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Pubblicazioni recenti - cardiorenal
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The role of kidney injury molecule-1 in predicting cardiorenal syndrome type 1 after diuretic treatment.
Arch Med Sci Atheroscler Dis2019 ;4():e208-e214. doi: 10.5114/amsad.2019.87305.
Atici Adem, Emet Samim, Toprak Ilkim Deniz, Cakmak Ramazan, Akarsu Murat, Tukek Tufan,
Abstract
Introduction:
Cardiorenal syndrome (CRS) is defined as acute or chronic dysfunction in the heart and kidney due to important interactions between the heart and kidney disease. The aim of this study was to evaluate prediction of CRS type 1 by measuring kidney injury molecule-1 (KIM-1) and to establish early diagnosis of acute kidney injury (AKI).
Material and methods:
During 2015-2016, 146 patients who were admitted to the emergency service with acute decompensated HF were included in the study. We investigated urinary KIM-1 levels in 146 consecutive patients with decompensated heart failure before and after diuretic treatment. Statistical analyses were performed using the Statistical Package for the Social Sciences (SPSS - version 21.0)/Windows Statistical Software. values less than < 0.05 were considered significant.
Results:
There was a moderate negative correlation between the percentage change of creatinine values and the percentage change of KIM-1 values ( = -0.357, = 0.016). There was no statistically significant relationship between KIM-1 and the development of CRS type 1 ( = 0.011).
Conclusions:
No statistically significant relationship was observed between KIM-1 levels and the development of CRS type 1. In addition, there was no correlation between mortality in patients and KIM-1 values. It is thought that KIM-1 is not a potential prognostic indicator because renal tubular damage is only one of many factors in the pathophysiology of CRS type 1 and heart failure.
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Cardiac Inflammation after Ischemia-Reperfusion of the Kidney: Role of the Sympathetic Nervous System and the Renin-Angiotensin System.
Cell Physiol Biochem2019 ;53(4):587-605. doi: 10.33594/000000159.
Panico Karine, Abrahão Mariana V, Trentin-Sonoda Mayra, Muzi-Filho Humberto, Vieyra Adalberto, Carneiro-Ramos Marcela S,
Abstract
BACKGROUND/AIMS:
To investigate the role of the sympathetic nervous system (SNS) and renin-angiotensin system (RAS) in renal ischemia/reperfusion-induced (I/R) cardiac inflammatoryprofile.
METHODS:
Left kidney ischemia was induced in male C57BL/6 mice for 60 min, followed by reperfusion for 12 days, and treatment with or without atenolol, losartan, or enalapril. The expression of vimentin in kidney and atrial natriuretic factor (ANF) in the heart has been investigated by RT-PCR. In cardiac tissue, levels of ?-adrenoreceptors, adenylyl cyclase, cyclic AMP-dependent protein kinase (PKA), noradrenaline, adrenaline (components of SNS), type 1 angiotensin II receptors (ATR), angiotensinogen/Ang II and renin (components of RAS) have been measured by Western blotting and HPLC analysis. A panel of cytokines - tumour necrosis factor (TNF-?), interleukin IL-6, and interferon gamma (IFN-?) - was selected as cardiac inflammatory markers.
RESULTS:
Renal vimentin mRNA levels increased by >10 times in I/R mice, indicative of kidney injury. ANF, a marker of cardiac lesion, increased after renal I/R, the values being restored to the level of Sham group after atenolol or enalapril treatment. The cardiac inflammatory profile was confirmed by the marked increase in the levels of mRNAs of TNF-?, IL-6, and IFN-?. Atenolol and losartan reversed the upregulation of TNF-? expression, whereas enalapril restored IL-6 levels to Sham levels; both atenolol and enalapril normalized IFN-? levels. I/R mice showed upregulation of ?-adrenoreceptors, adenylyl cyclase, PKA and noradrenaline. Renal I/R increased cardiac levels of ATR, which decreased after losartan or enalapril treatment. Renin expression also increased, with the upregulation returning to Sham levels after treatment with SNS and RAS blockers. Angiotensinogen/Ang II levels in heart were unaffected by renal I/R, but they were significantly decreased after treatment with losartan and enalapril, whereas increase in renin levels decreased.
CONCLUSION:
Renal I/R-induced cardiac inflammatory events provoked by the simultaneous upregulation of SNS and RAS in the heart, possibly underpin the mechanism involved in the development of cardiorenal syndrome.
© Copyright by the Author(s). Published by Cell Physiol Biochem Press.
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Changes in Estimated Glomerular Filtration after Balloon Pulmonary Angioplasty for Chronic Thromboembolic Pulmonary Hypertension.
Cardiorenal Med2019 Sep;():1-10. doi: 10.1159/000502254.
Darocha Szymon, Banaszkiewicz Marta, Pietrasik Arkadiusz, Siennicka Anna, Piorunek Mateusz, Grochowska Emilia, Pi?ka Micha?, Dobosiewicz Anna, Florczyk Micha?, Pietura Rados?aw, Torbicki Adam, Kurzyna Marcin,
Abstract
BACKGROUND:
Balloon pulmonary angioplasty (BPA) is a novel treatment option for inoperable or persistent chronic thromboembolic pulmonary hypertension (CTEPH). Little is known about renal function in CTEPH patients undergoing BPA.
OBJECTIVES:
The aim of this study was to assess the frequency of contrast-induced acute kidney injury (CI-AKI) in patients with CTEPH undergoing BPA and to evaluate the relationship between hemodynamic and renal function.
METHODS:
A total of 41 CTEPH patients were included and 250 consecutive BPA sessions were analyzed for frequency of CI-AKI. The serum creatinine (SC) concentration was measured and the glomerular filtration rate (GFR) was estimated using the Modification of Diet in Renal Disease equation before and 72 h after each BPA procedure. CI-AKI was defined as an increase of 25% or 0.5 mg/dL in SC from the baseline value within 48-72 h of contrast administration. SC and GFR were assessed before and after 3-6 months of completing the BPA treatment and correlated with hemodynamic parameters.
RESULTS:
The SC concentration and GFR did not change significantly within 72 h after BPA (+1%, p = 0.921, and +4%, p = 0.112, respectively). CI-AKI was noted in 2 cases (0.8%). Significant improvement was noted in GFR (75.4 ± 21.2 vs. 80.9 ± 22.4 mL/min/1.73 m2; p = 0.012) in addition to improvement in right atrial pressure (RAP; 9.1 ± 4.1 to 5.0 ± 2.2 mm Hg; p < 0.001), mean pulmonary artery pressure (49.1 ± 10.7 to 29.8 ± 8.3 mm Hg; p < 0.001), cardiac index (CI; 2.42 ± 0.6 to 2.70 ± 0.6 L/min/m2; p = 0.004), and pulmonary vascular resistance (9.42 ± 3.6 to 4.4 ± 2.3 Wood units; p < 0.001). In a subpopulation of 12 patients with impaired renal function at baseline, the relative increase in GFR was significantly correlated with relative improvement in CI (r = 0.060; p = 0.037), RAP (r = -0.587; p = 0.044), and mixed venous saturation (r = 0.069; p = 0.012).
CONCLUSIONS:
Hemodynamically effective BPA procedures improve renal function in patients with CTEPH with a minimal risk of CI-AKI in the course of treatment.
© 2019 S. Karger AG, Basel.
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[Prognostic value of acute cardiorenal syndrome in patients with acute cardiac pathology].
Kardiologiia2019 Sep;59(8S):44-55. doi: 10.18087/cardio.2678.
Mezhonov E M, Vyalkina Ju A, Shalaev S V,
Abstract
AIM:
To assess the prevalence and prognostic value of AKI in patients with acute decompensation of chronic heart failure (ADCHF) with a reduced ejection fraction (HFrEF) and with preserved ejection fraction (HFpEF) or acute coronary syndrome (ACS), to identify predictors of AKI.
MATERIALS AND METHODS:
In a prospective study included 863 patients, of which 141 with ADCHF, 446 - non-ST-elevation acute coronary syndromes (NSTE-ACS) and 276 - ST-segment elevation myocardial infarction (STEMI). AKI was diagnosed according to KDIGO recommendations. The end point was defined as death from cardiovascular causes.
RESULT:
During the follow-up from 1 to 37 months (median follow-up was 18 months) for patients with ADCHF in 24,8 % an endpoint was reported. For patients with ACS, the observation time ranged from 1 day to 14 months (median follow-up was 12 months), in 4,3 % - NSTE-ACS, 10,9 % - STEMI the end point was recorded. AKI developed in 14,8 % of patients with ADCHF HFpEF and 11,2 % ADCHF HFrEF, in 23,1 % - STEMI and 21,4 % - NSTE-ACS. AKI increases the risk of death from cardiovascular causes in patients with ADCHF HFrEF (OR 95 % 98,750 (11,158-873,976), ?<0,001) and STEMI (OR 95 % 5,395 (2,451-11,878), p<0,001), but did not increase the risk of an endpoint occurrence in patients with ADCHF HFpEF (OR 95 % 1,875 (0,221-15,930), ?=0,565) and NSTE-ACS (OR 95 % 1,199 (0,421-3,412), ?=0,734). The multivariate analysis revealed risk factors for the development of AKI in patients with ADCHF HFrEF: high albuminuria (AU) from 30 mg / l (OR 95 % 5,763 (1,338-24,819), ?=0,019), GFR<45 ml / min initially at admission to hospital (OR 95 % 76,593 (1,193-36,446), p=0,031), age>75 years (OR 15,933 (1,020-248,856), ?=0,048). In patients with STEMI: age>75 years (OR 95 % 3,248 (1,476-7,146), p=0,003), female gender (OR 95 % 2,321 (1,190-4,526), p=0,013), acute heart failure (AHF) Killip IV (OR 95 % 10,334 (1,777-60,110), p=0,009). Risk factors for the development of AKI in patients with NSTE-ACS: age>75 years (OR 95 % 1,761 (1,051-2,949), ?=0,032), PCI on RCA (OR 95 % 2,565 (1,193-5,517), ?=0,016).
CONCLUSION:
In patients with ADCHF HFrEF and STEMI development AKI is associated with a poor prognosis, but does not affect the prognosis of patients with ADCHF HFpEF and NSTE-ACS. AKI in patients with ADCHF HFrEF can be predicted using predictors: GFR<45 ml / min, AU more than 30 mg / l and age>75 years. In patients with STEMI, the predictors of AKI were age>75 years, female gender, AHF Killip IV, and in patients with NSTE-ACS age>75 years, PCI on RCA.
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Caspase-1 as Molecular Key in Cardiac Remodeling during Cardiorenal Syndrome Type 3 in the Murine Model.
Curr Mol Med2019 Sep;():. doi: 10.2174/1566524019666190916153257.
Trentin-Sonoda Mayra, Fratoni Frayli Maltoni, da Cruz Junho Carolina Victoria, Silva Wellington Caio, Panico Karine, Carneiro-Ramos Marcela Sorelli,
Abstract
BACKGROUND:
Renal ischemia/reperfusion induces a systemic inflammatory response that is directly related to the development of cardiac hypertrophy due to cardiorenal syndrome type 3. Classic inflammatory pathways have been extensively investigated in cardiovascular diseases, including the participation of inflammasome in caspase-1-dependent IL-1? cleavage.
OBJECTIVE:
In this study, we aim to understand how caspase-1 participates in cardiac remodeling induced by apoptosis.
METHODS:
Wildtype and caspase-1 knockout animals were submitted to a renal ischemia/reperfusion protocol. Briefly, left kidney ischemia was induced in male C57BL/6 mice for 60 min, followed by reperfusion for 15 days. Gene expression has been investigated by Real Time PCR. Caspase activity was also evaluated.
RESULTS:
Lack of caspase-1 was sufficient to prevent the inflammatory response and cardiac dysfunction (such as an increase of QJ interval), however, caspase-1 knockout mice subjected to the renal ischemia/reperfusion protocol still developed cardiac hypertrophy. Assessment of caspase 3/7 and 9 activity suggests that the apoptotic response observed in this model is interleukin-1?-independent. The unexpected hypertrophy can be explained by the nuclear role of caspase-1 and inactivation of the transcription factor GATA-binding factor 4.
CONCLUSION:
Our data corroborates important findings on the role of caspase-1 in the development of cardiac hypertrophy and remodeling, even in the absence of inflammation.
Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
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Differential Regulation of ANP and BNP in Acute Decompensated Heart Failure: Deficiency of ANP.
JACC Heart Fail2019 Sep;():. doi: S2213-1779(19)30404-4.
Reginauld Shawn H, Cannone Valentina, Iyer Seethalakshmi, Scott Christopher, Bailey Kent, Schaefer Jacob, Chen Yang, Sangaralingham S Jeson, Burnett John C,
Abstract
OBJECTIVES:
This study investigated the differential regulation of circulating atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in patients with acute decompensated heart failure (ADHF) and tested the hypothesis that a relative deficiency of ANP exists in a subgroup of patients with ADHF.
BACKGROUND:
The endocrine heart releases the cardiac hormones ANP and BNP, which play a key role in cardiovascular (CV), renal, and metabolic homeostasis. In heart failure (HF), both plasma ANP and BNP are increased as a compensatory homeostatic response to myocardial overload.
METHODS:
ANP and BNP concentrations were measured in a small group of patients with ADHF (n = 112). To support this study's goal, a total of 129 healthy subjects were prospectively recruited to establish contemporary normal values for ANP and BNP. Plasma 3',5'cyclic guanosine monophosphate (cGMP), ejection fraction (EF), and body mass index (BMI) were measured in these subjects.
RESULTS:
In cases of ADHF, 74% of patients showed elevated ANP and BNP. Importantly, 26% of patients were characterized as having normal ANP (21% of this subgroup had normal ANP and elevated BNP). Cyclic GMP was lowest in the ADHF group with normal levels of ANP (p < 0.001), whereas BMI and EF were inversely related to ANP levels (p = 0.003).
CONCLUSIONS:
Among a subgroup of patients hospitalized with ADHF, the presence of an ANP deficiency is consistent with a differential regulation of ANP and BNP and suggests the existence of a potentially compromised compensatory cardiac endocrine response. These findings have implications for the pathophysiology, diagnostics, and therapeutics of human HF.
Copyright © 2019 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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Native T1 time and extracellular volume fraction in differentiation of normal myocardium from non-ischemic dilated and hypertrophic cardiomyopathy myocardium: A systematic review and meta-analysis.
Int J Cardiol Heart Vasc2019 Dec;25():100422. doi: 10.1016/j.ijcha.2019.100422.
Minegishi Shintaro, Kato Shingo, Takase-Minegishi Kaoru, Horita Nobuyuki, Azushima Kengo, Wakui Hiromichi, Ishigami Tomoaki, Kosuge Masami, Kimura Kazuo, Tamura Kouichi,
Abstract
Background:
Both native T1 time and extracellular volume (ECV) fraction have been shown to be important measures for the detection of myocardial fibrosis. However, ECV determination requires the administration of an intravenous contrast agent, whereas native T1 mapping can be performed without a contrast agent.
Methods:
Here, we conducted a meta-analysis of myocardial native T1 data obtained for non-ischemic cardiomyopathy (NIC) patients and controls. A literature review included studies that applied T1 mapping using modified Look-Locker inversion recovery to measure myocardial fibrosis, and the results were validated by comparing datasets for dilated cardiomyopathy (DCM) or hypertrophic cardiomyopathy (HCM) patients and healthy controls (HCs).
Results:
We identified 16 eligible studies. Pooled mean differences (MDs) and 95% confidence intervals (CIs) were estimated as follows. Native T1 at 1.5-T, DCM vs. HC: MD?=?45.26 (95% CI: 30.92-59.59); HCM vs. HC: MD?=?47.09 (95% CI: 32.42-61.76). Native T1 at 3.0-T, DCM vs. HC: MD?=?82.52 (95% CI: 47.60-117.44); HCM vs. HC: MD?=?115.87 (95% CI: 50.71-181.04). ECV at 1.5-T, DCM vs. HC: MD?=?4.26 (95% CI: 3.06-5.46); HCM vs. HC: MD?=?1.49 (95% CI: -1.45-4.43). ECV at 3.0-T, DCM vs. HC: MD?=?8.40 (95% CI: 2.94-13.86); HCM vs. HC: MD?=?8.02 (95% CI: 5.45-1-0.59).
Conclusion:
In conclusion, native T1 values were significantly different between NIC patients and controls. Native T1 mapping may be a useful noninvasive method to detect diffuse myocardial fibrosis in NIC patients.
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Doxorubicin induces trans-differentiation and MMP1 expression in cardiac fibroblasts via cell death-independent pathways.
PLoS One2019 ;14(9):e0221940. doi: 10.1371/journal.pone.0221940.
Narikawa Masatoshi, Umemura Masanari, Tanaka Ryo, Hikichi Mayu, Nagasako Akane, Fujita Takayuki, Yokoyama Utako, Ishigami Tomoaki, Kimura Kazuo, Tamura Kouichi, Ishikawa Yoshihiro,
Abstract
Although doxorubicin (DOX)-induced cardiomyopathy causes lethal heart failure (HF), no early detection or effective treatment methods are available. The principal mechanisms of cardiotoxicity are considered to involve oxidative stress and apoptosis of cardiomyocytes. However, the effect of DOX on cardiac fibroblasts at non-lethal concentrations remains unknown. The aim of this study was to investigate the direct effect of doxorubicin on the activation of cardiac fibroblasts independent of cell death pathways. We first found that DOX induced ?-SMA expression (marker of trans-differentiation) at a low concentration range, which did not inhibit cell viability. DOX also increased MMP1, IL-6, TGF-? and collagen expression in human cardiac fibroblasts (HCFs). In addition, DOX promoted Akt and Smad phosphorylation. A Smad inhibitor prevented DOX-induced ?-SMA and IL-6 protein expression. An PI3K inhibitor also prevented MMP1 mRNA expression in HCFs. These findings suggest that DOX directly induces fibrotic changes in HCFs via cell death-independent pathways. Furthermore, we confirmed that these responses are organ- and species-specific for HCFs based on experiments using different types of human and murine fibroblast cell lines. These results suggest potentially new mechanisms of DOX-induced cardiotoxicity from the viewpoint of fibrotic changes in cardiac fibroblasts.
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Primary versus secondary cardiorenal prevention in type 2 diabetes: Which newer antihyperglycaemic drug matters?
Diabetes Obes Metab2019 Sep;():. doi: 10.1111/dom.13881.
Giugliano Dario, Ceriello Antonio, De Nicola Luca, Perrone-Filardi Pasquale, Cosentino Francesco, Esposito Katherine,
Abstract
We are observing a resurgence of major diabetic vascular complications after a period of dramatic decrease in 1990-2010?years. The classical division of the cardiovascular prevention in primary (with an event) and secondary (without an event) is largely used to describe the cardiovascular risk in type 2 diabetes (T2D); however, there is evidence that the diabetic cardiovascular risk may range from the highest one in patients with a previous cardiovascular event to a mild one in patients with the main risk factors at target. Herein, we present details of the 14 cardiovascular outcome trials (CVOTs) published so far, including the total population investigated, and their separation into primary (T2D + multiple risk factors) and secondary prevention (T2D + established CVD) population as detailed within the trials; and summarize evidence for the effects of dipeptidyl peptidase-4 inhibitors (DPP-4i), glucagon-like peptide-1 receptor agonists (GLP1-RA) and sodium glucose co-transporter-2 inhibitors (SGLT-2i) versus placebo on risk of MACE, HF and DKD. In primary prevention, SGLT-2i reduce both the risk of hospitalization for HF and progression of DKD; in secondary prevention, SGLT-2i are effective on the three endpoints, DPP-4i are neutral, while GLP1-RA show mixed results. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
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Inhibition of the renin-angiotensin system in the cardiorenal syndrome with anaemia: a double-edged sword.
J Hypertens2019 Sep;():. doi: 10.1097/HJH.0000000000002111.
Vlahakos Demetrios V, Tsioufis Costas, Manolis Athanasios, Filippatos Gerasimos, Marathias Katerina P, Papademetriou Vasilios, Mancia Giuseppe,
Abstract
: The term 'cardiorenal syndrome' (CRS) was introduced to describe problems related to the simultaneous existence of heart and renal insufficiency. The prevalence of anaemia in CRS is high and increases the risk of hospitalizations and death. Renin-angiotensin system (RAS) inhibition is the cornerstone therapy in cardiovascular and renal medicine. As angiotensin II regulates both glomerular filtration rate (GFR) and erythropoiesis, RAS inhibition can further deteriorate renal function and lower hematocrit or cause anaemia in patients with heart failure. The aim of this review is to explore the relationship among CRS, anemia and administration of angiotensin-converting enzyme inhibitor (ACEi) or angiotensin receptor blocker (ARB) and summarize the evidence suggesting that RAS inhibition may be considered an iatrogenic cause of deterioration of CRS with anemia. It should be emphasized however, that RAS inhibition reduces mortality in both groups with and without worsening of renal function, and therefore, no patient with CRS should be denied an ACEi or ARB trial without careful evaluation.
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Piperine ameliorates the severity of fibrosis via inhibition of TGF??/SMAD signaling in a mouse model of chronic pancreatitis.
Mol Med Rep2019 Oct;20(4):3709-3718. doi: 10.3892/mmr.2019.10635.
Choi Ji-Won, Lee Sung-Kon, Kim Myoung-Jin, Kim Dong-Gu, Shin Joon-Yeon, Zhou Ziqi, Jo Il-Joo, Song Ho-Joon, Bae Gi-Sang, Park Sung-Joo,
Abstract
Chronic pancreatitis (CP) is characterized by recurrent pancreatic injury, resulting in inflammation and fibrosis. Currently, there are no drugs for the treatment of pancreatic fibrosis associated with CP. Piperine, a natural alkaloid found in black pepper, has been reported to show anti?inflammatory, anti?oxidative, and antitumor activities. Although piperine exhibits numerous properties in regards to the regulation of diverse diseases, the effects of piperine on CP have not been established. To investigate the effects of piperine on CP in vivo, we induced CP in mice through the repetitive administration of cerulein (50 µg/kg) six times at 1?h intervals, 5 times per week, for a total of 3 weeks. In the pre?treatment groups, piperine (1, 5, or 10 mg/kg) or corn oil were administrated orally at 1 h before the first cerulein injection, once a day, 5 times a week, for a total of 3 weeks. In the post?treatment groups, piperine (10 mg/kg) or corn oil was administered orally at 1 or 2 week after the first cerulein injection. Pancreases were collected for histological analysis. In addition, pancreatic stellate cells (PSCs) were isolated to examine the anti?fibrogenic effects and regulatory mechanisms of piperine. Piperine treatment significantly inhibited histological damage in the pancreas, increased the pancreatic acinar cell survival, reduced collagen deposition and reduced pro?inflammatory cytokines and chemokines. In addition, piperine treatment reduced the expression of fibrotic mediators, such as ??smooth muscle actin (??SMA), collagen, and fibronectin 1 in the pancreas and PSCs. Moreover, piperine treatment reduced the production of transforming growth factor (TGF)?? in the pancreas and PSCs. Furthermore, piperine treatment inhibited TGF???induced pSMAD2/3 activation but not pSMAD1/5 in the PSCs. These findings suggest that piperine treatment ameliorates pancreatic fibrosis by inhibiting TGF??/SMAD2/3 signaling during CP.
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Successful Peritoneal Dialysis for the Treatment of Inotrope-Dependent End-Stage Heart Failure.
Int Heart J2019 Sep;():. doi: 10.1536/ihj.18-550.
Sugiura Emiyo, Dohi Kaoru, Tanimura Muneyoshi, Kumagai Naoto, Ishikawa Eiji, Ito Masaaki,
Abstract
Extra- and/or intracorporeal renal replacement therapy can improve the cardiorenal hemodynamics in patients with advanced heart failure (HF) refractory to medical therapy and renal failure. Here, we report the case of a 51-year-old woman with inotrope-dependent end-stage HF and chronic renal failure due to anthracycline-induced cardiomyopathy, in whom the induction of hemodiafiltration and subsequent chronic peritoneal dialysis (PD) provided a dramatic improvement of her cardiac hemodynamics from restrictive to almost normal physiology assessed by echocardiography and cardiac catheterization. The patient returned to office work with New York Heart Association functional class I-II symptoms for at least 3 years with continuous ambulatory PD after hospital discharge.
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Prognostic Value of Cysteine-Rich Protein 61 Combined with N-Terminal Pro-B-Type Natriuretic Peptide for Mortality in Acute Heart Failure Patients with and without Chronic Kidney Disease.
Cardiorenal Med2019 Aug;():1-11. doi: 10.1159/000501929.
Liu Chen, Liang Weihao, He Xin, Owusu-Agyeman Marvin, Wu Zexuan, Zhou Yuanyuan, Cao Yalin, Zhang Chongyu, Liu Jian, Jiang Jingzhou, Dong Bin, Xue Ruicong, Wu Dexi, Dong Yugang, Zhao Jingjing,
Abstract
BACKGROUND:
The ability of most biomarkers, such as N-terminal pro-B-type natriuretic peptide (NT-proBNP), to predict prognosis in heart failure can be affected by the state of renal function; therefore, there is the need for a biomarker that can predict prognosis accurately without the influence of renal function. The prognostic value of cysteine-rich protein 61 (CYR61/CCN1) in acute heart failure (AHF) patients has been proven.
METHODS:
A total of 248 patients hospitalized with AHF were recruited in this study, and serum CCN1 levels, NT-proBNP levels, and other necessary data of patients were collected upon admission. The correlation of serum CCN1 with estimated glomerular filtration rate (eGFR) was investigated, and the logistic regression model was used to investigate the prognostic value of serum CCN1 for 3-month mortality.
RESULTS:
Fifty-four of 248 patients died (21.8%) during a 3-month follow-up. Serum CCN1 had no significant correlation with eGFR (rho = -0.088, p = 0.167). In the overall population and patients without chronic kidney disease, results showed that both serum CCN1 and NT-proBNP were significantly associated with 3-month mortality. In patients with chronic kidney disease, serum CCN1 was significantly associated with 3-month mortality in logistic regression analysis (odds ratio = 2.40, p = 0.002) while NT-proBNP was not. Further in tertile group comparison, in patients with chronic kidney disease, higher tertile levels of serum CCN1 had a significantly higher risk of 3-month mortality compared to the lower tertile ones (odds ratio = 4.17, p = 0.013), but that of NT-proBNP did not.
CONCLUSION:
Serum CCN1 level is not associated with eGFR, and it maintains the prognostic value in AHF patients with chronic kidney disease. CCN1 could be a potential novel prognostic biomarker in AHF patients with chronic kidney disease.
© 2019 S. Karger AG, Basel.
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Implication of Acute Kidney Injury in Heart Failure.
Heart Fail Clin2019 Oct;15(4):463-476. doi: S1551-7136(19)30038-8.
Ronco Claudio, Bellasi Antonio, Di Lullo Luca,
Abstract
Patients with acute or chronic decompensated heart failure (ADHF) present with various degrees of heart and kidney dysfunction characterizing cardiorenal syndrome (CRS). CRS can be generally defined as a pathophysiologic disorder of the heart and kidneys whereby acute or chronic dysfunction of 1 organ may induce acute or chronic dysfunction of the other. ADHF is a challenge in the management of heart failure. This review provides an overview the pathophysiology of type 1 CRS together with new approaches to treatment in patients with heart failure with worsening renal function or acute kidney disease.
Copyright © 2019 Elsevier Inc. All rights reserved.
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Cardiorenal Interactions, Diuretic Resistance, and Acute Heart Failure: Renal Response vs Renal Function.
Can J Cardiol -
Preeminent Role of the Cardiorenal Axis in the Antihypertensive Response to an Arteriovenous Fistula: An Analysis.
Am J Physiol Heart Circ Physiol2019 Aug;():. doi: 10.1152/ajpheart.00354.2019.
Clemmer John S, Pruett William Andrew, Hester Robert L, Lohmeier Thomas E,
Abstract
Percutaneous creation of a small central arteriovenous (AV) fistula is currently being evaluated for the treatment of uncontrolled hypertension (HT). Although the mechanisms that contribute to the antihypertensive effects of the fistula are unclear, investigators have speculated that chronic blood pressure (BP) lowering may be due to: 1) reduced total peripheral resistance (TPR), 2) increased secretion of atrial natriuretic peptide (ANP), and/or 3) suppression of renal sympathetic nerve activity (RSNA). We used an established integrative mathematical model of human physiology to investigate these possibilities from baseline conditions that mimic sympathetic overactivity and impaired renal function in patients with resistant HT. After simulating a small fistula there were sustained increases in cardiac output, atrial pressures, and plasma ANP concentration (3-fold), without suppression of RSNA; at 8 weeks BP was reduced 14 mmHg along with a 32% fall in TPR. In contrast, when this simulation was repeated while clamping ANP at baseline BP decreased only 4 mmHg, despite a comparable fall in TPR. Further, when chronic resetting of atrial mechanoreceptors was prevented during the fistula RSNA decreased 7% and, along with the same 3-fold increase in ANP, BP fell 19 mmHg. This exaggerated fall in BP occurred with a similar decrease in TPR when compared to the above simulations. These findings suggest that ANP, but not TPR, is a key determinant of long-term BP lowering after the creation of an AV fistula and support a contribution of suppressed RSNA if resetting of the atrial-renal reflex is truly incomplete.
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[Cardiovascular pharmacotherapy and coronary revascularization in end-stage renal failure].
Herz2019 Aug;():. doi: 10.1007/s00059-019-04846-6.
Lauder L, Ewen S, Emrich I E, Böhm M, Mahfoud F,
Abstract
There is a close physiological relationship between the kidneys and the heart. Cardiovascular diseases are the most prevalent cause of death in patients with chronic kidney disease (CKD), whereas CKD may directly accelerate the progression of cardiovascular diseases and is considered to be a cardiovascular risk factor. In patients with mild CKD, i.e. an estimated glomerular filtration rate (eGFR) >60?ml/min/1.73?m, treatment of coronary artery disease and chronic heart failure is not essentially different from patients with preserved renal function; however, as most pivotal trials have systematically excluded patients with advanced renal failure, many treatment recommendations in this patient group are based on observational studies, post hoc subgroup analyses and meta-analyses or pathophysiological considerations, which are not supported by controlled studies. Therefore, prospective randomized studies on the management of heart failure and coronary artery disease are needed, which should specifically focus on the growing number of patients with advanced renal functional impairment.
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Association between food insecurity, cardiorenal syndrome and all-cause mortality among low-income adults.
Nutr Health2019 Aug;():260106019869069. doi: 10.1177/0260106019869069.
Banerjee Srikanta, Radak Timothy,
Abstract
BACKGROUND:
Food insecurity is known to be a major public health issue. There is limited data on food insecurity and chronic disease in the general population.
AIM:
We aimed to assess effect of food insecurity on mortality of individuals with chronic disease like cardiorenal syndrome (CRS).
METHODS:
The study was conducted on participants aged 20 years or older in the United States living below the 130% Federal Poverty Level. We assessed food insecurity utilizing the Household Food Security Survey Module in NHANES survey for the years 1999 to 2010 with mortality follow-up. Prospective analysis was performed using complex samples Cox regression with adjustment for known confounders to determine the relationship of food insecurity and CRS.
RESULTS:
Prevalence of food insecurity among the low-income population was 16.1% among males and 21.7% among females. The mean follow-up was 6.5 years. For all-cause mortality, the overall unadjusted hazard ratio (HR) of food insecurity to no food insecurity was 1.28 (95% confidence interval [CI], 1.18-1.37, p < 0.001). Adjusted HR was elevated, 2.81 (CI 1.57-5.05, p < 0.001), among participants who were CRS-positive and food insecure but closer to 1.0 (2.48 CI 1.73-3.55, p < 0.001) among those who were CRS-positive and food secure, after controlling for medical and demographic risk factors.
CONCLUSIONS:
Food insecurity is associated with higher mortality than food security. Food insecurity also may modify the effect of CRS on all-cause mortality in a representative general population. Social policy, when addressing food insecurity, should be inclusive among those with specific chronic diseases.
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A comprehensive analysis of the effects of rivaroxaban on stroke or transient ischaemic attack in patients with heart failure, coronary artery disease, and sinus rhythm: the COMMANDER HF trial
Eur Heart J2019 Jun;():. doi: 10.1093/eurheartj/ehz427.
Mehra Mandeep R, Vaduganathan Muthiah, Fu Min, Ferreira Joao Pedro, Anker Stefan D, Cleland John G F, Lam Carolyn S P, van Veldhuisen Dirk J, Byra William M, Spiro Theodore E, Deng Hsiaowei, Zannad Faiez, Greenberg Barry,
Abstract
Aims:
Stroke is often a devastating event among patients with heart failure with reduced ejection (HFrEF). In COMMANDER HF, rivaroxaban 2.5?mg b.i.d. did not reduce the composite of first occurrence of death, stroke, or myocardial infarction compared with placebo in patients with HFrEF, coronary artery disease (CAD), and sinus rhythm. We now examine the incidence, timing, type, severity, and predictors of stroke or a transient ischaemic attack (TIA), and seek to establish the net clinical benefit of treatment with low-dose rivaroxaban.
Methods and results:
In this double-blind, randomized trial, 5022 patients who had HFrEF(?40%), elevated natriuretic peptides, CAD, and who were in sinus rhythm were treated with rivaroxaban 2.5?mg b.i.d. or placebo in addition to antiplatelet therapy, after an episode of worsening HF. The primary neurological outcome for this post hoc analysis was time to first event of any stroke or TIA. Over a median follow-up of 20.5 (25th?75th percentiles 20.0?20.9) months, 150 all-cause stroke (127) or TIA (23) events occurred (ischaemic stroke in 82% and haemorrhagic stroke in 11% of stroke events). Overall, 47.5% of first-time strokes were either disabling (16.5%) or fatal (31%). Prior stroke, low body mass index, geographic region, and the CHA2DS2-VASc score were predictors of stroke/TIA. Rivaroxaban significantly reduced the primary neurological endpoint of all-cause stroke or TIA compared with placebo by 32% (1.29 events vs. 1.90 events per 100 patient-years), adjusted for the time from index HF event to randomization and stratified by geographic region (adjusted hazard ratio 0.68, 95% confidence interval 0.49?0.94), with a number needed to treat of 164 patients per year to prevent one stroke/TIA event. The principal safety endpoint of fatal bleeding or bleeding into a critical space, occurred at a similar rate on rivaroxaban and placebo (0.44 events vs. 0.55 events per 100 patient-years).
Conclusion:
Patients with HFrEF and CAD are at risk for stroke or TIA in the period following an episode of worsening heart failure in the absence of atrial fibrillation. Most strokes are of ischaemic origin and nearly half are either disabling or fatal. Rivaroxaban at a dose of 2.5?mg b.i.d. reduced rates of stroke or TIA compared with placebo in this population.
Trial Registration:
COMMANDER HF (A Study to Assess the Effectiveness and Safety of Rivaroxaban in Reducing the Risk of Death, Myocardial Infarction, or Stroke in Participants with Heart Failure and Coronary Artery Disease Following an Episode of Decompensated Heart Failure); ClinicalTrials.gov NCT01877915.
The Author(s) 2019. Published by Oxford University Press on behalf of the European Society of Cardiology.
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Improved home BP profile with dapagliflozin is associated with amelioration of albuminuria in Japanese patients with diabetic nephropathy: the Yokohama add-on inhibitory efficacy of dapagliflozin on albuminuria in Japanese patients with type 2 diabetes study (Y-AIDA study).
Cardiovasc Diabetol2019 Aug;18(1):110. doi: 10.1186/s12933-019-0912-3.
Kinguchi Sho, Wakui Hiromichi, Ito Yuzuru, Kondo Yoshinobu, Azushima Kengo, Osada Uru, Yamakawa Tadashi, Iwamoto Tamio, Yutoh Jun, Misumi Toshihiro, Aoki Kazutaka, Yasuda Gen, Yoshii Taishi, Yamada Takayuki, Ono Syuji, Shibasaki-Kurita Tomoko, Hosokawa Saho, Orime Kazuki, Hanaoka Masaaki, Sasaki Hiroto, Inazumi Kohji, Yamada Taku, Kobayashi Ryu, Ohki Kohji, Haruhara Kotaro, Kobayashi Yusuke, Yamanaka Takeharu, Terauchi Yasuo, Tamura Kouichi,
Abstract
BACKGROUND:
The Y-AIDA study was designed to investigate the renal- and home blood pressure (BP)-modulating effects of add-on dapagliflozin treatment in Japanese individuals with type 2 diabetes mellitus (T2DM) and albuminuria.
METHODS:
We conducted a prospective, multicenter, single-arm study. Eighty-six patients with T2DM, HbA1c 7.0-10.0%, estimated glomerular filtration rate (eGFR)???45 mL/min/1.73 m, and urine albumin-to-creatinine ratio (UACR)???30 mg/g creatinine (gCr) were enrolled, and 85 of these patients were administered add-on dapagliflozin for 24 weeks. The primary and key secondary endpoints were change from baseline in the natural logarithm of UACR over 24 weeks and change in home BP profile at week 24.
RESULTS:
Baseline median UACR was 181.5 mg/gCr (interquartile range 47.85, 638.0). Baseline morning, evening, and nocturnal home systolic/diastolic BP was 137.6/82.7 mmHg, 136.1/79.3 mmHg, and 125.4/74.1 mmHg, respectively. After 24 weeks, the logarithm of UACR decreased by 0.37?±?0.73 (P?
CONCLUSIONS:
In Japanese patients with T2DM and diabetic nephropathy, dapagliflozin significantly improved albuminuria levels and the home BP profile. Improved morning home systolic BP was associated with albuminuria reduction. Trial registration The study is registered at the UMIN Clinical Trials Registry (UMIN000018930; http://www.umin.ac.jp/ctr/index-j.htm ). The study was conducted from July 1, 2015 to August 1, 2018.
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