title: HLA phenotypes as promoters of cardiovascular remodelling in subjects with arterial hypertension.
abstract: The objective of this study was to investigate the association between human leukocyte antigens (HLA) phenotypes and cardiovascular remodelling, as expressed by left ventricular mass (LVM) and carotid intima-media thickness (IMT), in hypertensives. We examined 153 subjects with arterial hypertension and 61 normotensive controls living in the greater Athens area. The population was classified into three groups and specifically group I (normotensives), group II with Grade 1 hypertension and group III with Grade 2 or 3 hypertension. HLA class I and class II antigens were studied by microlymphocytotoxic technique. Carotid IMT and LVM were determined by ultrasonography. The prevalence of HLA DQ7 in the hypertensive cohort was 27.4% that was significantly smaller than the 52.5% among the controls (P = 0.002). The HLA DR11 was found in 24.0% of the hypertensives and in 52.5% of the controls (P < 0.001). Group III hypertensives with HLA DR11 exhibited significantly higher LVM/h in comparison to the hypertensives without this HLA (199.0 +/- 28.8 vs 171.2+44.1g/m, P = 0.009). This association was not present in groups I and II. Similarly, group III hypertensives with HLA DQ7 were characterized by higher IMT in comparison to those without this HLA (0.94 +/- 0.19 vs 0.83 +/- 0.23 mm, P = 0.048). HLA DR17 was associated with higher IMT in both groups II and III (1.00 +/- 0.19 vs 0.82 +/- 0.19 mm, P = 0.046 and 1.01 +/- 0.23 vs 0.84 +/- 0.22 mm, P = 0.049, respectively) but not in group I. In conclusion, certain HLA phenotypes may be related to the levels of arterial blood pressure. Moreover, it seems that these HLA phenotypes may identify subjects with arterial hypertension that are more prone to develop cardiovascular hypertrophy.
authors.affiliation: 4th Department of Internal Medicine, Evangelismos State General Hospital, Athens, Greece. andreadise@usa.net
authors.forename: E J
authors.initials: EJ
authors.lastname: Diamantopoulos
authors.forename: E A
authors.initials: EA
authors.lastname: Andreadis
authors.forename: C V
authors.initials: CV
authors.lastname: Vassilopoulos
authors.forename: I G
authors.initials: IG
authors.lastname: Vlachonikolis
authors.forename: K E
authors.initials: KE
authors.lastname: Tarassi
authors.forename: N A
authors.initials: NA
authors.lastname: Chatzis
authors.forename: G I
authors.initials: GI
authors.lastname: Tsourous
authors.forename: C A
authors.initials: CA
authors.lastname: Papasteriades
mesh_terms: D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000235:genetics*; D002340:Carotid Artery Diseases / Q000453:epidemiology / Q000235:genetics*; D016022:Case-Control Studies; D005260:Female; D005819:Genetic Markers / Q000235:genetics; D020022:Genetic Predisposition to Disease; D006680:HLA Antigens / Q000235:genetics*; D006801:Humans; D006973:Hypertension / Q000453:epidemiology / Q000235:genetics*; D017379:Hypertrophy, Left Ventricular / Q000453:epidemiology / Q000235:genetics*; D015994:Incidence; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D011336:Probability; D011379:Prognosis; D012016:Reference Values; D018570:Risk Assessment; D012680:Sensitivity and Specificity; D017539:Tunica Intima / Q000503:physiopathology; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D005819:Genetic Markers; D006680:HLA Antigens