High prevalence of cardiac hypertophy without detectable signs of fibrosis in patients with untreated active acromegaly: an<i> in</i> <i>vivo</i> study using magnetic resonance imaging

Bogazzi, Fausto; Lombardi, Massimo; Strata, Elisabetta; Aquaro, Giovanni Donato; Bello, Vitantonio Di; Cosci, Chiara; Sardella, Chiara; Talini, Enrica; Martino, Enio

doi:10.1111/j.1365-2265.2007.03047.x

Cited by 60 publications

(55 citation statements)

References 49 publications

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“…In the later stages, cardiac extracellular collagen deposition, diastolic and systolic dysfunction due to cardiac remodeling, and heart failure become prominent. Later stages can be observed in older patients, in untreated acromegaly, or in cases of prolonged elevated serum GH levels . Valvular regurgitations are also frequent, the mitral valve being affected in most cases .…”

Section: Discussionmentioning

confidence: 99%

Left ventricular twist is impaired in acromegaly: Insights from the three‐dimensional speckle tracking echocardiographic MAGYAR‐Path Study

Kormányos

Domsik

Kalapos

et al. 2017

J of Clinical Ultrasound

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Section: Discussionmentioning

confidence: 99%

Left ventricular twist is impaired in acromegaly: Insights from the three‐dimensional speckle tracking echocardiographic MAGYAR‐Path Study

Kormányos

Domsik

Kalapos

et al. 2017

J of Clinical Ultrasound

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“…Patients with Acro frequently have hypertrophic cardiomyopathy (Lie & Grossman 1980, Colao et al 2004, Melmed 2006, Bogazzi et al 2008b, considered due to a direct effect of GH/IGF-1 excess , Ciulla et al 1999, Colao et al 2004. Mice-overexpressing bovine (b) GH have many features of patients with Acro, including heart hypertrophy and impaired energetic metabolism .…”

Section: Introductionmentioning

confidence: 99%

Regulation of cardiac fatty acids metabolism in transgenic mice overexpressing bovine GH

Bogazzi¹,

Raggi²,

Ultimieri³

et al. 2009

Journal of Endocrinology

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Cardiac energy metabolism depends mainly on fatty acid (FA) oxidation; however, regulation of FA metabolism in acromegalic (Acro) heart is unknown. The aim of the study was to evaluate cardiac expression of key proteins of FA metabolism in young and elder transgenic mice overexpressing bovine GH Acro. Expression of proteins regulating FA entry into the cells, their uptake by mitochondria and beta-oxidation were evaluated by western blot, while FA content by Fourier transform infrared microspectrometry. Regulatory mechanisms of key steps of FA metabolism were also studied. The expression of plasma-membrane FA carriers (fatty acid-binding protein and fatty acid transport protein-1) and acylCoA synthetase was higher in young and lower in elder Acro than in corresponding controls; likewise, expression of cytoplasm to mitochondria-1 (CPT-1), the key enzyme of mitochondrial FA uptake, and that of medium-chain acyl-CoA dehydrogenase and long-chain acyl-CoA dehydrogenase, two regulatory beta-oxidation dehydrogenases, followed a similar pattern. FA content was lower in young and higher in elder Acro than in wild-type, suggesting an increased utilisation in young animals. GH regulated expression of key proteins of FA metabolism through changes in peroxisome proliferator-activated receptor alpha (PPARalpha) expression, which varied accordingly. GH effect was confirmed by treatment of Acro mice with a receptor antagonist, which abolished changes in key proteins of FA metabolism in young Acro. GH increased phosphorylation of AMP-activated protein kinase and anti-acetyl-CoA-carboxylase, two regulatory kinases, leading to lower CPT-1 inhibition by malonyl-CoA, and intervened in regulating PPARalpha expression through the ERK 1/2 pathway. In conclusion, chronic GH excess increased FA metabolism in the young age, whereas its action was overwhelmed in elder ages likely by GH-independent mechanisms, leading to reduced expression of key enzyme of FA metabolism.

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“…LV systolic function can be preserved in cases with no active heart failure 8. Ventricular dilatation often occurs, but was not seen in this case.…”

Section: Investigationsmentioning

confidence: 55%

Acromegaly-induced cardiomyopathy with dobutamine-induced outflow tract obstruction

Abdelsalam

Nippoldt

2016

BMJ Case Reports

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SUMMARYA 50-year-old man with a history of acromegaly was referred for preoperative cardiac evaluation preceding trans-sphenoidal resection of a pituitary macroadenoma. Dobutamine stress echocardiography was negative for myocardial ischaemia. Resting left ventricular (LV) LV ejection fraction (LVEF) was 64% and there was hypertrophy of ventricular septum (18 mm) without resting LV outflow tract obstruction. With 40 mg/kg/min of dobutamine, the LVEF became hyperdynamic at 80%, and there was a maximal instantaneous LV outflow tract gradient of 77 mm Hg. There was no delayed myocardial enhancement on cardiac MRI and the pattern of hypertrophy was concentric. Acromegaly-induced cardiomyopathy can mimic hypertrophic cardiomyopathy in the setting of dobutamine provocation. Because cardiomyopathy is an important cause of mortality in acromegaly, diagnosis and appropriate management are critical to improve survival. BACKGROUND

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High prevalence of cardiac hypertophy without detectable signs of fibrosis in patients with untreated active acromegaly: an in vivo study using magnetic resonance imaging

Cited by 60 publications

References 49 publications

Left ventricular twist is impaired in acromegaly: Insights from the three‐dimensional speckle tracking echocardiographic MAGYAR‐Path Study

Left ventricular twist is impaired in acromegaly: Insights from the three‐dimensional speckle tracking echocardiographic MAGYAR‐Path Study

Regulation of cardiac fatty acids metabolism in transgenic mice overexpressing bovine GH

Acromegaly-induced cardiomyopathy with dobutamine-induced outflow tract obstruction

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