Antihypertensive Drugs and Inflammation in Acute Ischemic Stroke as a Predictor Factor of Future Cardiovascular Mortality

Benbir, Gülçin; İnce, Birsen; Kumral, Emre; Öngen, Zeki; Kültürsay, Hakan; Tokgözoğlu, Lâle; Oto, Ali̇; Tüzün, Hasan

doi:10.1007/s10753-010-9290-4

Cited by 7 publications

(4 citation statements)

References 32 publications

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“…A complete medical history was obtained from all subjects, including diabetes mellitus (DM), alcohol intake, cigarette smoking, weight, height, body mass index (BMI), systolic blood pressure (SBP), and diastolic blood pressure (DBP). BMI was calculated as following formula: BMI = Weight (kg)/(Height (m) × Height (m)) [ 11 ]. Biochemical variables including serum creatinine, total cholesterol (TC), total triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) were acquired from patient’s medical chart.…”

Section: Methodsmentioning

confidence: 99%

Serum apelin is associated with left ventricular hypertrophy in untreated hypertension patients

Ding

Zhang

et al. 2015

J Transl Med

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BackgroundApelin is an endogenous ligand for the G protein-coupled receptor APJ. The association between apelin and cardiac modeling has been reported. However, if serum apelin affect the left ventricular hypertrophy (LVH) prevalence in hypertensive patients remains unknown.MethodsWe enrolled 344 untreated hypertensive patients. The presence of LVH was determined by echocardiography. The blood was drawn from these patients and serum apelin level was detected. To study the direct effect of apelin on cardiac hypertrophy, cardiomyocytes were cultured and were transfected with apelin gene. Morphometric analysis and measurement of protein contain per cell were then performed.ResultsWe observed a significantly lower serum apelin level in hypertensive patients with LVH compared with those without LVH. Receiver operating characteristic analyses shows that serum apelin level is robust in discriminating patients with LVH from those without. Our in vitro study showed that cellular protein content and cellular size was increased by Ang II treatment, which can be markedly inhibited by the apelin over-expression in cultured cardiomyocytes.ConclusionOur clinical date established a link between apelin and LVH, suggesting serum apelin may be used as a predicator for LVH prevalence in hypertensive patients. The direct evidence in vitro suggest apelin pathway is involved in the cardiomyocyte adaption to hypertrophic stimuli.

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Section: Methodsmentioning

confidence: 99%

Serum apelin is associated with left ventricular hypertrophy in untreated hypertension patients

Ding

Zhang

et al. 2015

J Transl Med

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“…A high level of inflammation (assessed by hs-CRP) in hypertensive patients with acute ischemic stroke has been linked to an increased risk of future cardiovascular mortality [34]. A study on normotensive subjects revealed that adhesion molecules, particularly the sE-selectin, relates to obesity (waist and hip ratio), whereas the relationship between adhesion molecules and BP in hypertensive subjects is adhesion molecule-specific and varies with sex and age, which may partially explain inconsistencies found in the literature [35].…”

Section: Multivariate Analysis Of the Effects Of Vitamin Supplementatmentioning

confidence: 99%

Blood Pressure Reduction is Associated With the Changes in Oxidative Stress and Endothelial Activation in Hypertension, Regardless of Antihypertensive Therapy

Mihalj

Tadžić²,

Včev³

et al. 2016

Kidney Blood Press Res

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Background/Aims: Hypertensive patients present with increased oxidative stress and frequently receive angiotensin II (ANGII) receptor type I blockers (ARB) for blood pressure (BP) reduction. Recent studies revealed an important role of ANGII in maintaining vascular oxidative homeostasis, including sustaining normal sodium dismutase activity. This study aimed to investigate the effects of antihypertensive therapy and also vitamin C/E supplementation on BP, oxidative stress and endothelial activation in patients with essential hypertension. Methods: Newly discovered patients received ARB/olmesartan or the Ca²⁺-channel blocker (CCB)/amlodipine, and additionally vitamin C/E or placebo throughout weeks 9-16. ELISA was used to determine 8-iso-prostaglendin F2-alpha (8iPGF2α) and endothelial activation markers. Results: In both groups BP was normalized during first 8 weeks of therapy. Vitamins C/E had no additional BP-lowering effect. The vitamins C/E supplementation was not effective in reducing absolute values of 8iPGF2α; however; the magnitude of 8iPGF2α reduction was significantly greater in patients taking vitamins C/E in the CCB group. Although plasma 8iPGF2α positively correlated to BP, a significant decrease occurred during an additional 8 weeks of treatment. There were no changes in endothelial activation markers related to the specific action of ARB or CCB. Conclusions: Present study suggests that observed oxidative stress is a consequence of hypertension. BP reduction is associated with the observed decrease in oxidative stress and changes in endothelial activation regardless of antihypertensive therapy.

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“…Moreover, advanced endothelial dysfunction is associated with future cardiovascular events in high-risk patients (75). Inflammatory mediators, such as hs-CRP and fibrinogen, involved in the atherothrombotic process, are important predictors of future cardiovascular mortality in patients with acute ischemic stroke (76). CRP is the most extensively studied marker of inflammation, and is a novel plasma marker of atherothrombotic disease (77).…”

Section: Endothelial Dysfunction In Inflammation Following Ischemic S...mentioning

confidence: 99%

Inflammation in the pathogenesis of ischemic stroke

Pei

You

2015

Front Biosci

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Ischemic stroke is a common cause of permanent disability in adults worldwide. Inflammation plays a significant role in the pathogenesis of ischemic stroke and its mechanism is complex. Both pro-inflammatory and anti-inflammatory mediators are involved in the pathogenesis of ischemic stroke, an imbalance of which leads to inflammation. Inflammatory cells from both the innate and acquired immune systems are involved in ischemic stroke-related inflammation; processes that are linked by the action of interleukin-17A (IL-17A). Although most inflammatory cells promote inflammation, T regulatory cells (Tregs) may have a protective function at the early stages of an ischemic injury, but a negative role during later stages. However, the precise mechanism of inflammation in ischemic stroke remains elusive; further understanding of it may provide new ideas for the prevention and treatment of ischemic stroke. In this review, we discuss the role of pro-inflammatory and anti-inflammatory mediators and related immune cells in the pathogenesis of ischemic stroke.

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Antihypertensive Drugs and Inflammation in Acute Ischemic Stroke as a Predictor Factor of Future Cardiovascular Mortality

Cited by 7 publications

References 32 publications

Serum apelin is associated with left ventricular hypertrophy in untreated hypertension patients

Serum apelin is associated with left ventricular hypertrophy in untreated hypertension patients

Blood Pressure Reduction is Associated With the Changes in Oxidative Stress and Endothelial Activation in Hypertension, Regardless of Antihypertensive Therapy

Inflammation in the pathogenesis of ischemic stroke

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