Racial difference in endothelial function: role of the infective burden.
There is much evidence to suggest the existence of racial differences between blacks and whites in the behaviour of endothelial function. Infective state, sustained by viral or bacterial agents, may injure the endothelial surface favouring the onset and progression of atherosclerotic process, mainly by an inflammatory mechanism. The aim of the study was to investigate endothelial function, expressed as brachial flow-mediated vasodilation (FMV), in black and white healthy subjects, along with antibody titer to cytomegalovirus, hepatitis virus (B, C), herpes virus-1 and 2, Epstein-Barr, Chlamydia pneumoniae and the expression of adhesion molecules. We enrolled 22 young (mean age 27+/-8 years) healthy subjects of black race (10 males) and 20 healthy young subjects (10 males, mean age 28+/-9 years) of white race. Total infectious burden (TIB) was defined as the number of serological positive infections. Black subjects have a reduced brachial FMV (6.9+/-3.5% versus 11.6+/-3.0%, p<0.01) and increased values of hsCRP (0.35+/-0.15 mg/dL versus 0.07+/-0.08 mg/dL, p<0.05), white cells (8578+/-1041/mmc versus 5833+/-998/mmc, p<0.01) and adhesion molecules (respectively: sVCAM-1 945+/-142 versus 779+/-93, sICAM-1 534+/-107 ng/mL versus 325+/-80 ng/mL; both p<0.01) in comparison to white subjects. The total infectious burden in black race was significantly higher than in white race (5+/-1 versus 2+/-1, p<0.01). At the univariate analysis, brachial FMV was significantly related to the levels of adhesion molecules (respectively: sVCAM-1 r=-0.49; sICAM-1 r=-0.50, both p<0.05), hsCRP (r=-0.47, p<0.05) and white blood cells (r=-0.43, p<0.05). TIB was associated with brachial FMV (r=-0.64, p<0.05), sVCAM-1 (r=0.55, p<0.05) and hsCRP (r=0.47, p<0.05). At the multivariate analysis the only predictive variables for brachial FMV were hsCRP, TIB and brachial diameter (respectively: beta=-0.49, -0.19, -0.54, all p<0.05). This study confirms that endothelial reactivity is impaired in young African black patients; moreover its behavior is strictly related to the inflammatory state and to the total infectious burden.
Marchesi
Simona
S
Internal Medicine Section, Department of Clinical and Experimental Medicine, University of Perugia, Italy. simonamarchesi@yahoo.it
Lupattelli
Graziana
G
Sensini
Alessandra
A
Lombardini
Rita
R
Brozzetti
Matteo
M
Roscini
Anna Rita
AR
Siepi
Donatella
D
Mannarino
Elmo
E
Vaudo
Gaetano
G
D000328:Adult; D050197:Atherosclerosis / Q000208:ethnology / Q000503:physiopathology; D044383:Black People; D001916:Brachial Artery / Q000502:physiology*; D002097:C-Reactive Protein / Q000032:analysis; D002690:Chlamydia Infections / Q000150:complications*; D004730:Endothelium, Vascular / Q000502:physiology / Q000821:virology*; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000208:ethnology; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008297:Male; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D014664:Vasodilation / Q000502:physiology*; D014777:Virus Diseases / Q000150:complications* / Q000208:ethnology; D044465:White People
D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein