Changes In Brachial Artery Diameter Research Articles

Cardiovascular Responses to Dynamic Handgrip Exercise in Patients with Heart Failure with Preserved Ejection Fraction

BackgroundHeart failure with preserved ejection fraction (HFpEF) is associated with symptoms of exercise intolerance, which may correspond to disease‐related changes in the peripheral circulation. A small muscle mass (dynamic handgrip, HG) exercise that evokes minimal cardiopulmonary stress was utilized to concomitantly evaluate exercising muscle blood flow and conduit vessel endothelium‐dependent vasodilation in patients with HFpEF compared to hypertensive controls (CON).MethodsWe evaluated heart rate (HR), stroke volume (SV), cardiac output (CO), mean arterial pressure (MAP), and brachial artery blood velocity and diameter in CON (n = 25, 52 ± 7 y, BMI 30 ± 6 kg/m2) and patients with HFpEF (n = 25, 69 ± 10 y, BMI 33 ± 6 kg/m2) during dynamic HG exercise (15, 30, and 45% MVC, 1 contraction/sec). Brachial artery blood flow and vascular conductance were determined to quantify the hemodynamic response to HG exercise, and changes in brachial artery diameter were evaluated to assess conduit vessel vasodilatory capacity.ResultsWhile HR modestly increased in both groups at 45% MVC (10 ± 2 and 8 ± 2 bpm compared to rest, HFpEF and Control), SV and CO were unchanged across exercise intensities in both groups. Brachial artery blood flow was similar between groups at the lowest exercise intensity (15% MVC: 145 ± 41 vs. 158 ± 17 ml/min, HFpEF vs. CON) but was blunted by 20–40% in HFpEF patients at higher work rates (30% MVC: 229 ± 8 vs. 274 ± 23 ml/min, 45% MVC: 283 ± 17 vs. 399 ± 34 ml/min, HFpEF vs. CON). Brachial artery vascular conductance increased to a similar degree in both groups at 15 and 30% MVC, but was blunted by ~20% at the highest exercise intensity (45% MVC: 2.74 ± 0.21 vs. 3.54 ± 0.30 ml/min/mmHg, HFpEF vs. CON). Brachial artery shear rate was similar between HFpEF and CON at all exercise intensities. Brachial artery diameter increased across work rates in both HFpEF (15% MVC: 3 ± 1%, 30% MVC: 6 ± 1%, 45% MVC: 8 ± 1%) and CON (15% MVC: 2 ± 1%, 30% MVC: 4 ± 1%, 45% MVC: 7 ± 1%), and there was no difference between groups.ConclusionsThese results provide evidence for impaired skeletal muscle blood flow during small muscle mass exercise in patients with HFpEF that cannot be attributed to a disease‐related alteration in central hemodynamics. However, brachial artery vasodilation in response to the step‐wise, sustained shear stimulus evoked during exercise was similar between groups, suggesting a preservation of endothelium‐dependent dilation in patients with HFpEF compared to their hypertensive counterparts. Together, these findings suggest an overall derangement in the regulation of muscle blood flow during exercise in patients with HFpEF that is not attributable to disease‐related changes in endothelial function.Support or Funding InformationThis project is funded in part by the National Institutes of Health (HL118313) and the U.S. Department of Veterans Affairs (RX001697, RX001418, E6910R).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

To study the endothelial dysfunction by brachial artery flow mediated dilatation in coronary artery disease patients

Background: Brachial artery flow mediated dilatation (BAFMD), assessed by high resolution ultrasonography, reflects endothelium dependent vasodilator function. BAFMD is diminished in patients with atherosclerosis and with coronary risk factors and improves with risk reduction therapy.Methods: Study was conducted on 50 patients of coronary artery disease from In-patients who were admitted in the Department of Medicine and 25 healthy control without cardiovascular disease risk factors. All patients having established CAD i.e. Acute coronary syndrome and past history of CABG/angioplasty were included in study. Those morbidly ill and patients with evidence of chronic inflammatory or malignant disease were excluded. Doppler ultrasound of brachial artery was performed in all of them to assess baseline lumen diameter and flow mediated dilatation (i.e. percent change in brachial artery diameter after occlusion cuff release). Patients were divided into two groups; first group was classified as those having BAFMD less than 7.5% and the second group consisted patients having BAFMD less than 10%.Results: Flow mediated dilatation in cases was 6.87±5.48% as compared to the control group in which it was 13.08±3.40% and was statistically significant (P value 0.000002). Brachial artery flow mediated dilatation was abnormal in 80% cases at a cut off value <10% significant abnormalities; i.e. BAFMD <7.5% was found in 66% patients.Conclusions: Endothelial function as assessed by FMD is significantly impaired in patient of coronary artery disease. Hence it may be used as an important screening tool in people having cardiovascular disease risk factors and may play as a crucial role in preventive cardiology.

Clinical Study of Plasma Lipocalin-2 and Endothelial Function

Recent animal studies suggested that lipocalin-2 plays a key role in the development of hypertension, atherosclerosis and endothelial dysfunction. Lipocalin-2 knockout mice are resistant to the harmful effects of high fat diet and do not develop hypertension or atherosclerosis. We therefore hypothesised that lipocalin-2 is also related to endothelial function in man. We measured plasma lipocalin-2 concentration and brachial artery flow-mediated dilatation (FMD) in 245 subjects (201 men, 44 women; mean age±SD, 68±9 y), of whom 151 had hypertension, 80 had diabetes mellitus and 240 were on lipid lowering therapy. Lipocalin-2 was measured using a highly-specific ELISA, with intra- and interassay coefficients of variation of 3.8-6.0% and 3.1–5.2% respectively. Brachial artery diameter and flow velocity were measured using a 7.5MHz ultrasound probe. Scans were taken at baseline, 5 minutes after tourniquet inflation and after sublingual glyceryl trinitrate spray. The percentage change in brachial artery diameter following reactive hyperaemia was calculated. The coefficient of variation of FMD determination was 5%. The median (IQR) plasma lipocalin-2 concentration was 50 (29-75) ng/mL. There was no sex difference. Plasma lipocalin-2 level correlated with serum creatinine (ρ=0.23, p<0.001) but not FMD (ρ=0.005, p=0.94). Instead, FMD decreased with age (ρ=-0.14, p=0.03). It is also lower in individuals with diabetes (p=0.044). Endothelial function decreases with age and diabetes, but is unrelated to plasma lipocalin-2 level. This suggests that plasma lipocalin-2 level is not a major determinant of endothelial function. However, plasma lipocalin-2 is a marker for renal dysfunction.

Changes in brachial artery endothelial function and resting diameter with moderate-intensity continuous but not sprint interval training in sedentary men.

Moderate-intensity continuous training (MICT) improves peripheral artery function in healthy adults, a phenomenon that reverses as continued training induces structural remodeling. Sprint interval training (SIT) elicits physiological adaptations similar to MICT, despite a lower exercise volume and time commitment; however, its effect on peripheral artery function and structure is largely unexplored. We compared peripheral artery responses to 12 wk of MICT and SIT in sedentary, healthy men (age = 27 ± 8 yr). Participants performed MICT (45 min of cycling at 70% peak heart rate; n = 10) or SIT (3 × 20-s "all out" cycling sprints with 2 min of recovery; n = 9), and responses were compared with a nontraining control group (CTL, n = 6). Allometrically scaled brachial flow-mediated dilation (FMD) increased 2.2% after 6 wk of MICT and returned to baseline levels by 12 wk, but did not change in SIT or CTL (group × time interaction, P = 0.04). Brachial artery diameter increased after 6 and 12 wk (main effect, P = 0.03), with the largest increases observed in MICT. Neither training protocol affected popliteal relative FMD and diameter, or central and lower limb arterial stiffness (carotid distensibility, central and leg pulse wave velocity) (P > 0.05 for all). Whereas earlier and more frequent measurements are needed to establish the potential presence and time course of arterial responses to low-volume SIT, our findings suggest that MICT was superior to the intense, but brief and intermittent SIT stimulus at inducing brachial artery responses in healthy men.NEW & NOTEWORTHY We compared the effects of 12 wk of moderate-intensity continuous training (MICT) and sprint interval training (SIT) on peripheral artery endothelial function and diameter, and central and lower limb stiffness in sedentary, healthy men. Whereas neither training program affected the popliteal artery or stiffness indexes, we observed changes in brachial artery function and diameter with MICT but not SIT. Brachial artery responses to SIT may follow a different time course or may not occur at all.

High Dietary Sodium Reduces Low‐Flow‐Mediated Constriction in Salt‐Resistant Adults

High dietary sodium has been shown to impair flow‐mediated dilation independent of blood pressure (BP). Low flow‐mediated (LFC) constriction has been proposed as a complementary measure of vascular function in humans. Therefore, the purpose of this study was to test the hypothesis that a high sodium diet would reduce brachial artery LFC in salt‐resistant adults. Additionally, we sought to determine if sex differences existed in the LFC response to high dietary sodium. Twenty healthy, normotensive adults (12 males, 28.8±1.8 yrs; 8 females, 29.8±2.2 yrs) participated in a controlled feeding study. Following a run‐in diet, participants completed 7 days of a low sodium (LS) diet (20mmol sodium/day) and 7 days of a high sodium (HS) diet (300mmol sodium/day) in random order. Diets were designed to be eucaloric and consistent in macronutrient distribution and potassium content. On the last day of the LS and HS diets, a 24‐hour urine was collected and 24‐hour ambulatory BP was assessed. Subjects were classified as salt‐resistant as defined by a change in 24‐hour ambulatory mean arterial pressure (MAP) of ≤5mmHg between the LS and HS diets. On day 7 of the LS and HS diet, LFC was assessed by ultrasound. LFC was calculated as the % change in brachial artery diameter following a 5‐minute distal cuff occlusion. By design, 24‐hour MAP was not different between LS and HS conditions (85±1 vs 84±1 mmHg, p&gt;0.05) whereas urinary sodium excretion (34.8±6.0mmol/24hr vs 269.7±21.6 mmol/24hr, p&lt;0.01) and serum sodium concentration (137.9±0.6mmol/L vs 140.2±0.3mmol/L, p&lt;0.01) increased significantly on the HS diet. LFC was significantly attenuated on the HS diet compared to LS (2.2±0.3% vs 3.3±0.3%). LFC was reduced by HS in both men and women (men: LS 3.8±0.4% vs HS 2.6±0.4%; women: LS 2.6±0.5% vs HS 1.5±0.5%; p&lt;0.05). These data demonstrate that high dietary sodium impairs LFC in salt‐resistant adults providing additional evidence for the adverse vascular effects of dietary sodium independent of BP.Support or Funding InformationResearch funded by NIH grant R01 HL104106

Endothelial dysfuncton and 2 type diabetes: novel markers for earlier diagnostics

Aim. To assess clinical significance of the novel ultrasound and biochemical markers of endothelial dysfunction (ED) in men with 2 type diabetes (DM2). Material and methods. Totally, 200 males studied, with DM2, of those 112 selected (mean age 51,7±6,7 y.) with normal vascular reactivity by Celermajer D. (1994). function of endothelium was assessed by ultrasound study of arterial vessel reactivity of brachial artery (BA) during the test with reactive hyperaemia and proteomic markers of ED — nitric oxide, endothelial nitric oxide synthase type 3 (NOS3), adhesion molecules ICAM-1, VCAM-1, p-selectin, e-selectin, resistin, osteoprotegerin, immune-enzyme assay. Patients were selected to 2 groups by presence or absence of polymorphism с.582+353_379del gene eNOS3. Results . Regardless the absence of ED signs by standard test with reactive hyperaemia, patients with deletion of 27 pair of nucleotides in 4 intron of non-coding area of eNOS3 gene had increased concentrations of adhesion molecules VCAM-1 by 27% and ICAM-1 by 22,9%, as the decrease of eNOS3 by 55,7%, that followed by slowed maximum vasodilation of BA during the test, comparing to the males not having this polymorphism. The significant positive correlations found of the time of maximum vasodilation development with proteomic markers of ED ICAM-1 and VCAM-1. Conclusion. For the first time, a complex of parameters established — time to maximum BA dilation with increased concentration of proteomic markers ICAM-1, VCAM-1 and decrease of eNOS3 that points on the role of ED earlier than BA diameter changes during the reactive hyperaemia test.

Vascular ultrasound measures before pregnancy and pregnancy complications: A prospective cohort study

ABSTRACTObjectives: To examine the relationship between pre-pregnancy indicators of cardiovascular risk and pregnancy complications and outcomes. Study design: Data from 359 female participants in the Cardiovascular Risk in Young Finns Study were linked with the national birth registry. Flow-mediated dilatation (FMD; maximum change in the left brachial artery diameter after rest and hyperemia); carotid intima-media thickness (IMT); Young’s elastic modulus (YEM); and carotid artery distensibility (Cdist) at the visit prior to the pregnancy were examined as predictors of hypertensive disorders, birthweight, and gestational age using multivariable linear regression with adjustment for confounders (age, BMI, smoking, and socioeconomic status). Results: No relations were seen between FMD, IMT, or the stiffness indices, and hypertensive disorders. Higher pre-pregnancy FMD was associated with lower gestational age, while increased Cdist was associated with reduced birthweight-for-gestational-age. Conclusions: Some cardiovascular ultrasound measures of pre-pregnancy may predict pregnancy complications, but the association is likely to be small.

Reproducibility of Brachial Vascular Changes with Alterations in End-Tidal Carbon Dioxide

The purpose of this study was to examine the reproducibility of the peripheral vascular response to hypercapnia. Healthy college-aged men (n = 7) and women (n = 10) underwent an iso-oxic 10-mm Hg increase in PetCO2 for 12 min. Brachial artery diameter changes were measured using ultrasound imaging. Two tests were completed on day 1 with 15 min of rest between tests. Tests were repeated on day 2. Paired t-tests, Bland–Altman plots and intra-class correlations (ICCs) determined reproducibility. There were no significant differences in peak dilation within day (5.33 ± 3.73% vs. 4.52 ± 2.49%, p = 0.378). The within-day ICC was poor (0.213). Within-day time-to-peak dilation did not significantly differ (660.0 ± 231.8 s vs. 602.7 ± 259.9 s, p = 0.379), and the ICC was fair (0.416, p = 0.113). Between-day peak dilation did not significantly differ (5.24 ± 3.84% vs. 4.71 ± 3.17%, p = 0.123), and the ICC was fair (0.419). Hypercapnia-induced brachial artery dilation is similar within day and between days. The ICC for peak dilation suggests the methodology is not reproducible.

Comparison of brachial dilatory responses to hypercapnia and reactive hyperemia

Flow-mediated dilation (FMD) relies on reactive hyperemia to stimulate the endothelium to release nitric oxide, causing smooth muscle relaxation. Hypercapnia also produces vasodilation, which is thought to be nitric oxide-independent. The purpose of this study was to compare and contrast the effects of hypercapnia and reactive hyperemia as stimuli for brachial artery dilation.On separate days, twenty-five participants underwent vasodilation studies via reactive hyperemia or hypercapnia (i.e. 10 mmHg increase in end-tidal carbon dioxide [PetCO2)]). During both studies changes in brachial artery diameter were recorded using continuous ultrasound imaging. Heart rate (HR) was measured throughout both tests. Resting HR (63 ± 11 versus 68 ± 14 beats min−1, p = 0.0027) and baseline brachial artery diameter measurements (4.57 ± 1.51 versus 5.28 ± 1.86 mm, p = 0.022) were significantly different between reactive hyperemia and hypercapnia, respectively. HR at peak dilation (65 ± 11 versus 76 ± 14 beats min−1, p < 0.0001), peak vessel dilation (8.68 ± 4.50 versus 5.28 ± 1.86%, p = 0.002), and time to peak dilation (90.8 ± 120.1 versus 658.3 ± 226.6 s, p < 0.0001) were also significantly different between reactive hyperemia and hypercapnia.The dynamics by which reactive hyperemia and hypercapnia stimulate vasodilation appear to differ. Hypercapnia produces a smaller and slower vasodilatory effect than reactive hyperemia. Further research is necessary to better understand the mechanisms of vasodilation under hypercapnic conditions.

Microvascular Dysfunction as Opposed to Conduit Artery Disease Explains Sex-specific Chest Pain in Emergency Department Patients With Low to Moderate Cardiac Risk

PurposeChest pain is a common emergency department (ED) presentation that is often unexplained. Recent evidence suggests that disease of the microvessels (arterioles) as opposed to the coronary artery (conduit artery) could explain one third of these cases, particularly in women. Brachial artery reactivity (BAR) is a validated surrogate measure of coronary artery vasomotion. ObjectivesThe goal of this study was to compare brachial artery conduit vessel function (BAR) and microvascular function (postischemic peak reactive hyperemia [RH]) in subjects with and without chest pain and grouped according to sex. MethodsThis prospective cohort study was conducted from January through March 2010. Cases were patients admitted to an ED chest pain center with low to moderate risk of acute coronary syndrome; they were eligible for study if their creatinine level was <2.0 mg/dL and systolic blood pressure was >100 mm Hg or <180 mm Hg. Asymptomatic healthy volunteers on no medications were recruited as control subjects. BAR as a change in brachial artery diameter in response to transient forearm ischemia (endothelium-dependent vasodilation) and RH as a change in flow velocities were measured with a high-resolution ultrasound. Telephone follow-up visits were made at 1 month for recurrence of chest pain and recidivism. FindingsA total of 57 patients and 21 control subjects were enrolled; there was 100% follow-up at 1 month. Most patients (86%) had at least 1 cardiac risk factor. Neither BAR nor RH varied significantly between patients and control subjects (P > 0.05). Symptomatic men had lower mean BAR than women (2.67% vs 6.22%; P < 0.01), even when normalized for shear stress (P = 0.01). Conversely, women with chest pain had lower RH compared with men (2.85 vs 4.61; P = 0.01). The sex-specific differences adjusted for age and Framingham risk scores persisted for BAR (P = 0.003) and RH (P = 0.002). Of 57 patients, 53% had recurrent pain, and 4 returned to the hospital within 1 month. ImplicationsDifferences in BAR and RH in patients ruled out for myocardial infarction suggest that the pathophysiology of acute chest pain might be sex-specific. Men with chest pain exhibited lower BAR, indicating peripheral conduit artery dysfunction. Conversely, women with chest pain exhibited lower postischemic peak hyperemia, indicative of peripheral microvascular dysfunction. Sex differences in pathophysiology of chest pain and vascular dysfunction could inform development of effective therapeutics for patients with recurrent or persistent chest pain in the absence of obstructive coronary artery disease.

Risk factors and longevity

Aim. To assess clinical significance of the novel ultrasound and biochemical markers of endothelial dysfunction (ED) in men with 2 type diabetes (DM2). Material and methods. Totally, 200 males studied, with DM2, of those 112 selected (mean age 51,7±6,7 y.) with normal vascular reactivity by Celermajer D. (1994). function of endothelium was assessed by ultrasound study of arterial vessel reactivity of brachial artery (BA) during the test with reactive hyperaemia and proteomic markers of ED — nitric oxide, endothelial nitric oxide synthase type 3 (NOS3), adhesion molecules ICAM-1, VCAM-1, p-selectin, e-selectin, resistin, osteoprotegerin, immune-enzyme assay. Patients were selected to 2 groups by presence or absence of polymorphism с.582+353_379del gene eNOS3. Results . Regardless the absence of ED signs by standard test with reactive hyperaemia, patients with deletion of 27 pair of nucleotides in 4 intron of non-coding area of eNOS3 gene had increased concentrations of adhesion molecules VCAM-1 by 27% and ICAM-1 by 22,9%, as the decrease of eNOS3 by 55,7%, that followed by slowed maximum vasodilation of BA during the test, comparing to the males not having this polymorphism. The significant positive correlations found of the time of maximum vasodilation development with proteomic markers of ED ICAM-1 and VCAM-1. Conclusion. For the first time, a complex of parameters established — time to maximum BA dilation with increased concentration of proteomic markers ICAM-1, VCAM-1 and decrease of eNOS3 that points on the role of ED earlier than BA diameter changes during the reactive hyperaemia test.

CO-28: Flow-mediated dilatation (FMD) and endothelium-independent dilation (EID) in patients with multifocal fibromuscular dysplasia: a cross-sectional study

Background Fibromuscular dysplasia (FD) is a rare idiopathic, segmental, non-atherosclerotic non-inflammatory vascular disease, which occurs mostly in middle-aged patients and affects medium-sized arteries (renal and carotid arteries). We previously showed that FD is a general arterial disease with focal exacerbation of the trait. However, whether endothelial dysfunction may be involved in the pathophysiology of FD is unclear. Abstract CO-28 – Table FD EH HS Age, yrs 52 ± 9 52 ± 9 52 ± 9 Women, n (%) 43 (86%) 43 (86%) 42 (84%) Caucasian, n (%) 38 (76%) 38 (76%) 42 (84%) Office SBP, mmHg 125 ± 15*** 121 ± 12*** 113 ± 10 Antihypertensive drugs, n (range) 2 (1-4) 2 (1-4) 0 BA structure External diameter, mm 3.91 ± 0.72° 4.19 ± 0.69 4.00 ± 0.64 Distensibility, μm 114 ± 64 115 ± 57 135 ± 73 IMT, μm 319 ± 79 330 ± 85 303 ± 97 Internal diameter, mm 3.34 ± 0.64 3.56 ± 0.66 3.47 ± 0.57 FMD Basal BA diameter; mm 3.86 ± 0.70*° 4.17 ± 0.63 4.02 ± 0.65 BA diameter (hand ischemia), mm 3.91 + 0.71°° 4.22 + 0.64 4.04 + 0.61 BA diameter (hand hyperhemia), mm 3.98 ± 0.73*° 4.29 ± 0.63 4.16 ± 0.62 Change in BA diameter, % 2.39 [0.31; 5.41] 2.85 [–0.23; 6.15] 2.67 [0.20; 5.73] Basal BA flow velocity, cm/s 7.70 ± 5.99 7.39 ± 5.98 7.66 ± 8.53 BA flow velocity (ischemia), cm/s 3.71 ± 5.25 2.68 ± 5.01 0.98 ± 2.54 BA flow velocity (hyperhemia) cm/s 73 ± 29 69 ± 27 78 ± 38 EID Basal BA diameter, mm 3.92 ± 0.69°° 4.22 ± 0.67 4.07 ± 0.67 Post-GTN BA diameter, mm 4.43±0.69**°° 4.82 ± 0.61 4.74 ± 0.71 Change in BA diameter, % 13.8 [7.9;19.0] 15.3 [10.2; 18.9] 18.4 [12.9;21.1] Post-GTN BA flow velocity, cm/s 7.27 ± 8.12 5.56 ± 6.84 4.76 ± 10.29 * P < 0.05, ** P < 0.01, *** P < 0.001 vs. HS Full-size table Table options View in workspace Download as CSV Methods In a cross sectional study, we compared the endothelial function between 50 patients with multifocal FD of renal/carotid arteries confirmed by CT-angiography, 50 essential hypertensive (EH) patients matched for age, sex, ethnicity and BP and 50 healthy subjects (HS) matched for age, sex and ethnicity. Exclusion criteria were: tobacco consumption, hypercholesterolemia, diabetes, aspirin or statin treatment. Brachial artery (BA) FMD after release of hand ischemia and glyceryl trinitrate (GTN)-induced EID were measured using a high-resolution radiofrequency – based echotracking system blind to the diagnosis. Results FD, EH and HS were well matched. FD and EH had significantly higher SBP than HS despite antihypertensive treatments. BA external diameter was significantly lower in FD than in both HS and EH before, during and after hand ischemia and after GTN. BA intima media thickness (IMT), internal diameter and distensibility did not differ between the 3 groups. The percent changes in BA diameter after release of hand ischemia (FMD) or GTN administration (EID) did not significantly differ between the 3 groups. BA flow velocity did not significantly differ in any experimental condition. Conclusions In conclusion, despite showing similar acute vasodilatory responses to flow and GTN, FD patients differed from EH and HS in terms arterial morphology with smaller BA diameter associated with similar IMT. The similarity of the IMT between the groups, combined with the reduction of the BA diameter in FD patients suggests that the BA underwent inward eutro-phic remodeling despite normal blood flow velocity. This paradoxical remodeling may suggest a chronic defect in the endothelium-dependent pathways involved in arterial remodeling in FD patients.

Time-course of vascular dysfunction of brachial artery after transradial access for coronary angiography.

Prior studies have demonstrated endothelial and smooth muscle brachial artery dysfunction after transradial cardiac catheterization for diagnostic coronary angiography. The duration of this vascular dysfunction is unknown. To determine the time-course of endothelial and smooth muscle cell dysfunction in the upstream brachial artery after transradial cardiac catheterization. We studied 22 consecutive patients with suspected coronary artery disease (age 64.4 ± 7.7 years) undergoing diagnostic transradial cardiac catheterization. Using high-resolution vascular ultrasound, we measured ipsilateral brachial artery diameter changes during reactive hyperemia (endothelium-dependent dilatation) and administration of sublingual nitroglycerin (endothelium-independent dilatation). The measurements were taken at baseline (before cardiac catheterization), 6 h, 24 h, 1 week, and 1 month postprocedure. The contralateral brachial artery served as a control. Ipsilateral brachial artery diameter during endothelium-dependent dilatation decreased significantly compared with the contralateral diameters at 6 h and 24 h after transradial cardiac catheterization (3.22 vs. 4.11 and 3.29 vs. 4.11, respectively, P < 0.001). The administration of nitroglycerin did not affect this difference. At 1 week and 1 month postprocedure there was no significant difference in diameter of the ipsilateral versus the contralateral brachial artery. As expected the contralateral brachial artery showed no significant changes in diameter. Our results showed that transradial cardiac catheterization causes transient vascular endothelial and smooth muscle dysfunction of the ipsilateral brachial artery, which resolves within 1 week postprocedure. These findings strongly suggest the absence of systemic vascular dysfunction after transradial catheterization both immediately postprocedure as well as 1 week postprocedure. © 2015 Wiley Periodicals, Inc.

Association between anthropometry, cardiometabolic risk factors, & early life factors & adult measures of endothelial function: Results from the New Delhi Birth Cohort.

Background & objectives:Abnormal endothelial function represents a preclinical marker of atherosclerosis. This study was conducted to evaluate associations between anthropometry, cardiometabolic risk factors, and early life factors and adult measures of endothelial function in a young urban Indian cohort free of clinical cardiovascular disease.Methods:Absolute changes in brachial artery diameter following cuff inflation and sublingual nitroglycerin (400 µg) were recorded to evaluate endothelium-dependent and -independent measures of endothelial function in 600 participants (362 men; 238 women) from the New Delhi Birth Cohort (2006-2009). Data on anthropometry, cardiometabolic risk factors, medical history, socio-economic position, and lifestyle habits were collected. Height and weight were recorded at birth, two and 11 yr of age. Age- and sex-adjusted linear regression models were developed to evaluate these associations.Results:The mean age of participants was 36±1 yr. Twenty two per cent men and 29 per cent women were obese (BMI > 30 kg/m2). Mean systolic blood pressure (SBP) was 131±14 and 119±13 mmHg, and diabetes prevalence was 12 and 8 per cent for men and women, respectively. Brachial artery diameter was higher for men compared with women both before (3.48±0.37 and 2.95±0.35 cm) and after hyperaemia (3.87±0.37 vs. 3.37±0.35 cm). A similar difference was seen before and after nitroglycerin. Markers of increased adiposity, smoking, SBP, and metabolic syndrome, but not early life anthropometry, were inversely associated with endothelial function after adjustment for age and sex.Interpretation & conclusions:The analysis of the current prospective data from a young urban Indian cohort showed that cardiometabolic risk factors, but not early life anthropometry, were associated with worse endothelial function.

0101 Work Hours, Job Strain, and Occupation with Endothelial Function: The Multi-Ethnic Study of Atherosclerosis (MESA)

ObjectivesTo investigate associations of work hours, job control, job demands, job strain, and occupational category with endothelial function, a predictor of cardiovascular disease (CVD).MethodCurrently employed participants free of CVD (n...

Abstract 226: Importance of Measuring the Time Course of Flow Mediated Dilation When Assessing Endothelial Function in Obese African Americans

Flow mediated dilation (FMD) is a noninvasive technique to assess endothelial function in humans. In most studies FMD is reported as the percent change in brachial artery diameter at 60 seconds after cuff deflation relative to baseline (%FMD at 60 seconds). Recently the availability of automated computer-based edge detection allows measurement of peak dilation during the entire time course of brachial dilation post-hyperemia. Considering that changes in arterial diameter in response to shear stress is a continuous process and that peak dilation may differ in pathological states and occur at any arbitrary time point, we examined the time course of brachial artery FMD after a 5-min period of ischemia in 38 obese African American women (42±9.3 years old, BMI 39±6, % body fat 48.2±4.3, SBP 131±13, DBP 83±8 mm Hg, HR 77±12 bpm). Results were analyzed using brachial analyzer software (Medical Imaging Applications LLC). Baseline brachial artery diameter was 3.95±0.55 mm, the time to peak was 48.93 ±13.82 seconds. The percent change in FMD (%FMD) obtained at peak diameter was greater (4.7±3.19 mm) than %FMD at 60 seconds (3.23±4.33 mm); mean difference = 1.4 (95% CI, 0.54-2.4, P=0.003). A large proportion (79%) of true peak diameters fell outside the 60 seconds time frame typically used to assess FMD, Figure. Our results suggest that the peak vasodilator effect occurs before 60±5 seconds in the majority of our population. Therefore, the evaluation of FMD as a continuous measurement has greater accuracy and less variability for the evaluation of FMD compared with an arbitrary time point.

Cardiovascular impacts and micro-environmental exposure factors associated with continuous personal PM2.5 monitoring

The US Environmental Protection Agency's (US EPA) Detroit Exposure and Aerosol Research Study (DEARS) has provided extensive data on human exposures to a wide variety of air pollutants and their impact on human health. Previous analyses in the DEARS revealed select cardiovascular (CV) health outcomes such as increase in heart rate (HR) associated with hourly based continuous personal fine particulate matter (PM2.5) exposures in this adult, non-smoking cohort. Examination of time activity diary (TAD), follow-up questionnaire (FQ) and the continuous PM2.5 personal monitoring data provided the means to more fully examine the impact of discreet human activity patterns on personal PM2.5 exposures and changes in CV outcomes. A total of 329 343 min-based PM2.5 personal measurements involving 50 participants indicated that ∼75% of these total events resulted in exposures <35 μg/m(3). Cooking and car-related events accounted for nearly 10% of the hourly activities that were identified with observed peaks in personal PM2.5 exposures. In-residence cooking often resulted in some of the highest incidents of 1 min exposures (33.5-17.6 μg/m(3)), with average peaks for such events in excess of 209 μg/m(3). PM2.5 exposure data from hourly based personal exposure activities (for example,, cooking, cleaning and household products) were compared with daily CV data from the DEARS subject population. A total of 1300 hourly based lag risk estimates associated with changes in brachial artery diameter and flow-mediated dilatation (BAD and FMD, respectively), among others, were defined for this cohort. Findings indicate that environmental tobacco smoke (ETS) exposures resulted in significant HR changes between 3 and 7 h following the event, and exposure to smells resulted in increases in BAD on the order of 0.2-0.7 mm/μg/m(3). Results demonstrate that personal exposures may be associated with several biological responses, sometimes varying in degree and direction in relation to the extent of the exposure.

Contribution of nitric oxide to brachial artery vasodilation during progressive handgrip exercise in the elderly

The reduction in nitric oxide (NO)-mediated vascular function with age has largely been determined by flow-mediated dilation (FMD). However, in light of recent uncertainty surrounding the NO dependency of FMD and the recognition that brachial artery (BA) vasodilation during handgrip exercise is predominantly NO-mediated in the young, we sought to determine the contribution of NO to BA vasodilation in the elderly using the handgrip paradigm. BA vasodilation during progressive dynamic (1 Hz) handgrip exercise performed at 3, 6, 9, and 12 kg was assessed with and without NO synthase (NOS) inhibition [intra-arterial N(G)-monomethyl-l-arginine (l-NMMA)] in seven healthy older subjects (69 ± 2 yr). Handgrip exercise in the control condition evoked significant BA vasodilation at 6 (4.7 ± 1.4%), 9 (6.5 ± 2.2%), and 12 kg (9.5 ± 2.7%). NOS inhibition attenuated BA vasodilation, as the first measurable increase in BA diameter did not occur until 9 kg (4.0 ± 1.8%), and the change in BA diameter at 12 kg was reduced by ∼30% (5.1 ± 2.2%), with unaltered shear rate ( 407 ± 57, l-NMMA: 427 ± 67 s(-1)). Although shifted downward, the slope of the relationship between BA diameter and shear rate during handgrip exercise was unchanged ( 0.0013 ± 0.0004, l-NMMA: 0.0011 ± 0.007, P = 0.6) as a consequence of NOS inhibition. Thus, progressive handgrip exercise in the elderly evokes a robust BA vasodilation, the magnitude of which was only minimally attenuated following NOS inhibition. This modest contribution of NO to BA vasodilation in the elderly supports the use of the handgrip exercise paradigm to assess NO-dependent vasodilation across the life span.

Non-cancer atherosclerotic effects associated with environmental and therapeutic radiation doses: The Chernobyl thyroid cancer children study

The Chernobyl disaster, which took place on April 26th 1986 at the nuclear plant in northern Ukraine, represents the largest everhappened nuclear accident. About fivemillion people were exposed to radioactive contamination in Belarus, Russian Federation and Ukraine, with an estimated individual radiation dose ranging from few mSv to some hundred mSv [1]. The main health effect observed was an increase in the incidence of thyroid cancer in the young, but a number of non-cancer end points have been reported [2]. Recently, studies on the atomic bomb survivors in Japan demonstrated that moderate doses of ionizing radiations may contribute to excess cardiovascular disease risk [3], as confirmed also by a metaanalysis [4]. However, cardiovascular effects of low–moderate doses are still largely unexplored [5]. The aim of the present study was to assess the proatherosclerotic effects of radiation exposure in survivors of Chernobyl disaster, subsequently diagnosed with papillary thyroid cancer and treated with radioiodine ablation. Forty-six volunteers were enrolled: 23 subjects who were children (≤8 years old) living in the Chernobyl area in Belarus at the time of the nuclear blast in 1986 (group E-exposed), subsequently diagnosed and treated with radioiodine ablation for papillary thyroid cancer; 23 nonexposed (NE) healthy subjects, matched with E for age, gender and cardiovascular risk factors. All subjects underwent carotid intima–media thickness assessment (CIMT), aortic and carotid stiffnessmeasurement, andperipheral blood testing forEPCevaluation. In a subset of 28 subjects (14 subjects from each group), endothelial function was assessed by brachial artery flow-mediated dilation (FMD). A volume of 100 μL peripheral blood was immunostained with the following monoclonal antibodies: PERcP-conjugated human antiCD34, fluorescein-conjugated human anti-kinase insert domain receptor (KDR), human anti-CD133, or isotype control, and then analyzed by flow-cytometry. Carotid–femoral pulse wave velocity (PWV) was performed (SphygmoCor, AtCor Medical, Sydney, Australia) [6]. Common carotid artery ultrasound scans analyzed by means of Carotid Studio (Cardiovascular Suite; Quipu srl, Pisa, Italy), an algorithm for the automatic evaluation of the instantaneous carotid diameter, CIMT, distensibility coefficient and stiffness [7]. Non-invasive ultrasound assessment of brachial endothelial function was performed as previously described [6]. An automated system for real-time detection of brachial artery diameter by analysis of B-mode ultrasound image sequences was used (FMD Studio, Cardiovascular Suite: Quipu srl, Pisa, Italy). Endothelium-dependent dilation was induced by reactive hyperemia following a 5-min forearm cuff occlusion at 300 mm Hg. Endothelium-independent dilation was obtained by sublingual administration of 25 μg glyceryl-trinitrate (GTN). The baseline characteristics of the study participants are given in Table 1. In E mean total radiation dose was 47.3 ± 16.1 mCi (range 30–200 mCi). All E subjects were treated with L-thyroxin: their median TSH was 0.018 μg/mL (25–75 percentile: 0.007–0.462). Subpopulations of putative EPCs (CD34 + KDR+, CD34+ CD133+, CD34 + CD133 + KDR+) expressed as cell numbers per 10 cytometric events, were significantly decreased in E group when compared to NE group (Table 2, Fig. 1). E and NE presented similar carotid diameter, CIMT, distensibility and stiffness, as well as similar carotid–femoral PWV (Table 2). PP amplification from carotid to brachial site was significantly higher in E than in NE even after considering age, height and heart rate as covariates (P = 0.04). Carotid AIx was also higher in E than in NE (Table 2). E and NE showed similar brachial artery diameter, absolute and percent hyperemic change in diameter and shear rate, whereas in E response to GTN was significantly greater than in NE (Table 2). Themain result of this study is that in a group of young survivors of the Chernobyl nuclear disaster, subsequently treated with radioiodine ablation for thyroid cancer, the number of EPCs was significantly reduced in comparison to healthy volunteers, suggesting a reduced endothelial regeneration and repair capacity. This selective alteration, International Journal of Cardiology 168 (2013) 4255–4592

Lack of Correlation Between Cerebral Vasomotor Reactivity and Flow-Mediated Dilation in Subjects Without Vascular Disease

Cerebral vasomotor reactivity (CVR) represents the capability of cerebral vessels to modify their caliber in response to a stimulus. Impaired CVR is associated with an increased risk for ischemic events in patients with carotid disease. Endothelial dysfunction is considered an important pathogenic factor for atherosclerosis and can be noninvasively assessed by flow-mediated vasodilation (FMD) evaluation. We aimed to evaluate both CVR and FMD in patients without histories of vascular disease in order to define a possible correlation. FMD was measured as brachial artery flow and diameter changes induced by transient ischemia. CVR to hypercapnia was assessed in all subjects by means of a breath-holding test and, in 20 subjects, by an additional CO2 inhalation test. In 30 healthy volunteers (60% women, mean age 56 ± 6 years), CVR and FMD did not appear to be correlated (p = 0.444). A strong association between CO2-induced CVR and breath-holding index was observed (p < 0.001). CVR and FMD represent 2 different modalities that evaluate vasomotor function. According to our data, they did not appear to correlate, probably due to physiologic differences between cerebral and peripheral vascular districts and the vasodilatory stimulus used. The carbon dioxide-induced CVR and breath-holding index appeared to be significantly associated.