1. |
|
|
2. |
|
|
3. |
|
|
4. |
|
|
5. |
|
|
6. |
|
|
7. |
- Schuermans, A., et al.
(författare)
-
Exercise in patients with repaired tetralogy of Fallot: a systematic review and meta-analysis
- 2023
-
Ingår i: Heart. - : BMJ. - 1355-6037 .- 1468-201X. ; 109:13, s. 984-991
-
Forskningsöversikt (refereegranskat)abstract
- ObjectiveChildren and adults with repaired tetralogy of Fallot (rTOF) have an impaired exercise capacity, a less active lifestyle and an increased long-term risk of adverse outcomes compared with healthy peers. This study aimed to summarise the current evidence for the effectiveness and safety of exercise training interventions in patients with rTOF. MethodsPubMed/MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials (CENTRAL), Web of Science, Scopus and reference lists of relevant articles were searched for prospective studies published by November 2021. Random-effects meta-analysis and descriptive synthesis were performed to assess the effectiveness and safety of exercise training in patients with rTOF. ResultsOf the 9677 citations identified, 12 articles were included that reported on 10 unique studies and covered 208 patients with rTOF (range of mean/median age: 7.4-43.3 years). All studies implemented 2 to 7 aerobic or respiratory training sessions per week with durations ranging from 6 to 26 weeks. Meta-analysis of the included randomised controlled trials showed that exercise training was associated with a significant improvement in peak VO2 (pooled mean difference: +3.1 mL/min/kg; 95% CI: 0.76 to 5.36 mL/min/kg, p=0.019). Cardiac imaging studies revealed no subclinical adverse remodelling after the exercise interventions. No serious adverse events including arrhythmias were reported in these studies. ConclusionCurrent evidence suggests that exercise training can improve exercise capacity in patients with rTOF with a low risk for adverse events. Exercise prescription may be a safe and effective tool to help improving outcomes in patients with rTOF. PROSPERO registration numberCRD42021292809.
|
|
8. |
|
|
9. |
|
|
10. |
- Gumuser, Esra D., et al.
(författare)
-
Clonal Hematopoiesis of Indeterminate Potential Predicts Adverse Outcomes in Patients With Atherosclerotic Cardiovascular Disease
- 2023
-
Ingår i: Journal of the American College of Cardiology. - 0735-1097. ; 81:20, s. 1996-2009
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Clonal hematopoiesis of indeterminate potential (CHIP)—the age-related clonal expansion of blood stem cells with leukemia-associated mutations—is a novel cardiovascular risk factor. Whether CHIP remains prognostic in individuals with established atherosclerotic cardiovascular disease (ASCVD) is less clear. Objectives: This study tested whether CHIP predicts adverse outcomes in individuals with established ASCVD. Methods: Individuals aged 40 to 70 years from the UK Biobank with established ASCVD and available whole-exome sequences were analyzed. The primary outcome was a composite of ASCVD events and all-cause mortality. Associations of any CHIP (variant allele fraction ≥2%), large CHIP clones (variant allele fraction ≥10%), and the most commonly mutated driver genes (DNMT3A, TET2, ASXL1, JAK2, PPM1D/TP53 [DNA damage repair genes], and SF3B1/SRSF2/U2AF1 [spliceosome genes]) with incident outcomes were compared using unadjusted and multivariable-adjusted Cox regression. Results: Of 13,129 individuals (median age: 63 years) included, 665 (5.1%) had CHIP. Over a median follow-up of 10.8 years, any CHIP and large CHIP at baseline were associated with adjusted HRs of 1.23 (95% CI: 1.10-1.38; P < 0.001) and 1.34 (95% CI: 1.17-1.53; P < 0.001), respectively, for the primary outcome. TET2 and spliceosome CHIP, especially large clones, were most strongly associated with adverse outcomes (large TET2 CHIP: HR: 1.89; 95% CI: 1.40-2.55; P <0.001; large spliceosome CHIP: HR: 3.02; 95% CI: 1.95-4.70; P < 0.001). Conclusions: CHIP is independently associated with adverse outcomes in individuals with established ASCVD, with especially high risks observed in TET2 and SF3B1/SRSF2/U2AF1 CHIP.
|
|