Myocardial injury and coronary microvascular disease in sickle cell disease

Kaur, Kiranveer; Huang, Ying; Raman, Subha V.; Kraut, Eric H.; Desai, Payal

doi:10.3324/haematol.2020.271254

Cited by 7 publications

(11 citation statements)

References 13 publications

(14 reference statements)

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“…One hypothesis stresses the potential role of repeated microvascular ischaemic events related to sickling 8,9 . However, there is scarce evidence of microvascular myocardial injury linked to sickling in clinical studies 10 . If significant, these sickling‐induced ischaemic events should induce contractile dysfunction and an increase in the most sensitive laboratory indicators of acute myocardial ischaemia during vaso‐occlusive crises.…”

Section: Introductionmentioning

confidence: 99%

“…In a recent retrospective study in a subset of 22 patients with SCD, Kaur et al. found that elevated troponin I predicted the presence of cardiomyopathy with a sensitivity of 88% and specificity of 57% using cardiac magnetic resonance imaging as the gold standard 10 …”

Section: Introductionmentioning

confidence: 99%

“…In a recent retrospective study in a subset of 22 patients with SCD, Kaur et al found that elevated troponin I predicted the presence of cardiomyopathy with a sensitivity of 88% and specificity of 57% using cardiac magnetic resonance imaging as the gold standard. 10 Left ventricular global longitudinal strain (LVGLS) is more sensitive than LVEF in detection of impairment of LV systolic function, and it is now a widely accessible technique to evaluate LV function with high reproducibility. 13 Impaired microvascular function and microvascular obstruction after myocardial infarction are associated with LVGLS decreases in the general population.…”

mentioning

confidence: 99%

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Left ventricular global longitudinal strain and acute myocardial injury in patients with sickle cell disease admitted to the intensive care unit for vaso‐occlusive crisis

Roger,

Denormandie,

Gobe

et al. 2024

Br J Haematol

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SummaryIn patients with sickle cell disease (SCD), SCD‐related cardiomyopathy may be partly due to repeated ischaemic events related to sickling during vaso‐occlusive crises, but few clinical studies support this hypothesis. We evaluated the incidence of acute myocardial ischaemia during vaso‐occlusive crises as assessed by the left ventricular global longitudinal strain (LVGLS) and high‐sensitive cardiac troponin T (hs‐cTnT). We included adult patients with SCD admitted to the intensive care unit (ICU) for vaso‐occlusive crisis. We collected hs‐cTnT and measured LVGLS with echocardiography at admission (day 1), day 2, day 3 and ICU discharge. Among 55 patients included, considering only the first hospitalization of patients admitted several times, 3 (5%) had elevated hs‐cTnT at ≥1 time point of the ICU stay. It was ≤2 times the upper limit of normal in two of these patients. LVGLS was altered at ≥1 time point of the ICU stay in 13 (24%) patients. Both hs‐cTnT and LVGLS were abnormal at ≥1 time point of the hospital stay in 2 (4%) patients. Acute myocardial injury as assessed by troponin elevation and LVGLS impairment was a rare event during vaso‐occlusive crises.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Left ventricular global longitudinal strain and acute myocardial injury in patients with sickle cell disease admitted to the intensive care unit for vaso‐occlusive crisis

Roger,

Denormandie,

Gobe

et al. 2024

Br J Haematol

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“…Nosso grupo de pacientes classificados com escores de alto risco era relativamente baixo e esse efeito pode ter sido perdido.Seria interessante a avaliação de grupos maiores para verificar a possibilidade da utilização desse biomarcador na estimativa de gravidade. Kaur e cols255 . realizaram um estudo retrospectivo e mostraram uma correlação entre os níveis de troponina I e as alterações da perfusão miocárdica na RM.…”

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“…O corte normal foi inferior a 0,6 ng/ml. Em sete casos a troponina I foi positiva (15,9%).Nlemadim255 , estudando crianças com DF na Nigéria, encontrou elevação da troponina T em 17,6% das crianças em estado de equilíbrio. Houve detecção de Troponina T em 82,4% dos pacientes durante crise vaso-oclusiva e foi com alterações eletrocardiográficas sugestivas de isquemia miocárdica.…”

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Biomarcadores cardíacos em pacientes adultos com doenças falciformes

Fonseca¹

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À professora Sandra Fátima Menosi Gualandro, pela enorme paciência e carinho. Você sempre será um exemplo pessoal de integridade e dedicação. Nosso ambulatório só existe pela sua visão e persistência.À Daniela Menosi Gualandro, uma pessoa, médica e pesquisadora brilhante, agradeço pela ideia inicial do trabalho e pelo suporte nas dúvidas e nas análises.Ao Professor Vanderson Rocha, a excelência científica e o currículo incomparável escondem o seu grande diferenciala noção de que cada vida importa, que cada paciente que perdemos não é uma derrota mas sim uma pergunta a ser respondida.Ao Professor Rogério de Souza, pelos conselhos e auxílio em momentos tão difíceis. Não existe limite para seu sucesso e isso é resultado de sua inteligência e dedicação.À Professora Vera Maria Cury Salemi. Pela imensa disponibilidade, generosidade e carinho. Você não titubeou um instante em me auxiliar.Ao Professor Bruno Caramelli pelo apoio irrestrito e auxílio na parte técnica e administrativa Ao Renato de Aguiar Hortegal, pela ajuda na realização dos ecocardiogramas. Sua dedicação, conhecimento e disponibilidade são impressionantes.À Camila Rocon de Lima Andreta. Não tivemos contato pessoal, mas em cada conversa ou mensagem conheci uma pessoa que empenhou seu precioso tempo e conhecimento me auxiliando na leitura dos ecocardiogramas. Não há como recompensar, só agradecer imensamente.Ao Marcelo Dantas Tavares de Melo, pelo auxílo na leitura dos ecocardiogramas e pelas ideias de análise.A Iara Keiko Yokomizo, pelo auxílio na coleta, preservação e organização das amostras. Além da competência que todos conhecem você sempre me auxiliou com o seu carinho e palavras de incentivo.

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CRISPR technology in human diseases

Feng,

Li,

Zhou

et al. 2024

MedComm

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Gene editing is a growing gene engineering technique that allows accurate editing of a broad spectrum of gene‐regulated diseases to achieve curative treatment and also has the potential to be used as an adjunct to the conventional treatment of diseases. Gene editing technology, mainly based on clustered regularly interspaced palindromic repeats (CRISPR)–CRISPR‐associated protein systems, which is capable of generating genetic modifications in somatic cells, provides a promising new strategy for gene therapy for a wide range of human diseases. Currently, gene editing technology shows great application prospects in a variety of human diseases, not only in therapeutic potential but also in the construction of animal models of human diseases. This paper describes the application of gene editing technology in hematological diseases, solid tumors, immune disorders, ophthalmological diseases, and metabolic diseases; focuses on the therapeutic strategies of gene editing technology in sickle cell disease; provides an overview of the role of gene editing technology in the construction of animal models of human diseases; and discusses the limitations of gene editing technology in the treatment of diseases, which is intended to provide an important reference for the applications of gene editing technology in the human disease.

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Myocardial injury and coronary microvascular disease in sickle cell disease

Abstract: Not available.

Cited by 7 publications

References 13 publications

Left ventricular global longitudinal strain and acute myocardial injury in patients with sickle cell disease admitted to the intensive care unit for vaso‐occlusive crisis

Left ventricular global longitudinal strain and acute myocardial injury in patients with sickle cell disease admitted to the intensive care unit for vaso‐occlusive crisis

Biomarcadores cardíacos em pacientes adultos com doenças falciformes

CRISPR technology in human diseases

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