Microcirculation dysfunction in hypertrophic cardiomyopathy (Record no. 14342)

Metadata
000 -Etiqueta do registo
campo de controlo de comprimento fixo nam a22 4500
001 - Identificador do registo
Campo de controlo 14342
100 ## - Dados Gerais de Proc.
Dados gerais de processamento 20220311d2022 u||y0pory50 ba
200 ## - Título
Título próprio Microcirculation dysfunction in hypertrophic cardiomyopathy
Primeira menção de responsabilidade Sílvia Aguiar Oliveira Rosa
Outras menções de responsabilidade orient. Miguel Mota Carmo... [et al.]
210 ## - Publicação, Distribuição
Lugar da edição, distribuição, etc. Lisboa
Nome do editor, distribuidor, etc. NOVA Medical School, Universidade NOVA de Lisboa
Data da publicação, distribuição, etc. 2022
328 ## - Nota de dissertação ou tese
Especificações da dissertação ou tese e tipo de grau académico Tese de Doutoramento
Área cientifica do grau académico Medicina, Investigação Clínica
Ano do grau académico 2022
Instituição que confere o grau académico Faculdade de Ciências Médicas, Universidade NOVA de Lisboa
330 ## - Sumário ou Resumo
Texto da nota Background:Hypertrophic cardiomyopathy (HCM) is defined by the presence of left ventricular(LV)hypertrophy that cannot be solely explained by an increased afterload. The pathophysiologic mechanisms of this disease include coronary microvascular dysfunction and ischemia. The microvascular dysfunction is multifactorial, including reduced capillary density and vascular remodelling, fibrosis, myocyte disarray, and extravascular compression. Chronic and recurrent myocardial ischemia leads to fibrosis, which may culminate in myocardial dysfunction. Despite the recognition of microvascular dysfunction in HCM, further investigation is needed to delineate the interrelationships between microvascular dysfunction,fibrosis and prognosis.Objectives:The present research aimed to study the coronary microvascular dysfunctionin HCM using a multimodality approach, in order to identify predictors of microvascular dysfunction and to assess the association between microvascular dysfunction withtissue abnormalities and clinical manifestations. Methods:This prospective study enrolled83adult patients with HCM,withoutobstructiveepicardial coronary artery disease, submitted to the assessment of coronary microcirculation by:Echocardiography to evaluatecoronary flow velocity reserve (CFVR)(normal cut-off value ≥2.0), during adenosine-induced hyperemia;CMRto assess the ischemic burden by perfusion imaging during regadenoson-induced hyperemia;Cardiac catheterization to determine index of microcirculatory resistance(IMR)(normal cut-off value ≤22.0) and coronaryflow reserve (CFR) (normal cut-off value ≥2.0), during adenosine-induced hyperemia.Echocardiographic protocol included the assessment of myocardial deformation by two-dimensional(2D)longitudinal strain and three-dimensional(3D)longitudinal, circumferential and radial strain, area strain, torsion and twist.CMR protocol also included parametric mapping(to assess native T1, extracellular volume (ECV) and T2), late gadolinium enhancement (LGE) and three-dimensional longitudinal, circumferential and radial strains analysis.12-lead electrocardiogram, 24 hours Holter recording and cardiopulmonary exercise testing (CPET) were performed to assess arrhythmias and functional capacity. Results:EchocardiographyEighty-three patients underwent echocardiographic study. Mean age 55.0(14.4)years,50(60%)patientswere male; 59(71%) had nonobstructive HCM.CFVRin the left anterior descending artery(LAD)was 1.81(0.49) and CFVRin the posterior descending(PD)was 1.73(0.55); CFVR LAD was <2.0in 49(59%)patients and CFVR PD was <2.0in 43(52%).Greater LV maximum wall thickness (MWT) (β-estimate: -0.040, 95%CI: -0.071;-0.010, p=0.010) and female gender (β-estimate: -0.379, 95%CI: -0.640;-0.118, p=0.005)were independently associated with impaired CFVR.Lower CFVR PD was associated with impaired global longitudinal strain (GLS)2D (β-estimate: -3.240,95%CI: -4.634;-1.846, p<0.001), GLS 3D (β-estimate:-2.559,95%CI:-3.932;-1.186, p<0.001) and area strain (β-estimate: -3.044, 95%CI: -5.373;-0.716, p=0.011).Lower values of CFVR PD were relatedtoworsemyocardialglobal work index(β-estimate:267.824,95%CI: 75.964;459.683,p=0.007);global constructive work(β-estimate:217.300,95%CI: 38.750;395.850,p=0.018) and global work efficiency(β-estimate:5.656,95%CI:2.229;9.084, p=0.002).Impaired CFVR LAD (β-estimate:2.826, 95%CI:0.913;4.739,p=0.004) and CFVR PD (β-estimate:2.801,95%CI:0.657;4.945,p=0.011) were found to be associated with lowertricuspid annular plane systolic excursion. Lowervalues of CFVRLAD (β-estimate:2.580, 95%CI:0.169;4.991,p=0.036)and CFVR PD (β-estimate:3.163, 95%CI:0.721;5.606,p=0.012)were associated with worsepeak oxygen uptakein CPET.Cardiovascular magnetic resonanceSeventy-five patients underwent CMR,meanage 54.6(14.8) years, 47(63%) males, 51(68%)patients had nonobstructive HCM, MWTwas 20.2(4.6)mm andLV ejection fraction 71.6(8.3)%. Perfusion defect in at least in one segment was noted in 68 (91%) patients and ischemic burden was 22.5(16.9)% of LV. Greater MWT was associated with the severity of ischemia (β-estimate:1.353,95%CI:0.182,2.523,p<0.024). Ischemic burden wasassociated with higher values of native T1 (β-estimate:9.018,95%CI:4.721,13.315,p<0.001). The association between ischemia and LGE was significant in subgroup analysis: MWT 15-20mm (β-estimate:1.941,95%CI:0.738,3.143,p=0.002), nonobstructive HCM (β-estimate:1.471, 95%CI:0.258,2.683,p=0.019), females (β-estimate:1.957,95%CI:0.423,3.492,p=0.015)and age <40 years (β-estimate:4.874,95%CI:1.155,8.594,p=0.016). Ischemia in ≥21% of LV was associated with LGE>15% (area under the curve0.766,sensitivity 0.724, specificity 0.659). Ischemia was also associated with atrial fibrillation/flutter (AF/AFL) (OR:1.481,95%CI:1.020,2.152,p=0.039), but no association was seen for nonsustained ventricular tachycardia. Ischemia was associated with shorter time to anaerobic threshold in CPET (β-estimate:-0.442,95%CI:-0.860,-0.023,p=0.039).Cardiac catheterizationFourteen patientsunderwent cardiac catheterizationwith a mean age of62.8(6.2)years, 8 (57.1%) males, 9 (64.3%) of whom had obstructive HCM. Among 4 patientswith an IMR >22.0, all had nonobstructive HCM and 2 had angina. CFR<2.0was reported in 8(57%)patients. Among 4 patients with IMR>22.0, perfusion defects were found in 2 of the 3 patients who underwent stress CMR.Increased ECV (>28%) was documented in2 of the patients with IMR>22 and in 3 of the patients with IMR≤22.0.LGE was >15% in 2 of the patients with IMR>22 and in 4 with IMR≤22.0. Conclusions: Coronary microvascular dysfunction isafrequentpathophysiological finding in HCM, and its evaluation has clinical relevance. In our cohort, greater MWT was linkedto depressed CFVR, and blunted CFVR associated with impaired biventricular systolic function and worse functional capacity.Ischemic burden, secondary to microvascular dysfunction, wasrelated to the severity of LV hypertrophy and impacts on various pathological and clinical features, includingtissue abnormalitiesandarrhythmic events.IMR assessment inHCMisfeasible and safe. Patients with abnormal IMR seemed to havemore significant tissue abnormalities in CMR.Our findings highlight the potential additional role of the evaluation ofcoronary microvascular dysfunction in patients with HCM,which may allow more accuraterisk stratificationfor arrhythmic events and progression to heart failure.
606 ## - Nome comum
Koha Internal code 22276
Elemento de entrada Cardiomyopathy, Hypertrophic
606 ## - Nome comum
Koha Internal code 4576
Elemento de entrada Microcirculation
606 ## - Nome comum
Koha Internal code 1603
Elemento de entrada Coronary Artery Disease
606 ## - Nome comum
Koha Internal code 4782
Elemento de entrada Myocardial Ischemia
606 ## - Nome comum
Koha Internal code 22278
Elemento de entrada Fibrosis
606 ## - Nome comum
Koha Internal code 30
Elemento de entrada Academic Dissertation
606 ## - Nome comum
Koha Internal code 5724
Elemento de entrada Portugal
700 ## - Responsabilidade principal
Koha Internal Code 22279
Palavra de ordem Rosa
Outra parte do nome Sílvia Aguiar Oliveira
702 ## - Responsabilidade secundária
Koha Internal Code 23689
Palavra de ordem Carmo
Outra parte do nome Miguel Mota
Código de função Orientador de tese
702 ## - Responsabilidade secundária
Código de função Orientador de tese
Koha Internal Code 12685
Palavra de ordem Fiarresga
Outra parte do nome António José
702 ## - Responsabilidade secundária
Código de função Orientador de tese
Koha Internal Code 22280
Palavra de ordem Lopes
Outra parte do nome Luís Rocha
702 ## - Responsabilidade secundária
Código de função Orientador de tese
Koha Internal Code 12704
Palavra de ordem Filipe
Outra parte do nome Carlos Manuel Nunes
801 ## - Fonte de origem
País Portugal
Agência NMS
Regras de catalogação RPC
856 ## - Localização e acesso electrónico
URL http://hdl.handle.net/10362/134275
090 ## - Números de controlo do sistema (Koha)
Número biblioitem do Koha (gerado automaticamente) 14342
942 ## - Elementos de entrada adicionados (Koha)
Tipo de item no Koha Documento Eletrónico
Suprimido Disponível no OPAC
Holdings
Removido (estado) Perdido (estado) Data de aquisição Identificador de recurso uniforme Origem do registo (biblioteca) (codificado) Código da organização que empresta ou é detentora (biblioteca) Localização da prateleira Código de barras Cota Tipo de circulação (não pode ser emprestado) Tipo de item e material
Disponível Disponível 2022-03-11 http://hdl.handle.net/10362/134275 Biblioteca NMS|FCM Biblioteca NMS|FCM online 20220051 RUN Normal Documento Eletrónico