Endothelial shear stress (ESS) has a possible effect on regulation of gene expression in the protection against atherosclerosis. During exercise, ESS should increase as systolic blood pressure and heart rate (HR) increase too; however, it is hard to determine ESS changes during exercise. Imaging ultrasound assessment of the brachial and the carotid arterial blood flow during exercise might help to estimate exercise-induced ESS. We present here the methodology at the Clinical Applied Physiology Laboratory to estimate exercise-induced ESS. We normally perform 2 exercise tests in 2 different visits. First, a cardiopulmonary exercise test with serial microblood sampling to determine blood lactate (La) levels on a stationary cycle ergometer to determine maximal oxygen consumption, maximal exercising HR, and lactate threshold curve. The second exercise test includes three 5-min steady state stages determined by La levels from test 1 (La <2 mmol/L, La 2–4 mmol/L, and La >4 mmol/L). During the second test, we position an ultrasound probe holder on either the arm or neck to image the brachial or carotid arteries, respectively. We obtain images and blood flow velocities through Doppler at each exercise stage and then we analyze the images using edge detection software to determine artery diameters. With these data, we are able to estimate ESS, flow direction, and the presence of turbulent flow.

Endothelial dysfunction is the first pathophysiological step of atherosclerosis, which is responsible for 90% of strokes. Exercise programs aim to reduce the risk of developing stroke; however, the majority of the beneficial factors of exercise are still unknown. Endothelial shear stress (ESS) is associated with endothelial homeostasis. Unfortunately, ESS has not been characterized during different exercise modalities and intensities in the carotid artery. Therefore, the purpose of this study was to determine exercise-induced blood flow patterns in the carotid artery. Fourteen apparently healthy young adults (males = 7, females = 7) were recruited for this repeated measures study design. Participants completed maximal oxygen consumption (VO2max) tests on a Treadmill, Cycle-ergometer, and Arm-ergometer, and 1-repetition maximum (1RM) tests of the Squat, Bench Press (Bench), and Biceps Curl (Biceps) on separate days. Thereafter, participants performed each exercise at 3 different exercise intensities (low, moderate, high) while a real-time ultrasound image and blood flow of the carotid artery was obtained. Blood flow patterns were assessed by estimating ESS via Womersley’s estimation and turbulence via Reynold’s number (Re). Data were analyzed using a linear mixed-effects model. Pairwise comparisons with Holm-Bonferroni correction were conducted with Hedge’s g effect size to determine the magnitude of the difference. There was a main effect of intensity, exercise modality, and intensity * exercise modality interaction on both ESS (p &lt; 0.001). Treadmill at a high intensity yielded the greatest ESS when compared to the other exercise modalities and intensities, while Bench Press and Biceps curls yielded the least ESS. All exercise intensities across all modalities resulted in turbulent blood flow. Clinicians must take into consideration how different exercise modalities and intensities affect ESS and Re of the carotid artery.

Background Recent studies have shown that the extent of extravalvular (extra-aortic valve) cardiac damage in patients with severe aortic stenosis (AS) have important prognostic implications for clinical outcomes after aortic valve replacement (AVR). Aims The aim of the present study is to evaluate the prognostic impact of a defined staging classification (“Généreux Staging Classification”) (GSC) characterizing the extent of extravalvular cardiac damage in patients with severe AS undergoing percutaneous transcatheter aortic valve implantation (TAVI). Methods A total of 102 consecutive patients, admitted in our institution between 2011–2017, with severe AS (echo-defined by peak aortic velocity, mean transvalvular gradient or aortic valve area) and symptoms related to AS (dyspnea, heart failure, angina or syncope) undergoing TAVI, were included. These patients were pooled and classified according to the presence or absence of cardiac damage as detected by echocardiography prior to TAVI, regarding the GSC: no extravalvular cardiac damage (Stage 0), left ventricular damage (Stage 1), left atrial or mitral valve damage (Stage 2), pulmonary vasculature or tricuspid valve damage (Stage 3), or right ventricular damage (Stage 4). Two-year outcomes were compared using Kaplan– Meier techniques and multivariable Cox proportional hazards models were used to identify 2-year predictors of mortality. Results Out of 102 patients, 57 were male (55.9%). Mean age was 83.46±4.23 years. 2 patients (2.1%) were classified as Stage 0; 20 patients (20.3%) as Stage 1; 55 patients (54.2%) as Stage 2; 22 (21.6%) as Stage 3; and 3 patients (2.9%) as Stage 4. Two-year mortality was 0.0% in Stage 0, 5.0% in Stage 1, 5.5% in Stage 2, and 44.0% in Stages 3–4. After multivariable and univariate analysis, stage of cardiac damage was independently associated as predictor for all-cause mortality at 2-years, after TAVI (HR 2.8 [1.3±6.2], p&lt;0.01). There were not another identificable predictors of 2-years death (age, sex, hypertension [78.5% of total patients], dislipemia [64.7%], diabetes [30.3%], smoking [78.5%], O2-chronic obstructive pulmonary disease [27.5% of total patients], renal insufficiency [78.5%], previous coronary artery disease [37.3%], peak aortic velocity, mean transvalvular gradient, and aortic valve area). Conclusions Given the strong association demonstrated in this study between advanced staging of cardiac damage and worse clinical outcomes after TAVI in short-middle term survival, consideration of the GSC in patients with severe AS in future recommendations for risk stratification might be useful. Two-year all-cause death in TAVI by GSC. Funding Acknowledgement Type of funding source: None

A randomized, double-blind, placebo-controlled, cross-over study where continuous therapeutic ultrasound (CUS; at 0.4 W/cm2), pulsed therapeutic ultrasound (PUS; at 20% duty cycle, 0.08 W/cm2), both at 1 MHz, and placebo (equipment on, no energy provided) were randomized and applied over the forearm of the non-dominant arm for 5 min in 10 young, healthy individuals. Absolute and peak forearm blood flow (FBF) were measured via Venous Occlusion Plethysmography. FBF was measured before, halfway, and after (immediately and 5 min after) the therapeutic ultrasound (TUS) intervention. Post-ischemic peak FBF was measured 10 min before and 10 min after the TUS intervention. A two-way repeated measures ANOVA (group × time) was selected to assess differences in FBF before, during, and after TUS treatment, and for peak FBF before and after TUS treatment. FBF increased 5 min after TUS in CUS compared to placebo (2.96 ± 1.04 vs. 2.09 ± 0.63 mL/min/100 mL of tissue, p < 0.05). PUS resulted in the greatest increase in Peak FBF at 10 min after US (Δ = 3.96 ± 2.02 mL/min/100 mL of tissue, p = 0.06). CUS at 1 MHz was an effective treatment modality for increasing FBF up to 5 min after intervention, but PUS resulted in the greatest increase in peak FBF at 10 min after intervention.

PURPOSE Endothelial function is highly regulated by the friction between blood flow and the endothelium. Endothelial shear stress (ESS) is defined as the dragging force generated by this interaction and it has been reported that low ESS affects nitric oxide bioavailability which in turn might increase blood pressure. Exercise programs are one of the best suited approaches to treat high blood pressure, however, there are no studies describing changes on ESS in the common carotid artery during upper‐body exercise, such as boxing training. Therefore, the purpose of this study was to quantify ESS in the common carotid artery during 60% and 95% of the maximal boxing exercise capacity in normotensive and pre‐hypertensive subjects. METHODS A total of 5 healthy normotensive and 5 pre‐hypertensive subjects matched by age, gender, height, and weight were recruited for this study. All 10 subjects performed two boxing exercise tests. The first was a graded maximal boxing test to estimate their maximal oxygen uptake (VO2max). The second one, performed 48 hours after the first evaluation, was a 2‐workload steady‐state boxing test at 60%VO2max and at 95%VO2max for 3 minutes each. A high‐definition Doppler ultrasound recorded common carotid artery diameters and blood flow velocities throughout each steady‐state condition. ESS was estimated using Womersley’s approximation. RESULTS There was a significant increase in antegrade ESS with higher workloads in both groups (p < 0.05 for all). No difference were found in anterograde ESS at baseline (Normotensive: 33.9±13.9 dynes/cm2, Pre‐HTA: 34.7±5.5 dynes/cm2; p = 0.936), at 60%VO2max (Normotensive: 51.3±19.1 dynes/cm2, Pre‐HTA: 49.6±7.6 dynes/cm2; p = 0.894, and at 95%VO2max (Normotensive: 72.9±30.9 dynes/cm2, Pre‐HTA: 85.2±12.5 dynes/cm2; p = 0.560) between both groups. Meanwhile, no retrograde blood flow was present at baseline for either groups, but it was identified at 60%VO2max (Normotensive: 8.1±0.7 dynes/cm2, Pre‐HTA: 7.8±7.8 dynes/cm2; p = 0.971) and 95%VO2max (Normotensive: 22.5±18.9 dynes/cm2, Pre‐HTA: 20.8±5.6 dynes/cm2; p = 0.891). CONCLUSION ESS increases in an exercise‐intensity manner during boxing training in normotensive and prehypertensive population. Boxing training might be beneficial in high blood pressure prevention due to increments on ESS.