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Self-care interventions that reduce hospital readmissions in patients with heart failure; towards the identification of change agents

- Toukhsati, Samia, Jaarsma, Tiny, Babu, Abraham, Driscoll, Andrea, Hare, David

  • Authors: Toukhsati, Samia , Jaarsma, Tiny , Babu, Abraham , Driscoll, Andrea , Hare, David
  • Date: 2019
  • Type: Text , Journal article , Review
  • Relation: Clinical Medicine Insights: Cardiology Vol. 13, no. (2019), p. 1-8
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  • Description: Unplanned hospital readmissions are the most important, preventable cost in heart failure (HF) health economics. Current professional guidelines recommend that patient self-care is an important means by which to reduce this burden. Patients with HF should be engaged in their care such as by detecting, monitoring, and managing their symptoms. A variety of educational and behavioural interventions have been designed and implemented by health care providers to encourage and support patient self-care. Meta-analyses support the use of self-care interventions to improve patient self-care and reduce hospital readmissions; however, efficacy is variable. The aim of this review was to explore methods to achieve greater clarity and consistency in the development and reporting of self-care interventions to enable ‘change agents’ to be identified. We conclude that advancement in this field requires more explicit integration and reporting on the behaviour change theories that inform the design of self-care interventions and the selection of behaviour change techniques. The systematic application of validated checklists, such as the Theory Coding Scheme and the CALO-RE taxonomy, will improve the systematic testing and refinement of interventions to enable ‘change agent/s’ to be identified and optimised.

Glycogen storage disease

- Kannourakis, George

  • Authors: Kannourakis, George
  • Date: 2002
  • Type: Text , Journal article
  • Relation: Seminars in Hematology Vol. 39, no. 2 (2002), p. 103-106
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  • Description: Glycogen storage disease (GSD) is a rare autosomal-recessive disorder characterized by hypoglycemia, hepatosplenomegaly, seizures, and failure to thrive in infants. Neutropenia and/or neutrophil dysfunction develops in GSD1b, but not in other types. GSD1b results from a deficiency of the glucose-6-phosphate translocase enzyme and the genetic defect maps to chromosome 11q23. Patients with GSD1b are susceptible to recurrent bacterial infections, commonly involving the perirectal area, ears, skin, and urinary tract, although life-threatening infections, such as septicemia, pneumonia, and meningitis occur less frequently. Although the exact mechanism of neutropenia in patients with GSD1b is not known, treatment with recombinant human granulocyte colony-stimulating factor (G-CSF) has reduced the incidence of infections and has improved the quality of life of these patients. Defects in neutrophil chemotaxis and intracellular bacterial killing have been described and appear to be corrected by the use of G-CSF. To date, no cases of myelodysplasia or acute myeloid leukemia have been observed in patients with GSD1b treated with G-CSF. A significant complication of cytokine therapy is the development of hypersplenism, requiring either a reduction in the dosage of G-CSF or splenectomy. Copyright 2002, Elsevier Science (USA). All rights reserved.

Angiotensin II, Sympathetic nerve activity and chronic heart failure

- Wang, Yutang, Seto, Sai-Wang, Golledge, Jonathan

  • Authors: Wang, Yutang , Seto, Sai-Wang , Golledge, Jonathan
  • Date: 2014
  • Type: Text , Journal article
  • Relation: Heart Failure Reviews Vol. 19, no. 2 (2014), p. 187-198
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  • Description: Sympathetic nerve activity has been reported to be increased in both humans and animals with chronic heart failure. One of the mechanisms believed to be responsible for this phenomenon is increased systemic and cerebral angiotensin II signaling. Plasma angiotensin II is increased in humans and animals with chronic heart failure. The increase in angiotensin II signaling enhances sympathetic nerve activity through actions on both central and peripheral sites during chronic heart failure. Angiotensin II signaling is enhanced in different brain sites such as the paraventricular nucleus, the rostral ventrolateral medulla and the area postrema. Blocking angiotensin II type 1 receptors decreases sympathetic nerve activity and cardiac sympathetic afferent reflex when therapy is administered to the paraventricular nucleus. Injection of an angiotensin receptor blocker into the area postrema activates the sympathoinhibitory baroreflex. In peripheral regions, angiotensin II elevates both norepinephrine release and synthesis and inhibits norepinephrine uptake at nerve endings, which may contribute to the increase in sympathetic nerve activity seen in chronic heart failure. Increased circulating angiotensin II during chronic heart failure may enhance the sympathoexcitatory chemoreflex and inhibit the sympathoinhibitory baroreflex. In addition, increased circulating angiotensin II can directly act on the central nervous system via the subfornical organ and the area postrema to increase sympathetic outflow. Inhibition of angiotensin II formation and its type 1 receptor has been shown to have beneficial effects in chronic heart failure patients. © 2012 Springer Science+Business Media New York.

Cardiovascular risk and androgenic anabolic steroids

- Sculthorpe, Nicholas, Grace, Fergal, Angell, Peter, Baker, Julien, George, Keith

  • Authors: Sculthorpe, Nicholas , Grace, Fergal , Angell, Peter , Baker, Julien , George, Keith
  • Date: 2013
  • Type: Text , Journal article
  • Relation: British Journal of Cardiac Nursing Vol. 7, no. 6 (2013), p. 266-275
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  • Description: Although several drugs are purported to improve exercise performance, androgenic anabolic steroids (AAS) are the most widespread. Furthermore, unlike other drugs, their use has expanded beyond competition, to non-competitive and recreational athletes. Correspondingly health professionals are more likely to come into contact with users of AAS than with users of other performance-enhancing drugs. While there are numerous reports outlining serious cardiovascular consequences to high-dose AAS abuse, this evidence is often limited by difficulties in gaining access to users due to the legal status of AAS. Additionally the co-abuse of other substances (as additional muscle mass enhancers, or to mitigate possible side effects) is a further confounding factor. This review examines the evidence for AAS having a negative effect on the cardiac and vascular tissue and the corresponding risk of developing cardiovascular disease. Possible mechanisms of action by which AAS bring about these changes are also discussed.

Genetics of blood pressure : Time to curate the collection

- Harrap, Stephen, Charchar, Fadi

  • Authors: Harrap, Stephen , Charchar, Fadi
  • Date: 2017
  • Type: Text , Journal article , Editorial
  • Relation: Journal of Hypertension Vol. 35, no. 7 (2017), p. 1360-1362
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  • Description: The genetics of blood pressure (BP) is all about discovery and understanding, but it is certainly not for the faint hearted. Despite heroic effort, the question we posed nearly 15 years ago [1] regarding the whereabouts of BP genes remains largely unanswered.

The efficacy of different modes of analgesia in postoperative pain management and early mobilization in postoperative cardiac surgical patients : A systematic review

- Nachiyunde, Brenda, Lam, Louisa

  • Authors: Nachiyunde, Brenda , Lam, Louisa
  • Date: 2018
  • Type: Text , Journal article , Review
  • Relation: Annals of Cardiac Anaesthesia Vol. 21, no. 4 (2018), p. 371-375
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  • Description: Cardiac surgery induces severe postoperative pain and impairment of pulmonary function, increases the length of stay (LOS) in hospital, and increases mortality and morbidity; therefore, evaluation of the evidence is needed to assess the comparative benefits of different techniques of pain management, to guide clinical practice, and to identify areas of further research. A systematic search of the Cochrane Central Register of Controlled Trials, DARE database, Joanna Briggs Institute, Google scholar, PUBMED, MEDLINE, EMBASE, Academic OneFile, SCOPUS, and Academic search premier was conducted retrieving 1875 articles. This was for pain management postcardiac surgery in intensive care. Four hundred and seventy-one article titles and 266 abstracts screened, 52 full text articles retrieved for critical appraisal, and ten studies were included including 511 patients. Postoperative pain (patient reported), complications, and LOS in intensive care and the hospital were evaluated. Anesthetic infiltrations and intercostal or parasternal blocks are recommended the immediate postoperative period (4-6 h), and patient-controlled analgesia (PCA) and local subcutaneous anesthetic infusions are recommended immediate postoperative and 24-72 h postcardiac surgery. However, the use of mixed techniques, that is, PCA with opioids and local anesthetic subcutaneous infusions might be the way to go in pain management postcardiac surgery to avoid oversedation and severe nausea and vomiting from the narcotics. Adequate studies in the use of ketamine for pain management postcardiac surgery need to be done and it should be used cautiously.

Higher long-term adherence to statins in rural patients at high atherosclerotic risk

- Peverelle, Matthew, Baradi, Arul, Paleri, Sarang, Lee, Yun, Sultani, Rohullah, Toukhsati, Samia, Hare, David, Janus, Edward, Wilson, Andrew

  • Authors: Peverelle, Matthew , Baradi, Arul , Paleri, Sarang , Lee, Yun , Sultani, Rohullah , Toukhsati, Samia , Hare, David , Janus, Edward , Wilson, Andrew
  • Date: 2019
  • Type: Text , Journal article
  • Relation: Journal of Clinical Lipidology Vol. 13, no. 1 (2019), p. 163-169
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  • Description: Background: Rural patients with atherosclerotic cardiovascular disease (ASCVD) experience greater cardiovascular morbidity and mortality than their urban counterparts. Statin therapy is a key component of ASCVD treatment. The extent to which there may be regional differences in long-term adherence to statins is unknown. Objective: To assess long-term rates of adherence to statins in a high-risk ASCVD cohort, and whether regional differences exist between rural and urban patients. Methods: Follow-up was conducted in patients who underwent coronary angiography at a single tertiary center between 2009 and 2013. Adherence was defined as consumption of prescribed statin ≥6 days per week. Patients were divided into remoteness areas (RAs), classified as RA1 (major city), RA2 (inner regional), and RA3 (outer regional) based on the Australian Standard Geographical Classification. Results: Five hundred twenty-five patients (69% male, mean age 64 ± 11 years) were followed-up after a median of 5.3 years. Baseline characteristics were similar between RAs. Overall adherence was 83%; however, rural patients were significantly more adherent to their statin therapy (80% in RA1, 83% in RA2, and 93% in RA3, P =.04). Living in RA3 independently predicted greater statin adherence than living in RA1 (odds ratio: 2.75, 95% CI: 1.1–7.8, P =.03). All-cause mortality was significantly higher in RA3 than other regional areas (6% RA1, 12% RA2, and 18% RA3, P =.01). Conclusions: Despite higher all-cause mortality, rural patients with ASCVD demonstrate significantly greater long-term adherence to statins than urban patients. Other factors, such as reduced access to health care and delayed diagnosis may explain the gap in outcomes between rural and urban patients.

Meaningful and effective consultation and the construction industry of Victoria, Australia

- Ayers, Gerard, Culvenor, John, Sillitoe, Jim, Else, Dennis

  • Authors: Ayers, Gerard , Culvenor, John , Sillitoe, Jim , Else, Dennis
  • Date: 2013
  • Type: Text , Journal article
  • Relation: Construction Management and Economics Vol. 31, no. 6 (2013), p. 542-567
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  • Description: Consultation between employers and employees is mandated under Australian occupational health and safety legislation. For consultation to be considered meaningful and effective, it is generally accepted that moral and ethical principles such as trust, honesty, commitment and respect need to be recognized and applied by individuals during consultation. It is also considered that an organization's level of cultural maturity is an important element in the ability of individuals to freely engage in meaningful and effective consultation. If the value of consultation is best reflected in the degree of input and control that workers have regarding the very decisions that affect them, and if the level of worker involvement is a reflection of an organization's level of cultural maturity, it is debateable whether the notion of applying moral and ethical principles during consultation, and the adoption of the paradigm of organizational and cultural maturity, have been successfully developed and embraced in the commercial and industrial sector of the construction industry of Victoria, Australia. © 2013 Taylor and Francis Group, LLC.
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Wnt signaling pathway inhibitor Sclerostin inhibits angiotensin II-induced aortic aneurysm and atherosclerosis

- Krishna, Smriti, Seto, Sai-Wang, Jose, Roby, Li, Jiaze, Morton, Susan, Biros, Erik, Wang, Yutang, Nsengiyumva, Vianne, Lindeman, Jan, Loots, Gabriela, Rush, Catherine, Craig, Jeffrey, Golledge, Jonathan

  • Authors: Krishna, Smriti , Seto, Sai-Wang , Jose, Roby , Li, Jiaze , Morton, Susan , Biros, Erik , Wang, Yutang , Nsengiyumva, Vianne , Lindeman, Jan , Loots, Gabriela , Rush, Catherine , Craig, Jeffrey , Golledge, Jonathan
  • Date: 2017
  • Type: Text , Journal article
  • Relation: Arteriosclerosis Thrombosis and Vascular Biology Vol. 37, no. 3 (2017), p. 553-566
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  • Description: Objective-Sclerostin (SOST) has been identified as an important regulator of bone formation; however, it has not been previously implicated in arterial disease. The aim of this study was to assess the role of SOST in aortic aneurysm (AA) and atherosclerosis using human samples, a mouse model, and in vitro investigations. Approach and Results-SOST protein was downregulated in human and mouse AA samples compared with controls. Transgenic introduction of human SOST in apolipoprotein E-deficient (ApoE(-/-)) mice (SOSTTg. ApoE(-/-)) and administration of recombinant mouse Sost inhibited angiotensin II-induced AA and atherosclerosis. Serum concentrations of several proinflammatory cytokines were significantly reduced in SOSTTg. ApoE(-/-) mice. Compared with controls, the aortas of mice receiving recombinant mouse Sost and SOSTTg. ApoE(-/-) mice showed reduced matrix degradation, reduced elastin breaks, and preserved collagen. Decreased inflammatory cell infiltration and a reduction in the expression of wingless-type mouse mammary virus integration site/beta-catenin responsive genes, including matrix metalloproteinase-9, osteoprotegerin, and osteopontin, were observed in the aortas of SOSTTg. ApoE(-/-) mice. SOST expression was downregulated and the winglesstype mouse mammary virus integration site/beta-catenin pathway was activated in human AA samples. The cytosinephosphate- guanine islands in the SOST gene promoter showed significantly higher methylation in human AA samples compared with controls. Incubation of vascular smooth muscle cells with the demethylating agent 5-azacytidine resulted in upregulation of SOST, suggesting that SOST is epigenetically regulated. Conclusions-This study identifies that SOST is expressed in the aorta and downregulated in human AA possibly because of epigenetic silencing. Upregulating SOST inhibits AA and atherosclerosis development, with potential important implications for treating these vascular diseases.

The effect of bronchial thermoplasty on airway volume measured 12 months post-procedure

- Langton, David, Banks, Ceri, Noble, Peter, Plummer, Virginia, Thien, Francis, Donovan, Graham

  • Authors: Langton, David , Banks, Ceri , Noble, Peter , Plummer, Virginia , Thien, Francis , Donovan, Graham
  • Date: 2020
  • Type: Text , Journal article
  • Relation: Erj Open Research Vol. 6, no. 4 (Oct 2020), p. 9
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  • Description: Bronchial thermoplasty induces atrophy of the airway smooth muscle layer, but the mechanism whereby this improves patient health is unclear. In this study, we use computed tomography (CT) to evaluate the effects of bronchial thermoplasty on airway volume 12 months post-procedure. 10 consecutive patients with severe asthma were evaluated at baseline by the Asthma Control Questionnaire (ACQ), and high-resolution CT at total lung capacity (TLC) and functional residual capacity (FRC). The CT protocol was repeated 4 weeks after the left lung had been treated by bronchial thermoplasty, but prior to right lung treatment, and then again 12 months after both lungs were treated. The CT data were also used to model the implications of including the right middle lobe (RML) in the treatment field. The mean patient age was 62.7 +/- 7.7 years and forced expiratory volume in 1 s (FEV1) 42.9 +/- 11.5% predicted. 12 months post-bronchial-thermoplasty, the ACQ improved, from 3.4 +/- 1.0 to 1.5 +/- 0.9 (p=0.001), as did the frequency of oral steroid-requiring exacerbations (p=0.008). The total airway volume increased 12 months after bronchial thermoplasty in both the TLC (p=0.03) and the FRC scans (p=0.02). No change in airway volume was observed in the untreated central airways. In the bronchial thermoplasty-treated distal airways, increases in airway volume of 38.4 +/- 31.8% at TLC (p=0.03) and 30.0 +/- 24.8% at FRC (p=0.01) were observed. The change in distal airway volume was correlated with the improvement in ACQ (r=-0.71, p=0.02). Modelling outputs demonstrated that treating the RML conferred no additional benefit. Bronchial thermoplasty induces long-term increases in airway volume, which correlate with symptomatic improvement.

Human Y Chromosome Exerts Pleiotropic Effects on Susceptibility to Atherosclerosis

- Eales, James, Maan, Akhlaq, Xu, Xiaoguang, Michoel, Tom, Hallast, Pille, Batini, C, Zadik, Daniel, Prestes, Priscilla, Molina, Elsa, Denniff, Matthew, Schroeder, Juliane, Bjorkegren, Johan, Thompson, John, Maffia, Pasquale, Guzik, Tomasz, Keavney, Bernard, Jobling, Mark, Samani, Nilesh, Charchar, Fadi, Tomaszewski, Maciej

  • Authors: Eales, James , Maan, Akhlaq , Xu, Xiaoguang , Michoel, Tom , Hallast, Pille , Batini, C , Zadik, Daniel , Prestes, Priscilla , Molina, Elsa , Denniff, Matthew , Schroeder, Juliane , Bjorkegren, Johan , Thompson, John , Maffia, Pasquale , Guzik, Tomasz , Keavney, Bernard , Jobling, Mark , Samani, Nilesh , Charchar, Fadi , Tomaszewski, Maciej
  • Date: 2019
  • Type: Text , Journal article
  • Relation: Arteriosclerosis, thrombosis, and vascular biology Vol. 39, no. 11 (2019), p. 2386-2401
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  • Description: OBJECTIVE: The male-specific region of the Y chromosome (MSY) remains one of the most unexplored regions of the genome. We sought to examine how the genetic variants of the MSY influence male susceptibility to coronary artery disease (CAD) and atherosclerosis. Approach and Results: Analysis of 129 133 men from UK Biobank revealed that only one of 7 common MSY haplogroups (haplogroup I1) was associated with CAD-carriers of haplogroup I1 had ≈11% increase in risk of CAD when compared with all other haplogroups combined (odds ratio, 1.11; 95% CI, 1.04-1.18; P=6.8×10-4). Targeted MSY sequencing uncovered 235 variants exclusive to this haplogroup. The haplogroup I1-specific variants showed 2.45- and 1.56-fold respective enrichment for promoter and enhancer chromatin states, in cells/tissues relevant to atherosclerosis, when compared with other MSY variants. Gene set enrichment analysis in CAD-relevant tissues showed that haplogroup I1 was associated with changes in pathways responsible for early and late stages of atherosclerosis development including defence against pathogens, immunity, oxidative phosphorylation, mitochondrial respiration, lipids, coagulation, and extracellular matrix remodeling. UTY was the only Y chromosome gene whose blood expression was associated with haplogroup I1. Experimental reduction of UTY expression in macrophages led to changes in expression of 59 pathways (28 of which overlapped with those associated with haplogroup I1) and a significant reduction in the immune costimulatory signal. CONCLUSIONS: Haplogroup I1 is enriched for regulatory chromatin variants in numerous cells of relevance to CAD and increases cardiovascular risk through proatherosclerotic reprogramming of the transcriptome, partly through UTY.

Short and long term mortality rates after a lower limb amputation

- Fortington, Lauren, Geertzen, Jan, Van Netten, Jaap, Postema, Klaas, Rommers, Gerardus, Dijkstra, Pieter

  • Authors: Fortington, Lauren , Geertzen, Jan , Van Netten, Jaap , Postema, Klaas , Rommers, Gerardus , Dijkstra, Pieter
  • Date: 2013
  • Type: Text , Journal article
  • Relation: European Journal of Vascular and Endovascular Surgery Vol. 46, no. 1 (July 2013), p. 124-131
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  • Description: Objective: To determine mortality rates after a first lower limb amputation and explore the rates for different subpopulations. Methods: Retrospective cohort study of all people who underwent a first amputation at or proximal to transtibial level, in an area of 1.7 million people. Analysis with Kaplan-Meier curves and Log Rank tests for univariate associations of psycho-social and health variables. Logistic regression for odds of death at 30-days, 1-year and 5-years. Results: 299 people were included. Median time to death was 20.3 months (95%CI: 13.1; 27.5). 30-day mortality = 22%; odds of death 2.3 times higher in people with history of cerebrovascular disease (95%CI: 1.2; 4.7, P = 0.016). 1 year mortality = 44%; odds of death 3.5 times higher for people with renal disease (95%CI: 1.8; 7.0, P < 0.001). 5-years mortality = 77%; odds of death 5.4 times higher for people with renal disease (95%CI: 1.8; 16.0,P = 0.003). Variation in mortality rates was most apparent in different age groups; people 75-84 years having better short term outcomes than those younger and older. Conclusions: Mortality rates demonstrated the frailty of this population, with almost one quarter of people dying within 30-days, and almost half at 1 year. People with cerebrovascular had higher odds of death at 30 days, and those with renal disease and 1 and 5 years, respectively.
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High-intensity interval training and cardiac autonomic control in individuals with metabolic syndrome: A randomised trial

- Ramos, Joyce, Dalleck, Lance, Borrani, Fabio, Beetham, Kassia, Mielke, Gregore, Dias, Katrin, Wallen, Matthew, Keating, Shelley, Fassett, Robert, Coombes, Jeff

  • Authors: Ramos, Joyce , Dalleck, Lance , Borrani, Fabio , Beetham, Kassia , Mielke, Gregore , Dias, Katrin , Wallen, Matthew , Keating, Shelley , Fassett, Robert , Coombes, Jeff
  • Date: 2017
  • Type: Text , Journal article
  • Relation: International Journal of Cardiology Vol. , no. (2017), p.
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  • Description: Background: Insulin resistance has been postulated to play a central role in the co-appearance of various cardiovascular disease risk factors constituting the metabolic syndrome (MetS). There is evidence that altered cardiac autonomic function (CAF) may precede the onset of insulin resistance. Exercise training has been shown to improve CAF in different populations, yet little is known regarding the exercise dose response for CAF. The aim of this study was to investigate the impact of different volumes of high-intensity interval training (HIIT) and traditional moderate-intensity continuous training (MICT) on CAF in participants with MetS. Methods: Individuals with MetS (n=56) were randomised into the following 16-week training interventions: i) MICT (n=16, 30min at 60-70%HRpeak, 5×/week); ii) 4HIIT (n=19, 4×4min bouts at 85-95%HRpeak, interspersed with 3min of active recovery at 50-70%HRpeak, 3×/week); or iii) 1HIIT (n=21, 1×4min bout at 85-95%HRpeak, 3×/week). R-R interval recorded for 5min in a supine position at pre- and post-intervention was used to derive linear (SDNN, RMSSD, pNN50, LF, HF, LF/HF) and non-linear (SD1, SD2, Alpha1, Alpha2, SampEn) heart rate variability (HRV) indices as measures of CAF. Group×time interaction effects were examined (ANCOVA) and Eta squared (η2) interaction effect sizes calculated. Results: While there were no significant between-group differences in CAF indices, there were small-to-medium group×time interaction effects on SDNN [F(2,52)=0.70, p=0.50, η2 =0.02], RMSSD [F(2,52)=1.35, p=0.27, η2 =0.03], HF power [F(2,52)=1.27, p=0.29, η2 =0.03], SD1 [F(2,52)=0.47, p=0.63, η2 =0.01], and SD2 [F(2,52)=0.41, p=0.67, η2 =0.01]. The following represent the relative percentage increases across these variables for 4HIIT, MICT, and 1HIIT respectively (SDNN, +30%, +17%, 9%; RMSSD, +30%, +22%, -2%; HF power, +69%, +18%, +7%; SD1, +30%, +22%,-2%; SD2, +22%, +14%, 4%). Conclusions: There were no significant between-group differences for the effects of exercise dose on CAF indices, however; high-volume HIIT demonstrated the greatest magnitude of effect for improving CAF in individuals with MetS. © 2017 Elsevier Ireland Ltd.

Neural suppression of miRNA-181a in the kidney elevates renin expression and exacerbates hypertension in Schlager mice

- Jackson, Kristy, Gueguen, Cindy, Lim, Kyungjoon, Eikelis, Nina, Stevenson, Emily, Charchar, Fadi, Lambert, Gavin, Burke, Sandra, Paterson, Madeleine, Marques, Francine, Head, Geoffrey

  • Authors: Jackson, Kristy , Gueguen, Cindy , Lim, Kyungjoon , Eikelis, Nina , Stevenson, Emily , Charchar, Fadi , Lambert, Gavin , Burke, Sandra , Paterson, Madeleine , Marques, Francine , Head, Geoffrey
  • Date: 2020
  • Type: Text , Journal article
  • Relation: Hypertension Research Vol. 43, no. 11 (2020), p. 1152-1164
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  • Description: BPH/2J mice are a genetic model of hypertension with overactivity of the sympathetic nervous system (SNS) and renin–angiotensin system (RAS). BPH/2J display higher renal renin mRNA and low levels of its negative regulator microRNA-181a (miR-181a). We hypothesise that high renal SNS activity may reduce miR-181a expression, which contributes to elevated RAS activity and hypertension in BPH/2J. Our aim was to determine whether in vivo administration of a renal-specific miR-181a mimic or whether renal denervation could increase renal miR-181a abundance to reduce renal renin mRNA, RAS activity and hypertension in BPH/2J mice. Blood pressure (BP) in BPH/2J and normotensive BPN/3J mice was measured via radiotelemetry probes. Mice were administered miR-181a mimic or a negative control (1–25 nmol, i.v., n = 6–10) with BP measured for 48 h after each dose or they underwent renal denervation or sham surgery (n = 7–9). Injection of 5–25 nmol miR-181a mimic reduced BP in BPH/2J mice after 36–48 h (−5.3 ± 1.8, −6.1 ± 1.9 mmHg, respectively, P < 0.016). Treatment resulted in lower renal renin and inflammatory marker (TLR4) mRNA levels in BPH/2J. The mimic abolished the hypotensive effect of blocking the RAS with enalaprilat (P < 0.01). No differences between mimic or vehicle were observed in BPN/3J mice except for a higher level of renal angiotensinogen in the mimic-treated mice. Renal miR-181a levels that were lower in sham BPH/2J mice were greater following renal denervation and were thus similar to those of BPN/3J. Our findings suggest that the reduced renal miR-181a may partially contribute to the elevated BP in BPH/2J mice, through an interaction between the renal sympathetic nerves and miR-181a regulation of the RAS. © 2020, The Japanese Society of Hypertension.
  • Description: This work was supported by a grant from the National Health & Medical Research Council of Australia (NHMRC, Project grant 1065714) and in part by the Victorian Government’s OIS Program. Investigators were supported by NHMRC/National Heart Foundation (NHF) Postdoctoral Fellowships (NHMRC APP1091688 to KLJ, NHMRC APP1052659 and NHF PF12M6785 and 101185 to FZM) and NHMRC Research Fellowships (APP1042492 to GWL and APP1002186 to GAH).

Tripartite motif-containing 55 identified as functional candidate for spontaneous cardiac hypertrophy in the rat locus cardiac mass 22

- Prestes, Priscilla, Marques, Francine, Lopez-Campos, Guillermo, Booth, Scott, McGlynn, Maree, Lewandowski, Paul, Delbridge, Lea, Harrap, Stephen, Charchar, Fadi

  • Authors: Prestes, Priscilla , Marques, Francine , Lopez-Campos, Guillermo , Booth, Scott , McGlynn, Maree , Lewandowski, Paul , Delbridge, Lea , Harrap, Stephen , Charchar, Fadi
  • Date: 2016
  • Type: Text , Journal article
  • Relation: Journal of Hypertension Vol. 34, no. 5 (May 2016), p. 950-958
  • Relation: http://purl.org/au-research/grants/nhmrc/1034371
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  • Description: Background:Left ventricular (LV) hypertrophy is a risk factor for cardiovascular death, but the genetic factors determining LV size and predisposition to hypertrophy are not well understood. We have previously linked the quantitative trait locus cardiac mass 22 (Cm22) on chromosome 2 with cardiac hypertrophy independent of blood pressure in the spontaneously hypertensive rat. From an original cross of spontaneously hypertensive rat with F344 rats, we derived a normotensive polygenic model of spontaneous cardiac hypertrophy, the hypertrophic heart rat (HHR) and its control strain, the normal heart rat (NHR).Methods and results:To identify the genes and molecular mechanisms underlying spontaneous LV hypertrophy we sequenced the HHR genome with special focus on quantitative trait locus Cm22. For correlative analyses of function, we measured global RNA transcripts in LV of neonatal HHR and NHR and 198 neonatal rats of an HHRxNHR F2 crossbred population. Only one gene within locus Cm22 was differentially expressed in the parental generation: tripartite motif-containing 55 (Trim55), with mRNA downregulation in HHR (P<0.05) and reduced protein expression. Trim55 mRNA levels were negatively correlated with LV mass in the F2 cross (r=-0.16, P=0.025). In exon nine of Trim55 in HHR, we found one missense mutation that functionally alters protein structure. This mutation was strongly associated with Trim55 mRNA expression in F2 rats (F=10.35, P<0.0001). Similarly, in humans, we found reduced Trim55 expression in hearts of subjects with idiopathic dilated cardiomyopathy.Conclusion:Our study suggests that the Trim55 gene, located in Cm22, is a novel candidate gene for polygenic LV hypertrophy independent of blood pressure.

A phase II trial for the efficacy of physiotherapy intervention for early-onset hip osteoarthritis: Study protocol for a randomised controlled trial

- Kemp, Joanne, Moore, Kate, Fransen, Marlene, Russell, Trevor, Crossley, Kay

  • Authors: Kemp, Joanne , Moore, Kate , Fransen, Marlene , Russell, Trevor , Crossley, Kay
  • Date: 2015
  • Type: Text , Journal article
  • Relation: Trials Vol. 16, no. 1 (2015), p. 1-8
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  • Description: Background: Early-onset hip osteoarthritis is commonly seen in people undergoing hip arthroscopy and is associated with increased pain, reduced ability to participate in physical activity, reduced quality of life and reduced range of motion and muscle strength. Despite this, the efficacy of non-surgical interventions such as exercise therapies remains unknown. The primary aim is to establish the feasibility of a phase III randomised controlled trial investigating a targeted physiotherapy intervention for people with early-onset hip osteoarthritis. The secondary aims are to determine the size of treatment effects of a physiotherapy intervention, targeted to improve hip joint range and hip-related symptoms in early-onset hip osteoarthritis following hip arthroscopy, compared to a health-education control. Methods: This protocol describes a randomised, assessor- and participant-blind, controlled clinical trial. We will include 20 participants who are (i) aged between 18 and 50 years; (ii) have undergone hip arthroscopy during the past six to 12 months; (iii) have early-onset hip osteoarthritis (defined as chondrolabral pathology) at the time of hip arthroscopy; and (iv) experience hip-related pain during activities. Primary outcome will be the feasibility of a phase III clinical trial. Secondary outcomes will be (i) perceived global change score; (ii) hip-related symptoms (measured using the Hip disability and Osteoarthritis Outcome Score (HOOS) pain subscale, activity subscale, and sport and recreation subscale); (iii) hip quality of life (measured using the HOOS quality of life subscale and International Hip Outcome tool; (iv) hip muscle strength and (v) hip range of motion. The physiotherapy intervention is semi-standardised, including joint and soft tissue mobilisation and stretching, hip and trunk muscle retraining and functional and activity-specific retraining and education. The control intervention encompasses individualised health education, with the same frequency and duration as the intervention. The trial primary end-point is the conclusion of the 12-week intervention, and follow-up measures will be collected at the 12-week post-baseline assessment. Discussion: The findings of this study will provide guidance regarding the feasibility of a full-scale phase III randomised controlled trial, prior to its undertaking. Trial registration: The trial protocol was registered with the Australian Clinical Trials Registry (number: 12614000426684) on 17 April 2014. © Kemp et al.

May measurement month 2019 the global blood pressure screening campaign of the International Society of Hypertension

- Beaney, Thomas, Schutte, Aletta, Stergiou, George, Borghi, Claudio, Burger, Dylan, Charchar, Fadi, Cro, Suzie, Diaz, Alejandro, Damasceno, Albertino, Espeche, Walter, Jose, Arun, Khan, Nadia, Kokubo, Yoshihiro, Maheshwari, Anuj, Marin, Marcos, More, Arun, Neupane, Dinesh, Nilsson, Peter, Patil, Mansi, Prabhakaran, Dorairaj, Ramirez, Agustin, Rodriguez, Pablo, Schlaich, Markus, Steckelings, Ulrike, Tomaszewski, Maciej, Unger, Thomas, Wainford, Richard, Wang, Jiguang, Williams, Bryan, Poulter, Neil, M. M. M. Investigators

Meta-analysis of genome-wide gene expression differences in onset and maintenance phases of genetic hypertension

- Marques, Francine, Campain, Anna, Yang, Yee, Morris, Brian

  • Authors: Marques, Francine , Campain, Anna , Yang, Yee , Morris, Brian
  • Date: 2010
  • Type: Text , Journal article
  • Relation: Hypertension Vol. 56, no. 2 (August 2010), p. 319-324
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  • Description: Gene expression differences accompany both the onset and established phases of hypertension. By an integrated genome-transcriptome approach we performed a meta-analysis of data from 74 microarray experiments available on public databases to identify genes with altered expression in the kidney, adrenal, heart, and artery of spontaneously hypertensive and Lyon hypertensive rats. To identify genes responsible for the onset of hypertension we used a statistical approach that sought to eliminate expression differences that occur during maturation unrelated to hypertension. Based on this adjusted fold-difference statistic, we found 36 genes for which the expression differed between the prehypertensive phase and established hypertension. Genes having possible relevance to hypertension onset included Actn2, Ankrd1, ApoE, Cd36, Csrp3, Me1, Myl3, Nppa, Nppb, Pln, Postn, Spp1, Slc21a4, Slc22a2, Thbs4, and Tnni3. In established hypertension 102 genes exhibited altered expression after Bonferroni correction (P<0.05). These included Atp5o, Ech1, Fabp3, Gnb3, Ldhb, Myh6, Lpl, Pkkaca, Vegfb, Vcam1, and reduced nicotinamide-adenine dinucleotide dehydrogenases. Among the genes identified, there was an overrepresentation of gene ontology terms involved in energy production, fatty acid and lipid metabolism, oxidation, and transport. These could contribute to increases in reactive oxygen species. Our meta-analysis has revealed many new genes for which the expression is altered in hypertension, so pointing to novel potential causative, maintenance, and responsive mechanisms and pathways.
  • Description: C1

Association between lipid profile and circulating concentrations of estrogens in young men

- Tomaszewski, Maciej, Maric, Christine, Zuzniewicz, Roman, Gola, Mateusz, Grzeszczak, Wladyslaw, Samani, Nilesh, Zukowska-Szczechowska, Ewa, Charchar, Fadi

Genetic variation within the Y chromosome is not associated with histological characteristics of the atherosclerotic carotid artery or aneurysmal wall

- Haitjema, Saskia, van Setten, Jessica, Eales, James, van der Laan, Sander, Gandin, Ilaria, de Vries, Jean-Paul, de Borst, Gert, Pasterkamp, Gerard, Asselbergs, Folkert, Charchar, Fadi, Wilson, James, de Jager, Saskia, Tomaszewski, Maciej, den Ruijter, Hester

  • Authors: Haitjema, Saskia , van Setten, Jessica , Eales, James , van der Laan, Sander , Gandin, Ilaria , de Vries, Jean-Paul , de Borst, Gert , Pasterkamp, Gerard , Asselbergs, Folkert , Charchar, Fadi , Wilson, James , de Jager, Saskia , Tomaszewski, Maciej , den Ruijter, Hester
  • Date: 2017
  • Type: Text , Journal article
  • Relation: Atherosclerosis Vol. 259, no. (2017), p. 114-119
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  • Description: Background and aims: Haplogroup I, a common European paternal lineage of the Y chromosome, is associated with increased risk of coronary artery disease in British men. It is unclear whether this haplogroup or any other haplogroup on the Y chromosome is associated with histological characteristics of the diseased vessel wall in other vascular manifestations of cardiovascular diseases showing a male preponderance. Methods: We examined Dutch men undergoing either carotid endarterectomy from the Athero-Express biobank (AE, n = 1217) or open aneurysm repair from the Aneurysm-Express biobank (AAA, n = 393). Upon resolving the Y chromosome phylogeny, each man was assigned to one of the paternal lineages based on combinations of single nucleotide polymorphisms of the male-specific region of the Y chromosome. We examined the associations between the Y chromosome and the histological characteristics of the carotid plaque and aneurysm wall, including lipid content, leukocyte infiltration and intraplaque haemorrhage, in all men. Results: A majority of men were carriers of either haplogroup I (AE: 28% AAA: 24%) or haplogroup R (AE: 59% AAA: 61%). We found no association between Y chromosomal haplogroups and histological characteristics of plaque collected from carotid arteries or tissue specimens of aneurysms. Moreover, the distribution of frequency for all Y chromosomal haplogroups in both cohorts was similar to that of a general population of Dutch men. Conclusions: Our data show that genetic variation on the Y chromosome is not associated with histological characteristics of the plaques from carotid arteries or specimens of aneurysms in men of Dutch origin. © 2017 Elsevier B.V.