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The high failure rate (46%) of peripheral intravenous catheters (PIVCs) is well-documented. There is limited research examining the effect of forces/pulls on PIVC complications. New breakaway connectors called force-activated separation devices (FASD) separate when a damaging force is placed on a PIVC. In a randomized, controlled trial, patients were assigned 1:1 to a control group receiving PIVC standard of care (SOC) or SOC with FASD added to the catheter. The primary outcome was total mechanical complications requiring a PIVC restart. Secondary outcomes were delay in therapy, PIVC restarts, and adverse events. Outcomes were compared in an intention-to-treat analysis (N = 302) and per-protocol analysis (N = 287). There were less total mechanical complications in FASD compared with SOC (22 vs 41, respectively; P.01). The treatment group was a predictor of total delay in therapy (minutes), indicating a greater estimated total delay in therapy in SOC than FASD (B = 69.53; 95% CI, 28.32-110.73; P = .001). There were more adverse events in SOC (127) than FASD (76; P = .001). Results were consistent in the per-protocol analysis. Use of a FASD showed a reduction in total mechanical complications. These results support use of the FASD as a safer and time-saving alternative to current SOC.

Background and Purpose: Reversible cerebral vasoconstriction syndrome (RCVS) is a well-established cause of stroke, but its demographics and outcomes have not been well delineated. Methods: Analysis of the United States Nationwide Inpatient Sample database (2016–2017) to characterize the frequency of hospitalizations for RCVS, demographic features, inpatient mortality, and discharge outcomes. Results: During the 2-year study period, 2020 patients with RCVS were admitted to Nationwide Inpatient Sample hospitals, representing 0.02 cases per 100 000 national hospitalizations. The mean age at admission was 47.6 years, with 85% under 65 years of age, and 75.5% women. Concomitant neurological diagnoses during hospitalization included ischemic stroke (17.1%), intracerebral hemorrhage (11.0%), subarachnoid hemorrhage (32.7%), seizure disorders (6.7%), and reversible brain edema (13.6%). Overall, 70% of patients were discharged home, 29.7% discharged to a rehabilitation facility or nursing home and 0.3% died before discharge. Patient features independently associated with the poor outcome of discharge to another facility or death were advanced age (odds ratio [OR], 1.04 [95% CI, 1.03–1.04]), being a woman (OR, 2.45 [1.82–3.34]), intracerebral hemorrhage (OR, 2.91 [1.96–4.31]), ischemic stroke (OR, 5.72 [4.32–7.58]), seizure disorders (OR, 2.61 [1.70–4.00]), reversible brain edema (OR, 6.26 [4.41–8.89]), atrial fibrillation (OR, 2.97 [1.83–4.81]), and chronic kidney disease (OR, 3.43 [2.19–5.36]). Conclusions: Projected to the entire US population, >1000 patients with RCVS are hospitalized each year, with the majority being middle-aged women, and about 300 required at least some rehabilitation or nursing home care after discharge. RCVS-related inpatient mortality is rare.

Cardiovascular disease (CVD) risk factors cluster in an individual. Exercise is universally recommended to prevent and treat CVD. Yet, clinicians lack guidance on how to design an exercise prescription (ExRx) for patients with multiple CVD risk factors. To address this unmet need, we developed a novel clinical decision support system to prescribe exercise (prioritize personalize prescribe exercise [P3-EX]) for patients with multiple CVD risk factors founded upon the evidenced-based recommendations of the American College of Sports Medicine (ACSM) and American Heart Association. To develop P3-EX, we integrated (1) the ACSM exercise preparticipation health screening recommendations; (2) an adapted American Heart Association Life’s Simple 7 cardiovascular health scoring system; (3) adapted ACSM strategies for designing an ExRx for people with multiple CVD risk factors; and (4) the ACSM frequency, intensity, time, and time principle of ExRx. We have tested the clinical utility of P3-EX within a university-based online graduate program in ExRx among students that includes physicians, physical therapists, registered dietitians, exercise physiologists, kinesiologists, fitness industry professionals, and kinesiology educators in higher education. The support system P3-EX has proven to be an easy-to-use, guided, and time-efficient evidence-based approach to ExRx for patients with multiple CVD risk factors that has applicability to other chronic diseases and health conditions. Further evaluation is needed to better establish its feasibility, acceptability, and clinical utility as an ExRx tool.

The Personal Impact of Epilepsy Scale (PIES) assesses patient functional status in subscales of (1) seizure impact, (2) medication effects, (3) moodsocial status, and (4) overall quality of life. This study was designed to determine the Minimal Clinically Important Change (MCID) in PIES subscale and total scores that demonstrate improvement.To ascertain the correspondence of PIES score change and clinical status change (improved, same, worse) in each PIES subscale and total score, we used two distinct retrospective anchor-based assessments of clinical status (patient self-assessment and trained rater assessment) across two clinic visits. Mean PIES scores were compared between clinical status groups, controlling for days between visits and initial clinical status. Personal Impact of Epilepsy Scale score change was quantified for each group to determine MCID. A small prospective proof-of-concept study was conducted in a separate subject group.Patient self-report anchor analysis demonstrated lower (better) PIES scores in the "improved" group vs the "worse" group on the moodsocial subscale (p .001) and total score (p = .002), with a similar trend on the seizure subscale (p = 0.056). Clinical rater anchor analysis demonstrated lower PIES scores in the "improved" vs "worse" group in the moodsocial subscale (p = .029) and a trend in total score (p = .082). For the "improved" group, the reduction in PIES scores between visits averaged across both anchor analyses was 8.14% for subscales and 8.67% for total score.Reduction of 8% on a PIES subscale or total score indicates meaningful improvement in patient clinical status, and is designated the MCID for this instrument. Personal Impact of Epilepsy Scale can be useful in day-to-day clinical care and as an outcome metric in clinical research.

We examined the association between contact with children and the clinical course of COVID-19 among COVID-19-positive adult patients. Participants completed a survey to assess demographics, medical information related to their COVID-19 diagnosis, contact with children at home and at the workplace. Patients were aged 45.68 ± 14.38 years, mostly female (72.1%), 842 were not hospitalized and 167 were hospitalized. At home, there were no differences between groups for the number of child contact hours or total child hours (hours × number of children) per week (Ps > 0.05). The number of children at home was greater among patients not hospitalized (P < 0.05), however this was no longer significant after controlling for covariates (P > 0.05). At the workplace, there were no differences between groups (all Ps > 0.05). Sub-group analysis found the proportion of patients that were treated in the intensive care unit (ICU) was greater among patients with no child contact (P < 0.05). A secondary analysis found that patients with no child contact had an increased likelihood of thromboembolism (P < 0.05) and a trend towards more overall COVID-19-related complications (P = 0.076). Overall, an association between contact with children and hospitalization was not found when adjusting for covariates. Sub-group analysis indicated a possible protective effect for more severe disease; however, these findings need further study.

Weight stigma induces cardiovascular health consequences for people with obesity. How stigma affects cardiovascular reactivity in individuals with both obesity and hypertension is not known.In a randomized experiment, we assessed the influence of two video exposures, depicting either weight stigmatizing (STIGMA) or non-stigmatizing (NEUTRAL) scenes, on cardiovascular reactivity [resting blood pressure (BP), heart rate (HR), ambulatory BP (ABP), and ambulatory HR (AHR)], among women with obesity and high BP (HBP; n=24) or normal BP (NBP; n=25). Systolic ABP reactivity was the primary outcome. Laboratory BP and HR were measured before/during/following the videos, and ABP and AHR were measured over 19 hours (10 awake hours, 9 sleep hours) upon leaving the laboratory. A repeated measures ANCOVA tested differences in BP and HR changes from baseline in the laboratory and over ambulatory conditions between the two groups after each video, controlling for body mass index, baseline BP and HR.Laboratory SBP/DBP increased 5.5+7.3/2.4+8.8mmHg more in women with HBP than NBP following the STIGMA versus NEUTRAL video (Ps0.05). For the primary outcome, ABP increased more in HBP than NBP over sleep (SBP/DBP=4.2+20.6/4.7+14.2mmHg; Ps0.05) following the STIGMA versus NEUTRAL video, as did HR during sleep (7.5+15.7bpm more in HBP than NBP; P0.05).Weight stigma increases cardiovascular reactivity among women with obesity and HBP in the laboratory and under ambulatory conditions.Registered at ClinicalTrials.gov (Identifier: NCT04161638).

Context:Compression socks have become increasingly popular with athletes due to perceived enhancement of exercise performance and recovery. However, research examining the efficacy of compression socks to reduce exercise-associated muscle damage has been equivocal, with few direct measurements of markers of muscle damage.Objective:To examine the influence of compression socks worn during a marathon on creatine kinase (CK) levels.Design:A randomized controlled trial.Setting:2013 Hartford Marathon, Hartford, CT.Participants:Adults (n = 20) randomized to control (CONTROL; n = 10) or compression sock (SOCK; n = 10) groups.Main Outcome Measures:Blood samples were collected 24 hours before, immediately after, and 24 hours following the marathon for the analysis of CK, a marker of muscle damage.Results:Baseline CK levels did not differ between CONTROL (89.3 [41.2] U/L) and SOCK (100.0 [56.2] U/L) (P = .63). Immediately following the marathon (≤1 h), CK increased 273% from baseline (P P = .60 for time × group). The day following the marathon (≤24 h), CK further increased 1094% from baseline (P P = .53 for time × group). These similar trends persisted despite controlling for potential covariates such as age, body mass index, and race finishing time (Ps > .29).Conclusions:Compression socks worn during a marathon do not appear to mitigate objectively measured markers of muscle damage immediately following and 24 hours after a marathon.

A single exercise session evokes immediate blood pressure (BP) reductions that persist for at least 24 h, termed postexercise hypotension (PEH). Self-monitoring of PEH may foster positive outcome expectations of exercise, and thus, enhance exercise adherence among adults with hypertension.To compare the efficacy of self-monitoring of exercise (EXERCISE) versus exercise and PEH (EXERCISE + PEH) to improve exercise adherence and BP control among adults with hypertension.Adults with high BP were randomized to EXERCISE (n = 12) or EXERCISE + PEH (n = 12). Participants underwent supervised, moderate intensity aerobic exercise training for 40-50 min/session, 3 days/week for 12 weeks and encouraged to exercise unsupervised at home at least 30 min/day, 1-2 days/week. EXERCISE + PEH also self-monitored BP before and after exercise. Adherence was calculated as [(no. of exercise sessions performed/no. of possible exercise sessions) × 100%]. BP was measured pre and posttraining.Healthy, middle-aged (52.3 ± 10.8 years) men (n = 11) and women (n = 13) with hypertension (136.2 ± 10.7/85.2 ± 8.9 mmHg) completed exercise training with 87.9 ± 12.1% adherence. EXERCISE + PEH demonstrated greater adherence to supervised training (94.3 ± 6.6%) than EXERCISE (81.6 ± 13.2%; P = 0.007). EXERCISE + PEH performed 32.6 ± 22.5 min/week more unsupervised home exercise than EXERCISE (P = 0.004), resulting in greater exercise adherence (107.3 ± 18.7%) than EXERCISE (82.7 ± 12.2%; P = 0.002). Post versus pretraining BP was reduced -7.4 ± 11.3/-4.9 ± 9.9 mmHg (P 0.025) with no statistical difference between EXERCISE (-5.2 ± 13.3/-3.6 ± 6.1 mmHg) and EXERCISE + PEH (-9.9 ± 11.3/-6.1 ± 6.9 mmHg; P 0.344).The current study is the first to demonstrate that PEH self-monitoring is an efficacious tool to improve exercise adherence among a small sample of adults with hypertension. Future research among a larger, more diverse sample is needed to confirm these novel findings and determine whether EXERCISE + PEH translates to better BP control relative to EXERCISE self-monitoring alone.

Venous thromboembolic (VTE) events such as deep vein thrombosis (DVT) and pulmonary embolism (PE) have been reported in otherwise low-risk healthy athletes following acute bouts of aerobic exercise.To review case reports and assess the commonalities of athletic individuals with VTE, as well as return-to-play (RTP) recommendations.We reviewed 47 reports (20 DVTs, 15 PEs, and 12 DVTs/PEs, 19 women) of trained individuals who were diagnosed with DVT and/or PE following aerobic exercise. We assessed frequency of VTE risk factors, presenting symptoms, and RTP recommendations.The age of women (24.6 ± 7.0 years) was lower (P .01) than of men (40.6 ± 13.6 years). Of the 19 women, 14 (73.7%) used oral contraceptives. Thirteen cases (27.7%) reported a recent period of prolonged inactivity (1 hour), and another 12 cases were found to have an antithrombin disorder following testing after diagnosis. The most frequently reported symptoms were muscle pain in 26 of 32 (81.3%) DVT or DVT/PE cases, and dyspnea in 21 of 27 (77.8%) PE or DVT/PE cases. Despite these common symptoms, the estimated time from first report of symptoms to confirmed diagnosis was 56.3 ± 118.7 days and 25 cases (53.2%) were initially misdiagnosed. Twenty-three cases (48.9%) did not report RTP recommendations, and those which did varied widely.Thirty-two cases (~70%) had at least one of three major risk factors, suggesting that many cases of VTE in athletes may be preventable with better education and awareness. The wide variety of RTP recommendations highlights the need for standardized guidelines in this population.

Background: Treatment options for acute ischemic stroke (AIS) now include mechanical thrombectomy. As a result, primary stroke centers (PSC) must quickly identify large vessel occlusion (LVO) patients, treat them with alteplase when appropriate and transfer them to a comprehensive stroke center (CSC) for potential mechanical thrombectomy. Given the need for expedited care in the emergency department, collaboration with emergency medical services (EMS) in the pre-hospital setting and timely administration of alteplase prior to transfer to the CSC have been identified as practice gaps. Purpose: To examine the effect of an educational stroke simulation session on the knowledge and confidence level of registered nurses (RN) and EMS providers who care for patients with acute stroke receiving alteplase. Methods: Simulations were 60 min, in groups of 4-5 RNs and 1-2 EMS providers, and focused on neurological assessment, administration of alteplase, and rapid transfer when a LVO is suspected and/or identified. Participants completed a pre and post simulation survey assessing confidence levels of nurse role actions and knowledge of stroke care (Table 1). A paired samples t-test examined differences in confidence levels and total percent of correctly answered questions on the survey, pre versus post simulation. A McNemar test examined differences in the proportion of participants that correctly answered each question on the test pre versus post simulation. Results: Following the stroke simulation, the confidence levels of nurses increased for all nurse role actions (all P sP sP Conclusions: Simulation based education can be an effective training tool for improving the knowledge and confidence of nursing and EMS providers in the management of AIS.

Thrombolytic treatment for patients who wake with acute ischemic stroke based on MRI DWI-FLAIR mismatch was added to AHA’s 2019 stroke guidelines. While changes were implemented to facilitate care in 2019, it was determined that managing each patient on a case-by-case basis would best use system resources. The spring of 2020 brought new challenges in delay to hospital arrival due to COVID-19. Purpose: Evaluate the current process of managing potential wake up treatment eligible patients. Methods: All ischemic stroke discharges during CT’s rise and peak of the pandemic were reviewed, January 1 - May 31, 2020. Records were reviewed to determine time of arrival, onset or last seen well, time found, NIHSS, treatment or hyperacute MRI done, and any contraindication based on wake up criteria. A chi-square of proportions or Fisher’s Exact test was used to examine the association between month of discharge and patient characteristics for categorical variables. A Kruskal-Wallis H test was used for the continuous NIHSS variable. Results: Since the first COVID-19 patients were admitted in early March, results from January and February were combined (Group 1 n=122) and compared to March, April and May (Group 2 n=143). There was a non-significant (p=0.48) increase from group 1 (62.3%) to group 2 (66.4%) in the percentage arriving more than 4.5 hours from onset or LSW. In addition, group 1 had higher NIHSSs than group 2 (median, IQR=6, 9 vs 3, 10, respectively), but this was not significant (p=0.27, H=1.21). This did however translate into fewer meeting wake up criteria for treatment during the rise and peak period (Group 1=6.6%, Group 2=2.8%; p=0.15). Use of hyperacute MRI was significantly higher in group 1 than group 2 (5.7% vs 0%, p=0.004) since no patients received a hyperacute MRI during peak pandemic. Conclusions: While more patients were expected to be eligible for acute thrombolytics using the wake up criteria due to delay in hospital arrival, this was not observed. Instead, patients arriving during the peak of the pandemic were less severe. Although a hyperacute MRI was still possible without confirmation of COVID-19 negative status, none were done. Enhancements to facilitate obtaining a hyperacute MRI are still needed regardless of reason for patient delay to hospital arrival.

Obesity affects approximately one-third of American adults. Recent evidence suggests that weight bias may be pervasive among both exercise and nutrition professionals working with adults who have obesity. However, the published literature on this topic is limited. This review aimed to (i) systematically review existing literature examining weight bias among exercise and nutrition professionals; (ii) discuss the implications of this evidence for exercise and nutrition professionals and their clients; (iii) address gaps and limitations of this literature; and (iv) identify future research directions. Of the 31 studies that met the criteria for this review, 20 examined weight bias among exercise professionals, of which 17 (85%) found evidence of weight bias among professionals practicing physical therapy (n = 4), physical education (n = 8) and personal/group fitness training (n = 5). Of 11 studies examining weight bias among nutrition professionals, eight (73%) found evidence of weight bias. These findings demonstrate fairly consistent evidence of weight bias among exercise and nutrition professionals. However, the majority of studies were cross-sectional (90%). Given that weight bias may compromise quality of care and potentially reinforce weight gain and associated negative health consequences in patients with obesity, it is imperative for future work to examine the causes and consequences of weight bias within exercise and nutrition professions using more rigorous study designs.

Serum creatine kinase (CK) levels are higher after eccentric, muscle-damaging exercise in statin-treated patients. This could contribute to the increased statin-associated muscle symptoms reported in physically active individuals.We tested the hypothesis in this pilot study that creatine (Cr) monohydrate supplementation would reduce the CK response to eccentric exercise in patients using statins to determine if Cr supplementation could be a strategy to mitigate statin-associated muscle symptoms in physically active individuals.Healthy, nonsmoking men (n = 5) and women (n = 14) were randomized to Cr monohydrate = atorvastatin 80 mg + 10 g Cr monohydrate (n = 10, age = 60 ± 7 years) or to placebo (PL) = atorvastatin 80 mg + PL (n = 9, age = 52 ± 6 years). After 4 weeks of treatment, subjects performed 45 minutes of eccentric exercise (downhill walking at a -15% grade). Serum CK levels, muscle soreness (visual analog scale after two squats), and muscle pain severity and interference (using the brief pain inventory) were measured before and after 4 weeks of treatment, and then for 4 consecutive days after downhill walking. Vitamin D, or serum 25(OH)D, was also measured at baseline.The PL group was younger (P = .01) but not otherwise different in blood lipids, vitamin D, CK, muscle visual analog scale, and pain scores before (all P .21) or after (all P .12) treatment. CK increased in all subjects after downhill walking (P .01), but neither the relative peak change (expressed as group mean difference with 95% confidence intervals: 43.52% [-196.41, 283.45]) nor the absolute peak change (67.38 U/L [-121.55, 256.31]) relative to baseline was different between groups (P = .46 and .71, respectively). A similar lack of treatment effect was observed for muscle soreness (11.03 mm [-9.49, 31.55]), pain severity (0.77 pts [-0.95, 2.50]), and pain interference (1.02 pts [-1.25, 3.29]) with P-values for group comparisons = 0.27, 0.36, and 0.35, respectively. However, subjects with "insufficient" Vitamin D 30 ng/mL (n = 10) had an ∼2-fold greater CK increase with eccentric exercise (nominal P-value = .04) than subjects with higher vitamin D levels.Cr monohydrate did not reduce CK increases after exercise in statin-treated subjects. We did observe that low vitamin D levels are associated with a greater CK response to eccentric exercise in statin-treated subjects.

Functional magnetic resonance imaging (fMRI) has not been used to assess the effects of statins on the brain. We assessed the effect of statins on cognition using standard neuropsychological assessments and brain neural activation with fMRI on two tasks.Healthy statin-naïve men and women (48±15 years) were randomized to 80 mg/day atorvastatin (n=66; 27 men) or placebo (n=84; 48 men) for 6 months. Participants completed cognitive testing while on study drug and 2 months after treatment cessation using alternative test and task versions.There were few changes in standard neuropsychological tests with drug treatment (all P.56). Total and delayed recall from the Hopkins Verbal Learning Test-Revised increased in both groups (P.05). The Stroop Color-Word score increased (P.01) and the 18-Point Clock Test decreased in the placebo group (P=.02) after drug cessation. There were, however, small but significant group-time interactions for each fMRI task: participants on placebo had greater activation in the right putamen/dorsal striatum during the maintenance phase of the Sternberg task while on placebo but the effect was reversed after drug washout (P.001). Participants on atorvastatin had greater activation in the bilateral precuneus during the encoding phase of the Figural Memory task while on-drug but the effect was reversed after drug washout (P.001).Six months of high dose atorvastatin therapy is not associated with measurable changes in neuropsychological test scores, but did evoke transient differences in brain activation patterns. Larger, longer-term clinical trials are necessary to confirm these findings and evaluate their clinical implications.

Considerable variability exists in the cardiometabolic disease biomarker response to exercise. We propose that a major contributor to this heterogeneity is underpowered studies due to small sample sizes. To test our hypothesis, we conducted a systematic review to identify meta-analyses/reviews of randomized controlled trials (RCT) and RCT that examined the cardiometabolic disease biomarker response to aerobic and resistance exercise.

Statins increase the creatine kinase release from skeletal muscle, a sign of muscle injury. This chapter discusses studies that examined the effect of statins on: (1) skeletal muscle strength, (2) aerobic exercise performance, (3) skeletal muscle and cardiac biomarkers during exercise, (4) training for athletic competition, and (5) physical activity adherence. The majority of evidence does not demonstrate a deleterious effect of statin therapy on exercise performance or training, although the populations that appear to be at greatest risk of exercise-induced statin-associated muscle symptoms (SAMS) include older adults and athletes, especially those participating in prolonged or intense forms of exercise.

Aerobic exercise reduces blood pressure (BP) on average 5-7 mmHg among those with hypertension; limited evidence suggests similar or even greater BP benefits may result from isometric handgrip (IHG) resistance exercise.We conducted a randomized controlled trial investigating the antihypertensive effects of an acute bout of aerobic compared with IHG exercise in the same individuals. Middle-aged adults (n = 27) with prehypertension and obesity randomly completed three experiments: aerobic (60% peak oxygen uptake, 30 min); IHG (30% maximum voluntary contraction, 4 × 2 min bilateral); and nonexercise control. Study participants were assessed for carotid-femoral pulse wave velocity pre and post exercise, and left the laboratory wearing an ambulatory BP monitor.SBP and DBP were lower after aerobic versus IHG (4.8 ± 1.8/3.1 ± 1.3 mmHg, P = 0.01/0.04) and control (5.6 ± 1.8/3.6 ± 1.3 mmHg, P = 0.02/0.04) over the awake hours, with no difference between IHG versus control (P = 0.80/0.83). Pulse wave velocity changes following acute exercise did not differ by modality (aerobic increased 0.01 ± 0.21 ms, IHG decreased 0.06 ± 0.15 ms, control increased 0.25 ± 0.17 ms, P 0.05). A subset of participants then completed either 8 weeks of aerobic or IHG training. Awake SBP was lower after versus before aerobic training (7.6 ± 3.1 mmHg, P = 0.02), whereas sleep DBP was higher after IHG training (7.7 ± 2.3 mmHg, P = 0.02).Our findings did not support IHG as antihypertensive therapy but that aerobic exercise should continue to be recommended as the primary exercise modality for its immediate and sustained BP benefits.

Exercise provides numerous physiological and psychological benefits for healthy older adults. However, most older adults in the United States are physically inactive. This chapter first summarizes the evidence demonstrating the resultant health benefits from exercise based on both epidemiological and interventional research. Second, this chapter introduces the concept of exercise prescription, presents the physical activity guidelines for older adults from various professional committees and organizations, and discusses special considerations when prescribing exercise for older adults. Last, this chapter highlights several of the behavioral theories that can be used to increase physical activity and reduce sedentary behavior among older adults.

BackgroundThere is a high prevalence of cardiovascular disease across diverse groups in the U.S. population, and increasing research has identified stigma as a potential barrier to cardiovascular disease prevention and treatment. This systematic review examines evidence linking discrimination and cardiovascular health among socially stigmatized groups.Study designSix databases were systematically reviewed from inception through February 2018 for studies with adult subjects, focusing on cardiovascular health indicators among social groups stigmatized because of their gender, race/ethnicity, age, body weight/obesity, or sexual orientation. The Newcastle-Ottawa Scale was used to evaluate the methodological quality and risk of bias for nonrandomized studies, and the Cochrane Collaboration 7-item domain for randomized controlled and experimental trials.ResultsThe search identified 84 eligible studies published between 1984 and 2017. Studies retrieved were categorized according to demonstrated links between stigma and cardiovascular disease risk factors including blood pressure (n = 45), heart rate variability (n = 6), blood/saliva cardiovascular biomarkers (n = 18), as well as other indicators of cardiovascular health (n = 15). Based on the findings from included studies, 86% concluded that there was a significant relationship among stigma or discrimination and cardiovascular health indicators among socially stigmatized groups. However, there were varying degrees of evidence supporting these relationships, depending on the type of discrimination and cardiovascular health indicator. The current evidence implies an association between perceived discrimination and cardiovascular health. However, a majority of these studies are cross-sectional (73%) and focus on racial discrimination (79%), while using a wide variety of measurements to assess social discrimination and cardiovascular health.ConclusionsFuture research should include longitudinal and randomized controlled trial designs, with larger and more diverse samples of individuals with stigmatized identities, using consistent measurement approaches to assess social discrimination and its relationship with cardiovascular health.

There are inconsistent findings regarding muscular weakness in individuals with statin-induced myalgia.We used rigorous muscle testing to compare findings from 3 investigations in 3 different study populations to determine if statin myalgia is associated with measurable weakness.In all 3 studies, we measured maximal isometric handgrip strength, resting respiratory exchange ratio (RER), and knee extensor isometric and isokinetic force. In 2 of the 3 studies, elbow flexor isometric and isokinetic force and knee endurance fatigue index were also assessed. Knee extensor and elbow flexor measurements were obtained using an isokinetic dynamometer. Resting RER was measured using a metabolic breath-by-breath collection method. Measurement outcomes were compared on vs off drug.In study 1, 18 participants fit the criteria for statin myalgia. Participants taking atorvastatin 80 mg daily had significantly lower muscle strength in 5 (P .05) of 14 measured variables. Participants on placebo (N = 10) with myalgia had significantly lower muscle strength in 4 (P .05) of 14 measured variables. In study 2, 18 participants tested positive for statin-induced myalgia when receiving simvastatin 20 mg daily and displayed no significant muscle strength changes (all P .05). In study 3, 11 patients with statin-induced myalgia completed the study and had a significant decrease in 2 (P .05) of 10 leg muscle strength variables. In all 3 studies, no significant changes were shown for handgrip strength or RER (all P .05).Our results indicate that after a short-term treatment with statin therapy, a rigorous muscle strength protocol does not show decrements of muscle strength in subjects with statin myalgia. Short-term treatment with statin therapy is not common in clinical practice. Thus, future studies should examine the effects of prolonged statin therapy on muscle strength.

Objectives To examine the effects of exercise training on cognitive function in individuals at risk of or diagnosed with Alzheimer's disease (AD). Design Meta‐analysis. Setting PubMed, Scopus, ClinicalTrials.gov, and ProQuest were searched from inception until August 1, 2017. Participants Nineteen studies with 23 interventions including 1,145 subjects with a mean age of 77.0 ± 7.5 were included. Most subjects were at risk of AD because they had mild cognitive impairment (64%) or a parent diagnosed with AD (1%), and 35% presented with AD. Intervention Controlled studies that included an exercise‐only intervention and a nondiet, nonexercise control group and reported pre‐ and post‐intervention cognitive function measurements. Measurements Cognitive function before and after the intervention and features of the exercise intervention. Results Exercise interventions were performed 3.4 ± 1.4 days per week at moderate intensity (3.7 ± 0.6 metabolic equivalents) for 45.2 ± 17.0 minutes per session for 18.6 ± 10.0 weeks and consisted primarily of aerobic exercise (65%). Overall, there was a modest favorable effect of exercise on cognitive function (d+ = 0.47, 95% confidence interval (CI) = 0.26–0.68). Within‐group analyses revealed that exercise improved cognitive function (d+w = 0.20, 95% CI = 0.11–0.28), whereas cognitive function declined in the control group (d+w = −0.18, 95% CI = −0.36 to 0.00). Aerobic exercise had a moderate favorable effect on cognitive function (d+w = 0.65, 95% CI = 0.35–0.95), but other exercise types did not (d+w = 0.19, 95% CI = −0.06–0.43). Conclusion Our findings suggest that exercise training may delay the decline in cognitive function that occurs in individuals who are at risk of or have AD, with aerobic exercise possibly having the most favorable effect. Additional randomized controlled clinical trials that include objective measurements of cognitive function are needed to confirm our findings.

Recent data suggest that rapid infusion of intravenous (IV) cold saline for Targeted Temperature Management (TTM) after cardiac arrest is associated with higher rates of rearrest, pulmonary edema, and hypoxia, with no difference in neurologic outcomes or survival when administered by Emergency Medical Services. We sought to determine the effects of IV cold saline administration in the hospital setting in postcardiac arrest patients to achieve TTM and its effect on clinical parameters and neurologic outcomes.A cohort of 132 patients who completed TTM after cardiac arrest in a single institution was retrospectively studied. Patients who did not receive cold saline were matched by age, gender, Glasgow coma scale, downtime, and presenting rhythm to patients who received cold saline. Demographics, cardiac rearrest, diuretic use, time to target temperature, and Cerebral Performance Category (CPC) scores were recorded among other variables. Patients who received cold saline achieved target temperature sooner (280 vs. 345 minutes, p = 0.05), had lower lactate levels on day 1 (4.2 ± 3.5 mM vs. 6.0 ± 4.9 mM, p = 0.019) and day 2 (1.3 ± 2.2 mM vs. 2.2 ± 3.2 mM, p = 0.046), increased incidence of pulmonary edema (51.5% vs. 31.8%, p = 0.006), and increased diuretic utilization (63.6% vs. 42.4%, p = 0.014). There was no significant difference in cardiac rearrest, arterial oxygenation, and CPC scores (ps 0.05).Infusion of IV cold saline is associated with shorter time to target temperature, increased incidence of pulmonary edema, and diuretic use, with no difference in cardiac rearrest, survival, and neurologic outcomes.

The effect of physical activity intensity on subjective well-being has not been well established. We examined this relationship among 419 healthy adults using objective and subjective physical activity measurements (sample size varied among well-being assessments). For accelerometers, light-intensity physical activity positively associated with psychological well-being ( n = 150) and negatively associated with depression ( n = 99); moderate intensity negatively associated with pain severity ( n = 419) and positively associated with psychological well-being; sedentary behavior negatively associated with psychological well-being and positively associated with depression ( ps

OBJECTIVE To investigate the effect of oral contraceptive (OC) use and compression socks on hemostatic activation in women flying cross-country to and from a marathon. DESIGN Prospective study. SETTING 2015 Boston Marathon. PARTICIPANTS Women were divided into non-OC using (CONTROL; n = 12), OC-using (OC; n = 15), and OC-using plus compression sock (OC + SOCK; n = 14) groups. INTERVENTION Women in OC + SOCK wore compression socks during flights to and from the marathon. MAIN OUTCOME MEASURES Venous blood samples were collected within 24 hours of arriving in Boston (EXPO), immediately after the marathon (RUN), and within 24 hours after a return flight home (Post-Flight) for analysis of thrombin-antithrombin complex (TAT), d-dimer, and tissue plasminogen activator (t-PA). RESULTS TAT did not increase with exercise (P = 0.48) and was not affected by group (P = 0.08) or the interaction between these 2 factors (P = 0.80). Group, time, and their interaction were significant for d-dimer (all P < 0.05) such that d-dimer increased with acute exercise to a greater extent (Δ d-dimer from expo to postrace = 909.5 ± 1021.9 ng/mL) in the OC + SOCK group relative to OC (Δ d-dimer = 240.0 ± 178.5 ng/mL; P = 0.02) and CONTROL (Δ d-dimer = 230.3 ± 120.3 ng/mL; P = 0.02). There was a significant effect of time, group, and the interaction on t-PA (all P < 0.01) such that t-PA increased with acute exercise to a greater extent (Δ t-PA from expo to postrace = 19.6 ± 10.0 ng/mL) in the CONTROL group relative to OC (Δ t-PA = 4.0 ± 1.8 ng/mL; P < 0.01) and OC + SOCK (Δ t-PA = 3.3 ± 1.2 ng/mL; P < 0.01). CONCLUSIONS Female runners using OCs did not exhibit disproportionately increased coagulation. The use of compression socks in women on OCs, surprisingly, resulted in a greater increase in d-dimer after exercise.

The mechanisms underlying statin-associated muscle symptoms (SAMS) are not understood. Mitochondrial dysfunction and atrogin-1 activation are among the leading possible explanations for SAMS. Interestingly, metformin can enhance mitochondrial function and may affect atrogin-1 expression. Therefore, we sought to perform a systematic search of the literature to explore the relationship among statins, metformin, and SAMS.

This review examined studies published within the last 16 months that investigated the relationship between statins and physical activity.These recent studies suggest that statins do not adversely affect cardiorespiratory fitness, muscle strength, athletic performance, or physical activity adherence. One recent study comparing patients with statin-associated myalgia and nonstatin-using controls did report that statins are associated with a slowing of time to peak power output, increased abdominal adiposity, and insulin resistance. Statin users also had different muscle gene expression than controls, but conclusions are limited by the design of that study.Previous reports suggest that statin-associated muscle symptoms such as myalgia, cramps, and weakness occur more frequently in physically active individuals, but the recent studies we reviewed do not provide additional support for this possibility. Well-designed clinical trials are needed to determine whether different statins or statin doses evoke statin-associated muscle symptoms or muscle damage that may reduce cardiorespiratory fitness and adherence to physical activity.

Objectives Two separate studies assessed the psychometric properties of a retrospective behavioral measure adapted for exercise called the Timeline Followback for Exercise (TLFB-E). Study one examined criterion, convergent, and predictive validity. Study two examined test–retest reliability. Design Validity data was collected at three time points (baseline, 2 months, and 6 months) as part of a randomized clinical trial on exercise engagement. Test-retest reliability was assessed via two participant interviews scheduled one month apart. Methods Study one participants ( N = 66) were college students 20.0 ± 1.4 yr. Validity of frequency, intensity, time, and type (FITT) of exercise as assessed on the TLFB-E was examined using Pearson r correlations with accelerometers, weekly exercise contracts between participants and researchers, question four of the College Alumni Questionnaire, and a health-related physical fitness battery. Study two participants were a different sample ( N = 40) of college students 18.63 ± 1.0 yr. Pearson r correlations determined reliability of the TLFB-E for exercise frequency, intensity, and time. Kappa statistic determined reliability of the TLFB-E for type of exercise. Results The TLFB-E displayed evidence of criterion validity when compared to accelerometers ( r = .35 to .39) and evidence of convergent validity when compared to weekly exercise contracts ( r = .65 to .80) and question four of the College Alumni Questionnaire ( r = .06 to .75). The TLFB-E displayed evidence of modest to adequate test-retest reliability ( r = .79 to .97) for exercise frequency, intensity, and time and moderate Kappa ( k = .49) for exercise type. Conclusions The TLFB-E produces evidence of reliable and valid scores among college students and improves upon other self-report, retrospective questionnaires by enabling daily collection of exercise FITT over a specified time period.

FURIN is a proprotein convertase subtilisin/kexin enzyme important in pro‐renin receptor processing, and FURIN (furin, paired basic amino acid cleaving enzyme) variants are involved in multiple aspects of blood pressure (BP) regulation. Therefore, we examined associations among FURIN variants and the immediate blood pressure (BP) response to bouts of aerobic exercise, termed postexercise hypotension (PEH). Obese (30.9 ± 3.6 kg m−2) Black‐ (n = 14) and White‐ (n = 9) adults 42.0 ± 9.8 year with hypertension (139.8 ± 10.4/84.6 ± 6.2 mmHg) performed three random experiments: bouts of vigorous (VIGOROUS) and moderate (MODERATE) intensity cycling and control. Subjects were then attached to an ambulatory BP monitor for 19 h. We performed deep‐targeted exon sequencing with the Illumina TruSeq Custom Amplicon kit. FURIN genotypes were coded as the number of minor alleles (#MA) and selected for additional statistical analysis based upon Bonferonni or Benjamini–Yekutieli multiple testing corrected P‐values under time‐adjusted linear models for 19 hourly BP measurements. After VIGOROUS over 19 h, as FURIN #MA increased in rs12917264 (P = 2.4E‐04) and rs75493298 (P = 6.4E‐04), systolic BP (SBP) decreased 30.4–33.7 mmHg; and in rs12917264 (P = 1.6E‐03) and rs75493298 (P = 9.7E‐05), diastolic BP (DBP) decreased 17.6–20.3 mmHg among Blacks only. In addition, after MODERATE over 19 h in FURIN rs74037507 (P = 8.0E‐04), as #MA increased, SBP increased 20.8 mmHg among Blacks only. Whereas, after MODERATE over the awake hours in FURIN rs1573644 (P = 6.2E‐04), as #MA increased, DBP decreased 12.5 mmHg among Whites only. FURIN appears to exhibit intensity and race‐dependent associations with PEH that merit further exploration among a larger, ethnically diverse sample of adults with hypertension.

Introduction: HMG-CoA reductase inhibitors (statins) are generally well-tolerated, although muscle weakness and pain have been reported in ~10% of statin users. However, many self-reported muscle side effects are non-specific. As mental health influences self-perception of pain, we sought to assess the effect of baseline well-being and depression on self-reported muscle pain and quality of life (QOL) after 6 months of atorvastatin (ATORVA) 80 mg/d or placebo in healthy, statin-naïve adults. Hypothesis: We hypothesized that lower levels of well-being and higher levels of depression would result in higher self-reported pain that interferes with QOL after statin therapy. Methods: The Psychological General Well-Being Index (Well-Being; n=82) and Beck Depression Inventory (Depression; n=55) were administered at baseline in subjects (aged 59.5+1.2 yrs) from STOMP (Effect of Statins on Skeletal Muscle Performance; Clinical Trials #NCT00609063). Muscle pain (Short-Form McGill Pain Questionnaire [SF-MPG]) and pain that interferes with QOL (Brief Pain Inventory [BPI]), were also measured before and after drug treatment. Results: At baseline, there were no group differences in Well-Being, Depression, or pain measures between groups (ps ≥0.05). Baseline Well-Being correlated with baseline BPI pain severity (r=-0.309, p

Hydroxy-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors or statins are well tolerated, but associated with various statin-associated symptoms (SAS), including statin-associated muscle symptoms (SAMS), diabetes mellitus (DM), and central nervous system complaints. These are "statin-associated symptoms" because they are rare in clinical trials, making their causative relationship to statins unclear. SAS are, nevertheless, important because they prompt dose reduction or discontinuation of these life-saving mediations. SAMS is the most frequent SAS, and mild myalgia may affect 5% to 10% of statin users. Clinically important muscle symptoms, including rhabdomyolysis and statin-induced necrotizing autoimmune myopathy (SINAM), are rare. Antibodies against HMG-CoA reductase apparently provoke SINAM. Good evidence links statins to DM, but evidence linking statins to other SAS is largely anecdotal. Management of SAS requires making the possible diagnosis, altering or discontinuing the statin treatment, and using alternative lipid-lowering therapy.

Marathon running evokes parallel increases in markers of coagulation and fibrinolysis (i.e. hemostatic activation) immediately following strenuous, endurance exercise such that hemostatic balance is maintained. However, other factors incident to marathon running (i.e. dehydration, travel) may disproportionately activate the coagulatory system, increasing blood clot risk after an endurance event in otherwise healthy individuals. We investigated the effect of compression socks on exercise-induced hemostatic activation and balance in endurance athletes running the 2013 Hartford Marathon.Adults (n = 20) were divided into compression sock (SOCK; n = 10) and control (CONTROL; n = 10) groups. Age, anthropometrics, vital signs, training mileage and finishing time were collected. Venous blood samples were collected 1 day before, immediately after and 1 day following the marathon for analysis of coagulatory (i.e. thrombin-antithrombin complex [TAT] and D-dimer) and fibrinolytic (i.e. tissue plasminogen activator [t-PA]) factors.Plasma D-dimer, TAT and t-PA did not differ between groups at baseline (p0.16). There were no significant group · time interactions (all p ≥ 0.17), however, average t-PA was lower in SOCK (8.9 ± 0.7 ng/mL) than CONTROL (11.2 ± 0.7 ng/mL) (p = 0.04). Average TAT also tended to be lower in SOCK (2.8 ± 0.2 µg/L) than CONTROL (3.4 ± 0.2 µg/L) (p = 0.07).Our results suggest that overall hemostatic activation (both coagulation and fibrinolysis) following a marathon tended to be lower with compression socks. Thus, compression socks do not adversely influence markers of hemostasis, appear safe for overall use in runners and may reduce exercise-associated hemostatic activation in individuals at risk for deep vein thrombosis.

Purpose/methods. The Boston Athletic Association’s annual marathon, also referred to as BAA in this article, continues to be a source of subjects for exercise and endurance performance research. We performed a systematic literature review of BAA studies published in the 7 years since our prior report. Results. We identified 20 articles published from January 2008 to February 2015. Nine were related to cardiology; six were related to exercise physiology; four were related to metabolism; and one was related to marathon qualifying times. As in our prior, report cardiovascular studies remained the dominant topic, but with risk factors for atherosclerosis and thrombosis as the present focus. Conclusion. Cardiac issues remain the largest subject area for BAA studies, but with more emphasis on the effect of prolonged exercise on atherosclerotic and thrombotic risk factors. This shift is associated with an increase in marathon participation by older, recreational runners at increased risk of cardiac compl...

Background Age-related macular degeneration (AMD) is the leading cause of vision loss and blindness in people over 65 years old in the United States and has been associated with cardiovascular risk and decreased survival. There is conflicting data, however, regarding the contribution of AMD to the prediction of stroke. Aim To determine whether AMD is a risk indicator for incident stroke in a meta-analysis of available prospective and retrospective cohort studies published in the English literature. Methods We performed a systematic literature search of all studies published in English with Pub Med and other databases from 1966 to August 2014, reporting stroke incidence in patients with macular degeneration. Two investigators independently extracted the data. A random effects model was used to report Odds ratios (OR), with corresponding 95% confidence intervals (CI). Meta-regression using a mixed linear model was used to understand potential heterogeneity amongst studies. Results We identified 9 studies that reported stroke incidence in patients with and without early AMD (N = 1,420,978). No significant association was found between early AMD with incident stroke. Combined, these 9 studies demonstrated random effects (OR, 1.12; CI, 0.86–1.47; I2 = 96%). Meta-regression on baseline covariates of age, sex, and year of publication did not significantly relate to heterogeneity. Conclusions We found no significant relationship between AMD and incident stroke. Further studies are needed to clarify other causes of decreased survival in patients with AMD.

Introduction. Vitamin D deficiency is associated with the onset and progression of hypertension and cardiovascular disease (CVD). However, mechanisms underlying vitamin D deficiency-mediated increased risk of CVD remain unknown. We sought to examine the differential effect of high-dose versus low-dose vitamin D supplementation on markers of arterial stiffness among ~40 vitamin D deficient adults with prehypertension.Methods. Participants were randomized to high-dose (4000 IU/d) versus low-dose (400 IU/d) oral vitamin D3 for 6 months. 24 hr ambulatory blood pressure (BP), carotid-femoral pulse wave velocity, and pulse wave analyses were obtained at baseline and after 6 months of vitamin D supplementation.Results. There were no changes in resting BP or pulse wave velocity over 6 mo regardless of vitamin D dose (allp>0.202). High-dose vitamin D decreased augmentation index and pressure by 12.3 ± 5.3% (p=0.047) and 4.0 ± 1.5 mmHg (p=0.02), respectively. However, these decreases in arterial stiffness were not associated with increases in serum 25-hydroxyvitamin D over 6 mo (p=0.425).Conclusion. High-dose vitamin D supplementation appears to lower surrogate measures of arterial stiffness but not indices of central pulse wave velocity.Clinical Trial Registration. This trial is registered with www.clinicaltrials.gov (Unique Identifier:NCT01240512).

In previous studies, we found an endothelial nitric oxide synthase gene ( NOS3 ) variant rs2070744 associated with the ambulatory blood pressure (BP) response following bouts of moderate and vigorous intensity acute exercise, termed post‐exercise hypotension (PEH). In a validation cohort, we sequenced NOS3 exons for associations with PEH. Obese (30.9 ± 3.6 kg . m −2 ) African American ( n = 14) [AF] and Caucasian ( n = 9) adults 42.0 ± 9.8 years with hypertension (139.8 ± 10.4/84.6 ± 6.2 mmHg) performed three random experiments: bouts of vigorous and moderate intensity cycling and control. Subjects were attached to an ambulatory BP monitor for 19 h. We performed deep‐targeted exon sequencing with the Illumina TruSeq Custom Amplicon kit. Variant genotypes were coded as number of minor alleles (#MA) and selected for additional statistical analysis based upon Bonferonni or Benjamini–Yekutieli multiple testing‐corrected P ‐values under time‐adjusted linear models for 19 hourly BP measurements for each subject. After vigorous intensity over 19 h, among NOS3 variants passing multiple testing thresholds, as the #MA increased in rs891512 ( P = 6.4E‐04), rs867225 ( P = 6.5E‐04), rs743507 ( P = 2.6E‐06), and rs41483644 ( P = 2.4E‐04), systolic (SBP) decreased from 17.5 to 33.7 mmHg; and in rs891512 ( P = 9.7E‐05), rs867225 ( P = 2.6E‐05), rs41483644 ( P = 1.6E‐03), rs3730009 ( P = 2.6E‐04), and rs77325852 ( P = 5.6E‐04), diastolic BP decreased from 11.1 mmHg to 20.3 mmHg among AF only. In contrast, after moderate intensity over 19 h in NOS3 rs3918164, as the #MA increased, SBP increased by 16.6 mmHg ( P = 2.4E‐04) among AF only. NOS3 variants exhibited associations with PEH after vigorous, but not moderate intensity exercise among AF only. NOS3 should be studied further for its effects on PEH in a large, ethnically diverse sample of adults with hypertension to confirm our findings.

Statins can produce myalgia or muscle pain, which may affect medication adherence. We measured the effects of statins on muscle strength in patients with previous statin myalgia. Leg isokinetic extension average power at 60° per second (−8.8 ± 10.5N-M, p = 0.02) and average peak torque at 60° per second (−14.0 ± 19.7N-M, p = 0.04) decreased slightly with statin use, but 8 of 10 other variables for leg strength did not change (all p >0.13). Handgrip, muscle pain, respiratory exchange ratio, and daily activity also did not change (all p >0.09). In conclusion, statin myalgia is not associated with reduced muscle strength or muscle performance.

The purpose of the present report was to examine whether proprotein convertase subtilisin/kexin type 9 (PCSK9) levels differ in individuals who do not exhibit expected reductions in low density lipoprotein cholesterol (LDL-C) with statin therapy. Eighteen nonresponder subjects treated with 80 mg atorvastatin treatment for 6 months without substantial reductions in LDL-C (ΔLDL-C: 2.6 ± 11.4%) were compared to age- and gender-matched atorvastatin responders (ΔLDL-C: 50.7 ± 8.5%) and placebo-treated subjects (ΔLDL-C: 9.9 ± 21.5%). Free PCSK9 was marginally higher in nonresponders at baseline(P=0.07)and significantly higher in atorvastatin responders after 6 months of treatment(P=0.04). The change in free PCSK9 over 6 months with statin treatment was higher(P<0.01)in atorvastatin responders (134.2 ± 131.5 ng/mL post- versus prestudy) than in either the nonresponders (39.9 ± 87.8 ng/mL) or placebo subjects (27.8 ± 97.6 ng/mL). Drug compliance was not lower in the nonresponders as assessed by pill counts and poststudy plasma atorvastatin levels. Serum PCSK9 levels, both at baseline and in response to statin therapy, may differentiate individuals who do versus those who do not respond to statin treatment.