British Heart Journal最新文献

{"title":"Intensive care of adults with congenital heart disease","authors":"P. Guedes Ramallo, L. Dos-Subirà","doi":"10.1136/heartjnl-2022-320926","DOIUrl":"https://doi.org/10.1136/heartjnl-2022-320926","url":null,"abstract":"Congenital heart diseases (CHD) are a variety of heart conditions that afflict an increasing number of adults. Significant advances in paediatric cardiology and paediatric cardiac surgery over the past decades have modified mortality trends and currently nearly 90% of children born with these defects reach adulthood. As a result, there are nowadays more adults than children living with CHD. However, these are repaired hearts with residual lesions that may require subsequent interventions over time and that are exposed to longterm complications, predominantly arrhythmias and heart failure. Moreover, the particular physiology of some CHD has a multisystemic impact that may lead to complications in organs far from the heart. Some of these cardiovascular and noncardiovascular complications are lifethreatening and require intensive care unit (ICU) admission. Such is the case of severe arrhythmias, acute pulmonary oedema, haemoptysis due to major aortopulmonary collateral arteries, acute cholecystitis due to gallstones in patients with cyanosis, infective endocarditis or stroke, among others. Approximately 16% of patients with adult congenital heart disease (ACHD) will require an ICU admission by the age of 40, particularly those with more complex forms of CHD. Management of these patients during this critical situation is challenging and requires a complete understanding of the anatomy, physiology and associated comorbidities to tailor an individualised approach that achieves the optimal care.","PeriodicalId":9311,"journal":{"name":"British Heart Journal","volume":"108 1","pages":"1424 - 1425"},"PeriodicalIF":0.0,"publicationDate":"2022-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41620222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Representation of women in heart failure trials: does it matter?","authors":"P. Parwani, H. V. Van Spall, M. Mamas","doi":"10.1136/heartjnl-2022-321094","DOIUrl":"https://doi.org/10.1136/heartjnl-2022-321094","url":null,"abstract":"Heart failure (HF) is a leading cause of hospitalisation, morbidity, and mortality in men and women, accounting for 46 076 annual HF deaths in women and 2.6 million women living with HF between 2015 and 2018 in the USA. Sex differences across the HF spectrum are well defined and pertain to risk factors, aetiology, provision of evidencebased therapies, referral to services, treatment response and clinical outcomes in both the acute and chronic HF syndrome setting. Much of our evidence base for the management of HF is derived from randomised clinical trials (RCTs) that inform best practice for the treatment of HF and shape guideline recommendations. The value of such trials in informing the management of HF in both men and women depends on representativeness of trial populations. Underenrolment of women in HF trials is well documented, including in landmark trials that have informed care. Since 2000, multiple studies have examined the recruitment of women in HF RCTs and reported that enrolment of women has varied between 21% and 29%, which is significantly below the prevalence of HF at the population level. In an attempt to quantify the representativeness in trials, recent studies have used the ratio of trial participation to disease prevalence ratio (PPR). A PPR <0.8 is considered low and indicates underrepresentation. A recent analysis of 740 cardiovascular trials (102 trials in HF) registered between 2010 and 2017 has shown the lowest PPR of 0.48 in HF trials. This is despite the fact that legislature such as the National Institutes of Health Revitalization Act stipulates the inclusion of women and men in clinical trials proportionate to the sexrelated prevalence of the disease under investigation, to provide data on the treatment effect of interventions/treatments studied in both women and men. Recent studies have tried to understand the factors responsible for low enrolment of women in HF trials. The low enrolment rates of women in cardiovascular clinical trials have historically been attributed to agerecruitment bias since cardiovascular disease is seen predominantly in older women. However, recent multivariable analyses have revealed trial characteristics such as ambulatory recruitment, sexspecific exclusion criteria, drug, device and surgical interventions, exclusively male trial leadership and trial coordination in North America, Europe and Asia to be independently associated with underenrolment of women in HFrEF RCTs. Moreover, poor awareness of HF trials, concerns around greater perceived risks from trial participation and childcare responsibilities have been reported as additional barriers to more equitable participation of women in clinical trials. It is important to highlight that randomised control trials led by women have greater odds of enrolling a representative sample of women and women steering committee members. 8 9 In the present study, Morgan et al have undertaken a systemic review of HF trials published in seven highimpact c","PeriodicalId":9311,"journal":{"name":"British Heart Journal","volume":"108 1","pages":"1508 - 1509"},"PeriodicalIF":0.0,"publicationDate":"2022-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45106748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early and long-term outcomes of conventional and valve-sparing aortic root replacement","authors":"M. Jahangiri, K. Mani, M. Acharya, R. Bilkhu, Paul Quinton, F. Schroeder, R. Morgan, M. Edsell","doi":"10.1136/heartjnl-2022-320870","DOIUrl":"https://doi.org/10.1136/heartjnl-2022-320870","url":null,"abstract":"Objective To determine the early and long-term outcomes of conventional aortic root (ARR) and valve-sparing root replacement (VSRR) using a standard perioperative and operative approach. Methods We present prospectively collected data of 609 consecutive patients undergoing elective and urgent aortic root surgery (470 ARR, 139 VSRR) between 2006 and 2020. Primary outcomes were operative mortality and incidence of postoperative complications. Secondary outcomes were long-term survival and requirement for reintervention. Median follow-up was 7.6 years (range 0.5–14.5). Results 189 patients (31%) had bicuspid aortic valves and 17 (6.9%) underwent redo procedures. Median cross-clamp time was 88 (range 54–208) min with cardiopulmonary bypass of 108 (range 75–296) min. In-hospital mortality was 10 (1.6%), with transient ischaemic attacks/strokes occurring in 1.1%. In-hospital mortality for VSRR was 0.7%. 12 patients (2.0%) required a resternotomy for bleeding and 14 (2.3%) received haemofiltration. Intensive care unit and hospital stay were 1.7 and 7.0 days, respectively. During follow-up, redo surgery for native aortic valve replacement was required in 1.4% of the VSRR group. Overall survival was 95.1% at 3 years, 93.1% at 5 years, 91.2% at 7 years and 88.6% at 10 years. Conclusions ARR and VSRR can be performed with low mortality and morbidity as well as a low rate of reintervention during the period of long-term follow-up, if performed by an experienced team with a consistent perioperative approach. This series provides contemporary evidence to balance the risks of aortic aneurysms and their rupture at diameters of <5.5 cm against the risks and benefits of surgery.","PeriodicalId":9311,"journal":{"name":"British Heart Journal","volume":"108 1","pages":"1858 - 1863"},"PeriodicalIF":0.0,"publicationDate":"2022-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44769496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How electrically silent is the pericardium?","authors":"Y. Birnbaum, B. Uretsky","doi":"10.1136/heartjnl-2021-320728","DOIUrl":"https://doi.org/10.1136/heartjnl-2021-320728","url":null,"abstract":"Acute pericarditis is a clinical inflamma-tory syndrome. The diagnosis is made when at least two of the following four criteria are present: (1) characteristic chest pain; (2) presence of pericardial friction rub; (3) ECG changes (up to 60% of patients); and (4) pericardial effusion (detected by imaging techniques in up to 60% of patients). 1 While it is commonly believed that diffuse ST segment elevation with concomitant ST depression in lead aVR (and V1) and with PR segment depression is typically detected in patients with acute pericarditis, this classic pattern is seen in less than 60% of patients. For example, Imazio et al 2 reported ST segment elevation in only 25% of their cohort of 240 patients with pericarditis. The classic ECG findings are seen mainly in the early phase (stage 1) of acute pericarditis and typically persist up to 2 weeks after symptom onset. 3 Later on, ST segment elevation resolves, and T waves become flat or inverted. These changes can persist for several weeks until complete resolution (stage 4). 3 However, it should be noted that similar ECG pattern with PR segment depression, diffuse ST elevation and ST depression in aVR can be seen with ‘early repolarisation’. 4 Thus, it could be that in some patients overdiag-nosis of acute pericarditis is made if diagnosis relies on the ECG in the presence of chest pain (that can be due to other aetiologies). the considered to be electric silent, inflammation limited to the not result in ST segment deviation. 1 3 Concomitant the 1 in","PeriodicalId":9311,"journal":{"name":"British Heart Journal","volume":"108 1","pages":"1428 - 1429"},"PeriodicalIF":0.0,"publicationDate":"2022-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49155240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fractional flow reserve versus angiography alone in guiding myocardial revascularisation: a systematic review and meta-analysis of randomised trials","authors":"A. Elbadawi, Ramy Sedhom, Alexander T. Dang, M. Gad, Faisal Rahman, E. Brilakis, I. Elgendy, H. Jneid","doi":"10.1136/heartjnl-2021-320768","DOIUrl":"https://doi.org/10.1136/heartjnl-2021-320768","url":null,"abstract":"Background Randomised trials evaluating the efficacy and safety of fractional flow reserve (FFR)-guided versus angiography-guided revascularisation among patients with obstructive coronary artery disease (CAD) have yielded mixed results. Aims To examine the comparative efficacy and safety of FFR-guided versus angiography-guided revascularisation among patients with obstructive CAD. Methods An electronic search of MEDLINE, SCOPUS and Cochrane databases without language restrictions was performed through November 2021 for randomised controlled trials that evaluated the outcomes of FFR-guided versus angiography-guided revascularisation. The primary outcome was major adverse cardiac events (MACE). Data were pooled using a random-effects model. Results The final analysis included seven trials with 5094 patients. The weighted mean follow-up duration was 38 months. Compared with angiography guidance, FFR guidance was associated with fewer number of stents during revascularisation (standardised mean difference=−0.80; 95% CI −1.33 to −0.27), but no difference in total hospital cost. There was no difference between FFR-guided and angiography-guided revascularisation in long-term MACE (13.6% vs 13.9%; risk ratio (RR) 0.97, 95% CI 0.85 to 1.11). Meta-regression analyses did not reveal any evidence of effect modification for MACE with acute coronary syndrome (p=0.36), proportion of three-vessel disease (p=0.88) or left main disease (p=0.50). There were no differences between FFR-guided and angiography-guided revascularisation in the outcomes all-cause mortality (RR 1.16, 95% CI 0.80 to 1.68), cardiovascular mortality (RR 1.27, 95% CI 0.50 to 3.26), repeat revascularisation (RR 0.99, 95% CI 0.81 to 1.21), recurrent myocardial infarction (RR 0.92, 95% CI 0.74 to 1.14) or stent thrombosis (RR 0.61, 95% CI 0.31 to 1.21). Conclusion Among patients with obstructive CAD, FFR-guided revascularisation did not reduce the risk of long-term adverse cardiac events or the individual outcomes. However, FFR-guided revascularisation was associated with fewer number of stents. PROSPERO registration number CRD42021291596.","PeriodicalId":9311,"journal":{"name":"British Heart Journal","volume":"108 1","pages":"1699 - 1706"},"PeriodicalIF":0.0,"publicationDate":"2022-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45164903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heartbeat: can cardiogenetics reduce adverse events due to catecholaminergic polymorphic ventricular tachycardia?","authors":"C. Otto","doi":"10.1136/heartjnl-2022-321248","DOIUrl":"https://doi.org/10.1136/heartjnl-2022-321248","url":null,"abstract":"genetic diagnosis of in in","PeriodicalId":9311,"journal":{"name":"British Heart Journal","volume":"108 1","pages":"816 - 818"},"PeriodicalIF":0.0,"publicationDate":"2022-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45575115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The British Cardiovascular Society Centenary Conference, 6–8 June 2022: the Vice President’s message","authors":"G. Ng","doi":"10.1136/heartjnl-2022-321317","DOIUrl":"https://doi.org/10.1136/heartjnl-2022-321317","url":null,"abstract":"","PeriodicalId":9311,"journal":{"name":"British Heart Journal","volume":"108 1","pages":"813 - 815"},"PeriodicalIF":0.0,"publicationDate":"2022-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"63983865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Man with recent myocardial infarction and heart failure","authors":"Dinkar Bhasin, Rahul Kumar, S. Bansal","doi":"10.1136/heartjnl-2022-320808","DOIUrl":"https://doi.org/10.1136/heartjnl-2022-320808","url":null,"abstract":"ryanodine receptor mutationcarrying relatives. Circ Arrhythm Electrophysiol 2012;5:748–56. 13 Sumitomo N, Harada K, Nagashima M, et al. Catecholaminergic polymorphic ventricular tachycardia: electrocardiographic characteristics and optimal therapeutic strategies to prevent sudden death. Heart 2003;89:66–70. 14 Ohno S, Hasegawa K, Horie M. Gender differences in the inheritance mode of RyR2 mutations in catecholaminergic polymorphic ventricular tachycardia patients. PLoS One 2015;10:e0131517. 15 Ackerman MJ, Priori SG, Willems S, et al. HRS/EHRA expert consensus statement on the state of genetic testing for the channelopathies and cardiomyopathies this document was developed as a partnership between the heart rhythm Society (HRS) and the European heart rhythm association (EHRA). Heart Rhythm 2011;8:1308–39. 16 Schwartz PJ. Cascades or waterfalls, the cataracts of genetic screening are being opened on clinical cardiology. J Am Coll Cardiol 2010;55:2577–9. 17 Richards S, Aziz N, Bale S, et al. Standards and guidelines for the interpretation of sequence variants: a joint consensus recommendation of the American College of medical genetics and genomics and the association for molecular pathology. Genet Med 2015;17:405–24. 18 Kawata H, Ohno S, Aiba T, et al. Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) Associated With Ryanodine Receptor (RyR2) Gene Mutations LongTerm Prognosis After Initiation of Medical Treatment. Circ J 2016;80:1907–15. 19 Rijnbeek PR, Witsenburg M, Schrama E, et al. New normal limits for the paediatric electrocardiogram. Eur Heart J 2001;22:702–11. 20 Rijnbeek PR, van Herpen G, Bots ML, et al. Normal values of the electrocardiogram for ages 1690 years. J Electrocardiol 2014;47:914–21. 21 Priori SG, Napolitano C, Memmi M, et al. Clinical and molecular characterization of patients with catecholaminergic polymorphic ventricular tachycardia. Circulation 2002;106:69–74. 22 Priori SG, Chen SRW. Inherited dysfunction of sarcoplasmic reticulum Ca2+ handling and arrhythmogenesis. Circ Res 2011;108:871–83. 23 MedeirosDomingo A, Bhuiyan ZA, Tester DJ, et al. The RYR2encoded ryanodine receptor/calcium release channel in patients diagnosed previously with either catecholaminergic polymorphic ventricular tachycardia or genotype negative, exerciseinduced long QT syndrome: a comprehensive open reading frame mutational analysis. J Am Coll Cardiol 2009;54:2065–74. 24 Kanda Y. Investigation of the freely available easytouse software ’EZR’ for medical statistics. Bone Marrow Transplant 2013;48:452–8. 25 Leinonen JT, Crotti L, Djupsjöbacka A, et al. The genetics underlying idiopathic ventricular fibrillation: a special role for catecholaminergic polymorphic ventricular tachycardia? Int J Cardiol 2018;250:139–45. 26 Nesta AV, Tafur D, Beck CR. Hotspots of human mutation. Trends Genet 2021;37:30276–6. 27 Roston TM, Vinocur JM, Maginot KR, et al. Catecholaminergic polymorphic ventricular tachycardia in children: analysis of therapeutic strat","PeriodicalId":9311,"journal":{"name":"British Heart Journal","volume":"108 1","pages":"847 - 898"},"PeriodicalIF":0.0,"publicationDate":"2022-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41381924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Response to: Correspondence on 'Cost-effectiveness of transcatheter edge-to-edge repair in secondary mitral regurgitation does need confirmation' by Armoiry and Connock","authors":"M. Garbi, Alfredo Mariani","doi":"10.1136/heartjnl-2022-321181","DOIUrl":"https://doi.org/10.1136/heartjnl-2022-321181","url":null,"abstract":"We read with interest the response of Armoiry and Connock to our editorial and to the Cohen et al paper it referred to. This response demonstrates the wide interest on costeffectiveness of transcatheter edgetoedge repair (TEER) in secondary mitral regurgitation. Armoiry and Connock generously conclude that the paper by Cohen et al ‘represents a valuable contribution’, although criticising it throughout the text. Regarding our editorial, we are sorry that Armoiry and Connock disagree with our statement that costeffectiveness of TEER in secondary mitral regurgitation does not need confirmation. Yet, our statement refers strictly to the UK NHS and is underpinned by the costeffectiveness analyses that informed the National Institute for Health and Care Excellence (NICE) guidelines recommendation: the NICE MitraClip model and Shore 2020. Although Armoiry and Connock state that in the UK ‘costeffectiveness is a key criterion to judge recommendation’ and although at current device cost, in the UK NHS, the incremental cost per qualityadjusted lifeyear (QALY) gained for TEER in secondary mitral regurgitation was significantly above the £20 000 threshold in both NICE analysis and Shore 2020, the NICE guidelines do recommend TEER in secondary mitral regurgitation; the recommendation (‘consider TEER’) is of similar strength with the European and American guidelines recommendation (class II). The NICE incremental cost per QALY gained threshold refers to a strong recommendation (‘offer TEER’), equivalent with a European and American recommendation class I. However, the existent clinical effectiveness evidence prevents all guidelines from making a strong recommendation. Further costeffectiveness confirmation would only be needed in case of new clinical effectiveness evidence supportive of a strong recommendation and of reduction of device cost in the UK NHS.","PeriodicalId":9311,"journal":{"name":"British Heart Journal","volume":"108 1","pages":"1073 - 1073"},"PeriodicalIF":0.0,"publicationDate":"2022-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45624687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correspondence on 'Cost-effectiveness of transcatheter edge-to-edge repair in secondary mitral regurgitation does need confirmation' by Cohen et al","authors":"X. Armoiry, M. Connock","doi":"10.1136/heartjnl-2022-321179","DOIUrl":"https://doi.org/10.1136/heartjnl-2022-321179","url":null,"abstract":"To the Editor: we have read with considerable interest the paper by Cohen et al estimating the costeffectiveness of the Mitraclip system in patients with secondary mitral regurgitation (SMR). Like other published works that adopted different healthcare perspectives, including the one by Baron et al, the costeffectiveness analysis conducted by Cohen et al was based on 2year data from the Coapt randomised controlled trial (RCT). Generating lifetime estimates of survival gain (1.57 years here) from the 2year data of Coapt requires extensive extrapolation of about 13 years beyond observed data and >95% of benefit reported in the percutaneous repair (PR) arm accrues in the extrapolation phase rather than the observation phase. The observed source data used for extrapolation can therefore exert a profound influence on estimation of gained benefit from PR. We were surprised that Cohen et al chose not to consider in their economic model the 3year data from Coapt which were released as oral presentation in 2019 and fully published in late 2020. Indeed, the 3year allcause mortality curve for the Mitraclip arm of Coapt reported by Mack et al 5 indicates a doubling in mean mortality rate in years 2–3 relative to years 1–2 (estimated using area under the curve as is done in costeffectiveness analysis). The upturn in mortality during years 2–3 in the PR arm is similarly reflected in the cumulative percentage mortality reported at years 1, 2 and 3 of 19%, 28.2% and 42.8%, respectively, that translates to a crude estimate of annual mortality rates of 19% over the first year, 9.2% over years 1–2, and 14.6% over years 2–3; an increase of 59% in rate for years 2–3 relative to years 1–2. It is therefore evident that using 3year mortality data instead of 2year will considerably influence estimated survival gains accrued in economic models. Consequently, we believe that the lifetime extrapolation beyond the observed 2year data is highly optimistic in the work by Cohen et al, particularly for the intervention arm, and that this has potential to impact the costeffectiveness in favour of the intervention. As a general principle, it would be expected that using longer rather than shorter followup results from trials is likely to reduce uncertainty in costeffectiveness estimates. This can optimise decisionmaking in territories such as the UK where costeffectiveness is a key criterion to judge recommendation of new technologies. In consequence, in our opinion, the 2year mortality data from Stone et al are likely to be unsuitable for reliable costeffectiveness analysis. Further prespecified analyses from Coapt at 4 and 5 years are eagerly awaited. Additionally, the generalisability of Cohen et al findings using US Coapt population as source of clinical inputs may be questionable since, as acknowledged by authors in the Limitation section, the inputs from the MitraFr RCT (undertaken in a French population and showing no advantage of PR relative to medical treatment alone) wer","PeriodicalId":9311,"journal":{"name":"British Heart Journal","volume":"108 1","pages":"1071 - 1071"},"PeriodicalIF":0.0,"publicationDate":"2022-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44480985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}