SOSTIENICI
Pubblicazioni recenti - dilated cardiomyopathy
-
Single-pass albumin dialysis and hemoadsorption for bilirubin and bile acids removal for a child with hyperbilirubinemia after ventricular assist device implantation.
J Artif Organs2022 Jan;():. doi: 10.1007/s10047-022-01309-4.
Hui Wun Fung, Lun Kin Shing, Hon Kam Lun,
Abstract
We report the successful management of hyperbilirubinemia using two different modalities of extracorporeal bilirubin removal therapy for a pediatric patient. A 13-year-old boy with dilated cardiomyopathy requiring veno-arterial extracorporeal membrane oxygenation (VA-ECMO) developed acute kidney injury and was dependent on continuous renal replacement therapy. He developed hyperbilirubinemia with a peak total bilirubin level of 786 ?mol/L after implantation of biventricular assist device (BiVAD). Extracorporeal bilirubin and bile acids removal using single-pass albumin dialysis (SPAD) with 4% albumin as dialysate brought down the bilirubin level to 672 ?mol/L after 21 h of therapy. Subsequently, he was started on two sessions of hemoadsorption using the Cytosorb® column which further lowered the total bilirubin level to 306 ?mol/ in 24 h and 173 ?mol/ after the treatment. No complication was encountered. Our case illustrated that both SPAD and hemoadsorption can effectively and safely reduce the serum bilirubin and bile acid levels in pediatric patients with BiVAD implantation. The ease of set-up, faster rate of bilirubin decline and capability of cytokine removal make hemoadsorption a favorable alternative to albumin dialysis.
© 2022. The Japanese Society for Artificial Organs.
Guarda su PubMed
-
Circadian REV-ERBs repress to activate NAMPT-dependent NAD biosynthesis and sustain cardiac function.
Nat Cardiovasc Res2022 Jan;1(1):45-58. doi: 10.1038/s44161-021-00001-9.
Dierickx Pieterjan, Zhu Kun, Carpenter Bryce J, Jiang Chunjie, Vermunt Marit W, Xiao Yang, Luongo Timothy S, Yamamoto Tsunehisa, Martí-Pàmies Íngrid, Mia Sobuj, Latimer Mary, Diwan Abhinav, Zhao Juanjuan, Hauck Amy K, Krusen Brianna, Nguyen Hoang C B, Blobel Gerd A, Kelly Daniel P, Pei Liming, Baur Joseph A, Young Martin E, Lazar Mitchell A,
Abstract
The heart is a highly metabolic organ that uses multiple energy sources to meet its demand for ATP production. Diurnal feeding-fasting cycles result in substrate availability fluctuations which, together with increased energetic demand during the active period, impose a need for rhythmic cardiac metabolism. The nuclear receptors REV-ERB? and ? are essential repressive components of the molecular circadian clock and major regulators of metabolism. To investigate their role in the heart, here we generated mice with cardiomyocyte (CM)-specific deletion of both s, which died prematurely due to dilated cardiomyopathy. Loss of markedly downregulated fatty acid oxidation genes prior to overt pathology, which was mediated by induction of the transcriptional repressor E4BP4, a direct target of cardiac REV-ERBs. E4BP4 directly controls circadian expression of and its biosynthetic product NAD via distal -regulatory elements. Thus, REV-ERB-mediated E4BP4 repression is required for expression and NAD production by the salvage pathway. Together, these results highlight the indispensable role of circadian REV-ERBs in cardiac gene expression, metabolic homeostasis and function.
Guarda su PubMed
-
Myocardial Rev-erb-Mediated Diurnal Metabolic Rhythm and Obesity Paradox.
Circulation2022 Jan;():. doi: 10.1161/CIRCULATIONAHA.121.056076.
Song Shiyang, Tien Chih-Liang, Cui Hao, Basil Paul, Zhu Ningxia, Gong Yingyun, Li Wenbo, Li Hui, Fan Qiying, Choi Jong Min, Luo Weijia, Xue Yanfeng, Cao Rui, Zhou Wenjun, Ortiz Andrea R, Stork Brittany, Mundra Vatsala, Putluri Nagireddy, York Brian, Chu Maoping, Chang Jiang, Jung Sung Yun, Xie Liang, Song Jiangping, Zhang Lilei, Sun Zheng,
Abstract
The nuclear receptor Rev-erb?/?, a key component of the circadian clock, emerges as a drug target for heart diseases, but the function of cardiac Rev-erb has not been studied in vivo. Circadian disruption is implicated in heart diseases, but it is unknown whether cardiac molecular clock dysfunction is associated with the progression of any naturally occurring human heart diseases. Obesity paradox refers to the seemingly protective role of obesity for heart failure, but the mechanism is unclear. We generated mouse lines with cardiac-specific Rev-erb?/? knockout (KO), characterized cardiac phenotype, conducted multi-omics (RNA-seq, ChIP-seq, proteomics, and metabolomics) analyses, and performed dietary and pharmacologic rescue experiments to assess the time-of-the-day effects. We compared the temporal pattern of cardiac clock gene expression with the cardiac dilation severity in failing human hearts. KO mice display progressive dilated cardiomyopathy (DCM) and lethal heart failure. Inducible ablation of Rev-erb?/? in adult hearts causes similar phenotypes. Impaired fatty acid oxidation in the KO myocardium, particularly in the light cycle, precedes contractile dysfunctions with a reciprocal overreliance on carbohydrate utilization, particularly in the dark cycle. Increasing dietary lipids or sugars supply in the dark cycle does not affect cardiac dysfunctions in KO mice. However, obesity coupled with systemic insulin resistance paradoxically ameliorates cardiac dysfunctions in KO mice, associated with rescued expression of lipid oxidation genes only in the light cycle in phase with increased fatty acids availability from adipose lipolysis. Inhibition of glycolysis in the light cycle and lipid oxidation in the dark cycle, but not vice versa, ameliorates cardiac dysfunctions in KO mice. Altered temporal patterns of cardiac Rev-erb gene expression correlate with the cardiac dilation severity in human hearts with DCM. The study delineates temporal coordination between clock-mediated anticipation and nutrient-induced response in myocardial metabolism at multi-omics levels. The obesity paradox is attributable to increased cardiac lipids supply from adipose lipolysis in the fasting cycle due to systemic insulin resistance and adiposity. Cardiac molecular chronotypes may be involved in human DCM. Myocardial bioenergetics downstream of Rev-erb may be a chronotherapy target in treating heart failure and DCM.
Guarda su PubMed
-
Design and rationale for a comparison study of Olmesartan and Valsartan On myocardial metabolism In patients with Dilated cardiomyopathy (OVOID) trial: study protocol for a randomized controlled trial.
Trials2022 Jan;23(1):36. doi: 10.1186/s13063-021-05970-7.
Jo Sua, Moon Hyeyeon, Park Kyungil, Sohn Chang-Bae, Kim Jeonghwan, Kwon Yong-Seop, Kim Su Hong,
Abstract
BACKGROUND:
Dilated cardiomyopathy (DCMP) is characterized by ventricular chamber enlargement and systolic dysfunction which may cause heart failure. Patients with DCMP have overactivation of the renin-angiotensin-aldosterone systems, which can also adversely affect myocardial metabolism in heart failure. The impairment of myocardial metabolism can contribute to the progression of left ventricular remodeling and contractile dysfunction in heart failure. Although angiotensin II receptor blockers (ARBs) have been used to treat patients with DCMP, there has been no direct comparison of the efficacy of these agents. The objective of this study is to compare the effects of olmesartan and valsartan on myocardial metabolism in patients with DCMP.
METHODS/DESIGN:
The OVOID study (a comparison study of Olmesartan and Valsartan On myocardial metabolism In patients with Dilated cardiomyopathy) is designed as a non-blinded, open-label, parallel-group, prospective, randomized, controlled, multicenter clinical trial. A total of 40 DCMP patients aged between 20 and 85?years will be randomly allocated into the olmesartan or the valsartan group. F-fluoro-2-deoxyglucose (FDG) cardiac positron emission tomography (PET) will be performed at baseline and six months after receiving the study agent. The primary endpoint is myocardial glucose consumption per square meter, measured using F-FDG PET 6 months after receiving the study agent.
DISCUSSION:
The purpose of this trial is to compare the efficacy between olmesartan and valsartan in improving myocardial metabolism in DCMP patients. This will be the first randomized comparative study investigating the differential effects of ARBs on heart failure.
TRIAL REGISTRATION:
ClinicalTrials.gov NCT04174456 . Registered on 18 November 2019.
© 2022. The Author(s).
Guarda su PubMed
-
An Explainable Machine Learning Approach Reveals Prognostic Significance of Right Ventricular Dysfunction in Nonischemic Cardiomyopathy.
JACC Cardiovasc Imaging2022 Jan;():. doi: S1936-878X(21)00902-5.
Fahmy Ahmed S, Csecs Ibolya, Arafati Arghavan, Assana Salah, Yankama Tuyen T, Al-Otaibi Talal, Rodriguez Jennifer, Chen Yi-Yun, Ngo Long H, Manning Warren J, Kwong Raymond Y, Nezafat Reza,
Abstract
OBJECTIVES:
We implemented an explainable machine learning (ML) model to gain insight into the association between cardiac magnetic resonance markers and adverse outcomes of cardiovascular hospitalization and all-cause death (composite endpoint) in patients with nonischemic dilated cardiomyopathy (NICM).
BACKGROUND:
Risk stratification of patients with NICM remains challenging. An explainable ML model has the potential to provide insight into the contributions of different risk markers in the prediction model.
METHODS:
An explainable ML model based on extreme gradient boosting (XGBoost) machines was developed using cardiac magnetic resonance and clinical parameters. The study cohorts consist of patients with NICM from 2 academic medical centers: Beth Israel Deaconess Medical Center (BIDMC) and Brigham and Women's Hospital (BWH), with 328 and 214 patients, respectively. XGBoost was trained on 70% of patients from the BIDMC cohort and evaluated based on the other 30% as internal validation. The model was externally validated using the BWH cohort. To investigate the contribution of different features in our risk prediction model, we used Shapley additive explanations (SHAP) analysis.
RESULTS:
During a mean follow-up duration of 40 months, 34 patients from BIDMC and 33 patients from BWH experienced the composite endpoint. The area under the curve for predicting the composite endpoint was 0.71 for the internal BIDMC validation and 0.69 for the BWH cohort. SHAP analysis identified parameters associated with right ventricular (RV) dysfunction and remodeling as primary markers of adverse outcomes. High risk thresholds were identified by SHAP analysis and thus provided thresholds for top predictive continuous clinical variables.
CONCLUSIONS:
An explainable ML-based risk prediction model has the potential to identify patients with NICM at risk for cardiovascular hospitalization and all-cause death. RV ejection fraction, end-systolic and end-diastolic volumes (as indicators of RV dysfunction and remodeling) were determined to be major risk markers.
Copyright © 2022 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
Guarda su PubMed
-
Myocardial inflammation and sudden death in the inherited cardiomyopathies.
Can J Cardiol2022 Jan;():. doi: S0828-282X(22)00047-2.
McKenna William J, Caforio Alida L P,
Abstract
The best studied of the inherited cardiomyopathies, hypertrophic (HCM), dilated (DCM) and arrhythmogenic (ACM), present overlapping clinical phenotypes with varying, often unrecognized risk of sudden death. Risk assessment is informed by patient sex and by the specific disease-causing variant. HCM and arrhythmogenic right ventricular cardiomyopathy (ARVC) remain important causes of sudden death. A phenotype mimicking DCM in patients with inherited ACM is associated with premature sudden death in families with overlapping DCM/ACM phenotypes. The role of inflammation as a determinant of disease development/progression and sudden death is poorly understood, but potentially important. Sudden death registries report myocarditis as the cause in 5-13%; examination of 30 hearts from ARVC sudden death victims found focal myocarditis in areas of myocyte necrosis in 20 (67%). The link to specific disease-causing variants remains to be explored including genetic determinants of the immune response. Clinical and experimental studies support immune/autoimmune mediated disease in DCM and ACM. Immunosuppression in biopsy-proven non-infectious myocarditis and inflammatory DCM is a treatment option. Recognition of ACM requires greater focus on distinguishing ACM from DCM. The potential to recognize disease prior to adverse events and to characterize patients who may benefit from immunosuppression and/or device therapy highlights the importance of more comprehensive genetic and immunological characterization of patients with myocarditis, and in those with a family history or clinical presentation of an inherited cardiomyopathy. This review will examine from a predominantly clinical perspective the potential importance of myocardial inflammation as a determinant of sudden death in inherited HCM, DCM and ACM.
Copyright © 2022. Published by Elsevier Inc.
Guarda su PubMed
-
Outcomes after heart transplantation in patients with cardiac sarcoidosis.
ESC Heart Fail2022 Jan;():. doi: 10.1002/ehf2.13789.
Asleh Rabea, Briasoulis Alexandros, Doulamis Ilias, Alnsasra Hilmi, Tzani Aspasia, Alvarez Paulino, Kuno Toshiki, Kampaktsis Polydoros, Kushwaha Sudhir,
Abstract
BACKGROUND:
The number of patients with sarcoidosis requiring heart transplantation (HT) is increasing. The aim of this study was to evaluate outcomes of isolated HT in patients with sarcoid cardiomyopathy and compare them to recipients with non-ischaemic restrictive or dilated cardiomyopathy.
METHODS AND RESULTS:
Adult HT recipients were identified in the UNOS Registry between 1990 and 2020. Patients were grouped according to diagnosis. The cumulative incidences for the all-cause mortality and rejection were compared using Fine and Gray model analysis, accounting for re-transplantation as a competing risk. Rejection was evaluated using logistic regression analysis. We also reviewed characteristics and outcomes of all HT recipients with previous diagnosis of sarcoid cardiomyopathy from a single centre. A total of 30 160 HT recipients were included in the present study (n = 239 sarcoidosis, n = 1411 non-ischaemic restrictive cardiomyopathy, and n = 28 510 non-ischaemic dilated cardiomyopathy). During a total of 194 733 patient-years, all-cause mortality at the latest follow-up was not significantly different when comparing sarcoidosis to non-ischaemic dilated cardiomyopathy [adjusted subhazard ratio (aSHR) 1.46, 95% confidence intervals (CIs): 0.9-2.4, P = 0.12] or restrictive cardiomyopathy (aSHR 1.12, 95% CI: 0.65-1.95, P = 0.67). Accordingly, multivariable analysis suggested that 1 year mortality was not significantly different between sarcoidosis and non-ischaemic dilated cardiomyopathy (aSHR 1.56, 95% CI: 0.9-2.7, P = 0.12) or restrictive cardiomyopathy (aSHR 1.15, 95% CI: 0.61-2.18, P = 0.66). No differences were observed regarding 30 day mortality, treated and hospitalized acute rejection, and 30 day death from graft failure after HT. Thirty-day mortality did not improve significantly in more recent HT eras whereas there was a trend towards improved 1 year mortality in the latest HT era (P = 0.06). Data from the single-centre case review showed excellent long-term outcomes with sirolimus-based immunosuppression.
CONCLUSIONS:
Short-term and long-term post HT outcomes among patients with sarcoid cardiomyopathy are similar to those with common types of non-ischaemic cardiomyopathy.
© 2021 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.
Guarda su PubMed
-
Identification of a novel missense mutation in the TPM1 gene via exome sequencing in a Chinese family with dilated cardiomyopathy: A case report and literature review.
Medicine (Baltimore)2022 Jan;101(2):e28551. doi: 10.1097/MD.0000000000028551.
Man Yilong, Yi Changying, Fan Meili, Yang Tianyu, Liu Peng, Liu Shiguang, Wang Guangxin,
Abstract
RATIONALE:
Dilated cardiomyopathy (DCM) is a cardiovascular disorder characterized by consecutive ventricular dilation and contractile dysfunction, often leading to congestive heart failure. DCM type 1Y (DCM1Y) is caused by a mutation in the TPM1 (tropomyosin 1) gene. To date, about thirty TPM1 gene mutations have been reported to be related to DCM1Y. However, mutational screening of the TPM1 gene is still far from being complete. Identification of TPM1 mutation is particularly important in the diagnosis of DCM1Y and will give more insights into the molecular pathogenesis of DCM1Y.
PATIENT CONCERNS:
A Chinese Han family with DCM phenotypes was examined.
DIAGNOSIS:
A novel missense mutation, c.340G?>?C in exon 3 of the TPM1 gene, was identified.
INTERVENTIONS:
Next-generation sequencing (NGS) of DNA samples was performed to detect the gene mutation in the proband, which was confirmed by Sanger sequencing.
OUTCOMES:
This novel heterozygous mutation results in the substitution of glutamic acid with glutamine (p.E114Q). Based on this finding and clinical manifestations, a final diagnosis of DCM1Y was made.
LESSONS:
We present evidence that p.E114Q mutation represents a novel TPM1 mutation in a Chinese Han family with DCM. Our data expand the mutation spectrum of the TPM1 gene and may facilitate the clinical diagnosis of DCM1Y.
Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.
Guarda su PubMed
-
Selection and outcome of ICD and CRT-D patients - Comparison of 4384 patients from the German Device Registry to randomized controlled trials.
J Cardiovasc Electrophysiol2022 Jan;():. doi: 10.1111/jce.15365.
Köbe Julia, Willy Kevin, Senges Jochen, Hochadel Matthias, Kleemann Thomas, Spitzer Stefan G, Andresen Dietrich, Jehle Joachim, Steinbeck Gerhard, Szendey Istvan, Butter Christian, Brachmann Johannes, Hoffmann Ellen, Eckardt Lars,
Abstract
BACKGROUND:
Registry data adds important information to randomized controlled trials (RCT) on real-life aspects of implantable cardioverter-defibrillator (ICD) patients with and without cardiac resynchronization therapy (CRT-D). This analysis of the prospectively conducted German Device Registry aims at comparing mortality rates, comorbidities, complication rates to results from RCT.
METHODS:
The German Device registry (DEVICE) prospectively collected data on ICD and CRT-D first implantations from 50 German centres. Demographic data, details on cardiac disease, electrocardiogram (ECG), medication, and data about procedure, complications and hospital stay were stored in electronic case report forms. One year after device implantation patients were contacted for follow-up.
RESULTS:
DEVICE included n=4384 first ICD/CRT-D implantations (29.3% CRT-D devices). We found a strong adherence to guidelines with over 90% of patients being on ß-blocker and ACE-inhibitor medication and adequate QRS width in the majority of CRT-D patients. Patients receiving a CRT-D were older (67.6±11.0 years vs. 63.9±13.4 years, p
CONCLUSION:
Despite relevant limitations of registry data, DEVICE highlights important differences between RCT and real-world registry data and the impact of comorbidities on mortality of ICD and CRT-D recipients. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
Guarda su PubMed
-
Exposure to Elevated Nitrogen Dioxide Concentrations and Cardiac Remodeling in Patients With Dilated Cardiomyopathy.
J Card Fail2022 Jan;():. doi: S1071-9164(21)00492-9.
Fecht Daniela, Chadeau-Hyam Marc, Owen Ruth, Gregson John, Halliday Brian P, Lota Amrit S, Gulliver John, Ware James S, Pennell Dudley J, Kelly Frank J, Shah Anoop S V, Miller Mark R, Newby David E, Prasad Sanjay K, Tayal Upasana,
Abstract
BACKGROUND:
Empirical evidence suggests a strong link between exposure to air pollution and heart failure incidence, hospitalizations, and mortality, but the biological basis of this remains unclear. We sought to determine the relationship between differential air pollution levels and changes in cardiac structure and function in patients with dilated cardiomyopathy.
METHODS AND RESULTS:
We undertook a prospective longitudinal observational cohort study of patients in England with dilated cardiomyopathy (enrollment 2009-2015, n?=?716, 66% male, 85% Caucasian) and conducted cross sectional analysis at the time of study enrollment. Annual average air pollution exposure estimates for nitrogen dioxide (NO) and particulate matter with diameter of 2.5 µm or less (PM) at enrolment were assigned to each residential postcode (on average 12 households). The relationship between air pollution and cardiac morphology was assessed using linear regression modelling. Greater ambient exposure to NO was associated with higher indexed left ventricular (LV) mass (4.3 g/m increase per interquartile range increase in NO, 95% confidence interval 1.9-7.0 g/m) and lower LV ejection fraction (-1.5% decrease per interquartile range increase in NO, 95% confidence interval -2.7% to -0.2%), independent of age, sex, socioeconomic status, and clinical covariates. The associations were robust to adjustment for smoking status and geographical clustering by postcode area. The effect of air pollution on LV mass was greatest in women. These effects were specific to NO exposure.
CONCLUSIONS:
Exposure to air pollution is associated with raised LV mass and lower LV ejection fraction, with the strongest effect in women. Although epidemiological associations between air pollution and heart failure have been established and supported by preclinical studies, our findings provide novel empirical evidence of cardiac remodeling and exposure to air pollution with important clinical and public health implications.
Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.
Guarda su PubMed
-
Molecular Mechanisms behind Persistent Presence of Parvovirus B19 in Human Dilated Myocardium.
Adv Exp Med Biol2022 Jan;():. doi: 10.1007/5584_2021_702.
Bironait? Daiva, Ka?ukauskien? Ieva, Bogomolovas Julius, Daunoravi?ius Dainius, Jakubauskas Art?ras, Vitkus Dalius, ?urauskas Edvardas, Ru?inskas K?stutis, Labeit Siegfried, Grabauskiene Virginija,
Abstract
The role of parvovirus B19 (PVB19) in the pathogenesis of idiopathic dilated cardiomyopathy (DCM) remains poorly understood. Therefore, we have measured the levels of inflammation, fibrosis, apoptosis, and necrosis in endomyocardial biopsies (EMBs) and sera of nonischemic PVB19-positive (n = 14) and PVB19-negative (n = 18) DCM patients. Chronic persistence of PVB19 in myocardium did not induce significant infiltration of T cells (CD3 and CD45Ro) and macrophages (CD68), and did not secrete TNF?, IL-6, and CRB. The fibrosis in PVB19-positive EMBs was also lower compared to the virus-negative ones, while ECM degrading matrix metalloproteinase MMP1 and gelatinase MMP2 were significantly (by twofold) upregulated. In addition, there was no activation of neither apoptotic nor necrotic pathways. However, levels of antiapoptotic mitochondrial Bcl-2 and heat shock protein 60 (Hsp60) in PVB19-positive biopsies were almost threefold lower than in PVB19-negative ones revealing impairment of mitochondria. Altogether, data indicate that persistence of PVB19 in myocardiums of nonischemic DCM patients can cause myocardial ECM remodeling through the MMPs, such as MMP1 and MMP2, and mitochondrial impairment. The correlative analysis of measured biomarkers suggested likely further activation of apoptotic cell death pathways rather than fibrosis. Data also suggest that antiviral therapy could be beneficial for PVB19-positive DCM patients by managing further pathological myocardial remodeling.
© 2022. Springer Nature Switzerland AG.
Guarda su PubMed
-
Coronary blood flow in heart failure: cause, consequence and bystander.
Basic Res Cardiol2022 Jan;117(1):1. doi: 10.1007/s00395-022-00909-8.
Heusch Gerd,
Abstract
Heart failure is a clinical syndrome where cardiac output is not sufficient to sustain adequate perfusion and normal bodily functions, initially during exercise and in more severe forms also at rest. The two most frequent forms are heart failure of ischemic origin and of non-ischemic origin. In heart failure of ischemic origin, reduced coronary blood flow is causal to cardiac contractile dysfunction, and this is true for stunned and hibernating myocardium, coronary microembolization, myocardial infarction and post-infarct remodeling, possibly also for the takotsubo syndrome. The most frequent form of non-ischemic heart failure is dilated cardiomyopathy, caused by genetic mutations, myocarditis, toxic agents or sustained tachyarrhythmias, where alterations in coronary blood flow result from and contribute to cardiac contractile dysfunction. Hypertrophic cardiomyopathy is caused by genetic mutations but can also result from increased pressure and volume overload (hypertension, valve disease). Heart failure with preserved ejection fraction is characterized by pronounced coronary microvascular dysfunction, the causal contribution of which is however not clear. The present review characterizes the alterations of coronary blood flow which are causes or consequences of heart failure in its different manifestations. Apart from any potentially accompanying coronary atherosclerosis, all heart failure entities share common features of impaired coronary blood flow, but to a different extent: enhanced extravascular compression, impaired nitric oxide-mediated, endothelium-dependent vasodilation and enhanced vasoconstriction to mediators of neurohumoral activation. Impaired coronary blood flow contributes to the progression of heart failure and is thus a valid target for established and novel treatment regimens.
© 2022. The Author(s).
Guarda su PubMed
-
Death-causing cardiac injuries after chronic alcohol intake identified by forensic medicine.
Rom J Morphol Embryol;62(2):553-561. doi: 10.47162/RJME.62.2.22.
Crauciuc Drago? Valentin, Stan Cristinel Ionel, Rî?canu Laura Adriana, Pîrvu Daniel Cristian, Bulgaru-Iliescu Diana,
Abstract
Ethyl alcohol is the most consumed drug, worldwide, with frequent consequences on the individual's health and lifestyle. Chronic alcoholism is a pathological state occurring after an excessive alcohol intake and may be observed in teenagers or very old individuals. The study performed by us investigated the changes caused by alcohol intake in the left ventricle myocardium in 77 bodies deceased at home under suspect circumstances and sent to the Institute of Forensic Medicine for establishing the cause of death. In all the individuals, there was determined high levels of blood Ethyl glucuronide, thus showing the alcohol intake up to 96 hours before death. The lesions present in the heart were represented by dilated cardiomyopathy, myocardial fibrosis, and myocardial infarction.
Guarda su PubMed
-
Hybrid epicardial ventricular tachycardia ablation with lateral thoracotomy in a patient with a history of left ventricular reconstruction surgery.
J Cardiol Cases2022 Jan;25(1):37-41. doi: 10.1016/j.jccase.2021.06.003.
Koya Taro, Watanabe Masaya, Kamada Rui, Hagiwara Hikaru, Nakao Motoki, Kadosaka Takahide, Koizumi Takuya, Anzai Toshihisa,
Abstract
Although a hybrid procedure involving surgical access may be feasible for epicardial catheter ablation in individuals with prior cardiac surgery, surgical approaches in thoracotomy are important in patients with advanced adhesions. We performed an epicardial ventricular tachycardia (VT) ablation in a patient with dilated phase hypertrophic cardiomyopathy after left ventricular reconstruction. We gained surgical epicardial access via lateral thoracotomy based on the anticipated VT circuit in the apical anteroseptal area, which was estimated using prior endocardial mapping. The remaining epicardial myocardium around the surgical incision was involved in the central isthmus, and the VT was eliminated by radiofrequency catheter ablation. .
© 2021 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
Guarda su PubMed
-
Bridging patients in cardiogenic shock with a paracorporeal pulsatile biventricular assist device to heart transplantation-a single-centre experience.
Eur J Cardiothorac Surg2022 Jan;():. doi: ezab547.
Michel Sebastian, Buchholz Stefan, Buech Joscha, Veit Tobias, Fabry Thomas, Abicht Jan, Thierfelder Nikolaus, Mueller Christoph, Rosenthal Laura Lily, Pabst von Ohain Jelena, Haas Nikolaus, Hörer Jürgen, Hagl Christian,
Abstract
OBJECTIVES:
We evaluated the outcome of patients in cardiogenic shock receiving a paracorporeal pulsatile biventricular assist device as a bridge to transplantation.
METHODS:
We performed a retrospective single-centre analysis of all patients who received a Berlin Heart Excor® at our institution between 2004 and 2019.
RESULTS:
A total of 97 patients (90 adults, 7 paediatric) were analysed. Eighty-four patients were in Interagency Registry for Mechanically Assisted Circulatory Support level 1 (80 adults, 4 paediatric). Diagnoses were dilated cardiomyopathy (n = 41), ischaemic cardiomyopathy (n = 17) or myocardial infarction (n = 4), myocarditis (n = 15), restrictive cardiomyopathy (n = 2), graft failure after heart transplant (n = 7), postcardiotomy heart failure (n = 5), postpartum cardiomyopathy (n = 3), congenital heart disease (n = 1), valvular cardiomyopathy (n = 1) and toxic cardiomyopathy (n = 1). All patients were in biventricular heart failure and had secondary organ dysfunction. The mean duration of support was 63 days (0-487 days). There was a significant decrease in creatinine values after assist device implantation (from 1.83 ± 0.79 to 1.12 ± 0.67 mg/dl, P = 0.001) as well as a decrease in bilirubin values (from 3.94 ± 4.58 to 2.65 ± 3.61 mg/dl, P = 0.084). Cerebral stroke occurred in 16 patients, bleeding in 15 and infection in 13 patients. Forty-eight patients died on support, while 49 patients could be successfully bridged to transplantation. Thirty-day survival and 1-year survival were 70.1% and 41.2%, respectively.
CONCLUSIONS:
A pulsatile biventricular assist device is a reasonable therapeutic option in cardiogenic shock, when immediate high cardiac output is necessary to rescue the already impaired kidney and liver function of the patient.
© The Author(s) 2022. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.
Guarda su PubMed
-
Advances in understanding the state of titin truncation variants in dilated cardiomyopathy.
Pflugers Arch -
The risk of all-cause mortality, heart outcomes, cancer, and neurodegenerative disorders with cobalt-chrome-containing total hip arthroplasty implants : an analysis of the National Joint Registry.
Bone Joint J2022 Jan;():1-9. doi: 10.1302/0301-620X.104B.BJJ-2021-0397.R1.
Deere Kevin, Matharu Gulraj S, Ben-Shlomo Yoav, Wilkinson J Mark, Blom Ashley W, Sayers Adrian, Whitehouse Michael R,
Abstract
AIMS:
A recent report from France suggested an association between the use of cobalt-chrome femoral heads in total hip arthroplasties (THAs) and an increased risk of dilated cardiomyopathy and heart failure. Cobalt-chrome is a commonly used material in orthopaedic implants. If the reported association is causal, the consequences would be significant given the millions of joint replacements and other orthopaedic procedures in which cobalt-chrome is used annually. We examined whether cobalt-chrome-containing THAs were associated with an increased risk of all-cause mortality, heart outcomes, cancer, and neurodegenerative disorders in a large national database.
METHODS:
Data from the National Joint Registry was linked to NHS English hospital inpatient episodes for 374,359 primary THAs with up to 14.5 years follow-up. We excluded any patients with bilateral THAs, knee replacements, indications other than osteoarthritis, aged under 55 years, and diagnosis of one or more outcome of interest before THA. Implants were grouped as either containing cobalt-chrome or not containing cobalt-chrome. The association between implant construct and the risk of all-cause mortality and incident heart failure, cancer, and neurodegenerative disorders was examined.
RESULTS:
There were 158,677 individuals (42.4%) with an implant containing cobalt-chrome. There were 47,963 deaths, 27,332 heart outcomes, 35,720 cancers, and 22,025 neurodegenerative disorders. There was no evidence of an association that patients with cobalt-chrome implants had higher rates of any of the outcomes.
CONCLUSION:
Cobalt-chrome-containing THAs did not have an increased risk of all-cause mortality, or clinically meaningful heart outcomes, cancer or neurodegenerative disorders into the second decade post-implantation. Our findings will help reassure clinicians and the increasing number of patients receiving primary THA worldwide that the use of cobalt-chrome containing implants is not associated with significant adverse systemic effects.
Guarda su PubMed
-
G3bp1 - microRNA-1 axis regulates cardiomyocyte hypertrophy.
Cell Signal2022 Jan;91():110245. doi: S0898-6568(22)00005-5.
Alikunju Saleena, Niranjan Nandita, Mohsin Maha, Sayed Nazish, Sayed Danish,
Abstract
Adaptation of gene expression is one of the most fundamental response of cardiomyocytes to hypertrophic stimuli. G3bp1, an RNA binding protein with site-specific endoribonuclease activity regulates the processing of pre-miR-1 stem-loop, and thus levels of cardiomyocyte -enriched mature miR-1. Here, we examine the role of G3bp1 in regulating gene expression in quiescent cardiomyocytes and those undergoing growth-factor induced hypertrophy. Further, we determine if these changes are facilitated through G3bp1-mediated regulation of miR-1 in these cardiomyocytes. Using isolated cardiomyocytes with knockdown of endogenous G3bp1, we performed high throughput RNA sequencing to determine the change in cardiac transcriptome. Then, using gain and loss of function approach for both, G3bp1 and miR-1, alone or in combination we examine the G3bp1-miR-1 signaling in regulating gene expression and Endothelin (ET-1) -induced cardiomyocyte hypertrophy. We show that knockdown of endogenous G3bp1 results in inhibition of genes involved in calcium handling, cardiac muscle contraction, action potential and sarcomeric structure. In addition, there is inhibition of genes that contribute to hypertrophic and dilated cardiomyopathy development. Conversely, an increase is seen in genes that negatively regulate the Hippo signaling, like Rassf1 and Arrdc3, along with inflammatory genes of TGF-? and TNF pathways. Knockdown of G3bp1 restricts ET-1 induced cardiomyocyte hypertrophy. Interestingly, concurrent silencing of G3bp1 and miR-1 rescues the change in gene expression and inhibition of hypertrophy seen with knockdown of G3bp1 alone. Similarly, expression of exogenous G3bp1 reverses the miR-1 induced inhibition of gene expression. Intriguingly, expression of Gfp tagged G3bp1 results in perinuclear accumulations of G3bp1-Gfp, resembling Stress Granules. Based on our results, we conclude that G3bp1 through its regulation of mature miR-1 levels plays a critical role in regulating the expression of essential cardiac-enriched genes and those involved in development of cardiomyocyte hypertrophy.
Copyright © 2022 Elsevier Inc. All rights reserved.
Guarda su PubMed
-
Biventricular non-compaction cardiomyopathy and tricuspid hypoplasia in a novel gene variant.
Cardiol Young2022 Jan;():1-5. doi: 10.1017/S1047951121004923.
Safi Sanam, Sanders Stephen P, Zhao Melissa, Carreon Chrystalle Katte,
Abstract
A maternally inherited novel pathogenic non-POU domain-containing octamer-binding gene variant c.767G>T, p.R256I [NM_001145408], manifested in a male infant as dilated cardiomyopathy with severe left ventricular dysfunction and dilation, biventricular non-compaction, tricuspid hypoplasia, and hydrocephaly. To the best of our knowledge, no previous non-POU domain-containing octamer-binding gene variants with biventricular non-compaction have been associated with tricuspid valve hypoplasia. Hence, this case introduces a new pathogenic variant observed in the non-POU domain-containing octamer-binding gene and adds to the range of cardiac phenotypes identified in non-POU domain-containing octamer-binding gene variants.
Guarda su PubMed
-
Identification of cardiomyopathy-related core genes through human metabolic networks and expression data.
BMC Genomics2022 Jan;23(1):47. doi: 10.1186/s12864-021-08271-0.
Rong Zherou, Chen Hongwei, Zhang Zihan, Zhang Yue, Ge Luanfeng, Lv Zhengyu, Zou Yuqing, Lv Junjie, He Yuehan, Li Wan, Chen Lina,
Abstract
BACKGROUND:
Cardiomyopathy is a complex type of myocardial disease, and its incidence has increased significantly in recent years. Dilated cardiomyopathy (DCM) and ischemic cardiomyopathy (ICM) are two common and indistinguishable types of cardiomyopathy.
RESULTS:
Here, a systematic multi-omics integration approach was proposed to identify cardiomyopathy-related core genes that could distinguish normal, DCM and ICM samples using cardiomyopathy expression profile data based on a human metabolic network. First, according to the differentially expressed genes between different states (DCM/ICM and normal, or DCM and ICM) of samples, three sets of initial modules were obtained from the human metabolic network. Two permutation tests were used to evaluate the significance of the Pearson correlation coefficient difference score of the initial modules, and three candidate modules were screened out. Then, a cardiomyopathy risk module that was significantly related to DCM and ICM was determined according to the significance of the module score based on Markov random field. Finally, based on the shortest path between cardiomyopathy known genes, 13 core genes related to cardiomyopathy were identified. These core genes were enriched in pathways and functions significantly related to cardiomyopathy and could distinguish between samples of different states.
CONCLUSION:
The identified core genes might serve as potential biomarkers of cardiomyopathy. This research will contribute to identifying potential biomarkers of cardiomyopathy and to distinguishing different types of cardiomyopathy.
© 2022. The Author(s).
Guarda su PubMed
