotensin-converting Enzyme Insertion/deletion Genotype in Elderly Hypertensive Patients. J Am Coll Cardiol. 1998;32(2):444-50. PubMed PMID: 9708474.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Endothelial cell damage and angiotensin-converting enzyme insertion/deletion genotype in elderly hypertensive patients. AU - Kario,K, AU - Matsuo,T, AU - Kobayashi,H, AU - Kanai,N, AU - Hoshide,S, AU - Mitsuhashi,T, AU - Ikeda,U, AU - Nishiuma,S, AU - Matsuo,M, AU - Shimada,K, PY - 1998/8/26/pubmed PY - 1998/8/26/medline PY - 1998/8/26/entrez SP - 444 EP - 50 JF - Journal of the American College of Cardiology JO - J Am Coll Cardiol VL - 32 IS - 2 N2 - OBJECTIVES: The purpose of this study was to investigate the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) genotype and endothelial cell dysfunction or hypercoagulable state in elderly hypertensive patients. BACKGROUND: Angiotensin-converting enzyme (ACE) insertion/ deletion (I/D) polymorphism was recently reported to be associated with various cardiovascular diseases. However, the precise mechanism of this association remains unknown, and some confounding factors might also affect the association. Endothelial cell dysfunction and coagulation activation play important roles in both the atherosclerotic process and the onset of cardiovascular events. METHODS: We identified the ACE I/D genotype and measured the plasma levels of markers of endothelial cell damage (von Willebrand factor [vWF] and thrombomodulin) and of coagulation activation (prothrombin fragment F1 + 2 [F1 + 2]) in 318 asymptomatic elderly patients with hypertension, aged 59-93 years. RESULTS: The vWF level was significantly higher in those with the DD genotype (n = 54) than in those with the II genotype (n = 131, p < 0.0001) or with the ID genotype (n = 133, p < 0.0001). The TM levels were also higher in patients with the ID genotype (p < 0.005) and the DD genotype (p < 0.01) than in those with the II genotype. There were no differences in F1 + 2 level among the groups. Positive correlations of systolic blood pressure with levels of both vWF and thrombomodulin were found predominantly in patients with the II genotype (both p < 0.001), but no correlation was noted in those with the DD genotype. CONCLUSIONS: Considering the increased plasma levels of both endothelial cell-derived markers in the hypertensive patients with ACE DD genotype, we speculate that the ACE D allele is a risk factor for the development of hypertensive cardiovascular disease associated with endothelial cell damage. SN - 0735-1097 UR - https://www.unboundmedicine.com/medline/citation/9708474/Endothelial_cell_damage_and_angiotensin_converting_enzyme_insertion/deletion_genotype_in_elderly_hypertensive_patients_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0735-1097(98)00251-4 DB - PRIME DP - Unbound Medicine ER -