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Contains fulltext : 252160.pdf (Publisher’s version ) (Open Access)

Funding Acknowledgements Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): Canadian Institute of Health Research Michael Smith Foreign Study Supplement Background Image and performance enhancing drugs (IPED) cause cardiac enlargement and dysfunction. Previous work has not assessed impact of user status (current [CU] vs. past [PU]) or allometric scaling cardiac dimensions for individual differences in fat-free mass (FFM). Purpose To investigate CU and PU of IPED and allometric scaling on LV and RV remodeling in strength-trained athletes. Methods Thirty-four (29 ± 6 years; 82% male) strength-trained athletes were recruited. Fourteen were CU, 9 PU and 11 non-users (NU) of IPEDs. Participants underwent bioelectric impedance body composition analysis, IPED and training questionnaire and 2D echocardiography with strain imaging. All structural data was allometrically scaled to FFM according to the laws of geometric similarity. Results CU and PU had significantly higher FFM compared to NU (82.4 ± 10.1 kg vs. 72.0 ± 6.3 kg vs. 58.2 ± 14.0 kg). Absolute values of all RV and LV size were larger between CU and NU. LV mean wall thickness (MWT) was larger in CU compared to PU but there were no differences between PU and NU. Allometric scaling eliminated all differences with exception of LV mass and LVMWT. LVEF was significantly lower in CU and PU compared to NU (55 ± 3 vs. 57 ± 4 vs. 61 ± 4) whilst LV GLS was lower in CU compared to PU and NU and LV GCS was lower in CU compared to NU but not PU. There was no significant difference between groups for RV functional indices. Conclusion Strength-trained athletes currently using IPEDs have bi-ventricular enlargement as well as reduced LV function. Allometric scaling highlights that increased size is partially associated with a larger FFM, with exception of LVMWT which is independently increased through IPED use. PUs demonstrate reverse structural remodeling whilst functional differences partially remain. CU PU NU RVD1 (mm) 45 ± 5* 43 ± 6 37 ± 6 Scaled RVD1 (mm/kg^0.33) 10.5 ± 0.9 10.4 ± 1.5 9.7 ± 1.0 LVd (mm) 58 ± 7* 55 ± 4 50 ± 4 Scaled LVd (mm/kg^0.33) 13.4 ± 1.2 13.3 ± 0.7 13.1 ± 0.6 MWT (mm) 10 ± 1*” 8 ± 1 8 ± 1 Scaled MWT (mm/kg^0.33) 2.3 ± 0.2*” 2.0 ± 0.1 2.0 ± 0.2 LVEDV (ml) 169 ± 42* 135 ± 28 116 ± 28 Scaled LVEDV (ml/kg) 2.0 ± 0.4 1.9 ± 0.3 2.0 ± 0.2 LV Mass (g) 255 ± 85*” 179 ± 30 137 ± 40 LV mass index (g/kg) 3.1 ± 0.8* 2.5 ± 0.3 2.4 ± 0.4 * CU and NU “ CU and PU ^ PU and NU Abstract Figure. Myocardial strain imaging

Funding Acknowledgements Type of funding sources: None. Background. Despite introduction of pharmacological therapies to improve outcomes of pulmonary hypertension (PH), poor long-term survival remains present. Cardiac rehabilitation may be an alternative strategy to improve survival. However, no study directly linked CR to mortality in PH patients. Therefore, adopting a retrospective observational study using a large electronic medical record (EMR) database, the objective of this study was to compare mortality between patients with primary PH with CR versus a propensity-matched control group of PH without CR. Methods. The retrospective analysis was conducted on December 14, 2020 using anonymized data within TriNetX, a global federated health research network with access to EMRs from participating academic medical centres, specialty physician practices, and community hospitals, predominantly in the United States. All patients were aged ≥18 years with primary PH recorded in EMRs at least 18-months before the search date to allow for 1-year follow-up from CR. Using logistic regression, patients with PH with an EMR of CR were 1:1 propensity score-matched with PH patients without CR for age, sex, race, diseases of the respiratory system, disease of the circulatory system, hypertensive disease, heart failure, diabetes mellitus, chronic kidney disease, cerebrovascular disease, cardiovascular procedures and cardiovascular medications. Results. In total, 70,875 patients with primary PH met the inclusion criteria for the control group and 637 patients with primary PH met the inclusion criteria for the CR and exercise cohort (Table 1). Using the propensity score-matched cohort, and excluding patients with outcomes outside the measurement window, mortality at 1-year from CR was proportionally lower with mortality of 13.9% (n = 87 of 628 patients) in the CR and exercise cohort compared to 21.0% (n = 133 of 632 patients) in the controls (OR 0.60, 95% CI 0.45-0.81). Conclusion. In conclusion, the present study of 1,264 patients with primary PH suggests that CR is associated with 40% lower odds of 1-year mortality, when compared to propensity score-matched patients without CR or exercise programmes. Abstract Figure.

Contains fulltext : 249141.pdf (Publisher’s version ) (Closed access) Whilst the athlete's heart has been extensively described, less work has focused on the potential for elite athletes to demonstrate further cardiac remodelling upon an increase in training volume. Moreover, little work explored potential side-specific cardiac remodelling. Therefore, we examined the impact of an increase in training volume across 9-months in elite rowers on left- and right-sided cardiac structure, function and mechanics (i. e. longitudinal, radial and circumferential strain, twist and strain-volume loops). As part of the preparations to the 2012 Olympic Games, twenty-seven elite rowers (26.4±3.7years, 19 male) underwent echocardiography prior to and post (9 months) an increase in training volume (24 to 30-35 h weekly). Training increased left ventricular structure, including wall thickness, diameter, volume, mass and LV twist (all p0.05). The 9-month intervention showed no change in right ventricular/atrial structure, function or mechanics (all p>0.05). In conclusion, our data revealed that 9-month increased training volume in elite rowers induced left-sided (but not right-sided) structural remodelling, concomitant with an increase in left ventricular twist, with some changes larger in women. 01 februari 2022

Contains fulltext : 233804.pdf (Publisher’s version ) (Open Access) 01 april 2021

Repeated ventricular exposure to alterations in workload may relate to subsequent cardiac remodeling. We examined whether baseline acute changes in right (RV) and left ventricular (LV) function relate to chronic cardiac adaptation to 12-week exercise training. Twenty-one healthy individuals performed 12-week high-intensity endurance running training under hypoxia (fraction of inspired oxygen: 14.5%). Resting transthoracic echocardiography was performed before and after the training programme to assess ventricular structure, function and mechanics (including strain-area/volume loops). In addition, we examined systolic cardiac function during recumbent exercise under hypoxia at baseline (heart rate of 110-120 bpm, 'stress echocardiography'). Fifteen individuals completed training (22.0±2.4y, 10 male). Hypoxic exercise training increased RV size, including diameter and area (all p0.05). Regarding the RV strain-area loop, lower systolic and diastolic slopes were found post-training (p0.05). To answer our primary aim, we found that a greater increase in RV fractional area change during baseline stress echocardiography (r=-0.67, P=0.01) inversely correlated with adaptation in RV basal diameter following 12-week training. In conclusion, 12-week high-intensity running hypoxic exercise training induced right-sided structural remodeling, which was, in part, related to baseline increase in RV fractional area change to acute exercise. These data suggest that acute cardiac responses to exercise may relate to subsequent RV remodeling after exercise training in healthy individuals.

Contains fulltext : 235286.pdf (Publisher’s version ) (Open Access) BACKGROUND: Acute exercise promotes transient exercise-induced cardiac fatigue, which affects the right ventricle and to a lesser extent the left ventricle. Hypoxic exposure induces an additional increase in right ventricular (RV) afterload. Therefore, exercise in hypoxia may differently affect both ventricles. The aim of this study was to investigate the acute effects of a bout of high-intensity exercise under hypoxia versus normoxia in healthy individuals on right- and left-sided cardiac function and mechanics. METHODS: Twenty-one healthy individuals (mean age, 22.2 ± 0.6 years; 14 men) performed 45-min high-intensity running exercise under hypoxia (fraction of inspired oxygen 14.5%) and normoxia (fraction of inspired oxygen 20.9%) in a randomized order. Pre- and post-exercise echocardiography, at rest and during low-to-moderate intensity recumbent exercise ("stress"), was performed to assess RV and left ventricular (LV) cardiac function and mechanics. RV structure, function, and mechanics were assessed using conventional two-dimensional, Doppler, tissue Doppler, speckle-tracking echocardiographic, and novel strain-area loops. RESULTS: Indices of RV systolic function (RV fractional area change, Tricuspid annular plane systolic excursion, RV s', and RV free wall strain) and LV function (LV ejection fraction and LV global longitudinal strain) were significantly reduced after high-intensity running exercise (P .05). CONCLUSIONS: There was no impact of hypoxia on the magnitude of exercise-induced cardiac fatigue in the right and left ventricles after a 45-min bout of high-intensity exercise. This finding suggests that any potential increase in loading conditions does not automatically exacerbate exercise-induced cardiac fatigue in this setting.

BACKGROUND: Acute exercise leads to an immediate drop in blood pressure (BP), also called post-exercise hypotension (PEH). Exercise in hypoxia is related to additional vasodilation, potentially contributing to more profound PEH. Therefore, we investigated the impact of hypoxia versus normoxia on the magnitude of PEH. Second, we examined whether these changes in PEH relate to the BP-lowering effects of 12-week exercise training under hypoxia. METHODS: In this prospective study, 21 healthy individuals (age 22.2 ±â€Š3.0 years, 14 male) performed a 45-minute high-intensity running exercise on 2 different days in a random order, under hypoxia (fraction of inspired oxygen 14.5%) and normoxia (fraction of inspired oxygen 20.9%). BP was examined pre-exercise (t = 0) and at t = 15, t = 30, t = 45, and t = 60 minutes post-exercise. Afterward, subjects took part in a 12-week hypoxic running exercise training program. Resting BP was measured before and after the 12-week training program. RESULTS: Acute exercise induced a significant decrease in systolic BP (systolic blood pressure [SBP], P = .001), but not in diastolic BP (diastolic blood pressure [DBP], P = .113). No significant differences were observed in post-exercise BP between hypoxic and normoxic conditions (SBP, P = .324 and DBP, P = .204). Post-exercise changes in SBP, DBP, and mean arterial pressure significantly correlated to the 12-week exercise training-induced changes in SBP (r = 0.557, P = .001), DBP (r = 0.615, P 

Contains fulltext : 220897.pdf (Publisher’s version ) (Open Access) AIM: To minimize termination of resuscitation (TOR) in potential survivors, the desired positive predictive value (PPV) for mortality and specificity of universal TOR-rules are >/=99%. In lack of a quantitative summary of the collective evidence, we performed a diagnostic meta-analysis to provide an overall estimate of the performance of the basic and advanced life support (BLS and ALS) termination rules. DATA SOURCES: We searched PubMed/EMBASE/Web-of-Science/CINAHL and Cochrane (until September 2019) for studies on either or both TOR-rules in non-traumatic, adult cardiac arrest. PRISMA-DTA-guidelines were followed. RESULTS: There were 19 studies: 16 reported on the BLS-rule (205.073 patients, TOR-advice in 57%), 11 on the ALS-rule (161.850 patients, TOR-advice in 24%). Pooled specificities were 0.95 (0.89-0.98) and 0.98 (0.95-1.00) respectively, with a PPV of 0.99 (0.99-1.00) and 1.00 (0.99-1.00). Specificities were significantly lower in non-Western than Western regions: 0.84 (0.73-0.92) vs. 0.99 (0.97-0.99), p

Funding Acknowledgements No financial support Background Chronic exercise training leads to cardiac remodelling; the so-called Athlete’s Heart. Previous studies are often limited by a cross-sectional design whilst longitudinal training studies are often constrained to the assessment of non-athletes. Echocardiography provides comprehensive assessment of mechanics and may give additional insight into short-term changes in training volume in the elite athlete. Purpose To examine the impact of a short-term (9 months) increase in training volume on cardiac structure and mechanics in elite international competing rowers. Methods As part of the work-up to the 2012 Olympic Games, twenty-seven elite rowers (26.4 ± 3.7 years, 19 male) underwent baseline echocardiography prior to and post (9-months) a planned increase in training volume. Conventional echocardiographic indices including mechanics of all cardiac chambers were assessed. Results In response to increased training volume, there was a significant increase in left ventricular (LV) size (IVSd 9.2 ± 1.2 to 9.7 ± 1.1 mm, p = 0.001; PWd 8.3 ± 1.3 to 8.7 ± 1.4 mm, p = 0.013), LVIDd (56.5 ± 4.6 to 57.9 ± 4.2 mm, p = 0.001), and LVMi (90.2 ± 17.8 to 100.8 ± 17.1 g/m2, p = 0.000), see table. There was a significant increase in LV twist (9.2 ± 4.5 to 11.2 ± 4.7 °, p = 0.04; basal rotation -4.4 ± 3.1 to -4.5 ± 3.4 °, p = 0.84; apical rotation 5.8 ± 3.4 to 7.1 ± 3.7 °, p = 0.011), see figure, however, there were no changes in any other conventional indices of function or any other cardiac mechanics. There was a significant increase in left atrial (LA) volume (58.8 ± 15.2 to 65.3 ± 17.6 mm, p = 0.01) whilst no changes were observed in right heart structure. Conclusion An increase in exercise training volume in elite rowers across 9-months induced mild balanced structural remodelling of the LV and LA with a concomitant increase in LV twist. Contradictory to findings in non-athletes, there was no increase in right ventricular or atrial structure or function which may be representative of the elite athlete status and possibly already at threshold for physiological adaptation. Abstract P784 Figure.

Contains fulltext : 202688.pdf (Publisher’s version ) (Closed access) AIMS: Pulmonary hypertension (PH) is associated with high morbidity and mortality and the predictive capacity of traditional functional echocardiographic measures is poor. Recent studies assessed the predictive capacity of right ventricular longitudinal strain (RVLS). Diversity in methods between these studies resulted in conflicting outcomes. The purpose of this systematic review and meta-analysis was to determine the independent prognostic value of RVLS for PH-related events and all-cause mortality. METHODS AND RESULTS: A systematic search in Pubmed (MEDLINE), Embase, the Cochrane Library, and Web of Science was performed to identify studies that examined the prognostic value of RVLS in patients with PH. Studies reporting Cox regression based hazard ratios (HRs) for a combined endpoint of mortality and PH-related events or all-cause mortality for echocardiographic derived RVLS were included. A weighted mean of the multivariate HR was used to determine the independent predictive value of RVLS. Eleven studies met our criteria, including 1169 patients with PH (67% female, 0.6-3.8 years follow-up). PH patients with a relative reduction of RVLS of 19% had a significantly higher risk for the combined endpoint [HR 1.22, 95% confidence interval (CI) 1.07-1.40], while patients with a relative reduction of RVLS of 22% had a significantly higher risk for all-cause mortality (HR 2.96, 95% CI 2.00-4.38). CONCLUSION: This systematic review and meta-analysis showed that RVLS has independent prognostic value for a combined endpoint and all-cause mortality in patients with PH. Collectively, these findings emphasize that RVLS may have value for optimizing current predictive models for clinical events or mortality in patients with PH.