High-output Cardiac Failure: A Forgotten Phenotype in Clinical Practice.

INTRODUCTION: The knowledge on High-Output Cardiac Failure (HOCF) has greatly improved in the last two decades. One of the advances was the identification of a new phenotype of HOCF, characterized by the absence of ventricular dilation, already associated with liver disease, Arteriovenous Fistulas (AVF), lung disease, myelodysplastic syndromes, and obesity. However, it has been noted that any aetiology can present with one of the two phenotypes, depending on the evolution. OBJECTIVE: The study aims to describe, through an integrative review, the physiopathology and aetiologies of HOCF and to discuss phenotypes associated with this condition. METHODS: Revisions, guidelines, case-controls, cohort studies and clinical studies were searched in MEDLINE and LILACS, using the connectives in the "cardiac output, high" database (MeSH Terms) OR "high cardiac output" (All Fields). DISCUSSION: Two distinct phenotypes are currently described in the HOCF, regardless of the aetiology: 1) one with enlarged cardiac chambers; and 2) with normal heart chambers. The mechanisms related to HOCF are vasodilation, arteriovenous shunts that cause increased microvascular density, Reduced Systemic Vascular Resistance (RSVR), and high metabolism. These mechanisms lead to activation of the renin-angiotensin-aldosterone system, sodium and water retention, activation of neprilysin, of the sodium-glucose-2 transporter, which promote interstitial fibrosis, ventricular remodeling and a consequent increase in cardiac output >8L/min. CONCLUSION: Many aetiologies of HOCF have been described, and some of them are potentially curable. Prompt recognition of this condition and proper treatment may lead to better outcomes.

Liver stiffness as measured by transient elastography is a predictor of outcomes in patients with chronic heart failure with reduced, mid-range, and recovered left-ventricular ejection fraction.

Background: Transient elastography is a noninvasive method for assessing liver stiffness (LS), which can reflect right-sided filling pressure associated with passive liver congestion in patients with HF. Methods: A prospective, single-center observational study in which LS was measured in consecutive ambulatory patients with heart failure with reduced, mid-range, and recovered left ventricular ejection fraction, between March 2018 and June 2019. Mean follow up was 219 ± 86 days. The primary endpoint was time to first event, which was defined as a composite of cardiovascular death or HF hospitalization. Results: Eighty-five patients were included in the final analysis. Mean age was 62 ± 10 and 68% were male. Mean ejection fraction and median NT-proBNP were, respectively, 38.7 ± 14.3% and 1140 pg/mL (interquartile range 224.3-2810.3). The median LS for the entire population was 6.3 (2.5-41.2) kPa. LS correlated with NT-proBNP (r = 0.46; p < 0.0001), total bilirubin (r = 0.47; p < 0.001), direct bilirubin (r = 0.43; p = 0.0001), gama-glutamyl-transpeptidase (r = 0.54; p < 0.0001), and alkaline phosphatase (r = 0.39; p = 0.0004). A Receiver Operating Characteristic (ROC) curve was performed and a cut point of 5.9 kPa showed sensitivity of 80% and specificity of 64.1% with area under the curve of 0.73. Using Cox proportional hazard model (independent variables: LS as a continuous variable, age, gender, NT-proBNP, LVEF, and creatinine), only LS was independently associated with the primary endpoint (hazard ratio 1.05, 95% confidence interval 1.01-1.09; for each increment of one unit of LS). Conclusion: LS correlates with biomarkers of myocardial stretch and several liver function tests and is an independent predictor of outcomes in ambulatory patients with HF.

Growth differentiation factor-15, a novel systemic biomarker of oxidative stress, inflammation, and cellular aging: Potential role in cardiovascular diseases.

Growth differentiation factor-15 (GDF-15) is a cytokine upregulated in multiple pathological conditions where oxidative stress, endothelial dysfunction, tissue aging, and chronic inflammation are the hallmarks. GDF-15 has many sources of production, including cardiac and vascular myocytes, endothelial cells, adipocytes and macrophages in response to metabolic stress, oncogenic transformation and the burden of proinflammatory cytokines or reactive oxygen species. Although the main sources of GDF-15 are extracardiac tissues, it has been shown to be elevated in many cardiac disorders. In experimental models of heart disease, GDF-15 release is induced after an ischemic insult and in pressure overload scenarios. Likewise, in recent years, an increasing body of evidence has emerged linking GDF-15 to the risk of mortality in acute coronary syndromes, atrial fibrillation and heart failure. Additionally, GDF-15 has been shown to add prognostic information beyond other conventional biomarkers such as natriuretic peptides and cardiac troponins. Further studies are needed to assess whether the incorporation of GDF-15 into clinical practice can improve cardiovascular outcomes.

Sagittal abdominal diameter as a marker of visceral obesity in older primary care patients.

BACKGROUND: Longevity, combined with a higher prevalence of obesity, particularly visceral obesity, has been associated with an increased risk of cardiovascular diseases. Insulin resistance (IR) is an important link between visceral obesity and cardiovascular diseases. An important association has been found between sagittal abdominal diameter, visceral obesity and IR. The objective of this study is to evaluate sagittal abdominal diameter as a marker of visceral obesity and correlate it with IR in older primary health care patients. METHODS: A cross-sectional study was performed with 389 patients over 60 years of age (70.6 ± 6.9), of whom 74% were female. Their clinical, anthropometric and metabolic profiles were assessed and their fasting serum insulin level was used to calculate the homeostasis model assessment insulin resistance (HOMA-IR). Sagittal abdominal diameter was measured in the supine position at the midpoint between the iliac crest and the last rib with abdominal calipers. RESULTS: Sagittal abdominal diameter was significantly correlated with anthropometric measures of general and visceral obesity and with HOMA-IR in both genders. There was no change in the association between sagittal abdominal diameter and HOMA-IR after adjusting for age, sex, diabetes and hypertension. CONCLUSION: It is feasible to use sagittal abdominal diameter in older primary care patients as a tool to evaluate visceral obesity, which is an indicator of cardiovascular risk.