Cardiorenal Syndrome Type 1: Renal Dysfunction in Acute Decompensated Heart Failure.
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ABSTRACT:
SUBMITTER: Prins KW
PROVIDER: S-EPMC4855293 | biostudies-literature | 2015 Sep
REPOSITORIES: biostudies-literature
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Cardiorenal Syndrome Type 1: Renal Dysfunction in Acute Decompensated Heart Failure.
Prins Kurt W KW Thenappan Thenappan T Markowitz Jeremy S JS Pritzker Marc R MR
Journal of clinical outcomes management : JCOM 20150901 10
<h4>Objective</h4>To present a review of cardiorenal syndrome type 1 (CRS1).<h4>Methods</h4>Review of the literature.<h4>Results</h4>Acute kidney injury occurs in approximately one-third of patients with acute decompensated heart failure (ADHF) and the resultant condition was named CRS1. A growing body of literature shows CRS1 patients are at high risk for poor outcomes, and thus there is an urgent need to understand the pathophysiology and subsequently develop effective treatments. In this revi ...[more]
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Project description:BackgroundAcute cardiorenal syndrome (ACRS) is associated with adverse outcomes in patients with acute decompensated heart failure (ADHF). Intrarenal venous blood flow can be assessed using Doppler ultrasound and has prognostic significance in ADHF. Although intrarenal Doppler (IRD) may be sensitive to renal congestion, an association between IRD parameters and ACRS has not been demonstrated in an ADHF population.MethodsHospitalized patients with ADHF (n = 21) or acute coronary syndrome (ACS; n = 21) were prospectively enrolled. Patients underwent echocardiography, including IRD, using a standard cardiac ultrasound transducer. Intrarenal venous flow was quantified with the renal venous stasis index (RVSI), defined as the duration of absent venous flow time divided by cardiac cycle duration. The primary outcome was acute kidney injury (AKI) as assessed using the Kidney Disease: Improving Global Outcomes (KDIGO) criteria.ResultsADHF patients had a similar cardiac index (2.0 ± 0.6 vs 2.1 ± 0.4 L/min per m2, P = 0.91) but higher estimated central venous pressure (13.0 ± 3.2 vs 4.6 ± 2.4 mm Hg, P < 0.001) measured using echocardiography, compared with ACS patients. IRD was abnormal in all ADHF patients and normal in all ACS patients (RVSI 0.62 ± 0.20 vs 0.0 ± 0, P < 0.001). AKI stage II/III occurred in 10 of 21 ADHF patients (48%) vs 0 of 21 ACS patients (P < 0.001), with a mean rise in serum creatinine of 97.7 ± 79.3 vs 16.8 ± 10.9 μmol/L (P < 0.001), respectively. RVSI was correlated with AKI severity in ADHF patients (r = 0.57; P = 0.004).ConclusionsRVSI is associated with AKI among ADHF patients and may be a useful diagnostic biomarker for ACRS in this setting. Further studies are needed to validate this finding and evaluate the potential efficacy of IRD-guided decongestive therapy in this setting.
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Project description:BackgroundWorsening renal function is common among patients hospitalized for acute decompensated heart failure (ADHF). When this occurs, subsequent management decisions often pit the desire for effective decongestion against concerns about further worsening renal function. There are no evidence-based treatments or guidelines to assist in these difficult management decisions. Ultrafiltration is a potentially attractive alternative to loop diuretics for the management of fluid overload in patients with ADHF and worsening renal function.Methods and resultsThe National Heart, Lung, and Blood Institute Heart Failure Clinical Research Network designed a clinical trial to determine if ultrafiltration results in improved renal function and relief of congestion compared with stepped pharmacologic care when assessed 96 hours after randomization in patients with ADHF and cardiorenal syndrome. Enrollment began in June 2008. This paper describes the rationale and design of the Cardiorenal Rescue Study in Acute Decompensated Heart Failure (CARRESS-HF).ConclusionsTreating the signs and symptoms of congestion in ADHF is often complicated by worsening renal function. CARRESS-HF compares treatment strategies (ultrafiltration vs stepped pharmacologic care) for the management of worsening renal function in patients with ADHF. The results of the CARRESS-HF trial are expected to provide information and evidence as to the most appropriate approaches for treating this challenging patient population.
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Project description:BackgroundCongestion is the most frequent cause for hospitalization in acute decompensated heart failure. Although decongestion is a major goal of acute therapy, it is unclear how the clinical components of congestion (eg, peripheral edema, orthopnea) contribute to outcomes after discharge or how well decongestion is maintained.Methods and resultsA post hoc analysis was performed of 496 patients enrolled in the Diuretic Optimization Strategy Evaluation in Acute Decompensated Heart Failure (DOSE-AHF) and Cardiorenal Rescue Study in Acute Decompensated Heart Failure (CARRESS-HF) trials during hospitalization with acute decompensated heart failure and clinical congestion. A simple orthodema congestion score was generated based on symptoms of orthopnea (≥2 pillows=2 points, <2 pillows=0 points) and peripheral edema (trace=0 points, moderate=1 point, severe=2 points) at baseline, discharge, and 60-day follow-up. Orthodema scores were classified as absent (score of 0), low-grade (score of 1-2), and high-grade (score of 3-4), and the association with death, rehospitalization, or unscheduled medical visits through 60 days was assessed. At baseline, 65% of patients had high-grade orthodema and 35% had low-grade orthodema. At discharge, 52% patients were free from orthodema at discharge (score=0) and these patients had lower 60-day rates of death, rehospitalization, or unscheduled visits (50%) compared with those with low-grade or high-grade orthodema (52% and 68%, respectively; P=0.038). Of the patients without orthodema at discharge, 27% relapsed to low-grade orthodema and 38% to high-grade orthodema at 60-day follow-up.ConclusionsIncreased severity of congestion by a simple orthodema assessment is associated with increased morbidity and mortality. Despite intent to relieve congestion, current therapy often fails to relieve orthodema during hospitalization or to prevent recurrence after discharge.Clinical trial registrationURL: http://www.clinicaltrials.gov. Unique identifiers: NCT00608491, NCT00577135.
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Project description:The study of trimethylamine oxide (TMAO), a metabolite of gut microbiota, and heart failure and chronic kidney disease has made preliminary achievements and been summarized by many researchers, but its research in the field of cardiorenal syndrome is just beginning. TMAO is derived from the trimethylamine (TMA) that is produced by the gut microbiota after consumption of carnitine and choline and is then transformed by flavin-containing monooxygenase (FMO) in the liver. Numerous research results have shown that TMAO not only participates in the pathophysiological progression of heart and renal diseases but also significantly affects outcomes in chronic heart failure (CHF) and chronic kidney disease (CKD), besides influencing the general health of populations. Elevated circulating TMAO levels are associated with adverse cardiovascular events such as HF, myocardial infarction, and stroke, patients with CKD have a poor prognosis as well. However, no study has confirmed an association between TMAO and cardiorenal syndrome (CRS). As a syndrome in which heart and kidney diseases intersect, CRS is often overlooked by clinicians. Here, we summarize the research on TMAO in HF and kidney disease and review the existing biomarkers of CRS. At the same time, we introduced the relationship between exercise and gut microbiota, and appropriately explored the possible mechanisms by which exercise affects gut microbiota. Finally, we discuss whether TMAO can serve as a biomarker of CRS, with the aim of providing new strategies for the detection, prognostic, and treatment evaluation of CRS.
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Project description:Cardiorenal syndromes (CRS) describe concomitant bidirectional dysfunction of the heart and kidneys in which 1 organ initiates, perpetuates, and/or accelerates decline of the other. CRS are common in heart failure and universally portend worsened prognosis. Despite this heavy disease burden, the appropriate diagnosis and classification of CRS remains problematic. In addition to the hemodynamic drivers of decreased renal perfusion and increased renal vein pressure, induction of the renin-angiotensin-aldosterone system, stimulation of the sympathetic nervous system, disruption of balance between nitric oxide and reactive oxygen species, and inflammation are implicated in the pathogenesis of CRS. Medical therapy of heart failure including renin-angiotensin-aldosterone system inhibition and β-adrenergic blockade can blunt these deleterious processes. Renovascular disease can accelerate the progression of CRS. Volume overload and diuretic resistance are common and complicate the management of CRS. In heart failure and CRS being treated with diuretics, worsening creatinine is not associated with worsened outcome if clinical decongestion is achieved. Adjunctive therapy is often required in the management of volume overload in CRS, but evidence for these therapies is limited. Anemia and iron deficiency are importantly associated with CRS and might amplify decline of cardiac and renal function. End-stage cardiac and/or renal disease represents an especially poor prognosis with limited therapeutic options. Overall, worsening renal function is associated with significantly increased mortality. Despite progress in the area of CRS, there are still multiple pathophysiological and clinical aspects of CRS that need further research to eventually develop effective therapeutic options.
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Project description:BackgroundHeart failure is one of the most common diseases of adults in Europe, with an overall prevalence of 1-2%. Among persons aged 60 and above, its prevalence is above 10% in men and 8% in women. Acute heart failure has a poor prognosis; it is associated with a high rate of rehospitalization and a 1-year mortality of 20-30%.MethodsThis review is based on pertinent literature, including guidelines, retrieved by a selective search in PubMed.ResultsThere are different types of acute heart failure; the basic diagnostic assessment is performed at once and consists of ECG, echocardiography, and the measurement of N-terminal pro-brain natriuretic peptide (NTproBNP) and troponin levels. The most common causes of decompensation are arrhythmia, valvular dysfunction, and acute cardiac ischemia, each of which accounts for 30% of cases. The potential indication for immediate revascularization should be carefully considered in cases where acute heart failure is due to coronary heart disease. The basic treatment of acute heart failure is symptomatic, with the administration of oxygen, diuretics, and vasodilators. Ino-tropic agents, vasopressors, and temporary mechanical support for the circulatory system are only used to treat cardiogenic shock.ConclusionThe treatment of acute heart failure is markedly less evidence-based than that of chronic heart failure. Newer treatment approaches that are intended to improve outcomes still need to be tested in multicenter trials.
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