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1.
J Cardiovasc Echogr ; 24(3): 67-71, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-28465908

RESUMO

Obesity represents a worldwide increasing health problem. Obesity, through complex and not fully understood pathogenetic mechanisms, induces different structural and functional changes of left heart chambers, right heart chambers, and arteries. Ultrasound techniques are the first choice for a comprehensive assessment of the cardiovascular adaptation to obesity. This review summarizes the up-to-date literature on the topic, with particular focus on the main clinical studies, which range over different cardiovascular adaptations to obesity, namely left ventricular mass, diastolic function, right ventricle structure and function, arterial stiffness, and intima-media thickness. Also, the importance of epicardial fat and of the degree of obesity is described. Finally, the role of weight loss and bariatric surgery and the study of cardiovascular obesity-induced abnormalities in children and adolescent are discussed.

2.
Echocardiography ; 27(8): 915-22, 2010 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-20572853

RESUMO

BACKGROUND: Although the guidelines consider severe left ventricular (LV) dilatation a class IIaC indication for surgery in asymptomatic patients with severe aortic regurgitation (AR) and normal LV function, the optimal management remains controversial. We aimed to assess the LV enlargement, hypertrophy and function, and the outcomes in these patients by the presence of severe LV dilatation at baseline. METHODS: From our 20-year database, we identified all asymptomatic patients with severe AR and LV ejection fraction (EF) >50% and ≥2 echocardiograms ≥1 year apart. LV end-diastolic diameter >70 mm or LV end-systolic diameter >50 mm or LV end-systolic diameter index >25 mm/m(2) defined severe LV dilatation. A composite end point included onset of symptoms or LV dysfunction. RESULTS: Eighty-four patients (52 ± 18 years, 61 men) were enrolled and followed-up for 7.1 ± 5.1 years. Two groups were defined: 22 patients with and 62 patients without severe LV dilatation at baseline. The progression of LV dilatation and hypertrophy, and the LVEF at last exam were similar in both groups. Twelve of 22 and 34 of 62 patients (P = 0.59) reached the end point. Vasodilators did not modify the progression of LV enlargement/hypertrophy. Ten of 22 and 25 of 62 patients (P = 0.45) underwent surgery and had similar postoperative LV diameters, mass, EF. CONCLUSIONS: The progression of LV enlargement/hypertrophy and outcomes in asymptomatic patients with severe AR, normal LV function, and severe LV dilatation or the postoperative LV parameters were not influenced by the severe LV dilatation, suggesting that a close follow-up could delay surgery in this population.


Assuntos
Insuficiência da Valva Aórtica/diagnóstico por imagem , Insuficiência da Valva Aórtica/mortalidade , Hipertrofia Ventricular Esquerda/diagnóstico por imagem , Hipertrofia Ventricular Esquerda/mortalidade , Volume Sistólico , Comorbidade , Dilatação Patológica/diagnóstico por imagem , Dilatação Patológica/mortalidade , Feminino , Humanos , Itália/epidemiologia , Estudos Longitudinais , Pessoa de Meia-Idade , Prevalência , Prognóstico , Medição de Risco , Fatores de Risco , Análise de Sobrevida , Taxa de Sobrevida , Ultrassonografia , Disfunção Ventricular Esquerda/diagnóstico por imagem , Disfunção Ventricular Esquerda/mortalidade
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