The Effects of Octreotide in Dilated Cardiomyopathy: An Open-label Trial in 12 Patients

Eryol, Namlk Kemal; Güven, Muhammed; Topsakal, Ramazan; Sungur, Murat; Özdoğru, İbrahіm; İnanç, Tuğrul; Oğuzhan, Abdurrahman

doi:10.1536/jhj.45.613

Cited by 7 publications

(6 citation statements)

References 35 publications

(40 reference statements)

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“…Cardiac SST showed a decreased expression at the peptide level in the tissue samples of patients with ischemic cardiomyopathy as compared to controls. In line with our present findings, octreotide treatment significantly improved cardiac function in eight patients with ischemic cardiomyopathy (NYHA class III, ejection fraction < 40%) (Eryol et al, 2004). Our present finding that SSTR1, SSTR2, and SSTR5 are expressed at the mRNA level in human left ventricle are supported by earlier data showing the mRNA expression of SSTR1, SSTR2, SSTR4, and SSTR5, but not SSTR3 in the human atria and ventricle (Smith et al, 2005).…”

Section: Discussionsupporting

confidence: 92%

Somatostatin and Its Receptors in Myocardial Ischemia/Reperfusion Injury and Cardioprotection

et al. 2021

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Little is known about the role of the neuropeptide somatostatin (SST) in myocardial ischemia/reperfusion injury and cardioprotection. Here, we investigated the direct cardiocytoprotective effect of SST on ischemia/reperfusion injury in cardiomyocyte cultures, as well as the expression of SST and its receptors in pig and human heart tissues. SST induced a bell-shaped, concentration-dependent cardiocytoprotection in both adult rat primary cardiomyocytes and H9C2 cells subjected to simulated ischemia/reperfusion injury. Furthermore, in a translational porcine closed-chest acute myocardial infarction model, ischemic preconditioning increased plasma SST-like immunoreactivity. Interestingly, SST expression was detectable at the protein, but not at the mRNA level in the pig left ventricles. SSTR1 and SSTR2, but not the other SST receptors, were detectable at the mRNA level by PCR and sequencing in the pig left ventricle. Moreover, remote ischemic conditioning upregulated SSTR1 mRNA. Similarly, SST expression was also detectable in healthy human interventricular septum samples at the protein level. Furthermore, SST-like immunoreactivity decreased in interventricular septum samples of patients with ischemic cardiomyopathy. SSTR1, SSTR2, and SSTR5 but not SST and the other SST receptors were detectable at the mRNA level by sequencing in healthy human left ventricles. In addition, in healthy human left ventricle samples, SSTR1 and SSTR2 mRNAs were expressed especially in vascular endothelial and some other cell types as detected by RNA Scope®in situ hybridization. This is the first demonstration that SST exerts a direct cardiocytoprotective effect against simulated ischemia/reperfusion injury. Moreover, SST is expressed in the heart tissue at the peptide level; however, it is likely to be of sensory neural origin since its mRNA is not detectable. SSTR1 and SSTR2 might be involved in the cardioprotective action of SST, but other mechanisms cannot be excluded.

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Section: Discussionsupporting

confidence: 92%

Somatostatin and Its Receptors in Myocardial Ischemia/Reperfusion Injury and Cardioprotection

et al. 2021

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“…injection of lanreotide SR, may improve exercise performance in acromegalic patients without significant changes in the GH and IGF-I plasma levels [41,42]. Previous studies showed that both neurosurgery [14,17,18] and medical treatment with somatostatin analogs [14][15][16][17]19] are effective in reducing cardiac mass, leading to systolic function improvement and increasing diastolic filling capacities. The cardiac remodelling seems to occur quite quickly (and as early as 3 months in some reports) and it is linked to the suppression of GH and IGF-I levels [15,16,18].…”

Section: Discussionmentioning

confidence: 99%

“…Continuing or relapsed hyperproduction of GH and IGF-I results in further deterioration of acromegalic heart damage, which may then leads to heart failure. Many studies suggest that this progression can be halted through biochemical control of acromegaly [14][15][16][17][18][19].…”

Section: Introductionmentioning

confidence: 99%

“…Although a definitive link between myocardial dysfunction and mortality due to cardiovascular disease has not been yet established, some authors support the finding that optimal biochemical control of acromegaly is associated with decreased cardiovascular mortality [22,23]. Both neurosurgery [14,17,18] or medical treatment with somatostatin analogs (SSA) [14][15][16][17]19] are effective in decreasing cardiac mass, leading to systolic function improvement and increasing diastolic filling capacities. Indeed, there is evidence in the literature to suggest that the improvement of acromegalic cardiomyopathy may occur during administration of octreotide regardless of ''normalization'' of GH/IGF-1 levels [16,24].…”

Section: Introductionmentioning

confidence: 99%

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The long-term cardiovascular outcome of different GH-lowering treatments in acromegaly

et al. 2007

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The aim of this longitudinal study was to evaluate the echocardiographic outcome of acromegalic heart disease in patients undergoing different therapeutic approaches, in order to investigate whether SSA could provide therapeutic advantages as compared with neurosurgery. In total of 36, consecutive patients undergoing SSA treatment after neurosurgery were enrolled in this study (Gr.Surg.-SSA). After 12 months of treatment, 21 patients had a controlled disease, while the remaining 15 patients displayed uncontrolled disease. Twelve acromegalic patients who did not undergo SSA treatment due to controlled disease after neurosurgery were enrolled as control group (Gr.Surg). The echocardiographic-Doppler study was performed before neurosurgery and after 12-months of follow-up. After follow-up, a significant reduction in serum GH and IGF-I values, Left Ventricular Mass index (LVMi) and LVH rate with an improvement in diastolic function was observed in both groups of patients. We found a significant reduction of LVMi either in patients with controlled disease or in those with poorly controlled disease undergoing SSA treatment. Diastolic function and of LVH percentage improved in all groups, but significantly so only in controlled patients, no significant difference in any echocardiographic parameters and in the prevalence of the LVH rate were observed between the three groups of patients at the end of follow-up. Therefore, our data appear to show that for echographic parameters medical treatment additive beneficial effects is compared to neurosurgery alone. SSA also appears to contribute to the improvement of acromegalic cardiomyopathy also in patients who did not achieve biochemical control of the disease.

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“…These results were not met by subsequent clinical placebo-controlled studies, leaving many unanswered questions concerning its use as drug cost-effectiveness, the administration method (continuous vs. pulsitile), treatment duration (>6 months), and possible colonic neoplastic evolution [ 81 ]. If GH is recommendable in case of deficiency [ 82 ], its use in iDCM remains a matter or investigation and evaluation in light, also, of a small clinical study with positive results testing the cardiovascular effect of octreotide [ 83 ], a somatostatin analog [ 84 ].…”

Section: Discussionmentioning

confidence: 99%

Insights from Second-Line Treatments for Idiopathic Dilated Cardiomyopathy

Luciani¹,

Monte

2017

JCDD

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Background: Dilated cardiomyopathy (DCM) is an independent nosographic entity characterized by left ventricular dilatation and contractile dysfunction leading to heart failure (HF). The idiopathic form of DCM (iDCM) occurs in the absence of coronaropathy or other known causes of DCM. Despite being different from other forms of HF for demographic, clinical, and prognostic features, its current pharmacological treatment does not significantly diverge. Methods: In this study we performed a Pubmed library search for placebo-controlled clinical investigations and a post-hoc analysis recruiting iDCM from 1985 to 2016. We searched for second-line pharmacologic treatments to reconsider drugs for iDCM management and pinpoint pathological mechanisms. Results: We found 33 clinical studies recruiting a total of 3392 patients of various durations and sizes, as well as studies that tested different drug classes (statins, pentoxifylline, inotropes). A metanalysis was unfeasible, although a statistical significance for changes upon treatment for molecular results, morphofunctional parameters, and clinical endpoints was reported. Statins appeared to be beneficial in light of their pleiotropic effects; inotropes might be tolerated more for longer times in iDCM compared to ischemic patients. General anti-inflammatory therapies do not significantly improve outcomes. Metabolic and growth modulation remain appealing fields to be investigated. Conclusions: The evaluation of drug effectiveness based on direct clinical benefit is an inductive method providing evidence-based insights. This backward approach sheds light on putative and underestimated pathologic mechanisms and thus therapeutic targets for iDCM management.

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The Effects of Octreotide in Dilated Cardiomyopathy: An Open-label Trial in 12 Patients

Cited by 7 publications

References 35 publications

Somatostatin and Its Receptors in Myocardial Ischemia/Reperfusion Injury and Cardioprotection

Somatostatin and Its Receptors in Myocardial Ischemia/Reperfusion Injury and Cardioprotection

The long-term cardiovascular outcome of different GH-lowering treatments in acromegaly

Insights from Second-Line Treatments for Idiopathic Dilated Cardiomyopathy

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