[Systemic endothelial dysfunction in patients with pseudoexfoliation syndrome]. / Systemische Endotheldysfunktion bei Patienten mit Pseudoexfoliationssyndrom.

BACKGROUND: Recent studies have shown that pseudoexfoliation syndrome (PEX) is not limited to the anterior segment of the eye, but also affects different structures, such as blood vessels, heart, liver and lungs. Vascular endothelial dysfunction is associated with an increased cardiovascular risk. The purpose of our study was to evaluate endothelial function of the brachial artery in patients with PEX. PATIENTS/MATERIALS AND METHODS: We prospectively examined 21 patients with PEX and 21 age- and sex-matched individuals in a control group. Brachial artery endothelial function was assessed by the response to flow-mediated dilation (FMD) and nitroglycerin-mediated dilation (NMD) using high resolution ultrasound. Dilation was expressed as the percent change in diameter relative to the baseline diameter. RESULTS: Patients with PEX had significantly lower FMD (1.9-2.8 versus 4.1-3.3 in the control group, p = 0.02). NMD in PEX patients was lower than in the control group (10.1-5.1 versus 10.8-5.8 in the control group, p < 0.69), but the difference was not statistically significant. CONCLUSIONS: Our study showed a statistically significant association between PEX and systemic vascular endothelial dysfunction. Larger clinical studies are needed to prove the higher cardiovascular risk in PEX patients.

Interaction between gene polymorphisms of renin-angiotensin system and metabolic risk factors in premature myocardial infarction.

The renin-angiotensin system is involved in the pathogenesis of coronary artery disease (CAD) and myocardial infarction (MI). The authors investigated the association of genetic variability in the renin-angiotensin system (RAS) with premature MI and interactive effects between gene polymorphisms and metabolic risk factors on MI risk. Their study compared 142 patients with MI younger than 55 years with 142 healthy subjects. Polymorphisms of angiotensin-I converting enzyme (ACE) gene (insertion/deletion), angiotensinogen gene (M235T), and angiotensin-II type-1 receptor (AGT1R) gene (A1166C) were tested. The ACE-DD (deletion/deletion) genotype conferred a twofold independent risk for MI (confidence interval [CI] = 1.1-3.7; p = 0.01) after adjustment for cardiovascular risk factors, whereas angiotensinogen-TT genotype and AGT1R-AA genotype were not independent risk factors for MI. An interactive effect on MI risk was found between ACE-DD and AGT1R-AA genotypes (odds ratio [OR]=2, 95% CI= 1-3.9), between ACE-DD and angiotensinogen-TT genotypes (OR = 2.7, 95% CI = 1-7.3), as well as among ACE-DD, angiotensinogen-TT, and AGT1R-AA genotypes (OR=4.8, 95% CI = 1-22.8). Similarly, metabolic risk factors interacted with angiotensinogen-TT genotype (OR= 2, 95% CI = 1.1-3.9) on MI risk. The ACE-DD genotype is an independent risk factor for MI in patients younger than 55 years. Additionally, the authors provide evidence of an interactive effect on MI risk between risk genotypes of RAS, as well as between the angiotensinogen-TT genotype and metabolic risk factors.