ABSTRACT
BACKGROUND: Microalbuminuria is associated with atherosclerosis and it is a strong and independent predictor of increased risk for cardiovascular morbidity and mortality. However, the underlying mechanisms of the association of albuminuria and cardiovascular disease are not well understood. We examined the association of endothelial dysfunction with microalbuminuria in non-diabetic and non-hypertensive patients with acute coronary syndromes (ACS). METHODS: We compared endothelial function by flow-mediated dilatation (FMD) and glyceryl trinitrate-mediated dilatation (GTN) and angiographic properties among 27 microalbuminuric and 106 normoalbuminuric patients. Severity of coronary arteriosclerosis was evaluated using the Gensini score and number of diseased vessels. RESULTS: We evaluated 133 patients (106 males; mean age 59 +/- 11 years). Microalbuminuria was present in 27 (20.3%) subjects. Patients with microalbuminuria and normoalbuminuria had similar baseline characteristics. FMD and GTN responses were not different in microalbuminuric patients compared with normoalbuminuric patients (FMD 8.2 +/- 5.3 vs. 7.9 +/- 6.5%, p = 0.54 and GTN 9.3 +/- 5.4 vs. 10.2 +/- 6.9%, p = 0.82). Microalbuminuria was not associated with endothelial dysfunction (p = 0.49). Morphological properties of coronary lesion were not different. CONCLUSION: The presence of microalbuminuria is not associated with endothelial dysfunction and severity of angiographic coronary atherosclerosis in non-diabetic and non-hypertensive patients with ACS.
Subject(s)
Acute Coronary Syndrome/complications , Acute Coronary Syndrome/physiopathology , Albuminuria/complications , Coronary Artery Disease/complications , Coronary Artery Disease/physiopathology , Endothelium, Vascular/physiopathology , Female , Humans , Male , Middle AgedABSTRACT
Endothelial dysfunction is major pathophysiologic mechanism in cardiac syndrome X (CSX), which causes a decrease in plasma nitrite oxide (NO) levels. It was demonstrated that nebivolol improves endothelial function and increases NO release. Despite this pathophysiologic relation, the effect of nebivolol therapy on endothelial function in patients with CSX is unknown. The aim of this study is to evaluate the effect of nebivolol on patients in CSX. Thirty-eight patients who were diagnosed with CSX were prospectively enrolled in the study. The treatment group consisted of 20 patients and the control group consisted of 18 patients. An oral 5-mg dose of nebivolol was given daily and maintained for 4 weeks in the treatment group. Ultrasonographic parameters (brachial artery flow-mediated dilatation [FMD], brachial artery lumen diameters) and inflammatory markers (high-sensitivity C-reactive protein [hsCRP], von Willebrand factor [vWf], and fibrinogen) were measured at baseline and end of the 4 weeks. Brachial baseline lumen diameter, brachial lumen diameter after reactive hyperemia, and FMD were 4.61 +/- 0.49 mm, 4.87 +/- 0.53 mm, and 5.6% +/- 2.3% at baseline. After the nebivolol therapy, there was a significant increase in both brachial artery baseline lumen diameter and lumen diameter after reactive hyperemia (P < 0.001 and P = 0.002). However, there was no significant change in FMD (5.6% +/- 2.2% vs 5.3% +/- 2.1%, P not significant). Levels of hsCRP, vWf, and fibrinogen were significantly decreased (hsCRP: 3.4 +/- 0.49 mg/dl vs 2.97 +/- 0.74 mg/dl, P = 0.001; vWf: 107 +/- 62 vs 86 +/- 58, P = 0.004; fibrinogen: 341 +/- 89 mg/dl vs 299 +/- 87 mg/ dl, P = 0.01) in the treatment group. Nebivolol therapy may have a favorable effect on endothelial function in CSX. Further studies are needed to confirm the clinical significance of nebivolol therapy in CSX.
Subject(s)
Adrenergic beta-Antagonists/therapeutic use , Benzopyrans/therapeutic use , Endothelium, Vascular/drug effects , Ethanolamines/therapeutic use , Microvascular Angina/drug therapy , Vasodilation/drug effects , Adult , Brachial Artery/drug effects , Brachial Artery/physiopathology , C-Reactive Protein/metabolism , Endothelium, Vascular/diagnostic imaging , Endothelium, Vascular/immunology , Endothelium, Vascular/physiopathology , Female , Fibrinogen/metabolism , Humans , Inflammation Mediators/blood , Male , Microvascular Angina/diagnostic imaging , Microvascular Angina/immunology , Microvascular Angina/physiopathology , Middle Aged , Nebivolol , Prospective Studies , Time Factors , Treatment Outcome , Ultrasonography , von Willebrand Factor/metabolismABSTRACT
OBJECTIVES: Endothelial dysfunction in coronary arteries is the main pathogenetic mechanism in patients with slow coronary flow (SCF). Angiotensin converting enzyme (ACE) gene polymorphism has important effects on endothelial function. However, angiographic studies investigating the relation between the ACE and angiotensin II type 1 receptor (ATIIR1) insertion (I)/deletion (D) polymorphism and SCF is limited. METHODS: Fifty-four patients with normal coronary arteries documented by coronary angiography with SCF in any coronary vessel, and 22 subjects with normal coronary arteries without SCF were included in this study. The ID (I/D), II, and DD genotypes were examined. RESULTS: Frequency of DD genotype was found higher in SCF group (50% vs. 27%, respectively; p = .055). Frequency of D allele was significantly higher in the SCF group (p < .05). Presence of DD genotypes increased the possibility of SCF 5.25 times compared to absence of DD genotype (OR, 5.25; 95% CI, 1.30-21.38, p < .05). There was no significant correlation of ATIIR1 gene polymorphism between the 2 groups. CONCLUSIONS: We demonstrated that DD genotype is a risk factor for SCF. Determination of ACE gene polymorphism in patients with SCF may be helpful in medical management and risk stratification.
