Assessing feasibility and sex-related inequity in the Cardiac Rehabilitation Quality Indicators in Manitoba.

The Cardiac Rehabilitation Quality Indicators (CRQIs) developed by the Canadian Cardiovascular Society provide a means to standardize program assessment and identify sex-related inequities. No formal evaluation of the CRQIs has been conducted in Manitoba. An environmental scan for the CRQIs was performed using data in the electronic medical record at two cardiac rehabilitation (CR) sites in Winnipeg for 2016-2019 referrals. Of the 8116 referrals, 7758 (5491 males and 2267 females) had geographical access and were eligible for CR. The Manitoba Centre for Healthcare Data Quality Policy framework informed the data quality assessment. Thirteen CRQIs were available; four were considered high quality; nine demonstrated moderate to significant missing data. In addition to missing values, potential misclassification of risk (CR-4) and physiologically implausible and invalid dates were assessed and identified (CR-13 and CR-17). Each site had a physician medical director (CR-31) and a documented emergency response strategy (CR-32). Only high-quality data were evaluated for sex-related differences using Chi-square and median tests. Women had lower enrollment (CR-3), and more women enrolled after the median of 41 days (CR-2b). Engagement with CR partners, including frontline staff, and utilizing strategies to assess and limit physiologically implausible values and dates will enhance data capture and quality.

Future directions for patient engagement in research: a participatory workshop with Canadian patient partners and academic researchers.

BACKGROUND: Patient engagement in research (also commonly referred to as patient or patient and public involvement in research) strives to transform health research wherein patients (including caregivers and the public) are regularly and actively engaged as multidisciplinary research team members (i.e. patient partners) working jointly towards improved health outcomes and an enhanced healthcare system. To support its mindful evolution into a staple of health research, this participatory study aimed to identify future directions for Canadian patient engagement in research and discusses its findings in the context of the international literature. METHODS: The study met its aim through a multi-meeting pan-Canadian virtual workshop. Participants (n = 30) included Strategy for Patient-Oriented Research-funded academic researchers and patient partners identified through a publicly available database, personal and professional networks and social media. All spoke English, could access the workshop virtually, and provided written informed consent. The workshop was composed of four, 1.5-3-h virtual meetings wherein participants discussed the current and preferred future states of Canadian patient engagement in research. Workshop discussions (i.e. data) were video and audio recorded. Themes were generated through an iterative process of inductive thematic analysis that occurred concurrently with the multi-week workshop. RESULTS: Our participatory and iterative process identified 10 targetable areas of focus for the future of Canadian patient engagement in research. Five were categorized as system-level (systemic integration; academic culture; engagement networks; funding models; compensation models), one as researcher-level (engagement processes), and four crossed both levels (awareness; diversity and recruitment; training, tools and education; evaluation and impact). System level targetable areas called for reshaping the patient engagement ecosystem to create a legitimized and supportive space for patient engagement to be a staple component of a learning health system. Researcher level targetable areas called for academic researchers and patient partners to collaboratively generate evidence and apply knowledge to inform values and behaviours necessary to foster and sustain supportive health research spaces that are accessible to all. CONCLUSIONS: Future directions for Canadian patient engagement in research span 10 interconnected targetable areas that require strong leadership and joint action between patient partners, academic researchers, and health and research institutions if patient engagement is to become a ubiquitous component of a learning health system.

Sirtuin 3 overexpression preserves maximal sarco(endo)plasmic reticulum calcium ATPase activity in the skeletal muscle of mice subjected to high fat - high sucrose feeding.

Sarco(endo)plasmic reticulum calcium (Ca2+) ATPase (SERCA) transports Ca2+ in muscle. Impaired SERCA activity may contribute to diabetic myopathy. Sirtuin (SIRT) 3 regulates muscle metabolism and function; however, it is unknown if SIRT3 regulates muscle SERCA activity or acetylation. We determined if SIRT3 overexpression enhances SERCA activity in mouse gastrocnemius muscle and if SIRT3 overexpression preserves gastrocnemius SERCA activity in a model of type 2 diabetes, induced by high fat - high sucrose (HFHS) feeding. We also determined if the acetylation status of SERCA proteins in mouse gastrocnemius is altered by SIRT3 overexpression or HFHS feeding. Wild-type (WT) and SIRT3 transgenic (SIRT3TG) mice, overexpressing SIRT3 in skeletal muscle, were fed a standard or HFHS diet for 4 months. SIRT3TG and WT mice developed obesity and glucose intolerance after 4 months of HFHS feeding. SERCA Vmax was higher in gastrocnemius of SIRT3TG mice compared with WT mice. HFHS-fed mice had lower SERCA1a protein levels and lower SERCA Vmax in their gastrocnemius than control-fed mice. The decrease in SERCA Vmax in gastrocnemius muscle due to HFHS feeding was attenuated by SIRT3 overexpression in HFHS-fed SIRT3TG mice. SERCA1a and SERCA2a acetylation in mouse gastrocnemius was not altered by genotype or diet. These findings suggest SIRT3 overexpression improves SERCA function in mouse skeletal muscle.

Frailty-aware care: giving value to frailty assessment across different healthcare settings.

Healthcare systems need to adapt to better serve an aging population with complex presentations. Frailty assessments are a potential means to address this heterogeneity in aging to identify individuals at increased risk for adverse health outcomes. Furthermore, frailty assessments offer an opportunity to optimize patient care in various healthcare settings. While the vast number of frailty assessment tools available can be a source of confusion for clinicians, each tool has features adaptable to the constraints and goals of different healthcare settings. This review discusses and compares barriers, facilitators, and the application of frailty assessments in primary care, the emergency department/intensive care unit and surgical care to cover a breadth of settings with different frailty assessment considerations. The implementation of frailty-aware care across healthcare settings potentiates better healthcare outcomes for older adults.

SKI activates the Hippo pathway via LIMD1 to inhibit cardiac fibroblast activation.

We have previously shown that overexpression of SKI, an endogenous TGF-ß1 repressor, deactivates the pro-fibrotic myofibroblast phenotype in the heart. We now show that SKI also functions independently of SMAD/TGF-ß signaling, by activating the Hippo tumor-suppressor pathway and inhibiting the Transcriptional co-Activator with PDZ-binding motif (TAZ or WWTR1). The mechanism(s) by which SKI targets TAZ to inhibit cardiac fibroblast activation and fibrogenesis remain undefined. A rat model of post-myocardial infarction was used to examine the expression of TAZ during acute fibrogenesis and chronic heart failure. Results were then corroborated with primary rat cardiac fibroblast cell culture performed both on plastic and on inert elastic substrates, along with the use of siRNA and adenoviral expression vectors for active forms of SKI, YAP, and TAZ. Gene expression was examined by qPCR and luciferase assays, while protein expression was examined by immunoblotting and fluorescence microscopy. Cell phenotype was further assessed by functional assays. Finally, to elucidate SKI's effects on Hippo signaling, the SKI and TAZ interactomes were captured in human cardiac fibroblasts using BioID2 and mass spectrometry. Potential interactors were investigated in vitro to reveal novel mechanisms of action for SKI. In vitro assays on elastic substrates revealed the ability of TAZ to overcome environmental stimuli and induce the activation of hypersynthetic cardiac myofibroblasts. Further cell-based assays demonstrated that SKI causes specific proteasomal degradation of TAZ, but not YAP, and shifts actin cytoskeleton dynamics to inhibit myofibroblast activation. These findings were supported by identifying the bi-phasic expression of TAZ in vivo during post-MI remodeling and fibrosis. BioID2-based interactomics in human cardiac fibroblasts suggest that SKI interacts with actin-modifying proteins and with LIM Domain-containing protein 1 (LIMD1), a negative regulator of Hippo signaling. Furthermore, we found that LATS2 interacts with TAZ, whereas LATS1 does not, and that LATS2 knockdown prevented TAZ downregulation with SKI overexpression. Our findings indicate that SKI's capacity to regulate cardiac fibroblast activation is mediated, in part, by Hippo signaling. We postulate that the interaction between SKI and TAZ in cardiac fibroblasts is arbitrated by LIMD1, an important intermediary in focal adhesion-associated signaling pathways. This study contributes to the understanding of the unique physiology of cardiac fibroblasts, and of the relationship between SKI expression and cell phenotype.

Intrauterine exposure to diabetes and risk of cardiovascular disease in adolescence and early adulthood: a population-based birth cohort study.

BACKGROUND: It is unclear whether intrauterine exposure to maternal diabetes is associated with risk factors for cardiovascular disease and related end points in adulthood. We examined this potential association in a population-based birth cohort followed up to age 35 years. METHODS: We performed a cohort study of offspring born between 1979 and 2005 (n = 293 546) and followed until March 2015 in Manitoba, Canada, using registry-based administrative data. The primary exposures were intrauterine exposure to gestational diabetes and type 2 diabetes mellitus. The primary outcome was a composite measure of incident cardiovascular disease events, and the secondary outcome was a composite of risk factors for cardiovascular disease in offspring followed up to age 35 years. RESULTS: The cohort provided 3 628 576 person-years of data (mean age at latest follow-up 20.5 [standard deviation 6.4] years, 49.3% female); 2765 (0.9%) of the offspring experienced a cardiovascular disease end point, and 12 673 (4.3%) experienced a cardiovascular disease risk factor. After propensity score matching, the hazard for cardiovascular disease end points was elevated in offspring exposed to gestational diabetes (adjusted hazard ratio [HR] 1.42, 95% confidence interval [CI] 1.12-1.79) but not type 2 diabetes (adjusted HR 1.40, 95% CI 0.98-2.01). A similar association was observed for cardiovascular disease risk factors (gestational diabetes: adjusted HR 1.92, 95% CI 1.75-2.11; type 2 diabetes: adjusted HR 3.40, 95% CI 3.00-3.85). INTERPRETATION: Intrauterine exposure to maternal diabetes was associated with higher morbidity and risk related to cardiovascular disease among offspring up to 35 years of age.

Cardiac structure and function in youth with type 2 diabetes in the iCARE cohort study: Cross-sectional associations with prenatal exposure to diabetes and metabolomic profiles.

OBJECTIVE: This study aimed to determine the degree of left ventricular (LV) dysfunction and its determinants in adolescents with type 2 diabetes (T2D). We hypothesized that adolescents with T2D would display impaired LV diastolic function and that these cardiovascular complications would be exacerbated in youth exposed to maternal diabetes in utero. METHODS: Left ventricular structure and function, carotid artery intima media thickness and strain, and serum metabolomic profiles were compared between adolescents with T2D (n = 121) and controls (n = 34). Sub-group analyses examined the role of exposure to maternal diabetes as a determinant of LV or carotid artery structure and function among adolescents with T2D. RESULTS: Adolescents with T2D were 15.1 ± 2.5 years old, (65% female, 99% Indigenous), had lived with diabetes for 2.7 ± 2.2 years, had suboptimal glycemic control (HbA1c = 9.4 ± 2.6%) and 58% (n = 69) were exposed to diabetes in utero. Compared to controls, adolescents with T2D displayed lower LV diastolic filling (early diastole/atrial filling rate ratio [E/A] = 1.9 ± 0.6 vs 2.2 ± 0.6, P = 0.012), lower LV relaxation and carotid strain (0.12 ± 0.05 vs 0.17 ± 0.05, P = .03) and elevated levels of leucine, isoleucine and valine. Among adolescents with T2D, exposure to diabetes in utero was not associated with differences in LV diastolic filling, LV relaxation, carotid strain or branched chain amino acids. CONCLUSIONS: Adolescents with T2D display LV diastolic dysfunction, carotid artery stiffness, and elevated levels of select branch chain amino acids; differences were not associated with exposure to maternal diabetes in utero.

Mechanisms for the transition from physiological to pathological cardiac hypertrophy.

The heart is capable of responding to stressful situations by increasing muscle mass, which is broadly defined as cardiac hypertrophy. This phenomenon minimizes ventricular wall stress for the heart undergoing a greater than normal workload. At initial stages, cardiac hypertrophy is associated with normal or enhanced cardiac function and is considered to be adaptive or physiological; however, at later stages, if the stimulus is not removed, it is associated with contractile dysfunction and is termed as pathological cardiac hypertrophy. It is during physiological cardiac hypertrophy where the function of subcellular organelles, including the sarcolemma, sarcoplasmic reticulum, mitochondria, and myofibrils, may be upregulated, while pathological cardiac hypertrophy is associated with downregulation of these subcellular activities. The transition of physiological cardiac hypertrophy to pathological cardiac hypertrophy may be due to the reduction in blood supply to hypertrophied myocardium as a consequence of reduced capillary density. Oxidative stress, inflammatory processes, Ca2+-handling abnormalities, and apoptosis in cardiomyocytes are suggested to play a critical role in the depression of contractile function during the development of pathological hypertrophy.

A focused review of myokines as a potential contributor to muscle hypertrophy from resistance-based exercise.

PURPOSE: Resistance exercise induces muscle growth and is an important treatment for age-related losses in muscle mass and strength. Myokines are hypothesized as a signal conveying physiological information to skeletal muscle, possibly to "fine-tune" other regulatory pathways. While myokines are released from skeletal muscle following contraction, their role in increasing muscle mass and strength in response to resistance exercise or training is not established. Recent research identified both local and systemic release of myokines after an acute bout of resistance exercise. However, it is not known whether myokines with putative anabolic function are mechanistically involved in producing muscle hypertrophy after resistance exercise. Further, nitric oxide (NO), an important mediator of muscle stem cell activation, upregulates the expression of certain myokine genes in skeletal muscle. METHOD: In the systemic context of complex hypertrophic signaling, this review: (1) summarizes literature on several well-recognized, representative myokines with anabolic potential; (2) explores the potential mechanistic role of myokines in skeletal muscle hypertrophy; and (3) identifies future research required to advance our understanding of myokine anabolism specifically in skeletal muscle. RESULT: This review establishes a link between myokines and NO production, and emphasizes the importance of considering systemic release of potential anabolic myokines during resistance exercise as complementary to other signals that promote hypertrophy. CONCLUSION: Investigating adaptations to resistance exercise in aging opens a novel avenue of interdisciplinary research into myokines and NO metabolites during resistance exercise, with the longer-term goal to improve muscle health in daily living, aging, and rehabilitation.

Acute Effect of High-Intensity Interval Versus Moderate-Intensity Continuous Exercise on Blood Pressure and Arterial Compliance in Middle-Aged and Older Hypertensive Women With Increased Arterial Stiffness.

Costa, EC, Kent, DE, Boreskie, KF, Hay, JL, Kehler, DS, Edye-Mazowita, A, Nugent, K, Papadopoulos, J, Stammers, AN, Oldfield, C, Arora, RC, Browne, RAV, and Duhamel, TA. Acute effect of high-intensity interval versus moderate-intensity continuous exercise on blood pressure and arterial compliance in middle-aged and older hypertensive women with increased arterial stiffness. J Strength Cond Res 34(5): 1307-1316, 2020-Hypertension and arterial stiffness are common in middle-aged and older women. This study compared the acute effect of high-intensity interval exercise (HIIE) and moderate-intensity continuous exercise (MICE) on blood pressure (BP) and arterial compliance in middle-aged and older hypertensive women with increased arterial stiffness. Nineteen women (67.6 ± 4.7 years) participated in this randomized controlled crossover trial. Subjects completed a control, MICE (30 minutes at 50-55% of heart rate reserve [HRR]), and HIIE (10 × 1 minute at 80-85% of HRR, 2 minutes at 40-45% of HRR) session in random order. Blood pressure and large and small arterial compliance (radial artery pulse wave analysis) were measured at baseline and 30, 60, 90, and 120 minutes after sessions. A p < 0.05 was considered statistically significant. Systolic BP was reduced in ∼10 mm Hg after MICE at 30 minutes and after HIIE at all time points (30, 60, 90, and 120 minutes) after exercise compared with the control session (p < 0.05). Only HIIE showed lower systolic BP levels at 60, 90, and 120 minutes after exercise compared with the control session (∼10 mm Hg; p < 0.05). No changes were observed in diastolic BP, or in large and small arterial compliance (p > 0.05). High-intensity interval exercise elicited a longer systolic postexercise hypotension than MICE compared with the control condition, despite the absence of acute modifications in large and small arterial compliance.

Resveratrol prevents palmitic-acid-induced cardiomyocyte contractile impairment.

Long-chain saturated fatty acids, especially palmitic acid (PA), contribute to cardiomyocyte lipotoxicity. This study tests the effects of PA on adult rat cardiomyocyte contractile function and proteins associated with calcium regulating cardiomyocyte contraction and relaxation. Adult rat cardiomyocytes were pretreated with resveratrol (Resv) and then treated with PA. For the reversal study, cardiomyocytes were incubated with PA prior to treatment with Resv. Cardiomyocyte contractility, ratio of rod- to round-shaped cardiomyocytes, and Hoechst staining were used to measure functional and morphological changes in cardiomyocytes. Protein expression of sarco-endoplasmic reticulum ATPase 2a (SERCA2a), native phospholamban (PLB) and phosphorylated PLB (pPLB ser16 and pPLB thr17), and troponin I (TnI) and phosphorylated TnI (pTnI) were measured. SERCA2a activity was also measured. Our results show that PA (200 µM) decreased the rate of cardiomyocyte relaxation, reduced the number of rod-shaped cardiomyocytes, and increased the number of cells with condensed nuclei; pre-treating cardiomyocytes with Resv significantly prevented these changes. Post-treatment with Resv did not reverse morphological changes induced by PA. Protein expression levels of SERCA2a, PLB, pPLBs, TnI, and pTnI were unchanged by PA or Resv. SERCA2a activity assay showed that Vmax and Iono ratio were increased with PA and pre-treatment with Resv prevented this increase. In conclusion, our results show that Resv protect cardiomyocytes from contractile dysfunction induced by PA.

Exercise-induced increases in the expression and activity of cardiac sarcoplasmic reticulum calcium ATPase 2 is attenuated in AMPKα2 kinase-dead mice.

Exercise enhances cardiac sarcoplasmic reticulum Ca2+-ATPase 2a (SERCA2a) function through unknown mechanisms. The present study tested the hypothesis that the positive effects of exercise on SERCA2a expression and function in the left ventricle is dependent on adenosine-monophosphate-activated protein kinase (AMPK) α2 function. AMPKα2 kinase-dead (KD) transgenic mice, which overexpress inactivated AMPKα2 subunit, and wild-type C57Bl/6 (WT) mice were randomized into sedentary groups or groups with access to running wheels. After 5 months, exercised KD mice exhibited shortened deceleration time compared with sedentary KD mice. In left ventricular tissue, the ratio of phosphorylated AMPKαThr172:total AMPKα was 65% lower (P < 0.05) in KD mice compared with WT mice. The left ventricle of KD mice had 37% lower levels of SERCA2a compared with WT mice. Although exercise increased SERCA2a protein levels in WT mice by 53%, this response of exercise was abolished in exercised KD mice. Exercise training reduced total phospholamban protein content by 23% in both the WT and KD mice but remained 20% higher overall in KD mice. Collectively, these data suggest that AMPKα influences SERCA2a and phospholamban protein content in the sedentary and exercised heart, and that exercise-induced changes in SERCA2a protein are dependent on AMPKα function.

CKD and Sedentary Time: Results From the Canadian Health Measures Survey.

RATIONALE & OBJECTIVE: Sedentary behavior and low physical activity are associated with incident diabetes, cardiovascular disease, and early mortality. Previous studies have examined associations between chronic kidney disease (CKD) and physical activity, but little is known about the role of sedentary time. STUDY DESIGN: Cross-sectional national survey. SETTING & PARTICIPANTS: A nationally representative sample of adults (n=8,444) participating in the Canadian Health Measures Survey's (CHMS) activity monitoring component (2007-2013). PREDICTOR: Estimated glomerular filtration rate (eGFR). OUTCOMES: Sedentary time (total sedentary minutes/total wear time) measured using triaxial accelerometry. ANALYTICAL APPROACH: Multivariable ordinal logistic regression for quartiles of sedentary time and linear regression for sedentary time measured on a continuous scale were performed in the entire study population and in the subgroup with CKD. RESULTS: Mean proportion of sedentary time ranged from 58% (least sedentary quartile: Q1) to 81% (most sedentary quartile: Q4). Lower eGFR, older age, lower serum albumin level, higher blood pressure, cardiovascular disease, diabetes, and higher body mass index were independently associated with a higher proportion of sedentary time. Patients with eGFRs < 45mL/min/1.73m2 had more than 4-fold higher likelihood of being sedentary (OR, 4.2; 95% CI, 2.5-7.3). Within the CKD subgroup, greater sedentary time was associated with diabetes (OR, 2.68; 95% CI, 1.56-4.59) and arthritis (OR, 2.32; 95% CI, 1.43-3.77) in adjusted analysis. LIMITATIONS: Cross-sectional design precluded evaluation of longitudinal outcomes and establishment of the causal nature of observed associations. Small sample of individuals with advanced CKD. CONCLUSIONS: In this cross-sectional survey, reduced eGFR was strongly and independently associated with greater sedentary time. This risk was further heightened by the presence of diabetes and arthritis. Studies to determine causes for sedentary behavior and assess the feasibility and value of interventions to reduce sedentary time in CKD are needed.

The systemic myokine response of decorin, interleukin-6 (IL-6) and interleukin-15 (IL-15) to an acute bout of blood flow restricted exercise.

PURPOSE: Blood flow restricted resistance exercise (BFR-RE) is an emerging hypertrophy training modality. A complete profile of its mechanisms of action has yet to be elucidated. Cytokines are universal intercellular messengers. Recent research has implicated certain cytokines (termed "myokines") in skeletal muscle hypertrophy pathways; however, little research has been conducted on the systemic myokine response to BFR-RE as potential hypertrophic biomarkers. Therefore, this project was conducted to determine any differences in the systemic myokine response between BFR-RE and control conditions. METHODS: The appearance of systemic myokines interleukin-6 (IL-6), interleukin-15 (IL-15), and decorin were measured following acute bouts of low-load resistance exercise, BFR-RE, and high-load resistance exercise in physically active young males to determine if BFR-RE modifies the exercise-induced systemic myokine response. RESULTS: No measurable levels of IL-6 were observed during the project. No significant effects were observed for IL-15. A significant time (11.91% increase pre to post exercise; p < 0.05) but no condition or condition by time effect was observed for decorin. CONCLUSION: These findings suggest that BFR-RE does not modify the systemic myokine appearance of IL-6, IL-15, or decorin when compared to control conditions.

Prevalence of frailty in Canadians 18-79 years old in the Canadian Health Measures Survey.

BACKGROUND: There is little certainty as to the prevalence of frailty in Canadians in younger adulthood. This study examines and compares the prevalence of frailty in Canadians 18-79 years old using the Accumulation of Deficits and Fried models of frailty. METHODS: The Canadian Health Measures Study data were used to estimate the prevalence of frailty in adults 18-79 years old. A 23-item Frailty Index using the Accumulation of Deficits Model (cycles 1-3; n = 10,995) was developed; frailty was defined as having the presence of 25% or more indices, including symptoms, chronic conditions, and laboratory variables. Fried frailty (cycles 1-2; n = 7,353) included the presence of ≥3 criteria: exhaustion, physical inactivity, poor mobility, unintentional weight loss, and poor grip strength. RESULTS: The prevalence of frailty was 8.6 and 6.6% with the Accumulation of Deficits and the Fried Model. Comparing the Fried vs. the Accumulation of Deficits Model, the prevalence of frailty was 5.3% vs. 1.8% in the 18-34 age group, 5.7% vs. 4.3% in the 35-49 age group, 6.9% vs. 11.6% in the 50-64 age group, and 7.8% vs. 20.2% in the 65+ age group. Some indices were higher in the younger age groups, including persistent cough, poor health compared to a year ago, and asthma for the accumulation of deficits model, and exhaustion, unintentional weight loss, and weak grip strength for the Fried model, compared to the older age groups. CONCLUSIONS: These data show that frailty is prevalent in younger adults, but varies depending on which frailty tool is used. Further research is needed to determine the health impact of frailty in younger adults.

A Single Session of Low-Volume High-Intensity Interval Exercise Reduces Ambulatory Blood Pressure in Normotensive Men.

Dantas, TCB, Farias Junior, LF, Frazão, DT, Silva, PHM, Sousa Junior, AE, Costa, IBB, Ritti-Dias, RM, Forjaz, CLM, Duhamel, TA, and Costa, EC. A single session of low-volume high-intensity interval exercise reduces ambulatory blood pressure in normotensive men. J Strength Cond Res 31(8): 2263-2269, 2017-The magnitude and duration of postexercise hypotension (PEH) may provide valuable information on the efficacy of an exercise approach to blood pressure (BP) control. We investigated the acute effect of a time-efficient high-intensity interval exercise (HIIE) on ambulatory BP. Twenty-one normotensive men (23.6 ± 3.6 years) completed 2 experimental sessions in a randomized order: (a) control (no exercise) and (b) low-volume HIIE: 10 × 1 minute at 100% of maximal treadmill velocity interspersed with 1 minute of recovery. After each experimental session, an ambulatory BP monitoring was initiated. Paired sample t-test was used to compare BP averages for awake, asleep, and 20-hour periods between the control and the low-volume HIIE sessions. A 2-way repeated measures analysis of variance was used to analyze hourly BP after both experimental sessions. Blood pressure averages during the awake (systolic: 118 ± 6 vs. 122 ± 6 mm Hg; diastolic: 65 ± 7 vs. 67 ± 7 mm Hg) and 20-hour (systolic: 115 ± 7 vs. 118 ± 6 mm Hg; diastolic: 62 ± 7 vs. 64 ± 7 mm Hg) periods were lower after the low-volume HIIE compared with the control (p ≤ 0.05). Systolic and diastolic PEH presented medium (Cohen's d = 0.50-0.67) and small (Cohen's d = 0.29) effect sizes, respectively. Systolic PEH occurred in a greater magnitude during the first 5 hours (3-5 mm Hg). No changes were found in asleep BP (p > 0.05). In conclusion, a single session of low-volume HIIE reduced ambulatory BP in normotensive men. The PEH occurred mainly in systolic BP during the first 5 hours postexercise.

Cardiovascular complications of type 2 diabetes in youth.

The prevalence of type 2 diabetes mellitus (T2DM) in youth has increased dramatically over the past decades. The literature also suggests that the progression from an impaired glucose tolerance state to established T2DM is more rapid in youth, compared to adults. The presence of significant cardiovascular complications in youth with T2DM, including cardiac, macrovascular, and microvascular remodeling, is another major issue in this younger cohort and poses a significant threat to the healthcare system. However, this issue is only now emerging as a major public health concern, with few data to support optimal treatment targets and strategies to reduce cardiovascular disease (CVD) risk in youth with T2DM. Accordingly, the purpose of this minireview is to better understand the cardiovascular complications in youth with T2DM. We briefly describe the pathophysiology from youth studies, including oxidative stress, inflammation, renin-angiotensin aldosterone system, and epigenetics, which link T2DM and CVD. We also describe the literature concerning the early signs of CVD in youth and potential treatment options to reduce cardiovascular risk.

The regulation of sarco(endo)plasmic reticulum calcium-ATPases (SERCA).

The sarco(endo)plasmic reticulum calcium ATPase (SERCA) is responsible for transporting calcium (Ca(2+)) from the cytosol into the lumen of the sarcoplasmic reticulum (SR) following muscular contraction. The Ca(2+) sequestering activity of SERCA facilitates muscular relaxation in both cardiac and skeletal muscle. There are more than 10 distinct isoforms of SERCA expressed in different tissues. SERCA2a is the primary isoform expressed in cardiac tissue, whereas SERCA1a is the predominant isoform expressed in fast-twitch skeletal muscle. The Ca(2+) sequestering activity of SERCA is regulated at the level of protein content and is further modified by the endogenous proteins phospholamban (PLN) and sarcolipin (SLN). Additionally, several novel mechanisms, including post-translational modifications and microRNAs (miRNAs) are emerging as integral regulators of Ca(2+) transport activity. These regulatory mechanisms are clinically relevant, as dysregulated SERCA function has been implicated in the pathology of several disease states, including heart failure. Currently, several clinical trials are underway that utilize novel therapeutic approaches to restore SERCA2a activity in humans. The purpose of this review is to examine the regulatory mechanisms of the SERCA pump, with a particular emphasis on the influence of exercise in preventing the pathological conditions associated with impaired SERCA function.

Prehabilitation program for elective coronary artery bypass graft surgery patients: a pilot randomized controlled study.

OBJECTIVE: To determine the feasibility of a cardiac prehabilitation (Prehab) program for patients waiting for elective coronary artery bypass graft (CABG). DESIGN: A two-group parallel randomized controlled trial. SETTING: Medical fitness facility. SUBJECTS: Seventeen preoperative elective CABG surgery patients were randomized to standard care (n = 9) or Prehab (n = 8). INTERVENTION: Standard care: three-hour preassessment appointment. Prehab: exercise and education classes for 60 minutes/day, twice weekly for at least four weeks. MAIN MEASURES: Data were collected at baseline, one week preoperatively, and three months postoperatively. The primary outcome measure was walking distance using a 6-minute walk test. Secondary outcome variables included 5-meter gait speed, and cardiac rehabilitation attendance three months postoperatively. RESULTS: Fifteen patients (standard care, n = 7; Prehab, n = 8) completed the study. No Prehab patients developed cardiac symptoms during study participation. Walking distance remained unchanged in the standard care group; whereas, the Prehab group increased their walking distance to mean ± SD 474 ±101 and 487 ±106 m at the preoperative and three month postoperative assessments (p < 0.05). Gait speed was unchanged in the standard care group, but improved in the Prehab group by 27% and 33% preoperatively and three months postoperatively, respectively (p < 0.05). Enrollment in cardiac rehabilitation three months postoperatively was higher for Prehab participants (100%) than standard care participants (43%; p < 0.05). CONCLUSION: These data provide evidence for the feasibility of a Prehab intervention to improve the health status of patients waiting for elective CABG surgery. A larger trial of 92 patients will be utilized to demonstrate the safety and efficacy of Prehab.

A scoping review of incidence and assessment tools for post-intensive care syndrome following cardiac surgery.

BACKGROUND: Post-intensive care syndrome is a new or worsening persistent deterioration in cognitive, mental, and/or physical health following a prolonged admission to an intensive care unit. Post-intensive care syndrome remains underexplored following cardiac surgery, with a lack of understanding of the incidence and tools used to measure the symptoms. A scoping review was conducted to determine the incidence and to identify the tools commonly used to measure symptoms of post-intensive care syndrome following cardiac surgery. METHODS: The electronic databases Medline (Ovid), EMBASE (Ovid), PsycINFO (Ovid), Scopus, and CINAHL (EBSCOhost) and Google Scholar were searched with keywords and controlled vocabulary to describe both cardiac surgery and post-intensive care syndrome (cardiac surgical procedures, heart surgery, and post-intensive care symptoms) and symptoms (delirium, depression, mobility and quality of life). Included were articles written in English and published after 2005 that described cognitive, mental, and physical symptoms of post-intensive care syndrome following cardiac surgery. 3,131 articles were found, with 565 duplicates, leaving 2,566 articles to be screened. Of these, seven unique studies were included. RESULTS: Five studies explored cognitive health, three mental health, one cognitive and mental health, and none physical health. No identified studies reported the overall incidence of post-intensive care syndrome following cardiac surgery. The incidence of cognitive health issues ranged from 21% to 38%, and mental health issues ranged from 16% to 99%. In total, 17 different tools were identified - 14 for cognitive health and three for mental health. No identified studies used the same tools to measure symptoms. No single tool was found to measure all three domains. CONCLUSION: This scoping review identified a literature gap specific to the incidence and inconsistency of assessment tools for post-intensive care syndrome in cardiac surgery patients. CLINICAL IMPLICATIONS: This work impacts clinical practice for the bedside nurse by raising awareness of an emerging health issue.