Acromegaly and the heart

Smallridge, Robert C.; Rajfer, Sol I.; Davia, James E.; Schaaf, Marcus

doi:10.1016/0002-9343(79)90477-7

Cited by 80 publications

(16 citation statements)

References 15 publications

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“…LV hypertrophy has been described in hypertensive [21, 22]as well as in normotensive patients, thus suggesting a possible independent anabolic effect of GH on the myocardium [23, 24]. Furthermore, alterations in LV function have been reported in acromegalic patients without any clinical signs of cardiac involvement, hypertension or coronary artery disease [24, 25].…”

Section: Discussionmentioning

confidence: 99%

Medium-Term Cardiovascular Effects of High-Dose Growth Hormone Treatment in Growth Hormone-Deficient Children

Radetti

Crepaz²,

Paganini³

et al. 1999

Horm Res Paediatr

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Aim: To investigate the possible cardiac morphofunctional alterations inducd by prolonged and high-dose GH therapy in a group of 14 children with isolated GH deficiency. Patients and Methods: Patients were evaluated at phase 1, after 1.1 ± 0.6 years of treatment with GH 0.93 ± 0.13 U/kg/week, and at phase 2, after 5.5 ± 2.1 years of therapy 0.89 ± 0.11 U/kg/week. At each phase left ventricular volume, mass and systolic function were evaluated by two-dimensional guided M-mode echocardiography; left ventricular diastolic function was assessed by PW-Doppler sampling of transmitral flow. Results: Phase 1: diastolic blood pressure was lower (p < 0.05) and fractional shortening was not adequate for the level of afterload (stress shortening index p < 0.05) in patients compared to controls. Phase 2: diastolic blood pressure was lower (p < 0.01) and mass and mass/volume ratio were increased (mass index p < 0.05, mass/ volume ratio p < 0.05) in patients compared to controls. The increased mass/volume ratio, together with the normal systolic blood pressure, explains the reduction in peak systolic stress (p < 0.005). Among the parameters of left ventricular diastolic function, the peak E velocity/total area under mitral valve tracing and the area under E velocity/total area under mitral value tracing ratios were significantly decreased (p < 0.05). Conclusion: After a mean period of 5 years on high-dose GH treatment in GH-deficient children, subclinical morphofunctional alterations in the left ventricle were found.

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Section: Discussionmentioning

confidence: 99%

Medium-Term Cardiovascular Effects of High-Dose Growth Hormone Treatment in Growth Hormone-Deficient Children

Radetti

Crepaz²,

Paganini³

et al. 1999

Horm Res Paediatr

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“…The early stage is characterized by functional abnormalities: enhanced myocardial contractility, decreased peripheral vascular resistance and increased cardiac output (hyperkinetic state) [22, 89, 98, 99]. In stage 1, ventricular wall thickening is not associated with cavity dilatation, so that relative wall thickness (left ventricular [LV] wall thickness/LV radius) increases and causes a reduction in wall stress and an increase in cardiac performance, according to the Laplace’s law (wall stress=LV pressure/LV relative wall thickness) [10, 22, 89, 99-106]. In this stage, the reduction of wall stress together with the positive effects of GH/IGF-1 on myocardial contractility and systemic vascular resistance produces an improvement in cardiac function.…”

Section: Clinical Evidence Of Gh Excess In Humansmentioning

confidence: 99%

The GH/IGF-1 Axis and Heart Failure

Castellano¹,

Affuso²,

Conza³

et al. 2009

CCR

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The growth hormone (GH)/insulin-like growth factor 1 (IGF-1) axis regulates cardiac growth, stimulates myocardial contractility and influences the vascular system. The GH/IGF-1 axis controls intrinsic cardiac contractility by enhancing the intracellular calcium availability and regulating expression of contractile proteins; stimulates cardiac growth, by increasing protein synthesis; modifies systemic vascular resistance, by activating the nitric oxide system and regulating non-endothelial-dependent actions. The relationship between the GH/IGF-1 axis and the cardiovascular system has been extensively demonstrated in numerous experimental studies and confirmed by the cardiac derangements secondary to both GH excess and deficiency. Several years ago, a clinical non-blinded study showed, in seven patients with idiopathic dilated cardiomyopathy and chronic heart failure (CHF), a significant improvement in cardiac function and structure after three months of treatment with recombinant GH plus standard therapy for heart failure. More recent studies, including a small double-blind placebo-controlled study on GH effects on exercise tolerance and cardiopulmonary performance, have shown that GH benefits patients with CHF secondary to both ischemic and idiopathic dilated cardiomyopathy. However, conflicting results emerge from other placebo-controlled trials. These discordant findings may be explained by the degree of CHF-associated GH resistance. In conclusion, we believe that more clinical and experimental studies are necessary to exactly understand the mechanisms that determine the variable sensitivity to GH and its positive effects in the failing heart.

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“…In many patients, heart failure occurs, and cardiovascular diseases are a major cause of death (8). Although diabetes mellitus, systemic hypertension, and coronary heart disease are especially frequent during acromegaly, alterations in cardiac function in acromegalic patients free of all these pathological conditions have suggested the existence of a cardiomyopathy specific for acromegaly (9)(10)(11)(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

“…In the mammalian heart, two forms of MHC (a and 13) are encoded by separate genes (22). They combine to give rise to three isomyosins consisting oftwo homodimers, VI (a, a) and V3 (13, ,B) with high and low ATPase activity, respectively, and one heterodimer V2 (a, 13) with intermediate activity (23)(24)(25). All three can be easily distinguished by their electrophoretical mobility (26,27).…”

Section: Introductionmentioning

confidence: 99%

Effects of chronic growth hormone hypersecretion on intrinsic contractility, energetics, isomyosin pattern, and myosin adenosine triphosphatase activity of rat left ventricle.

Timsit

Riou²,

Bertherat³

et al. 1990

J. Clin. Invest.

147

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We studied papillary muscle mechanics and energetics, myosin phenotype, and ATPase activities in left ventricles from rats bearing a growth hormone (GH)-secreting tumor. 18 wk after tumor induction, animals exhibited a dramatic increase in body weight (+101% vs. controls) but no change in the ventricular weight/body weight ratio. The maximum isometric force of papillary muscles normalized per cross-sectional area rose markedly (+42%, P < 0.05 vs. controls), whereas the maximum unloaded shortening velocity did not change. This was observed despite a marked isomyosin shift towards V3 (32±5% vs. 8±2% in controls, P < 0.001). Increased curvature of the force-velocity relationship (+64%, P < 0.05 vs. controls) indicated that the muscles contracted more economically, suggesting the involvement of V3 myosin. Total calcium-and actinactivated myosin ATPase activities assayed on quickly frozen left ventricular sections were similar in tumor-bearing rats and in controls. After alkaline preincubation, these activities only decreased in tumor-bearing rats, demonstrating that V3 enzymatic sites were involved in total ATPase activity. These data demonstrate that chronic GH hypersecretion in the rat leads to a unique pattern of myocardial adaptation which allows the muscle to improve its contractile performance and economy simultaneously, thanks to myosin phenoconversion and an increase in the number of active enzymatic sites. (J. Clin. Invest.

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Acromegaly and the heart

Cited by 80 publications

References 15 publications

Medium-Term Cardiovascular Effects of High-Dose Growth Hormone Treatment in Growth Hormone-Deficient Children

Medium-Term Cardiovascular Effects of High-Dose Growth Hormone Treatment in Growth Hormone-Deficient Children

The GH/IGF-1 Axis and Heart Failure

Effects of chronic growth hormone hypersecretion on intrinsic contractility, energetics, isomyosin pattern, and myosin adenosine triphosphatase activity of rat left ventricle.

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