5 research outputs found

    Atrial Mechanics in Hypertrophic Cardiomyopathy: Discriminating between Ventricular Hypertrophy and Fibrosis

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    Fundamento: A cardiomiopatia hipertrĂłfica (CMH) e a hipertrofia ventricular esquerda (HVE) secundĂĄria Ă  hipertensĂŁo arterial sistĂȘmica (HAS) podem estar associadas a anormalidades funcionais do ĂĄtrio esquerdo (AE). Objetivos: Caracterizar a mecĂąnica do AE na CMH e na HAS e avaliar qualquer correlação com a extensĂŁo da fibrose ventricular esquerda medida por ressonĂąncia magnĂ©tica cardĂ­aca (RMC) em pacientes com CMH. MĂ©todos: A função longitudinal do AE derivada do ecocardiograma bidimensional com speckle tracking foi adquirida a partir de cortes apicais de 60 pacientes com CMH e 34 indivĂ­duos controles, pareados por idade. Pacientes com CMH tambĂ©m foram submetidos Ă  RMC, com medida da extensĂŁo do realce tardio por gadolĂ­nio. A associação com parĂąmetros de strain do AE foi analisada. Valores p < 0,05 foram definidos como estatisticamente significativos. Resultados: A mĂ©dia da fração de ejeção do ventrĂ­culo esquerdo nĂŁo foi diferente entre os grupos. A razĂŁo E/e’ estava comprometida no grupo CMH e preservada no grupo controle. A mecĂąnica do AE estava significativamente reduzida na CMH em comparação aos pacientes com HAS. O strain rate do AE nas fases de reservatĂłrio (SRrAE) e na fase contrĂĄtil (SRctAE) foram os melhores parĂąmetros de discriminação de CMH com uma ĂĄrea sob a curva (AUC) de 0,8, seguido do strain do AE na fase de reservatĂłrio (SrAE) (AUC 0,76). O SRrAE e o SRctAE apresentaram elevada especificidade (89% e 91%, respectivamente), e o SrAE apresentou sensibilidade de 80%. Um decrĂ©scimo de 2,79% no strain rate do AE na fase de condução (SRcdAE) foi preditor de um aumento de 1 cm na extensĂŁo do RT pelo gadolĂ­nio (r2=0,42, ÎČ 2,79, p=0,027). ConclusĂ”es: O SRrAE e o SRctAE foram os melhores fatores de discriminação de HVE secundĂĄria Ă  CMH. O SRcdAE foi preditor do grau de fibrose ventricular esquerda avaliada por RMC. Esses achados sugerem que a mecĂąnica do AE pode ser um potencial preditor de gravidade de doença na CMH.Background: Hypertrophic cardiomyopathy (HCM) and left ventricular hypertrophy (LVH) secondary to systemic hypertension (HTN) may be associated with left atrial (LA) functional abnormalities. Objectives: We aimed to characterize LA mechanics in HCM and HTN and determine any correlation with the extent of left ventricular (LV) fibrosis measured by cardiac magnetic resonance (CMR) in HCM patients. Methods: Two-dimensional speckle tracking-derived longitudinal LA function was acquired from apical views in 60 HCM patients, 60 HTN patients, and 34 age-matched controls. HCM patients also underwent CMR, with measurement of late gadolinium enhancement (LGE) extension. Association with LA strain parameters was analyzed. Statistical significance was set at p<0.05. Results: Mean LV ejection fraction was not different between the groups. The E/e’ ratio was impaired in the HCM group and preserved in the control group. LA mechanics was significantly reduced in HCM, compared to the HTN group. LA strain rate in reservoir (LASRr) and in contractile (LASRct) phases were the best discriminators of HCM, with an area under the curve (AUC) of 0.8, followed by LA strain in reservoir phase (LASr) (AUC 0.76). LASRr and LASR-ct had high specificity (89% and 91%, respectively) and LASr had sensitivity of 80%. A decrease in 2.79% of LA strain rate in conduit phase (LASRcd) predicted an increase of 1cm in LGE extension (r2=0.42, ÎČ 2.79, p=0.027). Conclusions: LASRr and LASRct were the best discriminators for LVH secondary to HCM. LASRcd predicted the degree of LV fibrosis assessed by CMR. These findings suggest that LA mechanics is a potential predictor of disease severity in HCM

    Evaluation of a quality improvement intervention to reduce anastomotic leak following right colectomy (EAGLE): pragmatic, batched stepped-wedge, cluster-randomized trial in 64 countries

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    Background Anastomotic leak affects 8 per cent of patients after right colectomy with a 10-fold increased risk of postoperative death. The EAGLE study aimed to develop and test whether an international, standardized quality improvement intervention could reduce anastomotic leaks. Methods The internationally intended protocol, iteratively co-developed by a multistage Delphi process, comprised an online educational module introducing risk stratification, an intraoperative checklist, and harmonized surgical techniques. Clusters (hospital teams) were randomized to one of three arms with varied sequences of intervention/data collection by a derived stepped-wedge batch design (at least 18 hospital teams per batch). Patients were blinded to the study allocation. Low- and middle-income country enrolment was encouraged. The primary outcome (assessed by intention to treat) was anastomotic leak rate, and subgroup analyses by module completion (at least 80 per cent of surgeons, high engagement; less than 50 per cent, low engagement) were preplanned. Results A total 355 hospital teams registered, with 332 from 64 countries (39.2 per cent low and middle income) included in the final analysis. The online modules were completed by half of the surgeons (2143 of 4411). The primary analysis included 3039 of the 3268 patients recruited (206 patients had no anastomosis and 23 were lost to follow-up), with anastomotic leaks arising before and after the intervention in 10.1 and 9.6 per cent respectively (adjusted OR 0.87, 95 per cent c.i. 0.59 to 1.30; P = 0.498). The proportion of surgeons completing the educational modules was an influence: the leak rate decreased from 12.2 per cent (61 of 500) before intervention to 5.1 per cent (24 of 473) after intervention in high-engagement centres (adjusted OR 0.36, 0.20 to 0.64; P &lt; 0.001), but this was not observed in low-engagement hospitals (8.3 per cent (59 of 714) and 13.8 per cent (61 of 443) respectively; adjusted OR 2.09, 1.31 to 3.31). Conclusion Completion of globally available digital training by engaged teams can alter anastomotic leak rates. Registration number: NCT04270721 (http://www.clinicaltrials.gov)
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