natriuretic-peptide--c-type and Neoplasms

This review is devoted to the urgent problem of cardiology and oncology - the cardiotoxicity of chemotherapy drugs - anthracyclines, which are considered to be one of the most cardiotoxic and cause a variety of cardiotoxic effects. The review also examines the diagnosis, treatment or preventive treatment of this pathology. The urgency of the problem is associated with the possibility of early or late manifestations of cardiotoxicity, manifestations of cardiotoxicity against the background of cross treatment, manifestations of cardiotoxicity against the background of various concomitant diseases. The review identified 9 main categories of cardiovascular complications during chemotherapeutic treatment and presents the types of cardiotoxicity caused by the use of anthracyclines. The issue of heart failure as a manifestation of anthracycline cardiotoxicity and the approaches to early diagnosis of cardiac insufficiency were examined in detail. The recommendations of the European Society of Medical Oncology (ESMO) (2012), the recommendations the European Society of Cardiology (ESC) in 2016 regarding the diagnosis and treatment of these patients are reviewed. An overview of the literature on the treatment and diagnosis of this category of patients is presented, especially with concomitant diseases. Examination of the patients, the timing of the initiation of therapy, preventive treatment, medication correction of heart failure, the doses, the combinations of chemotherapeutic drugs are issues that are recommended for the multidisciplinary team to successfully manage these patients.

Topics: Anthracyclines; Antineoplastic Agents; Biomarkers; Cardiomyopathies; Cardiotonic Agents; Cardiotoxicity; Echocardiography; Elapid Venoms; Heart; Heart Failure; Humans; Ivabradine; Natriuretic Peptide, C-Type; Neoplasms; Survival Analysis; Trastuzumab; Trimetazidine; Troponin I

Cardiac natriuretic peptides consist of a family of six peptide hormones that are synthesised by three separate genes and then stored as three separate prohormones (i.e. 126 amino acid atrial natriuretic peptide (ANP), 108 amino acid B-type natriuretic peptide (BNP) and 103 amino acid C-type natriuretic peptide (CNP) prohormones). The ANP prohormone contains four peptide hormones: long-acting natriuretic peptide (LANP), vessel dilator, kaliuretic peptide and ANP. 2. Currently, the only natriuretic peptide available commercially to treat congestive heart failure (CHF) is BNP (Nesiritide/Natrecor; SCIOS, Sunnyvale, CA, USA), which causes a small increase in the urine volume of 90 38 mL/h compared with 67 27 mL/h and no significant natriuresis, but has beneficial haemodynamic effects in acute CHF individuals. These haemodynamic effects probably contribute to the side-effects of BNP in patients with acute CHF with a 27% incidence of hypotension and possibly to 22% worsening of renal function, defined as an increase in serum creatinine of 0.5 mg/dL, associated with a worse prognosis. A review of clinical trials suggests a twofold increased risk of death at 30 days post-nesiritide treatment, a finding that needs further investigation. 3. The best of the natriuretic peptides for treating chronic CHF is the vessel dilator, which increases urinary flow up to 13-fold and sodium excretion up to fourfold, without the previously mentioned side-effects. The natriuretic and diuretic effects of vessel dilators last 6 h, which would allow them to be used on a four times per day basis in treating chronic CHF. 4. Atrial natriuretic peptide does not cause significant improvement in acute renal failure (ARF) in humans. The only natriuretic peptide that significantly improves ARF is the vessel dilator. Even when ARF has been established for 2 days before treatment in an ischaemic ARF animal model, vessel dilator decreases serum creatinine from 8.2 0.5 to 0.98 0.12 mg/dL in 6 days. At day 6 of ARF, mortality decreases to 14% (from 88%) without the vessel dilator. After 6 days of treatment with the vessel dilator, the proximal and distal tubules regenerate. 5. In cancer, vessel dilator, LANP, kaliuretic peptide and ANP at 1 mmol/L, decrease up to 97% of human breast, pancreatic and prostate adenocarcinoma cells, as well as small cell and squamous cell lung cancer cells within 24 h. In vivo, vessel dilator, LANP and kaliuretic peptide completely stop the growth of human pancreati

Topics: Animals; Atrial Natriuretic Factor; Heart Failure; Humans; Natriuretic Peptide, Brain; Natriuretic Peptide, C-Type; Neoplasms; Renal Insufficiency