A prospective study on urinary microalbuminuria as surrogate marker of vascular endothelial dysfunction, in patients of ischemic stroke

Background: Presence of overt proteinuria has been independently linked to greater stroke risk. The objectives of this study were to determine the relationship between the for ischemic stroke and albuminurea as a marker for vascular events. Microalbuminuria, is an early marker of both kidney disease and endothelial dysfunction, may be associated with global vascular risk, but the nature and relationship between microalbuminuria and incident ischemic stroke has not been clearly defined. The purpose of this study was to assess the association of microalbuminuria and ischemic stroke.Methods: Study enrolled 150 admitted patients of acute ischemic stroke. The patients were assessed by questionnaire, microalbuminuria, creatinine clearance after detailed history taking and thorough clinical examination.Results: The combined common risk factors were HTN (80%), diabetes (33%) and smoking (53%). The hypertensive patients had 8 times higher risk of microalbuminuria as compared to normotensive patients (95% 1.8-31.0 p<0.05). Among diabetes patients had risk of microalbuminuria 30 times higher compared to euglycemic patients (95% CL 9.6-78.8 p<0.01). The smoker patients had 8 times risk of microalbuminuria (CL 95%-1.2-22.8 p<0.16). However, the patients who had dyslipidemia had risk of microalbuminuria 1.07 times who have normal lipid level, but it was statistically insignificance (98% CL 0.8-4.1 p>0.05). The 38 patients out of 46 patients who had microalbuminuria has high normal serum creatinine with creatinine clearance (45-59 mL/min/1.73 m2. (82% versus. 4.4% 30.44 mL/min/173m2). The risk of microalbuminuria was higher in patients who had high normal serum creatinine (1.4 mg/dL) with creatinine clearance of 45-59 mL/min/1.73 m2 versus normal serum creatinine 0.8 mg/dL.Conclusions: The finding of the study, show the microalbuminuria is an independent risk factor for vascular endothelial dysfunction, in patient of diabetes early renal dysfunction and HTN, extrapolating the vascular event (ischemic stroke).

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Particulate matter exposure induces persistent lung inflammation and endothelial dysfunction

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00048.2007 ◽

2008 ◽

Vol 295 (1) ◽

pp. L79-L85 ◽

Cited By ~ 114

Author(s):

Eiji Tamagawa ◽

Ni Bai ◽

Kiyoshi Morimoto ◽

Claire Gray ◽

Tammy Mui ◽

...

Keyword(s):

Air Pollution ◽

Particulate Matter ◽

Endothelial Dysfunction ◽

Total Dose ◽

Systemic Inflammation ◽

Lung Inflammation ◽

Vascular Endothelial ◽

Vascular Endothelial Dysfunction ◽

Vascular Events ◽

Acute And Chronic Exposure

Epidemiologic and animal studies have shown that exposure to particulate matter air pollution (PM) is a risk factor for the development of atherosclerosis. Whether PM-induced lung and systemic inflammation is involved in this process is not clear. We hypothesized that PM exposure causes lung and systemic inflammation, which in turn leads to vascular endothelial dysfunction, a key step in the initiation and progression of atherosclerosis. New Zealand White rabbits were exposed for 5 days (acute, total dose 8 mg) and 4 wk (chronic, total dose 16 mg) to either PM smaller than 10 μm (PM10) or saline intratracheally. Lung inflammation was quantified by morphometry; systemic inflammation was assessed by white blood cell and platelet counts and serum interleukin (IL)-6, nitric oxide, and endothelin levels. Endothelial dysfunction was assessed by vascular response to acetylcholine (ACh) and sodium nitroprusside (SNP). PM10 exposure increased lung macrophages ( P < 0.02), macrophages containing particles ( P < 0.001), and activated macrophages ( P < 0.006). PM10 increased serum IL-6 levels in the first 2 wk of exposure ( P < 0.05) but not in weeks 3 or 4. PM10 exposure reduced ACh-related relaxation of the carotid artery with both acute and chronic exposure, with no effect on SNP-induced vasodilatation. Serum IL-6 levels correlated with macrophages containing particles ( P = 0.043) and ACh-induced vasodilatation ( P = 0.014 at week 1, P = 0.021 at week 2). Exposure to PM10 caused lung and systemic inflammation that were both associated with vascular endothelial dysfunction. This suggests that PM-induced lung and systemic inflammatory responses contribute to the adverse vascular events associated with exposure to air pollution.

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Dynamics of fibrotic and vascular endothelial dysfunction markers in elderly hypertensive patients after ischemic stroke receiving beta-blockers

CARDIOVASCULAR THERAPY AND PREVENTION ◽

10.15829/1728-8800-2021-3087 ◽

2022 ◽

Vol 20 (8) ◽

pp. 3087

Author(s):

O. A. Osipova ◽

E. V. Gosteva ◽

O. N. Belousova ◽

S. G. Gorelik ◽

N. I. Klyushnikov ◽

...

Keyword(s):

Ischemic Stroke ◽

Endothelial Dysfunction ◽

Beta Blocker ◽

Enzyme Linked Immunosorbent Assay ◽

Average Dose ◽

Vascular Endothelial ◽

Vascular Endothelial Dysfunction ◽

Hypertensive Patients ◽

Elderly Hypertensive ◽

Elderly Hypertensive Patients

Aim. To compare the effect of beta-blocker therapy (bisoprolol and nebivolol) on the dynamics of fibrotic and vascular endothelial dysfunction markers in elderly hypertensive patients after ischemic stroke (IS).Material and methods. This prospective cohort study included 75 hypertensive patients who were admitted to the hospital due to IS. The mean age of patients was 67±6 years. The average National Institutes of Health Stroke Scale (NIHSS) score was 7±3. The followup period was 6 months. The control group consisted of 20 elderly people with hypertension without prior myocardial infarction. The patients were divided into groups based on received therapy: group 1 (n=38) — bisoprolol; group 2 (n=37) — nebivolol. The level of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) was determined by enzyme-linked immunosorbent assay (ELISAKit, USA). Vascular ultrasound was carried out using a LOGIQP9 (GE) system according to the Celermajer method.Results. After 6-month nebivolol, we revealed a decrease in the level of MMP-9 by 30,2% (p<0,01), TIMP-1 by 15,6% (p<0,05). After 6-month bisoprolol therapy, the level of MMP-9 decreased by 14,5% (p<0,05), while TIMP-1 did not change. Intergroup comparison found that when using nebivolol, there was a higher decrease in the level of MMP-9 by 15,7% (p<0,05), TIMP-1 by 9,7% (p<0,05), MMP-9/TIMP-1 by 7,8% (p<0,05) than with bisoprolol therapy. After 6-month bisoprolol therapy, there was a decrease in the proportion of patients with severe endothelial dysfunction (ED) by 7,9% (p<0,05). Two patients from the nebivolol group moved into mild ED category. The number of patients with moderate ED increased by 19% (p<0,01), while prevalence of severe ED decreased by 24,4% (p<0,01).Conclusion. The results obtained indicate that the beta-blocker nebivolol at an average dose of 8,55+1,75 mg/day significantly reduces the vascular fibrosis, normalizes the ratio of collagen synthesis and degradation markers, improves the vasodilation brachial artery properties in comparison with bisoprolol in elderly hypertensive patients after IS.

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Paradoxical absence of a prothrombotic phenotype in a mouse model of severe hyperhomocysteinemia

Blood ◽

10.1182/blood-2011-09-380568 ◽

2012 ◽

Vol 119 (13) ◽

pp. 3176-3183 ◽

Cited By ~ 23

Author(s):

Sanjana Dayal ◽

Anil K. Chauhan ◽

Melissa Jensen ◽

Lorie Leo ◽

Cynthia M. Lynch ◽

...

Keyword(s):

Endothelial Dysfunction ◽

Carotid Artery ◽

Inferior Vena ◽

Vena Cava ◽

Vascular Endothelial ◽

Vascular Endothelial Dysfunction ◽

Vascular Events ◽

Cerebral Arterioles ◽

Increased Susceptibility

Abstract Hyperhomocysteinemia confers a high risk for thrombotic vascular events, but homocysteine-lowering therapies have been ineffective in reducing the incidence of secondary vascular outcomes, raising questions regarding the role of homocysteine as a mediator of cardiovascular disease. Therefore, to determine the contribution of elevated homocysteine to thrombosis susceptibility, we studied Cbs−/− mice conditionally expressing a zinc-inducible mutated human CBS (I278T) transgene. Tg-I278T Cbs−/− mice exhibited severe hyperhomocysteinemia and endothelial dysfunction in cerebral arterioles. Surprisingly, however, these mice did not display increased susceptibility to arterial or venous thrombosis as measured by photochemical injury in the carotid artery, chemical injury in the carotid artery or mesenteric arterioles, or ligation of the inferior vena cava. A survey of hemostatic and hemodynamic parameters revealed no detectible differences between control and Tg-I278T Cbs−/− mice. Our data demonstrate that severe elevation in homocysteine leads to the development of vascular endothelial dysfunction but is not sufficient to promote thrombosis. These findings may provide insights into the failure of homocysteine-lowering trials in secondary prevention from thrombotic vascular events.

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