Testosterone treatment in chronic heart failure. Review of literature and future perspectives

Mounting evidence suggests that hormonal deficiencies (HD) have an important role in chronic heart failure (CHF). In particular, androgen depletion is common in men with CHF and is associated with increased morbidity and mortality. This review summarizes the current understanding of the complex relationship between CHF and testosterone, focusing on evidence derived from clinical trials that have investigated the role of testosterone in the treatment of CHF. A greater comprehension of this area will allow researchers and clinicians to plan future studies that improve current strategies to reduce mortality in this high-risk population. Online databases PubMed (Medline), Web of Science, and Scopus were searched for manuscripts published prior to June 2018 using key words "heart failure" AND "testosterone" OR "anabolism" OR "hormone" OR "replacement treatment”. Manuscripts were collated, studied and carried forward for discussion where appropriate. In summary, findings from the literature demonstrate that testosterone treatment in CHF is a promising topic that requires further investigation

Targeting the gut microbiome in coronary artery disease

Host-microbiota interactions via numerous inflammatory and metabolic pathways contribute to the pathogenesis of a multitude of diseases such as cardiovascular and metabolic diseases.1 Alterations in the microbial flora generate increased circulating levels of microbiota-dependent metabolites associated with disease risk.2 One such metabolite, trimethylamine N-oxide (TMAO), is formed from the metabolism of phosphatidylcholine or L-carnitine into trimethylamine by bacteria, which is converted to TMAO in the liver by flavin-containing monooxygenases (FMO).3 While TMAO is the most commonly studied gut microbiota-derived metabolite demonstrating associations with heart failure,3 myocardial infarction4 and heart disease,5 precursor metabolites to TMAO have also shown similar associations with cardiovascular disease (CVD) risk such as betaine,6 choline,6 γ-butyrobetaine7 and more recently, acetyl-L-carnitine and L-carnitine.8 Given that TMAO can be generated from two pathways; 1) betaine -> choline -> TMAO and 2) carnitine -> TMAO, this demonstrates that TMAO levels are determined from a multitude of sources including dietary (e.g., carnitine from red meat and choline from eggs), microbial flora, medications (e.g., antibiotics), liver flavin monooxygenase activity, as well as age, gender and ethnicity.9., 10., 11. [Opening paragraph

Multiple hormone deficiency syndrome: a novel topic in chronic heart failure.

[First paragraph] Heart failure (HF) is described as a clinical syndrome characterized by typical symptoms (e.g., ankle swelling, fatigue or dyspnea) or signs (e.g., peripheral edema, pulmonary crackles or elevated jugular venous pressure), in which structural and/or functional cardiac abnormalities induce an impairment of cardiac output or an increase of intracardiac pressures at rest and/or during stress [1,2]. Importantly, due to different underlying etiologies, demographics, co-morbidities, and response to therapies, the main terminology used to describe HF is based on measurement of left ventricle ejection fraction (EF). Classically, patients with normal EF (typically considered as ≥50%) are said to have HF with preserved EF (HFpEF), with those with reduced EF (typically considered as <40%) termed as HF with reduced EF (HFrEF). In the latest European Society of Cardiology guidelines, cases where EF lies between 40 and 49%, previously considered as a ‘gray area’, are now defined as HF with mid-range EF (HFmEF) [1]

Heart failure and trimethylamine N-oxide: time to transform a ‘gut feeling’ in a fact?

In the last few years, in the context of a growing interest in investigating novel pathways involved in heart failure (HF) pathophysiology, the association between the gastrointestinal (GI) system and HF represents an important model of attention, the so called ‘gut hypothesis’.Despite being classically identified as a ‘simple’ intestinal dysfunction, the main hypothesis is currently focused on the role of inflammation and oxidative stress as a consequence of the intestinal wall ischaemia and/or congestion induced by HF, determining a gut barrier dysfunction and resulting in an increased gut bacterial translocation.With this in mind, two main mechanisms have been proposed to link gut dysfunction and HF; (i) metabolism dependent, via gut-derived metabolites entering the systemic circulation and exerting pro-atherogenic effects and pro-inflammatory effects and (ii) metabolism independent, via bacterial components (e.g. lipopolysaccharides and endotoxins) translocating in the systemic circulation and contributing to the systemic inflammatory state with its well-known negative effects on HF. </p

Impact of acute choline loading on circulating trimethylamine N-oxide levels.

Despite recent efforts to reduce cardiovascular disease risk by dietary intervention,1few markers are useful to assess the efficiency and progress of this. Circulating levels of trimethylamine N-oxide (TMAO) are associated with poor outcomes of cardiovascular disease.2–6TMAO is generated via hepatic flavin monooxygenase 3 (FMO3) mediated oxidation of trimethylamine (TMA),7derived largely from carnitine and choline through gut microbial metabolism. These substrates are found in red meat and eggs, which are representative of a Western diet. Therefore, TMAO levels could be used to monitor the effect of dietary intervention, particularly for the consumption of a Western diet. In this study, we examined the effect of acute choline loading on TMAO levels in healthy adult volunteers

Prevention and treatment of peritoneal adhesions in patients affected by vascular diseases following surgery: a review of the literature.

Intra-abdominal adhesions are the most frequently occurring postoperative complication following abdomino-pelvic surgery. Abdominal and pelvic surgery can lead to peritoneal adhesion formation causing infertility, chronic pelvic pain, and intestinal obstruction. Laparoscopy today is considered the gold standard of care in the treatment of several abdominal pathologies as well as in a wide range of vascular diseases. Laparoscopy has several advantages in comparison to open surgery. These include rapid recovery times, shorter hospitalisation, reduced postoperative pain, as well as cosmetic benefits. The technological improvements in this particular surgical field along with the development of modern techniques and the acquisition of specific laparoscopic skills have allowed for its wider utilization in operations with fully intracorporeal anastomoses. Postoperative adhesions are caused by aberrant peritoneal healing and are the leading cause of postoperative bowel obstruction. The use of anti-adherence barriers is currently being advocated for their prevention. The outcome of the investigation showed adhesion formation inhibition without direct detrimental effects on anastomotic healing. Poor anasto-motic healing can provoke adhesions even in the presence of anti-adhesion barriers. This review gives a short overview on the current evidence on the pathophysiology and prevention of peritoneal adhesions

Bowel Angiodysplasia and Myocardial Infarction secondary to an ischaemic imbalance: a case report.

Angiodysplasia, defined as a vascular ectasia or arteriovenous malformation, is the most frequent cause of occult bleeding in patients older than 60 years and a significant association with several cardiac condition is described. Patients with anemia and negative findings on upper endoscopy and colonoscopy should be referred for further investigation of the small bowel. The investigation of choice, when available, is wireless capsule endoscopy. Several therapeutic options are available in this cases, as we reviewed in this report. We report a case of 78-year old man admitted to our Intensive Coronary Unit for dyspnea and chest pain. A diagnosis of non-ST-segment elevation acute coronary syndrome was made and a concomintant, significant anemia was found (hemoglobin 8.2 g/dl). No cororary disease was found by an angiography though the past medical history revealed systemic hypertension, chronic kidney disease (KDOQY stage III), and diabetes mellitus type II on insuline therapy. A Wireless Video capsule examination was positive for jejunum angiodysplasia and an argon plasma coagulation was chosen as terapeutic option. No subsequent supportive therapy and interventions were required in subsequent one year of follow-up

Combined use of trimethylamine N-oxide with BNP for risk stratification in heart failure with preserved ejection fraction: findings from the DIAMONDHFpEF study

Circulating levels of Trimethylamine N-oxide (TMAO), a gut microbiome-mediated metabolite related to Western diet1, 2 , have been shown to be associated with risk stratification and outcome in patients with heart failure (HF) with reduced ejection fraction (HFrEF) 3-6 . The aim of the present study was to assess the associations between TMAO with outcomes in patients with HF with preserved ejection fraction (HFpEF)

The impairment of the Growth Hormone/Insulin-like growth factor 1 (IGF-1) axis in heart failure: A possible target for future therapy

Hormonal abnormalities are quite common in chronic heart failure (CHF). The most studied hormonal axis in CHF is the impairment of Growth Hormone (GH)/Insulin Growth Factor-1(IGF-1), which in turn is defined either by a blunted response to GH stimulation test or low serum IGF-1 values. Several independent groups reported that the presence of an abnormal GH/IGF-1 status in CHF is associated with a more severe disease, impaired functional capacity and reduced Survival rates. After the first encouraging results, double -blind controlled trials showed a neutral effect of the GH administration in patients. However, further studies reported positive results, when a GH-therapy is implemented only in those patients presenting a GH deficiency (replacement therapy)

Biomarkers in Heart Failure: Clinical Insights

Heart failure (HF) is a clinical syndrome caused by structural and/or functional cardiac abnormalities and resulting from impaired cardiac output or an in-crease of intracardiac pressures at rest and/or during stress. Typical signs and symptoms of HF include ankle swelling, fatigue, dyspnea and peripheral edema, pulmonary crackles, or increased jugular venous pressure. Usually, patients with ejection fraction (EF) greater than or equal to 50% are defined as HF with preserved EF, where as those with EF less than 40% have HF with reduced EF. Patients with EF between 40% and 49% are now classified as HF with midrange EF