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AimsTo determine the impact of endurance training (ET) interventions on left ventricular (LV) chamber size, wall thickness, and mass in healthy adults.Methods and resultsElectronic databases including CINAHL, MEDLINE, PsycINFO, SPORTDiscus, Cochrane library, and EBM Reviews were searched up to 4 January 2022. Criteria for inclusion were healthy females and/or males (>18 years), ET intervention for ≥2 weeks, and studies reporting pre- and post-training LV structural parameters. A random-effects meta-analysis with heterogeneity, publication bias, and sensitivity analysis was used to determine the effects of ET on LV mass (LVM) and diastolic measures of interventricular septum thickness (IVSd), posterior wall thickness (PWTd), and LV diameter (LVDd). Meta-regression was performed on mediating factors (age, sex, training protocols) to assess their effects on LV structure. Eighty-two studies met inclusion criteria (n = 1908; 19–82 years, 33% female). There was a significant increase in LVM, PWTd, IVSd, and LVDd following ET [standardized mean difference (SMD) = 0.444, 95% confidence interval (CI): 0.361, 0.527; P < 0.001; SMD = 0.234, 95% CI: 0.159, 0.309; P < 0.001; SMD = 0.237, 95% CI: 0.159, 0.316; P < 0.001; SMD = 0.249, 95% CI:0.173, 0.324; P < 0.001, respectively]. Trained status, training type, and age were the only mediating factors for change in LVM, where previously trained, mixed-type training, young (18–35 years), and middle-aged (36–55 years) individuals had the greatest change compared with untrained, interval-type training, and older individuals (>55 years). A significant increase in wall thickness was observed in males, with a similar augmentation of LVDd in males and females. Trained individuals elicited an increase in all LV structures and ET involving mixed-type training and rowing and swimming modalities conferred the greatest increase in PWTd and LVDd.ConclusionLeft ventricular structure is significantly increased following ET. Males, young and trained individuals, and ET interventions involving mixed training regimes elicit the greatest changes in LV structure.

INTRODUCTION Pediatric heart transplant (HTx) recipients have reduced exercise capacity typically two-thirds of predicted values, the mechanisms of which are not fully understood. We sought to assess the cardiorespiratory responses to progressive exercise in HTx relative to controls matched for age, sex, body size, and work rate. METHODS Fourteen HTx recipients and matched controls underwent exercise stress echocardiography on a semisupine cycle ergometer. Hemodynamics, left ventricular (LV) dimensions, and volumes were obtained and indexed to body surface area. Oxygen consumption (V˙O2) was measured, and arteriovenous oxygen difference was estimated using the Fick Principle. RESULTS At rest, LV mass index (P = 0.03) and volumes (P < 0.001) were significantly smaller in HTx, whereas wall thickness (P < 0.01) and LV mass-to-volume ratio (P = 0.01) were greater. Differences in LV dimensions and stroke volume persisted throughout exercise, but the pattern of response was similar between groups as HR increased. As exercise progressed, heart rate and cardiac index increased to a lesser extent in HTx. Despite this, V˙O2 was similar (P = 0.82) at equivalent work rates as HTx had a greater change in arteriovenous oxygen difference (P < 0.01). CONCLUSIONS When matched for work rate, HTx had similar metabolic responses to controls despite having smaller LV chambers and an attenuated increase in hemodynamic responses. These findings suggest that HTx may increase peripheral O2 extraction as a compensatory mechanism in response to reduced cardiovascular function.

Background: Chronic endurance exercise training elicits desirable physiological adaptations in the cardiovascular system. The volume of exercise training required to generate healthy adaptations is unclear. This study assessed the effects of differing exercise training levels on arterial stiffness, compliance, and autonomic function. Methods: Eighty healthy adults (38.5 ± 9.7 years; 44% female) defined as endurance-trained (ET, n = 29), normally active (NA, n = 27), or inactive (IN, n = 24) participated. Cardiovascular markers, including hemodynamics, large arterial compliance and small arterial compliance (LAC and SAC), carotid-femoral pulse wave velocity (PWV), and spontaneous baroreceptor sensitivity (BRS) were assessed. Results: ET showed significantly greater LAC values (21.4 ± 6.5) than NA (16.9 ± 2.5; p = 0.002) and IN (14.7 ± 3.2 mL × mm Hg × 10; p = 0.028). Values for SAC and BRS were significantly higher in ET than IN (p < 0.001 and p = 0.028, respectively), but not NA. Compared to IN, PWV values for ET and NA were significantly lower (p < 0.003). After adjusting for covariates (age, sex, and SBP), significant associations with cardiovascular fitness status were noted for all markers but BRS. Conclusion: Endurance exercise increases LAC likely due to high-volume training; however, lower volumes of physical activity may be sufficient to positively benefit vascular health overall.

Objective Pediatric heart transplant recipients are at risk of posttransplant coronary artery disease known as cardiac allograft vasculopathy (CAV), and also may develop diastolic dysfunction. As CAV begins with a process of progressive intimal thickening, these occult diffuse changes may be detected using optical coherence tomography (OCT). We hypothesized that the development of CAV, as identified via OCT, may be a mechanism of declining ventricular function. Accordingly, the purpose of this study was to assess coronary artery intimal thickening and LV strain in children who have undergone heart transplantation. Methods In 17 children, we analyzed OCT images for coronary intima and media thickness, and cross-sectional area (CSA). We also performed speckle tracking imaging (STI) of the LV to determine longitudinal strain and strain rate, in addition to standard echocardiographic measures. Results Longitudinal diastolic strain rate was associated with maximum intima thickness (r = -.497, P = .042), intima CSA, (r = -.489, P = .047), maximum media thickness (r = -.503, P = .039), and media CSA (r = -.614, P = .009). The intima maximum thickness, intima/media, and intima/lumen ratios were associated with stroke volume index (Std. β = -0.487, P = .023 and Std. β = -0.488, P = .022, respectively). Conclusions These findings suggest coronary artery intimal thickening may be mechanistically linked to changes in ventricular function following cardiac transplantation.

OBJECTIVE To evaluate sex differences in left ventricular (LV) function after an ultramarathon, and the association of vascular and training indices with the magnitude of exercise-induced cardiac fatigue. DESIGN Descriptive field study. SETTING Fat Dog 100 Ultramarathon Trail Race, Canada. PARTICIPANTS Thirty-four (13 women) recreational runners (aged 28-56 years). INTERVENTIONS A 100-km or 160-km mountain marathon. MAIN OUTCOME MEASURES Baseline baroreceptor sensitivity, heart rate variability, and arterial compliance; Pre-exercise and postexercise echocardiographic evaluations of LV dimensions, volumes, Doppler flow velocities, tissue velocities, strain, and strain rate. RESULTS Finishers represented 17 men (44.8 ± 6.6 years) and 8 women (45.9 ± 10.2 years; P = 0.758). After ultraendurance exercise, significant reductions (P < 0.05) in fractional shortening (men: 40.9 ± 6.9 to 34.1 ± 7.6%; women: 42.5 ± 6.5 to 34.6 ± 7.9%) diastolic filling (E/A, men: 1.28 ± 0.68 to 1.26 ± 0.33; women: 1.55 ± 0.51 to 1.30 ± 0.27), septal and lateral tissue velocities (E'), and longitudinal strain (men: -21.02 ± 1.98 to -18.44 ± 0.34; women: -20.28 ± 1.90 to -18.44 ± 2.34) were observed. Sex differences were found for baseline cardiac structure and global function, peak late transmitral flow velocity, and estimates of LV filling pressures (P < 0.05). Regression analysis found that higher baseline arterial compliance was associated with lower reductions in cardiac function postexercise, to which sex was a significant factor for E' of the lateral wall. Faster race pace and greater lifetime ultramarathons were associated with lower reductions in LV longitudinal strain (P < 0.05). CONCLUSIONS Cardiac responses after an ultramarathon were similar between men and women. Greater evidence of exercise-induced cardiac fatigue was found to be associated with lower baseline arterial compliance and training status/experience. CLINICAL RELEVANCE These findings suggest that vascular health is an important contributor to the degree of cardiovascular strain incurred as the result of an acute bout of prolonged strenuous exercise.

Objective— Childhood obesity is associated with risk factors for cardiovascular disease. Arterial stiffness is considered one of the earliest detectable measures of vascular damage. There is controversy in the literature regarding the effects of childhood obesity on arterial stiffness. The objective of this study is to systematically review the literature and to conduct a meta-analysis comparing measures of central arterial stiffness in children and adolescents with obesity to healthy body mass index controls. Approach and Results— Literature searches were conducted using databases (eg, MEDLINE, EMBASE) and citations cross-referenced. Studies assessing central pulse wave velocity or β-stiffness index were included. A random effects meta-analysis of the standardized mean difference and 95% confidence intervals in arterial stiffness between children with obesity and control children was performed for each arterial stiffness measure. A total of 523 studies were identified. Fifteen case–control studies were included, with 2237 children/adolescents (1281 with obesity, 956 healthy body mass index controls) between 5 and 24 years of age. All studies measuring carotid and aortic β-stiffness index and 10/12 studies measuring central pulse wave velocity reported greater arterial stiffness in children/adolescents with obesity compared with controls. A random effects meta-analysis was performed revealing a significant effect of obesity on pulse wave velocity (standardized mean difference=0.718; 95% confidence interval=0.291–1.415), carotid β-stiffness index (0.862; 0.323–1.402), and aortic β stiffness index (1.017; 0.419–1.615). Conclusion— These findings indicate that child/adolescent obesity is associated with greater arterial stiffness. However, further research is needed to address confounders, such as pubertal status, that may affect this relationship in children. In the future, these techniques may be useful in risk stratification and guiding clinical management of obese children to optimize cardiovascular outcomes.

Early detection of hemorrhage remains an open problem. In this regard, blood pressure has been an ineffective measure of blood loss due to numerous compensatory mechanisms sustaining arterial blood pressure homeostasis. Here, we investigate the feasibility of causality detection in the heart rate and blood pressure interaction, a closed-loop control system, for early detection of hemorrhage. The hemorrhage was simulated via graded lower-body negative pressure (LBNP) from 0 to −40 mmHg. The research hypothesis was that a significant elevation of causal control in the direction of blood pressure to heart rate (i.e., baroreflex response) is an early indicator of central hypovolemia. Five minutes of continuous blood pressure and electrocardiogram (ECG) signals were acquired simultaneously from young, healthy participants (27 ± 1 years, N = 27) during each LBNP stage, from which heart rate (represented by RR interval), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) were derived. The heart rate and blood pressure causal interaction (RR↔SBP and RR↔MAP) was studied during the last 3 min of each LBNP stage. At supine rest, the non-baroreflex arm (RR→SBP and RR→MAP) showed a significantly (p < 0.001) higher causal drive toward blood pressure regulation compared to the baroreflex arm (SBP→RR and MAP→RR). In response to moderate category hemorrhage (−30 mmHg LBNP), no change was observed in the traditional marker of blood loss i.e., pulse pressure (p = 0.10) along with the RR→SBP (p = 0.76), RR→MAP (p = 0.60), and SBP→RR (p = 0.07) causality compared to the resting stage. Contrarily, a significant elevation in the MAP→RR (p = 0.004) causality was observed. In accordance with our hypothesis, the outcomes of the research underscored the potential of compensatory baroreflex arm (MAP→RR) of the heart rate and blood pressure interaction toward differentiating a simulated moderate category hemorrhage from the resting stage. Therefore, monitoring baroreflex causality can have a clinical utility in making triage decisions to impede hemorrhage progression.

Second-generation antipsychotic (SGA) medications, used to treat youth for a wide-range of mental health conditions, are associated with excessive weight gain and other comorbidities, placing these individuals at high risk for cardiovascular disease. Little is known about the effect of physical activity (PA) on cardiovascular risk in these children. Anthropometrics, fasting blood sample and self-report PA were obtained in 386 children diagnosed with mental health conditions (6-18 y). PA was classified as below (

An acute reduction in blood pressure observed after a single bout of exercise is termed post-exercise hypotension (PEH). In contrast to moderate intensity aerobic exercise, little is known about the PEH response following high-intensity interval exercise. The present purpose is to assess how sex and training status impact PEH following high-intensity interval exercise. Cardiac volumes and function via echocardiography were measured in 40 normotensive, endurance-trained (ET) and normally active (NA) men and women (Age ± SD = 30.5 ± 5.7) following high-intensity interval cycle exercise. Continuous measurements of ECG and beat-by-beat blood pressure were collected before and 30 min post-exercise for determination of cardiovagal baroreflex function (BRS and αLF), spectral analysis of heart rate and systolic blood pressure (SBP LF). Post-exercise systolic BP was significantly reduced from baseline, occurring to a greater degree in ET compared with NA (−12.9 vs. −5.3 mmHg, P = 0.008), while mean arterial pressure was similarly reduced in all groups (−4.6 mmHg, P = 0.003). Despite reduced SVI and TPRI, CI was increased post-exercise (P

Purpose The primary goal of pediatric heart transplantation (PHTx) is to improve the quality of life (QoL) of patients. National physical activity guidelines for adolescents recommend at least 60-90 minutes of moderate to vigorous physical activity per day. The Physical Activity Questionnaire (PAQ-C/A) for children and adolescents provides general estimates of physical activity levels. Measurement of peak aerobic capacity (VO2peak) using cardiopulmonary exercise testing (CPX) is the gold standard for assessing exercise capacity. Both physical activity and exercise capacity may be important factors that influence reporting a normal QoL. Our aim was to determine if there was a relationship between physical activity, exercise capacity, and QoL in a PHTx adolescent population. Methods This is a single centre retrospective chart review of adolescent (11-18 yrs) PHTx patients. Those who completed a maximal CPX test (RER>1.0), self-report physical activity (PAQ-C or PAQ-A) and QoL (PedsQL and PedsQL-Transplant) questionnaires, as part of their annual assessment, were eligible for inclusion. Results were compared to published age- and sex-matched healthy control data used in our laboratory. VO2peak and QoL were deemed to be normal if results were within two standard deviations of the mean. Pearson correlation coefficients were calculated. Medians and interquartile ranges are reported. Results Thirteen PHTx (10 males) completed a CPX and both QoL questionnaires. The median age was 14.9 yrs (12.3-17.5 yrs). VO2peak=34.5 mL/min/kg (30.2-43.4 mL/min/kg. Only 1 of 13 had an abnormal VO2peak. Total Peds QL score=84.8 (68.5-92.4) with 10 out 13 reporting a normal QoL. The Peds QL-Transplant score=90.5 (84.8-95.1). There was no significant correlation between VO2peak and QoL. The PAQ-C/PAQ-A was completed in 10 HTx. PAQ scores=2.38 (1.59-3.01). Only 2 of 13 met the cut-off point (>2.87) for adequate physical activity. There was a significant correlation between the Peds QL-Transplant QoL and the PAQ (r=0.69; p=0.04) Conclusion PHTx adolescents do not meet their required physical activity recommendations. Despite this, they have low normal exercise capacity and report a normal QoL. Efforts to engage adolescents to increase their physical activity should be encouraged.

High-intensity exercise induces marked physiological stress affecting the secretion of catecholamines. Sustained elevations in catecholamines are thought to desensitize cardiac beta receptors and may be a possible mechanism in impaired cardiac function following strenuous exercise. In addition, attenuated arterial-ventricular coupling may identify vascular mechanisms in connection with postexercise attenuations in ventricular function. Thirty-nine normally active (NA) and endurance-trained (ET) men and women completed an echocardiographic evaluation of left ventricular function before and after an acute bout of high-intensity interval exercise (15 bouts of 1:2 min work:recovery cycling: 100% peak power output and 50 W, respectively). Following exercise, time to peak twist and peak untwisting velocity were delayed ( P < 0.01) but did not differ by sex or training status. Interactions for sex and condition (rest vs. exercise) were found for longitudinal diastolic strain rate (men, 1.46 ± 0.19 to 1.28 ± 0.23 s−1 vs. women, 1.62 ± 0.25 to 1.63 ± 0.26 s−1; P = 0.01) and arterial elastance (men 2.20 ± 0.65 to 3.24 ± 1.02 mmHg·ml−1·m−2 vs. women 2.51 ± 0.61 to 2.93 ± 0.68 mmHg·ml−1·m−2; P = 0.04). No cardiac variables were found associated with catecholamine levels. The change in twist mechanics was associated with baseline aortic pulse-wave velocity ( r2 = 0.27, P = 0.001). We conclude that males display greater reductions in contractility in response to high-intensity interval exercise, independent of catecholamine concentrations. Furthermore, a novel association of arterial stiffness and twist mechanics following high-intensity acute exercise illustrates the influence of vascular integrity on cardiac mechanics.

Obesity-related cardiovascular disease in children is becoming more prevalent in conjunction with the rise in childhood obesity. Children with obesity are predisposed to an increased risk of cardiovascular morbidity and mortality in adulthood. Importantly, research in children with obesity over the last decade has demonstrated that children may exhibit early signs of cardiovascular dysfunction as a result of their excess adiposity, often independent of other obesity-related comorbidities such as dyslipidemia and insulin resistance. The clinical evidence is accumulating to suggest that the cardiovascular damage, once observed only in adults, is also occurring in obese children. The objective of this review is to provide a synopsis of the current research on cardiovascular abnormalities in children with obesity and highlight the importance and need for early detection and prevention programs to mitigate this potentially serious health problem.

The aim of this study was to systematically evaluate the incidence of infective endocarditis (IE) in right ventricle-to-pulmonary artery conduits and valves, comparing bovine jugular vein (BJV) valves with all others.Recent evidence suggests that the incidence of IE is higher in patients with congenital heart disease who have undergone implantation of BJV valves in the pulmonary position compared with other valves.Systematic searches of published research were conducted using electronic databases (MEDLINE, Embase, and CINAHL) and citations cross-referenced current to April 2016. Included studies met the following criteria: patients had undergone right ventricle-to-pulmonary artery conduit or percutaneous pulmonary valve implantation, and investigators reported on the type of conduit or valve implanted, method of intervention (surgery or catheter based), IE incidence, and follow-up time.Fifty studies (Levels of Evidence: 2 to 4) were identified involving 7,063 patients. The median cumulative incidence of IE was higher for BJV compared with other valves (5.4% vs. 1.2%; p 0.0001) during a median follow-up period of 24.0 and 35.5 months, respectively (p = 0.03). For patients with BJV valves, the incidence of IE was not different between surgical and catheter-based valve implantation (p = 0.83).There was a higher incidence of endocarditis with BJV valves than other types of right ventricle-to-pulmonary artery conduits. There was no difference in the incidence of endocarditis between catheter-based bovine valves and surgically implanted bovine valves, suggesting that the substrate for future infection is related to the tissue rather than the method of implantation.

Background Stress echocardiography has been advocated for the detection of abnormal myocardial function and unmasking diminished myocardial reserve in pediatric patients. The aim of this study was to create a simplified index of myocardial reserve, derived from the myocardial inotropic response to peak semisupine exercise in healthy children, and illustrate its applicability in a sample of pediatric oncology patients. Methods In this prospective analysis, children (7–18 years of age) with normal cardiac structure and function performed semisupine stress echocardiography to volitional fatigue. The quotient of wall stress at peak systole and heart rate–corrected velocity of circumferential fiber shortening were calculated at baseline and at peak exercise, the difference of which was termed the index of myocardial reserve (IMR). The IMR was also calculated in a retrospective sample of pediatric oncology patients with normal resting left ventricular function who had received anthracycline treatment and had performed the same exercise protocol to illustrate utility. Results Fifty healthy subjects (mean age, 13.2 ± 2.6 years) and 33 oncology patients (mean age, 12.7 ± 4.0 years) were assessed. In the healthy children at peak exercise, heart rate–corrected velocity of circumferential fiber shortening significantly increased (from 1.17 ± 0.17 to 1.58 ± 0.24 circ · sec −1 , P −2 , P Conclusions The authors have developed a novel IMR. Relative to the normal distribution of this IMR in healthy subjects, it is possible to identify patients with abnormal myocardial reserve. Thus, this study demonstrates the application of the IMR to aid in clinical decision making in individual patients.

The objective of this study is to compare arterial stiffness between those with spinal cord injury (SCI) and able-bodied (AB) individuals when matched for habitual level of physical activity.A total of 17 SCI and 17 AB individuals were matched for sex, age, weight, blood pressure, and levels of self-reported habitual physical activity (Godin-Shephard). Measures included central pulse wave velocity (PWV) (carotid-femoral PWV (cfPWV)) and lower limb PWV (femoral--toe PWV(ftPWV)) as well as large and small arterial compliance.The cfPWV was significantly elevated (7.3 ± 2.1 vs. 5.7 ± 1.4 m·s, P0.05) in SCI compared with AB. No other measures of arterial stiffness were different between the groups. Moderate to vigorous physical activity was significantly correlated with both large (r = 0.48, P0.05) and small (r = 0.65, P0.01) artery compliance, but not cfPWV or ftPWV.Both large and small artery compliance appear to be associated with habitual physical activity in physically active individuals with SCI. However, we did not show that physical activity is associated with PWV in physically active individuals with SCI. These findings suggest that factors other than physical inactivity may mediate the increase in arterial stiffness widely reported in the SCI population.

As sympathetic activity approximately doubles during intense lower body negative pressure (LBNP) of -60 mmHg or greater, we examined the relationship between surrogate markers of sympathetic activation and central arterial distensibility during severe LBNP. Eight participants were exposed to progressive 8-min stages of LBNP of increasing intensity (-20, -40, -60, and -80 mmHg), while recording carotid-femoral pulse wave velocity (cPWV), stroke volume (SV), heart rate, and beat-by-beat blood pressure. The spectral power of low frequency oscillations in SBP (SBP(LF)) was used as a surrogate indicator of sympathetically modulated vasomotor modulation. Total arterial compliance (C) was calculated as C = SV/pulse pressure. Both cPWV and C were compared between baseline, 50 % of the maximally tolerated LBNP stage (LBNP(50)), and the maximum fully tolerated stage of LBNP (LBNP(max)). No change in mean arterial pressure (MAP) occurred over LBNP. An increase in cPWV (6.5 ± 2.2; 7.2 ± 1.4; 9.0 ± 2.5 m/s; P = 0.004) occurred during LBNP(max). Over progressive LBNP, SBP(LF) increased (8.5 ± 4.6; 9.3 ± 5.8; 16.1 ± 12.9 mmHg(2); P = 0.04) and C decreased significantly (18.3 ± 6.8; 14.3 ± 4.1; 11.6 ± 4.8 ml/mmHg × 10; P = 0.03). The mean correlation (r) between cPWV and SBP(LF) was 0.9 ± 0.03 (95 % CI 0.79-0.99). Severe LBNP increased central stiffness and reduced total arterial compliance. It appears that increased sympathetic vasomotor tone during LBNP is associated with reduced aortic distensibility in the absence of changes in MAP.

BACKGROUND: The purpose of this study was to examine individual stroke volume-pulse pressure (PP) relationships in healthy young men and women. METHODS: Sixteen healthy men and women were assessed at baseline and during four 12-minute stages of progressive lower body negative pressure (LBNP) at -15, -30, -45, and -60 mm Hg. RESULTS: Throughout staged LBNP, systolic blood pressure (105 ± 7.8 vs. 103 ± 8.3 mm Hg) and mean arterial pressure were not statistically different (81 ± 5.6 vs. 83 ± 5.9 mm Hg). There was also a significant increase in diastolic blood pressure (69 ± 5.3 vs. 72 ± 5.9 mm Hg) and heart rate (63 ± 8.3 vs. 86 ± 14.2 bpm) as well as a decrease in PP (37 ± 5.7 vs. 31 ± 7.0 mm Hg) and stroke volume (80 ± 17.0 vs. 26.6 ± 10.0 mL). There was a strong positive relationship for LBNP versus stroke volume (r2 = 0.99), PP (r2 = 0.96), and heart rate (r2 = -0.92), as well as for stroke volume versus PP (r2 = 0.98) and stroke volume versus heart rate (r = -0.94). Substantial intersubject variability in the stroke volume and PP correlations were presented. Strong, significant correlations were only displayed for 38% of the participants, while heart rate and stroke volume was strongly associated in 63% of these individuals. CONCLUSIONS: This work highlights the limitations of using PP when assessing trauma patients because of large interindividual differences.

There is a growing interest in training for and competing in race distances that exceed the marathon; however, little is known regarding the vascular effects of participation in such prolonged events, which last multiple consecutive hours. There exists some evidence that cardiovascular function may be impaired following extreme prolonged exercise, but at present, only cardiac function has been specifically examined following exposure to this nature of exercise. The primary purpose of this study was to characterize the acute effects of participation in an ultra-marathon on resting systemic arterial compliance. Arterial compliance and various resting cardiovascular indices were collected at rest from 26 healthy ultra-marathon competitors using applanation tonometry (HDI CR-2000) before and after participation in a mountain trail running foot race ranging from 120-195 km which required between 20-40 continuous hours (31.2±6.8 h) to complete. There was no significant change in small artery compliance from baseline to post race follow-up (8.5±3.4-7.7±8.2 mL/mmHgx100, p=0.65), but large artery compliance decreased from 16.1±4.4 to 13.5±3.8 mL/mmHgx10 (p=0.003). Participation in extreme endurance exercise of prolonged duration was associated with acute reductions in large artery compliance, but the time course of this effect remains to be elucidated.

We aimed to compare the Finapres system, which is designed for accurate intra-arterial amplitude measurement, to the Caretaker system, which is designed for temporal accuracy of intra-arterial measurement, in regard to measurement of pulse transit time (PTT) at baseline and following an endurance exercise session. Pulse transit time was evaluated between the R-wave of the ECG and the foot of the arterial waveform using either the Finapres (fpPTT) or Caretaker (ctPTT). 23 participants were measured before and after completion of endurance exercise. When comparing PTT values before and after an exercise intervention within devices, ctPTT was significantly different following exercise (P=0.03); however, the Finapres obtained values did not differ significantly. Before exercise, there was no significant relationship between devices, however, after exercise a significant moderate correlation was observed (r=0.45, P=0.02). Significant differences existed between ctPTT and fpPTT (P 0.001). The Caretaker system appears to be more accurate at detecting changes in PTT occurring as a result of a single aerobic exercise session. This may be due to the servo-controller feedback loop in the waveform contour predicting algorithm within the Finapres system, which is not present in the Caretaker unit. The Finapres system also appears to have an inherent delay in pulse contour reporting.

Second-generation antipsychotics (SGA) are increasingly being used to treat children for a wide-range of mental health conditions, and are associated with cardiometabolic side effects such as rapid weight gain and elevated blood pressure (BP). The catechol-O-methyl transferase ( COMT) Val158Met variant is associated with BP in the general population. We recently reported higher BP in SGA-treated children with the Met allele, but no such association in SGA-naïve children. Methylation of the COMT promoter is another important regulatory factor governing COMT activity. The aim of this study was to investigate the interaction of the COMT Val158Met variant and COMT methylation on BP in children with mental health conditions. A cross-sectional population of SGA-treated (n=106) and SGA[[Unable to Display Character: –]]naïve children (n=122), ≤18 y of age, were assessed for markers of cardiometabolic health. Bisulfite pyrosequencing was used to quantify the methylation status of three CpG sites in the COMT promoter. Relationships between SGA treatment, COMT Val158Met genotype and COMT promoter methylation were assessed using general linear models. BMI was standardized for age and sex (zBMI) and systolic and diastolic BP standardized for age, sex, and height (zSBP, zDBP). When analyzed as one group, there were no significant effects of COMT genotype, SGA-treatment, or mental health diagnosis on mean methylation. In SGA-treated children, an interaction between mean methylation and COMT genotype was observed for zSBP ( p =0.015), where zSBP was positively related to methylation in children with the Val/Val genotype, but not in children with the Met allele. After adjustments for ethnicity, SGA-duration, and zBMI the effect was diminished ( p =0.109), with SGA-duration ( p =0.018) and zBMI ( p =0.032) accounting for the variation in zSBP. This association was not found in SGA-naïve children. These findings suggest COMT promoter methylation may influence the effect of the COMT Val158Met variant on blood pressure in SGA-treated children.

Heart transplant recipients are at increased risk for atherosclerosis and cardiac allograft vasculopathy, both initially presenting as intimal thickening. We aimed to determine the presence, extent, and anatomical characteristics of intimal thickness at coronary bifurcations in children using OCT. We measured the intimal thickness of coronary arteries in pediatric transplant recipients using OCT during routine cardiac catheterization. Intimal thickening was defined as (i) a percent change in contralateral intimal thickness greater than 50% when comparing the thickness at the bifurcation to the baseline thickness, and (ii) greater than 0.1 mm. We evaluated 153 unique coronary bifurcations in 31 children (58% boys, median 12.7 years). Intimal thickening was almost exclusively observed in the left coronary system (22 of 67 bifurcations) and rare in the right coronary system (2 of 86 bifurcations; P .001). There was a positive association between the relative size of the side branch and contralateral intimal thickening at coronary bifurcations (P = .009). Intimal thickening at coronary bifurcations is already present in the left coronary system in many pediatric transplant recipients. The correlation between intimal thickening and side branch size suggests that low shear stress and oscillating shear stress may have an important role in the development of intimal thickening at coronary bifurcations.

Childhood obesity is associated with progressive vascular dysfunction as manifest by arterial stiffness and elevated blood pressure with associated subsequent morbidity and mortality because of early cardiovascular events including myocardial infarction and stroke in adulthood. Consequently, the recent dramatic increases in childhood obesity around the world present a hitherto unforeseen public health concern. While coordinated primary prevention efforts remain an ongoing important focus of action, identification and treatment of modifiable cardiovascular risk factors in pediatric patients is necessary given the existing burden of disease and future health consequences. Lifestyle interventions remain a cornerstone of our therapeutic approach, however, medical therapy is needed in some cases and should not be underutilized based on patient age. Herein, we discuss the relationship between childhood obesity and hypertension with a key emphasis on the evolution of adaptive and maladaptive vascular changes in the genesis of overt cardiovascular disease.

After cervical spinal cord injury (SCI), orthostatic hypotension and intolerance commonly ensue. The cardiovagal baroreflex plays an important role in the acute regulation of blood pressure (BP) and is associated with the onset of presyncope. The cardiovagal baroreflex is dysfunctional after SCI; however, this may be influenced by either increased stiffening of the arteries containing the stretch-receptors (which has been shown in SCI) or a more downstream neural mechanism (i.e., solitary nucleus, sinoatrial node). Identifying where along this pathway baroreflex dysfunction occurs may highlight a potential therapeutic target. This study examined the relationship between spontaneous cardiovagal baroreflex sensitivity (BRS) and common carotid artery (CCA) stiffness in those with high level SCI before and after midodrine (alpha1-agonist) administration, as well as in able-bodied controls, to evaluate: (1) the role arterial stiffening plays mediating baroreflex function after SCI and (2) the effect of normalizing BP on these parameters. Three to five min recordings of beat-by-beat BP and heart rate, as well as 30 sec duration recordings of CCA diameter were used for analysis. All participants were tested supine and during upright-tilt. Arterial stiffness (β-stiffness index) was elevated in those with SCI when upright (+12%; p0.05). Further, β-stiffness index was negatively related to reduced BRS in those with SCI when upright (R2=0.55; p0.05), but not in able-bodied persons. Normalizing BP did not improve BRS or CCA stiffness. This study clearly shows that reduced BRS is closely related to increased arterial stiffness in the population with SCI.

We aimed to investigate the effects of a single session of prolonged strenuous exercise (PSE) on arterial stiffness by measuring pulse wave velocity (PWV) before and after competition in an ultramarathon. A total of 20 routine ultramarathon competitors (UM) completed baseline and postrace evaluation of central PWV (cPWV), upper-limb PWV (uPWV), and lower-limb PWV (lPWV) using carotid artery – femoral artery, carotid artery – finger, and femoral artery – toe segments, respectively. Fourteen additional age- and gender-matched normally active participants (NA) took part in the identical baseline evaluation but did not participate in the race. Average ultramarathon completion time was 30 h 47 min. Mean arterial blood pressure was reduced after exercise (before exercise (pre), 92 ± 7 mm Hg; after exercise (post), 84 ± 7 mm Hg; P < 0.001), whereas heart rate was increased (pre, 57 ± 10 beats·min–1; post, 73 ± 12 beats·min–1; P < 0.001). Also, lPWV (pre, 11.8 ± 3.6 m·s–1; post, 9.6 ± 2.6 m·s–1; P < 0.05) and uPWV (pre, 5.0 ± 0.53 m·s–1; post, 4.4 ± 0.8 m·s–1; P < 0.01) were reduced after exercise. No change in cPWV occurred (pre, 4.1 ± 0.8 m·s–1; post, 3.9 ± 1.3 m·s–1; P = 0.55). At baseline, the NA group had significantly increased cPWV in comparison with the UM group (UM, 4.1 ± 0.8 m·s–1; NA, 7.4 ± 1.3 m·s–1; P < 0.001). Acute participation in PSE influenced peripheral but not central arterial stiffness. Those who routinely participate in PSE have reduced central arterial stiffness as compared with normally active, age- and gender-matched controls.

All randomized controlled trials, prospective cohort, case–controlled, pre–post studies and case reports that assessed exercise interventions, which influence arterial structure and function after spinal cord injury (SCI), were included. To review systematically the evidence for exercise as a therapy to alter arterial function in persons with SCI. Literature searches were conducted for appropriate articles using several electronic databases (e.g. MEDLINE, EMBASE). Three independent reviewers evaluated each investigation's quality, using the Physiotherapy Evidence Database Scale for randomized controlled trials and Downs and Black Scale for all other studies. Results were tabulated and levels of evidence assigned. A total of 283 studies were found through the systematic literature search. Upon review of the articles, 27 were included. The articles were separated into those investigating arterial benefits, resulting from either acute bouts of exercise or long-term exercise interventions. The ability of both acute and long-term exercise interventions to improve arterial structure and function in those with SCI was supported by limited to moderate methodological quality. Upper body wheeling is the most commonly examined exercise therapy for improving arterial function. It appears from the evidence that a variety of exercise interventions, including passive exercise, upper body wheeling, functional electrical stimulation and electrically stimulated resistance exercise, can improve arterial function in those living with SCI. Although the quality and volume of evidence is low, the literature supports exercise as a useful intervention technique for improving arterial function in those with SCI.

Background Markers of temporal changes in central blood volume are required to non-invasively detect hemorrhage and the onset of hemorrhagic shock. Recent work suggests that pulse pressure may be such a marker. A new approach to tracking blood pressure, and pulse pressure specifically is presented that is based on a new form of pulse pressure wave analysis called Pulse Decomposition Analysis (PDA). The premise of the PDA model is that the peripheral arterial pressure pulse is a superposition of five individual component pressure pulses, the first of which is due to the left ventricular ejection from the heart while the remaining component pressure pulses are reflections and re-reflections that originate from only two reflection sites within the central arteries. The hypothesis examined here is that the PDA parameter T13, the timing delay between the first and third component pulses, correlates with pulse pressure. T13 was monitored along with blood pressure, as determined by an automatic cuff and another continuous blood pressure monitor, during the course of lower body negative pressure (LBNP) sessions involving four stages, -15 mmHg, -30 mmHg, -45 mmHg, and -60 mmHg, in fifteen subjects (average age: 24.4 years, SD: 3.0 years; average height: 168.6 cm, SD: 8.0 cm; average weight: 64.0 kg, SD: 9.1 kg). Results Statistically significant correlations between T13 and pulse pressure as well as the ability of T13 to resolve the effects of different LBNP stages were established. Experimental T13 values were compared with predictions of the PDA model. These interventions resulted in pulse pressure changes of up to 7.8 mmHg (SE = 3.49 mmHg) as determined by the automatic cuff. Corresponding changes in T13 were a shortening by -72 milliseconds (SE = 4.17 milliseconds). In contrast to the other two methodologies, T13 was able to resolve the effects of the two least negative pressure stages with significance set at p < 0.01. Conclusions The agreement of observations and measurements provides a preliminary validation of the PDA model regarding the origin of the arterial pressure pulse reflections. The proposed physical picture of the PDA model is attractive because it identifies the contributions of distinct reflecting arterial tree components to the peripheral pressure pulse envelope. Since the importance of arterial pressure reflections to cardiovascular health is well known, the PDA pulse analysis could provide, beyond the tracking of blood pressure, an assessment tool of those reflections as well as the health of the sites that give rise to them.

BACKGROUND: Using data from AMPLIFY, a phase III trial comparing apixaban with conventional anticoagulant treatment in patients with venous thromboembolism (VTE), we performed subgroup analyses to compare the efficacy and safety of these regimens in patients with and without active cancer at baseline. Active cancer was defined as cancer that was diagnosed or treated within the past 6 months. METHODS: Patients with symptomatic VTE were randomized to a 6-month course of apixaban (10mg BID for 7 days followed by 5mg BID) or conventional treatment consisting of enoxaparin (1mg/kg BID for at least 5 days) followed by doseadjusted warfarin (target INR, 2-3). Cancer patients for whom long-term low-molecular-weight heparin (LMWH) was planned were excluded. The primary efficacy outcome was symptomatic VTE or VTE-related death. The intent-to-treat efficacy analysis included all randomized subjects with a nonmissing primary endpoint. The primary safety outcome was ISTH-defined major bleeding up to 2 days after stopping study drug in all randomized subjects who received at least one dose of study medication. All outcomes were adjudicated by an independent committee blinded to treatment assignment. RESULTS: Of 5395 patients randomized, 169 (3.1%) had active cancer. Baseline characteristics in these patients were similar between the two treatment groups. The median duration of treatment was 167 and 168 days in the apixaban and warfarin groups, respectively. In patients with active cancer at entry, recurrent VTE occurred in 3 of 81 (3.7%) patients in the apixaban group and in 5 of 78 (6.4%) in the warfarin group (relative risk [RR], 0.56; 95% CI, 0.132.37); major bleeding occurred in 2 of 87 (2.3%) and 4 of 80 (5.0%) patients, respectively (RR, 0.45; 95% CI, 0.082.46). In patients without cancer at entry, recurrent VTE occurred in 56 of 2528 (2.2%) and in 66 of 2557 (2.6%) patients in the apixaban and warfarin group, respectively (RR, 0.86; 95% CI, 0.60-1.22), whereas major bleeding occurred in 13 of 2589 (0.5%) and in 45 of 2609 (1.7%) patients in the apixaban and warfarin group, respectively (RR, 0.29; 95% CI, 0.16-0.54). CONCLUSION: Although the number of cancer patients was small, the results in this pre-specified subgroup are consistent with the overall findings and suggest that apixaban is as effective as conventional therapy in VTE patients with active cancer, and is associated with less bleeding. Additional studies are needed to compare the efficacy and safety of apixaban and LMWH for VTE treatment in cancer patients. Pfizer, BMS

triglycerides were similar. Only global LV circumferential strain in the medium-risk tertile remained different when comparing the smaller T1D subgroups vs. controls (-19.4 1.6 vs. -18.8 1.7 %; p1⁄40.0312). CONCLUSION: Significant changes in myocardial function are evident in adolescent T1D of short to intermediate disease duration, suggesting these may be clinically useful preclinical markers of deterioration in cardiac performance to guide early intervention.

Background Left ventricular (LV) rotation is increasingly examined in those with heart disease. The available evidence measuring LV rotation in those with heart diseases has not been systematically reviewed. Methods To review systematically the evidence measuring LV rotational changes in various heart diseases compared to healthy controls, literature searches were conducted for appropriate articles using several electronic databases (e.g., MEDLINE, EMBASE). All randomized-controlled trials, prospective cohort and case–controlled studies that assessed LV rotation in relation to various heart conditions were included. Three independent reviewers evaluated each investigation’s quality using validated scales. Results were tabulated and levels of evidence assigned. Results A total of 1,782 studies were found through the systematic literature search. Upon review of the articles, 47 were included. The articles were separated into those investigating changes in LV rotation in participants with: aortic stenosis, myocardial infarction, hypertrophic cardiomyopathy, dilated cardiomyopathy, non-compaction, restrictive cardiomyopathy/ constrictive pericarditis, heart failure, diastolic dysfunction, heart transplant, implanted pacemaker, coronary artery disease and cardiovascular disease risk factors. Evidence showing changes in LV rotation due to various types of heart disease was supported by evidence with limited to moderate methodological quality. Conclusions Despite a relatively low quality and volume of evidence, the literature consistently shows that heart disease leads to marked changes in LV rotation, while rotational systolic-diastolic coupling is preserved. No prognostic information exists on the potential value of rotational measures of LV function. The literature suggests that measures of LV rotation may aid in diagnosing subclinical aortic stenosis and diastolic dysfunction.

Purpose: Orthostatic intolerance is more prevalent in women. The purpose of this investigation was to evaluate the physiological responses of orthostatic tolerant and intolerant females to progressive lower body negative pressure (LBNP) and to identify predictors of orthostatic tolerance. Methods: Following baseline measurements, eleven healthy, moderately active women (mean age 24 ± 3 yr) underwent an orthostatic challenge involving four 12-minute stages of progressive LBNP at -15, -30, -45 and -60 mmHg. Traditional haemodynamic characteristics, as well as baroreceptor sensitivity, were analyzed across all stages. Results: Five women became presyncopal during the test and were classified as low tolerant (LT) while the remaining six were classified as high tolerant (HT). LBNP by group (tolerance) interactions were significantly different for stroke volume (P=0.008) and the rate of decline (slope) of stroke volume (P=0.03). During the early stages of LBNP, the LT group displayed a higher stroke volume than the HT group (76.4 ± 8.6 vs. 60.0 ± 13.3 mL/beat; P=0.02) yet by the final stage, stroke volumes were similar (22.5 ± 11.9 vs. 22.7 ± 4.5 mL/beat, P = 0.99). Baroreceptor sensitivity, heart rate variability and blood pressure variability were not significantly different between the groups. Conclusions: The results of this investigation suggest that orthostatic intolerance in women can be identified during the initial stages of an LBNP challenge, as evidenced by a more rapid decline in stroke volume.