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Myocardial fibrosis mortality

Muhammad Naveed, Lei Han, Ghulam Jilany Khan, Sufia Yasmeen, Reyaj Mikrani, Muhammad Abbas, Li Cunyu, Zhou Xiaohui
Congestive heart failure (CHF) is a complicated pathophysiological syndrome, leading cause of hospitalization as well as mortalities in developed countries wherein an irregular function of the heart leads to the insufficient blood supply to the body organs. It is an accumulative slackening of various complications including myocardial infarction (MI), coronary heart disease (CAD), hypertension, valvular heart disease (VHD) and cardiomyopathy; its hallmarks include hypertrophy, increased interstitial fibrosis and loss of myocytes...
March 14, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
Andrew R Kompa, Jiayu Lu, Thomas J Weller, Darren J Kelly, Henry Krum, Thomas G von Lueder, Bing H Wang
BACKGROUND: Angiotensin receptor neprilysin inhibitor (ARNi) enhances beneficial natriuretic peptides by inhibiting their breakdown through neprilysin. Although the first-in-class ARNi sacubitril/valsartan (LCZ696) reduced mortality and morbidity in heart failure (HF) with reduced ejection fraction (EF) compared to angiotensin converting enzyme inhibitor (ACEi), mechanistic data on ARNi are scarce. ARNi may be superior to ACEi in attenuating adverse cardiac remodeling and dysfunction post-myocardial infarction (MI)...
May 1, 2018: International Journal of Cardiology
Lindsay T McDonald, Michael R Zile, Yuhua Zhang, An O Van Laer, Catalin F Baicu, Robert E Stroud, Jeffrey A Jones, Amanda C LaRue, Amy D Bradshaw
Myocardial fibrosis and the resultant increases in LV stiffness represent pivotal consequences of chronic pressure-overload (PO) that impact both functional capacity and the rates of morbid and mortal events. However, the time course and cellular mechanisms that underlie PO-induced fibrosis have not been completely defined. Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein shown to be required for insoluble collagen deposition and increased myocardial stiffness in response to murine PO...
March 9, 2018: American Journal of Physiology. Heart and Circulatory Physiology
Sophie I Mavrogeni, Petros P Sfikakis, Theodoros Dimitroulas, Loukia Koutsogeorgopoulou, Gikas Katsifis, George Markousis-Mavrogenis, Genovefa Kolovou, George D Kitas
Life expectancy in autoimmune rheumatic diseases (ARDs) remains lower compared to the general population, due to various comoborbidities. Cardiovascular disease (CVD) represents the main contributor to premature mortality. Conventional and biologic disease-modifying antirheumatic drugs (DMARDs) have considerably improved long-term outcomes in ARDs not only by suppressing systemic inflammation but also by lowering CVD burden. Regarding atherosclerotic disease prevention, EULAR has recommended tight disease control accompanied by regular assessment of traditional CVD risk factors and lifestyle changes...
March 7, 2018: Rheumatology International
Anbang Han, Yingdong Lu, Qi Zheng, Jian Zhang, YiZhou Zhao, Mingjing Zhao, Xiangning Cui
BACKGROUND/AIMS: Qiliqiangxin (QL), a traditional Chinese medicine, has been demonstrated to be effective and safe for the treatment of chronic heart failure. Left ventricular (LV) remodeling causes depressed cardiac performance and is an independent determinant of morbidity and mortality after myocardial infarction (MI). Our previous studies have shown that QL exhibits cardiac protective effects against heart failure after MI. The objective of this study was to explore the effects of QL on myocardial fibrosis in rats with MI and to investigate the underlying mechanism of these effects...
February 28, 2018: Cellular Physiology and Biochemistry
Kevin J Morine, Xiaoying Qiao, Sam York, Peter S Natov, Vikram Paruchuri, Yali Zhang, Mark J Aronovitz, Richard H Karas, Navin K Kapur
Background -Heart failure is a growing cause of morbidity and mortality worldwide. Transforming growth factor beta (TGF-β1) promotes cardiac fibrosis, but also activates counter-regulatory pathways that serve to regulate TGF-β1 activity in heart failure. Bone morphogenetic protein 9 (BMP9) is a member of the TGFβ family of cytokines and signals via the downstream effector protein Smad1. Endoglin is a TGFβ co-receptor that promotes TGF-β1 signaling via Smad3 and binds BMP9 with high affinity. We hypothesized that BMP9 limits cardiac fibrosis by activating Smad1 and attenuating Smad3 and further that neutralizing endoglin activity promotes BMP9 activity...
February 27, 2018: Circulation
Christoffer Stark, Pekka Taimen, Timo Savunen, Juha Koskenvuo
OBJECTIVE: We wanted to determine the impact of different doses of a pegylated and liposomal formulation of the cardiotoxic drug doxorubicin on cardiac function, fibrosis and survival in mice. The drug causes myocardial damage by producing reactive oxygen species, mitochondrial damage and lipid peroxidation. Thymosin beta 4 is a peptide with cardioprotective, anti-oxidant and anti-fibrotic properties and we further investigated whether the peptide could attenuate this drug-induced injury by measuring cardiac function and fibrosis...
February 21, 2018: BMC Research Notes
Guanghong Jia, Michael A Hill, James R Sowers
Heart failure and related morbidity and mortality are increasing at an alarming rate, in large part, because of increases in aging, obesity, and diabetes mellitus. The clinical outcomes associated with heart failure are considerably worse for patients with diabetes mellitus than for those without diabetes mellitus. In people with diabetes mellitus, the presence of myocardial dysfunction in the absence of overt clinical coronary artery disease, valvular disease, and other conventional cardiovascular risk factors, such as hypertension and dyslipidemia, has led to the descriptive terminology, diabetic cardiomyopathy...
February 16, 2018: Circulation Research
Maren Leifheit-Nestler, Felix Kirchhoff, Julia Nespor, Beatrice Richter, Birga Soetje, Michael Klintschar, Joerg Heineke, Dieter Haffner
Background: Fibroblast growth factor 23 (FGF23) is discussed as a new biomarker of cardiac hypertrophy and mortality in patients with and without chronic kidney disease (CKD). We previously demonstrated that FGF23 is expressed by cardiac myocytes, enhanced in CKD and induces cardiac hypertrophy via activation of FGF receptor 4 independent of its co-receptor klotho. The impact of FGF23 on cardiac fibrosis is largely unknown. Methods: By conducting a retrospective case-control study including myocardial autopsy samples from 24 patients with end-stage CKD and in vitro studies in cardiac fibroblasts and myocytes, we investigated the pro-fibrotic properties of FGF23...
February 7, 2018: Nephrology, Dialysis, Transplantation
Damien N Barnette, Thomas J Cahill, Mala Gunadasa-Rohling, Carolyn A Carr, Matthew Freeman, Paul R Riley
The role of proinflammation, and specifically TNF-α, on downstream fibrosis and healing after cardiac injury remains unknown. Using iRhom2-deficient mice, which lack myeloid-specific shedding of TNF-α, we reveal increased macrophages (MΦs) that were skewed towards a more proinflammatory (M1) state at day 4, followed by more reparative, antiinflammatory (M2) state at day 7 after myocardial infarction (MI). However, associated functional cytokine expression was significantly reduced in iRhom2-mutant M1 and M2 MΦs, respectively...
February 8, 2018: JCI Insight
Tom Gyllenhammar, Mikael Kanski, Henrik Engblom, Dirk M Wuttge, Marcus Carlsson, Roger Hesselstrand, Håkan Arheden
BACKGROUND: Patients with systemic sclerosis (SSc) have high cardiovascular mortality even though there is no or little increase in prevalence of epicardial coronary stenosis. First-pass perfusion on cardiovascular magnetic resonance (CMR) have detected perfusion defects indicative of microvascular disease, but the quantitative extent of hypoperfusion is not known. Therefore, we aimed to determine if patients with SSc have lower global myocardial perfusion (MP) at rest or during adenosine stress, compared to healthy controls, quantified with CMR...
January 30, 2018: BMC Cardiovascular Disorders
Pavel Zhabyeyev, Subhash K Das, Ratnadeep Basu, Mengcheng Shen, Vaibhav B Patel, Zamaneh Kassiri, Gavin Y Oudit
Chronic iron-overload results in heart and liver diseases and is a common cause of morbidity and mortality in patients with genetic hemochromatosis and secondary iron-overload. We investigated the role of tissue inhibitor of metalloproteinase-3 (TIMP3) in iron-overload mediated tissue injury by subjecting male mice lacking Timp3 ( Timp3 -/- ) and wildtype (WT) mice to 12 weeks of chronic iron-overload. While iron-overload in the WT group developed diastolic dysfunction, iron-overloaded Timp3 -/- mice showed worsened cardiac dysfunction coupled with systolic dysfunction...
January 26, 2018: American Journal of Physiology. Heart and Circulatory Physiology
Rong-Rong Zhao, Matthew Ackers-Johnson, Justus Stenzig, Chen Chen, Tao Ding, Yue Zhou, Peipei Wang, Shi Ling Ng, Peter Y Li, Gavin Teo, Pauline M Rudd, James W Fawcett, Roger S Y Foo
Background -Heart failure (HF) is a leading cause of mortality and morbidity, and the search for novel therapeutic approaches continues. In the monogenic disease mucopolysaccharidosis (MPS) VI, loss of function mutations in arylsulfatase B (ASB) leads to myocardial accumulation of chondroitin sulfate (CS) glycosaminoglycans (GAGs), manifesting as a myriad of cardiac symptoms. Here, we studied changes in myocardial CS in non-MPS failing hearts, and assessed its generic role in pathological cardiac remodeling...
January 25, 2018: Circulation
Toshikazu Sano, Daiki Ousaka, Takuya Goto, Shuta Ishigami, Kenta Hirai, Shingo Kasahara, Shinichi Ohtsuki, Shunji Sano, Hidemasa Oh
Rationale: Intracoronary administration of cardiosphere-derived cells (CDCs) in patients with single ventricles resulted in a short-term improvement in cardiac function. Objective: To test the hypothesis that CDC infusion is associated with improved cardiac function and reduced mortality in patients with heart failure. Methods and Results: We evaluated the effectiveness of CDCs using an integrated cohort study in 101 patients with single ventricles, including 41 patients that received CDC infusion and 60 controls treated with staged palliation alone...
January 24, 2018: Circulation Research
Manvir Kaur Hayer, Anna Marie Price, Boyang Liu, Shanat Baig, Charles Joseph Ferro, Jonathan Nicholas Townend, Richard Paul Steeds, Nicola Catherine Edwards
Patients with chronic kidney disease (CKD) have a disproportionately high risk of cardiovascular (CV) morbidity and mortality from the very early stages of CKD. This excess risk is believed to be the result of myocardial disease commonly termed uremic cardiomyopathy (UC). It has been suggested that interstitial myocardial fibrosis progresses with advancing kidney disease and may be the key mediator of UC. This longitudinal study reports data on the myocardial structure and function of 30 patients with CKD with no known cardiovascular disease and healthy controls...
December 11, 2017: American Journal of Cardiology
Kuo Zhang, Wenyao Wang, Shihua Zhao, Stuart D Katz, Giorgio Iervasi, A Martin Gerdes, Yi-Da Tang
BACKGROUND: Thyroid dysfunction and myocardial fibrosis are both associated with cardiovascular events in patients with dilated cardiomyopathy (DCM). HYPOTHESIS: The combination of thyroid hormone (TH) and myocardial fibrosis (detected by late gadolinium enhancement [LGE]) is an independent and incremental predictor of adverse events in DCM. METHODS: We consecutively enrolled 220 idiopathic DCM patients with thyroid function and LGE assessment at Fuwai Hospital (China) from January 2010 to October 2011 and followed up through December 2015...
January 23, 2018: Clinical Cardiology
Abeer Rababa H, Ashley Guillory, Rima Mustafa, Tamara Hijjawi
BACKGROUND: A common phenotype associated with heart failure is the development of cardiac hypertrophy. Cardiac hypertrophy occurs in response to stress, such as hypertension, coronary vascular disease, or myocardial infarction. The most critical pathophysiological conditions involved may include dilated hypertrophy, fibrosis and contractile malfunction. The intricate pathophysiological mechanisms of cardiac hypertrophy have been the core of several scientific studies, which may help in opening a new avenue in preventive and curative procedures...
January 11, 2018: Current Cardiology Reviews
Yasunori Suematsu, Wanghui Jing, Ane Nunes, Moti L Kashyap, Mahyar Khazaeli, Nosratola D Vaziri, Hamid Moradi
BACKGROUND: Chronic kidney disease (CKD) is associated with cardiac hypertrophy, fibrosis and increased risk of cardiovascular mortality. LCZ696 (Sacubitril/valsartan) is a promising agent which has shown significant potential in treatment of heart failure. We hypothesized that LCZ696 is more effective than valsartan alone in treatment of cardiovascular abnormalities associated with experimental CKD. METHODS AND RESULTS: Male Sprague Dawley rats underwent 5/6 nephrectomy and were subsequently randomized to no treatment (CKD), 30 mg/kg valsartan (VAL), or 60 mg/kg LCZ696 (LCZ)...
January 8, 2018: Journal of Cardiac Failure
Signe Holm Nielsen, Alan J Mouton, Kristine Y DeLeon-Pennell, Federica Genovese, Morten Karsdal, Merry L Lindsey
Cardiovascular Disease (CVD) is the most common cause of death in industrialized countries, and myocardial infarction (MI) is a major CVD with significant morbidity and mortality. Following MI, the left ventricle (LV) undergoes a wound healing response to ischemia that results in extracellular matrix (ECM) scar formation to replace necrotic myocytes. While ECM accumulation following MI is termed cardiac fibrosis, this is a generic term that does not differentiate between ECM accumulation that occurs in the infarct region to form a scar that is structurally necessary to preserve left ventricle (LV) wall integrity and ECM accumulation that increases LV wall stiffness to exacerbate dilation and stimulate the progression to heart failure...
December 13, 2017: Matrix Biology: Journal of the International Society for Matrix Biology
Che-Chung Yeh, Yanying Fan, Yanchun Xu, Yi-Lin Yang, Paul C Simpson, Michael J Mann
RATIONALE: We have hypothesized that post-infarction cardiac remodeling can be influenced by shifts in the balance between intracellular mediators of "pathologic" and "physiologic" hypertrophy. Although alpha1 adrenergic receptors (alpha1-ARs) mediate pro-adaptive hypertrophy during pressure overload, little is known about their role or downstream mediators after myocardial infarction. METHODS: We performed loss-of-function experiments via coronary ligation in alpha1A-AR knockout (AKO) mice...
2017: PloS One
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