scholarly journals Understanding endothelial dysfunction in preterm preeclampsia with severe features: utility of bedside brachial artery Doppler

2022 ◽  
Vol 226 (1) ◽  
pp. S425-S426
Author(s):  
Jenna L. Racine ◽  
Ryan Pewowaruk ◽  
Alejandro Roldan-Alzate ◽  
Ian Bird ◽  
Jason Austin ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Brachial Artery

Ascorbic Acid does not Improve Endothelium-Dependent Flow-mediated Dilatation of the Brachial Artery in Patients with Raynaud’s Phenomenon Secondary to Systemic Sclerosis

2003 ◽  
Vol 73 (1) ◽  
pp. 3-7 ◽  
Author(s):  
M. E. Mavrikakis ◽  
J. P. Lekakis ◽  
M. Papamichael ◽  
K. S. Stamatelopoulos ◽  
Ch. C. Kostopoulos ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Smooth Muscle ◽  
Systemic Sclerosis ◽  
Endothelial Dysfunction ◽  
Brachial Artery ◽  
Raynaud’S Phenomenon ◽  
Raynaud's Phenomenon ◽  
Water Soluble ◽  
Placebo Administration ◽  
Flow Mediated Dilatation

Previous studies have shown that patients with Raynaud’s phenomenon secondary to systemic sclerosis present abnormal endothelial function; the mechanisms responsible for the endothelial dysfunction are unknown but increased vascular oxidative stress could be a possible cause. The hypothesis that a potent water-soluble antioxidant can reverse endothelial dysfunction in these patients was tested in the present study. We examined 11 female patients with Raynaud’s phenomenon secondary to systemic sclerosis and ten healthy control women by ultrasound imaging of the brachial artery to assess flow-mediated (endothelium-dependent) and nitrate-induced (endothelium-independent) vasodilatation. Flow-mediated dilatation and nitrate-induced dilatation were significantly reduced in patients with Raynaud’s phenomenon, indicating abnormal endothelial and smooth muscle cell function. Patients with Raynaud’s phenomenon entered a double-blind, randomized, crossover placebo-controlled trial and received orally 2 g of ascorbic acid or placebo; vascular studies were repeated two hours after ascorbic acid or placebo administration. Flow-mediated dilatation did not improve after ascorbic acid (1.6 ± 2.2% to 2.2 ± 2.5%, ns) or placebo administration (1.2 ± 1,9% to 1.7 ± 1.4%, ns); also nitrate-induced dilatation was similar after ascorbic acid or placebo (16 ± 7.4% vs 17 ± 8%, ns), suggesting no effect of ascorbic acid on endothelial and vascular smooth muscle function. In conclusion, ascorbic acid does not reverse endothelial vasomotor dysfunction in the brachial circulation of patients with Raynaud’s phenomenon secondary to systemic sclerosis. The use of different antioxidants or different dosing of ascorbic acid may be required to show a beneficial effect on endothelial vasodilator function.

Abstract 2450: A Randomized Controlled Trial of Low Dose Hormone Therapy on Myocardial Ischemia in Postmenopausal Women with No Obstructive Coronary Artery Disease:Results from the NHLBI-sponsored WISE

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
C. Bairey Merz ◽  
Marian Olson ◽  
Candace McClure ◽  
James Symons ◽  
George Sopko ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Chest Pain ◽  
Coronary Artery ◽  
Endothelial Dysfunction ◽  
Myocardial Ischemia ◽  
Hormone Therapy ◽  
Postmenopausal Women ◽  
Brachial Artery ◽  
Low Dose

Background: Compared with men, women have more evidence of myocardial ischemia in the setting of no obstructive coronary artery disease (CAD). While low endogenous estrogen levels are associated with endothelial dysfunction, the role of low dose hormone therapy has not been fully evaluated in women suffering from myocardial ischemia and no obstructive CAD. Objective: This WISE ancillary trial evaluated the effect of low dose hormone therapy in postmenopausal women with myocardial ischemia and no obstructive CAD on: endothelial dysfunction, assessed by brachial artery reactivity, physical functional disability assessed by exercise testing, and quality of life assessed by cardiac symptoms and psychological questionnaires. Methods: Using a multicenter, randomized, placebo-controlled design, seventy-four participants with normal/minimally diseased epicardial coronary arteries (<50% luminal diameter stenosis) who fulfilled the inclusion criteria were planned to be randomized to receive either 1 mg norethindrone/10 mcg ethinyl estradiol (1/10 NA/EE) or placebo for twelve weeks. Baseline and exit brachial artery reactivity (BART), exercise stress testing, WISE psychosocial questionnaires, SF-36, blood lipids and hormone levels were evaluated. Results: Recruitment was closed prematurely due to failure to recruit in the year following publication of the Women’s Health Initiative hormone trial results. Of the 37 women randomized, 35 completed the study. While there was no difference in the frequency of chest pain between groups at the baseline visit, at study exit there was less frequent chest pain in the 1/10 NA/EE group compared to the placebo group (p=0.02). Women taking 1/10 NA/EE also showed a trend to improved BART and exercise tolerance, and had significantly fewer hot flashes/night sweats (p=0.003), less avoidance of intimacy (p=0.05), and borderline differences in sexual desire and vaginal dryness (p=0.06). Conclusion: Among postmenopausal women with myocardial ischemia and no obstructive CAD, hormone therapy with 1/10 NA/EE is associated with reduced chest pain symptoms, menopausal symptoms and improved quality of life with trends for improved endothelial function and exercise performance.

Fenofibrate improves endothelial function in the brachial artery and forearm resistance arterioles of statin-treated Type 2 diabetic patients

2010 ◽  
Vol 118 (10) ◽  
pp. 607-615 ◽  
Author(s):  
Sandra J. Hamilton ◽  
Gerard T. Chew ◽  
Timothy M.E. Davis ◽  
Gerald F. Watts
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Statin Therapy ◽  
Brachial Artery ◽  
Ldl Cholesterol ◽  
Density Lipoprotein ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Type 2 Diabetic

Dyslipidaemia contributes to endothelial dysfunction and CVD (cardiovascular disease) in Type 2 diabetes mellitus. While statin therapy reduces CVD in these patients, residual risk remains high. Fenofibrate corrects atherogenic dyslipidaemia, but it is unclear whether adding fenofibrate to statin therapy lowers CVD risk. We investigated whether fenofibrate improves endothelial dysfunction in statin-treated Type 2 diabetic patients. In a cross-over study, 15 statin-treated Type 2 diabetic patients, with LDL (low-density lipoprotein)-cholesterol <2.6 mmol/l and endothelial dysfunction [brachial artery FMD (flow-mediated dilatation) <6.0%] were randomized, double-blind, to fenofibrate 145 mg/day or matching placebo for 12 weeks, with 4 weeks washout between treatment periods. Brachial artery FMD and endothelium-independent NMD (nitrate-mediated dilatation) were measured by ultrasonography at the start and end of each treatment period. PIFBF (post-ischaemic forearm blood flow), a measure of microcirculatory endothelial function, and serum lipids, lipoproteins and apo (apolipoprotein) concentrations were also measured. Compared with placebo, fenofibrate increased FMD (mean absolute 2.1±0.6 compared with −0.3±0.6%, P=0.04), but did not alter NMD (P=0.75). Fenofibrate also increased maximal PIFBF {median 3.5 [IQR (interquartile range) 5.8] compared with 0.3 (2.1) ml/100 ml/min, P=0.001} and flow debt repayment [median 1.0 (IQR 3.5) compared with −1.5 (3.0) ml/100 ml, P=0.01]. Fenofibrate lowered serum cholesterol, triacylgycerols (triglycerides), LDL-cholesterol, apoB-100 and apoC-III (P≤0.03), but did not alter HDL (high-density lipoprotein)-cholesterol or apoA-I. Improvement in FMD was inversely associated with on-treatment LDL-cholesterol (r=−0.61, P=0.02) and apoB-100 (r=−0.54, P=0.04) concentrations. Fenofibrate improves endothelial dysfunction in statin-treated Type 2 diabetic patients. This may relate partly to enhanced reduction in LDL-cholesterol and apoB-100 concentrations.

scholarly journals Coenzyme Q10 improves endothelial dysfunction of the brachial artery in Type II diabetes mellitus

Diabetologia ◽  
2002 ◽  
Vol 45 (3) ◽  
pp. 420-426 ◽  
Author(s):  
G. F. Watts ◽  
D. A. Playford ◽  
K. D. Croft ◽  
N. C. Ward ◽  
T. A. Mori ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Endothelial Dysfunction ◽  
Brachial Artery ◽  
Coenzyme Q10 ◽  
Type Ii Diabetes ◽  
Type Ii Diabetes Mellitus ◽  
Type Ii

scholarly journals Flow-Mediated Dilatation of the Brachial Artery for Assessing Endothelial Dysfunction in Children with Moyamoya Disease

2020 ◽  
Vol 55 (3) ◽  
pp. 149-154
Author(s):  
Eun-Hee Kim ◽  
Hyung-Chul Lee ◽  
Jaeyeon Chung ◽  
Sang-Hwan Ji ◽  
Young-Eun Jang ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Moyamoya Disease ◽  
Brachial Artery ◽  
Flow Mediated Dilatation

Endothelial dysfunction is an independent factor responsible for vasospastic angina

2001 ◽  
Vol 101 (6) ◽  
pp. 707-713 ◽  
Author(s):  
Hiroki TERAGAWA ◽  
Masaya KATO ◽  
Junichi KUROKAWA ◽  
Togo YAMAGATA ◽  
Hideo MATSUURA ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Brachial Artery ◽  
Coronary Stenosis ◽  
Intima Media Thickness ◽  
Control Group ◽  
Test Results ◽  
Independent Factor ◽  
Atherosclerotic Changes ◽  
Significant Coronary Stenosis

In order to evaluate peripheral endothelial function in patients with vasospastic angina (VSA), we measured flow-mediated dilation (FMD) of the brachial artery in patients with VSA and compared it with FMD in patients without VSA. Endothelial dysfunction is considered one of the mechanisms underlying VSA. However, its exact role remains to be clarified. The study included 30 patients with positive spasm-provocational test results without evidence of significant coronary stenosis (VSA group) and 30 patients with negative spasm-provocational test results without evidence of significant coronary stenosis (control group). In each patient, brachial artery diameter responses to hyperemic flow and glyceryl trinitrate spray were measured using high-resolution ultrasound. The carotid intima-media thickness was also measured as a marker of systemic atherosclerosis. FMD was lower in the VSA group (4.8±0.5%) compared with the control group (9.4±0.7%, P < 0.0001). In the VSA group, FMD was not affected by coronary risk factors or the presence of atherosclerotic changes on coronary angiography. Glyceryl trinitrate-induced dilation did not differ between the two groups. The intima-media thickness was comparable between the VSA (0.85±0.04mm) and control groups (0.81±0.05mm). These findings indicated that peripheral endothelial function is impaired only in the VSA group, whereas the atherosclerotic changes were similar in the two groups. We conclude that endothelial dysfunction may be an independent factor responsible for the development of VSA.

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