Cerebrovascular carbon dioxide reactivity and flow-mediated dilation in young healthy South Asian and Caucasian European men

Copyright © 2020 the American Physiological Society South Asians living in the United Kingdom have a 1.5-fold greater risk of ischemic stroke than the general population. Impaired cerebrovascular carbon dioxide (CO2) reactivity is an independent predictor of ischemic stroke and cardiovascular mortality. We sought to test the hypothesis that cerebrovascular CO2 reactivity is reduced in South Asians. Middle cerebral artery blood velocity (MCA Vm) was measured at rest and during stepwise changes in end-tidal partial pressure of CO2 (PETCO2) in South Asian (n = 16) and Caucasian European (n = 18) men who were young (~20 yr), healthy, and living in the United Kingdom. Incremental hypercapnia was delivered via the open-circuit steady-state method, with stages of 4 and 7% CO2 (~21% oxygen, nitrogen balanced). Cerebrovascular CO2 reactivity was calculated as the change in MCA Vm relative to the change in PETCO2. MCA Vm was not different in South Asians [59 (9) cm/s, mean (standard deviation)] and Caucasian Europeans [61 (12) cm/s; P > 0.05]. Similarly, cerebrovascular CO2 reactivity was not different between the groups [South Asian 2.53 (0.76) vs. Caucasian European 2.61 (0.81) cm·s-1·mmHg-1; P > 0.05]. Brachial artery flow-mediated dilation was lower in South Asians [5.48 (2.94)%] compared with Caucasian Europeans [7.41 (2.28)%; P 0.05). Flow-mediated dilation was not correlated with cerebrovascular CO2 reactivity measures. In summary, cerebrovascular CO2 reactivity and flow-mediated dilation corrected for shear rate are preserved in young healthy South Asian men living in the United Kingdom. NEW & NOTEWORTHY Previous reports have identified an increased risk of ischemic stroke and peripheral endothelial dysfunction in South Asians compared with Caucasian Europeans. The main finding of this study is that cerebrovascular carbon dioxide reactivity (an independent predictor of ischemic stroke) is not different in healthy young South Asian and Caucasian European men

Walks4work: Rationale and study design to investigate walking at lunchtime in the workplace setting

Background: Following recruitment of a private sector company, an 8week lunchtime walking intervention was implemented to examine the effect of the intervention on modifiable cardiovascular disease risk factors, and further to see if walking environment had any further effect on the cardiovascular disease risk factors. Methods. For phase 1 of the study participants were divided into three groups, two lunchtime walking intervention groups to walk around either an urban or natural environment twice a week during their lunch break over an 8week period. The third group was a waiting-list control who would be invited to join the walking groups after phase 1. In phase 2 all participants were encouraged to walk during their lunch break on self-selecting routes. Health checks were completed at baseline, end of phase 1 and end of phase 2 in order to measure the impact of the intervention on cardiovascular disease risk. The primary outcome variables of heart rate and heart rate variability were measured to assess autonomic function associated with cardiovascular disease. Secondary outcome variables (Body mass index, blood pressure, fitness, autonomic response to a stressor) related to cardiovascular disease were also measured. The efficacy of the intervention in increasing physical activity was objectively monitored throughout the 8-weeks using an accelerometer device. Discussion. The results of this study will help in developing interventions with low researcher input with high participant output that may be implemented in the workplace. If effective, this study will highlight the contribution that natural environments can make in the reduction of modifiable cardiovascular disease risk factors within the workplace. © 2012 Brown et al.; licensee BioMed Central Ltd

The Effect of Water Immersion during Exercise on Cerebral Blood Flow

Introduction: Regular exercise induces recurrent increases in cerebrovascular perfusion. In peripheral arteries, such episodic increases in perfusion are responsible for improvement in arterial function and health. We examined the hypothesis that exercise during immersion augments cerebral blood flow velocity compared with intensity-matched land-based exercise. Methods: Fifteen normotensive participants were recruited (26 ± 4 yr, 24.3 ± 1.9 kg·m−2). We continuously assessed mean arterial blood pressure, HR, stroke volume, oxygen consumption, and blood flow velocities through the middle and posterior cerebral arteries before, during, and after 20-min bouts of water- and land-based stepping exercise of matched intensity. The order in which the exercise conditions were performed was randomized between subjects. Water-based exercise was performed in 30°C water to the level of the right atrium. Results: The water- and land-based exercise bouts were closely matched for oxygen consumption (13.3 mL·kg−1·min−1 (95% confidence interval (CI), 12.2–14.6) vs 13.5 mL·kg−1·min−1 (95% CI, 12.1–14.8), P = 0.89) and HR (95 bpm (95% CI, 90–101) vs 96 bpm (95% CI, 91–102), P = 0.65). Compared with land-based exercise, water-based exercise induced an increase in middle cerebral artery blood flow velocity (74 cm·s−1 (95% CI, 66–81) vs 67 cm·s−1 (95% CI, 60–74) P < 0.001), posterior cerebral artery blood flow velocity (47 cm·s−1 (95% CI, 40–53) vs 43 cm·s−1 (95% CI, 37–49), P < 0.001), mean arterial blood pressure (106 mm Hg (95% CI, 100–111) vs 101 mm Hg (95% CI, 95–106), P < 0.001), and partial pressure of expired CO2 (P ≤ 0.001). Conclusions: Our findings suggest that water-based exercise augments cerebral blood flow, relative to land-based exercise of similar intensity, in healthy humans

Diagnosis and Management of Congenital Coronary Arteriovenous Fistula in the Pediatric Patients Presenting Congestive Heart Failure and Myocardial Ischemia

Purpose: Four pediatric patients with congenital coronary arteriovenous fistula (CAVF) were reported to remind pediatric practitioners and cardiologists of its diagnosis and management. Materials and Methods: Four pediatric patients with congenital CAVF from June 1999 to November 2007 were include in this retrospective study. Study modalities included reviews of patients' profiles of clinical features, chest radiograph, Doppler echocardiography, cardiac catheterization with angiography, myocardial perfusion scan, and computed tomography. Results: All 4 patients were symptomatic. The clinical symptoms and signs were feeding problem, continuous murmur, tachycardia, tachypnea, cardiomegaly, and exertional chest pain. Myocardial enzyme was elevated in 1 patient. Echocardiography showed dilatation of the coronary artery in all 4 patients, and traced down its origin in 3 and drainage in 4. The Fistulas originated from the right coronary artery in 2 patients and left coronary artery in 2, and were drained into the right ventricle in 2, right atrium in 1, and pulmonary artery in 1. Single left coronary artery was found in I patient. The pulmonary-to-systemic blood flow ratios ranged from 1.2 to 2.5. Transcatheter coil occlusion was successfully performed in 4 patients through a coaxial delivery system. The symptoms and signs of congestive heart failure and myocardial ischemia disappeared after the procedure, Conclusion: Diagnosis of congenital CAVF could be achieved by appreciation or continuous murmur over area unusual for the ductus, and by scrupulous examination of echocardiography as well as angiography of the coronary artery through which coaxial transcatheter coil occlusion could be performed successfully

Conduit artery structure and function in lowlanders and native highlanders: relationships with oxidative stress and role of sympathoexcitation

Research detailing the normal vascular adaptions to high altitude is minimal and often confounded by pathology (e.g. chronic mountain sickness) and methodological issues. We examined vascular function and structure in: (1) healthy lowlanders during acute hypoxia and prolonged ( 2 weeks) exposure to high altitude, and (2) high-altitude natives at 5050 m (highlanders). In 12 healthy lowlanders (aged 32 ± 7 years) and 12 highlanders(Sherpa; 33 ± 14 years) we assessed brachial endothelium-dependent flow-mediated dilatation(FMD), endothelium-independent dilatation (via glyceryl trinitrate; GTN), common carotid intima–media thickness (CIMT) and diameter (ultrasound), and arterial stiffness via pulse wave velocity (PWV; applanation tonometry). Cephalic venous biomarkers of free radical-mediated lipid peroxidation (lipid hydroperoxides, LOOH), nitrite (NO2 –) and lipid soluble antioxidants were also obtained at rest. In lowlanders, measurements were performed at sea level (334 m) and between days 3–4 (acute high altitude) and 12–14 (chronic high altitude) following arrival to 5050 m. Highlanders were assessed once at 5050 m. Compared with sea level, acute high altitude reduced lowlanders’ FMD (7.9 ± 0.4 vs. 6.8 ± 0.4%; P = 0.004) and GTN-induced dilatation (16.6 ± 0.9 vs. 14.5 ± 0.8%; P = 0.006), and raised central PWV (6.0 ± 0.2 vs. 6.6 ± 0.3 m s−1; P = 0.001). These changes persisted at days 12–14, and after allometricallyscaling FMD to adjust for altered baseline diameter. Compared to lowlanders at sea level and high altitude, highlanders had a lower carotid wall:lumen ratio ( 19%, P 0.04), attributable to a narrower CIMT and wider lumen. Although both LOOH and NO2 – increased with high altitude in lowlanders, only LOOH correlated with the reduction in GTN-induced dilatation evident during acute (n = 11, r=−0.53) and chronic (n = 7, r=−0.69; P 0.01) exposure to 5050 m. In a follow-up, placebo-controlled experiment (n=11 healthy lowlanders) conducted in a normobaric hypoxic chamber (inspiredO2 fraction (FIO2 )=0.11; 6 h), a sustained reduction in FMD was evident within 1 h of hypoxic exposure when compared to normoxic baseline (5.7±1.6 vs. 8.0 ±1.3%; P < 0.01); this decline in FMD was largely reversed following α1-adrenoreceptor blockade. In conclusion, high-altitude exposure in lowlanders caused persistent impairment in vascular function, which was mediated partially via oxidative stress and sympathoexcitation. Although a lifetime of high-altitude exposure neither intensifies nor attenuates the impairments seen with short-term exposure, chronic high-altitude exposure appears to be associated with arterial remodelling