Implicación de la congestión venosa sistémica en la insuficiencia cardíaca

Gracia, Jorge; Marteles, Marta Sánchez; Calvo, Juan

doi:10.1016/j.rce.2016.10.012

Cited by 12 publications

(2 citation statements)

References 68 publications

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“…Cardiac filling pressures increase due to ventricular interdependence or due to chronically elevated left-sided filling pressures transmitted back through the pulmonary system into the right ventricle [5], resulting in systemic congestion. The excessive fluid is stored in the splanchnic venous system, which contains highly compliant capacitance veins that can store up to 65% of the total blood volume without repercussions on system hemodynamics [7,8]. In an attempt to increase the effective circulatory volume, sympathetic stimulation induces vasoconstriction of the splanchnic capacitance vessels and vasodilation of the hepatic veins [9].…”

Section: Introductionmentioning

confidence: 99%

Current animal models for the study of congestion in heart failure: an overview

et al. 2019

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Congestion (i.e., backward failure) is an important culprit mechanism driving disease progression in heart failure. Nevertheless, congestion remains often underappreciated and clinicians underestimate the importance of congestion on the pathophysiology of decompensation in heart failure. In patients, it is however difficult to study how isolated congestion contributes to organ dysfunction, since heart failure and chronic kidney disease very often coexist in the so-called cardiorenal syndrome. Here, we review the existing relevant and suitable backward heart failure animal models to induce congestion, induced in the left-(i.e., myocardial infarction, rapid ventricular pacing) or right-sided heart (i.e., aorta-caval shunt, mitral valve regurgitation, and monocrotaline), and more specific animal models of congestion, induced by saline infusion or inferior vena cava constriction. Next, we examine critically how representative they are for the clinical situation. After all, a relevant animal model of isolated congestion offers the unique possibility of studying the effects of congestion in heart failure and the cardiorenal syndrome, separately from forward failure (i.e., impaired cardiac output). In this respect, new treatment options can be discovered.

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Section: Introductionmentioning

confidence: 99%

Current animal models for the study of congestion in heart failure: an overview

et al. 2019

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“…In our study, the appetite assessment was undergone by SNAQ and showed that appetite loss was commonly seen in patients with CHF. In addition to the abnormality of cardiac and pulmonary function, the congestion of CHF may also cause the functional change in other organs, including liver, kidney, brain and gastrointestinal tract, which probably causes the appetite loss [ 30 ]. However, the relationship between CHF and pancreatic function is rarely reported.…”

Section: Discussionmentioning

confidence: 99%

Pancreatic exocrine insufficiency in patients with chronic heart failure and its possible association with appetite loss

2017

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BackgroundAppetite loss is one complication of chronic heart failure (CHF), and its association with pancreatic exocrine insufficiency (PEI) is not well investigated in CHF.AimWe attempted to detect the association between PEI and CHF-induced appetite.MethodsPatients with CHF were enrolled, and body mass index (BMI), left ventricular ejection fraction (LVEF), New York Heart Association (NYHA) cardiac function grading, B-type natriuretic peptide (BNP), serum albumin, pro-albumin and hemoglobin were evaluated. The pancreatic exocrine function was measured by fecal elastase-1 (FE-1) levels in the enrolled patients. Appetite assessment was tested by completing the simplified nutritional appetite questionnaire (SNAQ). The improvement of appetite loss by supplemented pancreatic enzymes was also researched in this study.ResultsThe decrease of FE-1 levels was found in patients with CHF, as well as SNAQ scores. A positive correlation was observed between SNAQ scores and FE-1 levels (r = 0.694, p < 0.001). Pancreatic enzymes supplement could attenuate the decrease of SNAQ scores in CHF patients with FE-1 levels <200 μg/g stool and SNAQ < 14.ConclusionsAppetite loss is commonly seen in CHF, and is partially associated with pancreatic exocrine insufficiency. Oral pancreatic enzyme replacement therapy attenuates the chronic heart failure-induced appetite loss. These results suggest a possible pancreatic-cardiac relationship in chronic heart failure, and further experiment is needed for clarifying the possible mechanisms.

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Intra-abdominal pressure and its relationship with markers of congestion in patients admitted for acute decompensated heart failure

et al. 2020

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Background: Systemic congestion is one of the mechanisms involved in acute decompensated heart failure (ADHF). Increased intraabdominal pressure (IAP), elicited by abdominal congestion, has been related to acute kidney injury and prognosis. Nonetheless, the link between diuretic response, surrogate markers of congestion and renal function remains poorly understood. Methods and results:We measured IAP in 43 patients from a non-interventional, exploratory, prospective, single center study carried out in patients admitted for ADHF. IAP was measured with an calibrated electronic manometer through a catheter inserted in the bladder. Normal IAP was defined as < 12 mmHg. At baseline, median IAP was 15 mmHg, with a reduction over the next 72 hours to a median of 12 mmHg. A higher IAP at admission was associated with higher baseline blood urea (83 mg/dL [62 -138] vs. 50 mg/dL [35 -65]; p=0.007) and creatinine (1.30 mg/dL vs 0.95 mg/dL; p=0.027), and with poorer diuretic response 72 hours after admission, either measured by diuresis (14.4 mL/mg vs. 21.6 mL/mg; [p = 0.005]) or natriuresis (1.2 mEqNa/mg vs. 2.0 mEqNa/mg; [p = 0.008]). A higher incidence for one-year all-cause mortality (45.0% vs 16.7%; log-rank test = 0.041) was observed among those patients with IAP>12mmHg at 72 hours. Conclusions:In patients with ADHF, higher IAP at admission is associated with poorer baseline renal function and impaired diuretic response. The persistence of IAP at 72 hours above 12 mm Hg associates to longer length of hospital stay and higher one-year all-cause mortality.

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Implicación de la congestión venosa sistémica en la insuficiencia cardíaca

Cited by 12 publications

References 68 publications

Current animal models for the study of congestion in heart failure: an overview

Current animal models for the study of congestion in heart failure: an overview

Pancreatic exocrine insufficiency in patients with chronic heart failure and its possible association with appetite loss

Intra-abdominal pressure and its relationship with markers of congestion in patients admitted for acute decompensated heart failure

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