Neurohormones and Cytokines in Heart Failure. Correlation With Coronary Flow Reserve

Coma-Canella, Isabel; Macı́as, Alfonso; Varo, Nerea; Ibarrola, A. Sánchez

doi:10.1016/s1885-5857(06)60414-3

Cited by 4 publications

(3 citation statements)

References 23 publications

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“…Direct effects include cytotoxicity mediated by both complement and antibody-dependent cells, and among indirect effects we could mention structural changes, apoptosis and sensitisation of malignant cells to chemotherapy [4]. During events of heart failure, higher levels of tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were observed, though this association might be related to a greater extent to their vasodilating compensating effect, unable to repair the endothelial damage seen in these situations [5]. Anyway, the occurrence of a complete atrioventricular block has been associated to immunity alterations, from the congenital block, in which an increased TNF-α level is observed, to the block associated to the administration of IFN-α and IL-2 [6].…”

Section: Discussionmentioning

confidence: 99%

Complete atrioventricular block induced by rituximab in monotherapy in an aged patient with non-Hodgkin’s diffuse large B-cell lymphoma

et al. 2008

Clin Transl Oncol

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Rituximab is a treatment option to non-Hodg kin's diffuse large B-cell lymphoma (NHDLBCL) in advanced stage and comorbility. It is known the cardiotoxicity effect of this drug, but there is no previous report describing a complete atrioventricular block (CAVB) secundary to treatment with Rituximab. We present an elderly woman treated with monotherapy with Rituximab who experienced a CAVB after administration of the fifth dose of this drug.

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Section: Discussionmentioning

confidence: 99%

Complete atrioventricular block induced by rituximab in monotherapy in an aged patient with non-Hodgkin’s diffuse large B-cell lymphoma

et al. 2008

Clin Transl Oncol

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“…0% in patients who received chemotherapy alone [64]. During events of heart failure, higher levels of tumour necrosis factor-(TNF-) and interleukin-6 (IL-6) were observed, though this association might be related to a greater extent to their vasodilating compensating effect, unable to repair the endothelial damage seen in these situations [65].…”

Section: Rituximabmentioning

confidence: 99%

Drug-Related Cardiotoxicity for the Treatment of Haematological Malignancies in Elderly

Malato

Saccullo²,

Fazio³

et al. 2010

CPD

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Several publications have focused on the cardiotoxicity of specific classes of hematological therapeutic agents such as antracyclines and cyclofosfamide. Cardiotoxicity of cancer chemotherapeutics is a problem for patients of all ages, but it increases with age. Toxicity can also develop months after the last chemotherapy dose, and late reactions can be seen years later when they present as new-onset cardiomyopathy. No data are available about the cardiotoxicity of non-chemotherapy agents currently used as preferred therapy for hematological malignancy in elderly. In this review we have provided a summary of the cardiovascular toxic effects produced by different drugs and therapeutic agents. Early identification of patients who are at risk for cardiotoxicity should be a primary goal for hematologists in the development of personalized antineoplastic therapeutic strategies or interventions. Thus, the discovery of new biomarkers to identify patients at a high risk for the development of these complications is a high priority. Although targeted therapies such as imatinib and anti-CD20 antibody such rituximab are considered less toxic and better tolerated by patients compared with classic chemotherapy drugs, certain cardiological complications can be very serious and as these agents have been in use for a limited period of time.

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“…HF and AF are the leading cause of morbidity and mortality worldwide affecting more than 30 million people [3,4]. A decrease in coronary blood flow during HF correlates with an increase in certain neurohormones, atrial and cerebral natriuretic peptides and cytokine (IL-6) with vasodilating effect, probably involved in compensatory mechanisms, which are not effective enough [5]. Coronary dilatory hypothalamic peptides, discovered and studied at the Institute of Biochemistry after H. Bunyanyan (NAS RA) can be used to protect the heart muscle [6,7].…”

Section: Introductionmentioning

confidence: 99%

The effect of hypothalamic peptides, neurohormone C and proline-rich peptide-1on the Ca2+-handling system in heartin pathophysiological conditions

Guevorkian

2020

Heliyon

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Institute of Biochemistry named after H. Buniatyan we discovered and studied hypothalamic peptides with coronary dilatory and antioxidant activities:neurohormone C (NC) and proline-rich peptide-1 (PRP-1). Both NC and PRP-1 exhibit cardioprotective effects, in part by restoring the calcium affinity for calcium-binding membrane proteins in cardiomyocytes. This affinity is diminished in the sarcoplasmic reticulum and mitochondriawith myocardial damage, heart failure, pancreatic necrosis and crush syndrome caused by isoproterenol. The peptides can also destroy the four detected toxic peptides and myocardial depressant factor, and protect against ischemiareperfusion injury. Further studies of these peptides may be promising for the treatment of patients at high risk of cardiovascular disease, regardless of pathology.

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Neurohormones and Cytokines in Heart Failure. Correlation With Coronary Flow Reserve

Cited by 4 publications

References 23 publications

Complete atrioventricular block induced by rituximab in monotherapy in an aged patient with non-Hodgkin’s diffuse large B-cell lymphoma

Complete atrioventricular block induced by rituximab in monotherapy in an aged patient with non-Hodgkin’s diffuse large B-cell lymphoma

Drug-Related Cardiotoxicity for the Treatment of Haematological Malignancies in Elderly

The effect of hypothalamic peptides, neurohormone C and proline-rich peptide-1on the Ca2+-handling system in heartin pathophysiological conditions

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