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Hypertrophy cardiomyopathy

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https://www.readbyqxmd.com/read/28108636/serelaxin-treatment-promotes-adaptive-hypertrophy-but-does-not-prevent-heart-failure-in-experimental-peripartum-cardiomyopathy
#1
Justus Nonhoff, Melanie Ricke-Hoch, Mirco Mueller, Britta Stapel, Tobias Pfeffer, Martina Kasten, Michaela Scherr, Constantin von Kaisenberg, Johann Bauersachs, Arash Haghikia, Denise Hilfiker-Kleiner
AIMS: Peripartum cardiomyopathy (PPCM) is a systolic left ventricular dysfunction developing in the peripartum phase in previously healthy women. Relaxin-2 is a pregnancy hormone with potential beneficial effects in heart failure patients. We evaluated Relaxin-2 as a potential diagnostic marker and/or a therapeutic agent in PPCM. METHODS AND RESULTS: In healthy peripartum women, serum Relaxin-2 levels (measured by ELISA in the second half of pregnancy) were elevated showing a decreasing trend in the first postpartum week and returned to non-pregnant levels thereafter...
January 20, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28105734/calcium-calmodulin-dependent-protein-kinase-mediates-the-intracellular-signaling-pathways-of-cardiac-apoptosis-in-mice-with-impaired-glucose-tolerance
#2
Marilen Federico, Enrique L Portiansky, Leandro Sommese, Francisco J Alvarado, Paula G Blanco, Carolina N Zanuzzi, John Dedman, Marcia Kaetzel, Xander H T Wehrens, Alicia Mattiazzi, Julieta Palomeque
Background The impact of cardiac apoptosis in pre-diabetic stages of diabetic cardiomyopathy is unknown. We described that myocytes from fructose-rich diet (FRD) animals exhibit arrhythmias produced by exacerbated Ca(2+) /calmodulin-protein kinase (CaMKII) activity, ryanodine receptors (RyR2) phosphorylation and sarcoplasmic reticulum (SR) Ca(2+) leak. We tested the hypothesis that this mechanism also underlies cardiac apoptosis in pre-diabetes. Methods and Results We generated a pre-diabetic model in mice fed with FRD...
January 20, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28100964/comparative-efficacy-of-nebivolol-and-metoprolol-to-prevent-tachycardia-induced-cardiomyopathy-in-a-porcine-model
#3
Alireza Nazeri, MacArthur A Elayda, Ana Maria Segura, Raymond F Stainback, Joanna Nathan, Vei-Vei Lee, Christina Bove, Luiz Sampaio, Brian Grace, Ali Massumi, Mehdi Razavi
Chronic tachycardia is a well-known cause of nonischemic cardiomyopathy. We hypothesized that nebivolol, a β-blocker with nitric oxide activity, would be superior to a pure β-blocker in preventing tachycardia-induced cardiomyopathy in a porcine model. Fifteen healthy Yucatan pigs were randomly assigned to receive nebivolol, metoprolol, or placebo once a day. All pigs underwent dual-chamber pacemaker implantation. The medication was started the day after the pacemaker implantation. On day 7 after implantation, each pacemaker was set at atrioventricular pace (rate, 170 beats/min), and the pigs were observed for another 7 weeks...
December 2016: Texas Heart Institute Journal
https://www.readbyqxmd.com/read/28090637/diltiazem-prevents-stress-induced-contractile-deficits-in-cardiomyocytes-but-does-not-reverse-the-cardiomyopathy-phenotype-in-mybpc3-knock-in-mice
#4
Frederik Flenner, Birgit Geertz, Silke Reischmann-Düsener, Florian Weinberger, Thomas Eschenhagen, Lucie Carrier, Felix W Friedrich
Left ventricular hypertrophy, diastolic dysfunction and fibrosis are main features of hypertrophic cardiomyopathy (HCM). Guidelines recommend β-adrenoceptor or Ca(2+) channel antagonists as pharmacological treatment. The Ca(2+) channel blocker diltiazem recently showed promising beneficial effects in pre-clinical HCM, particularly in patients carrying MYBPC3 mutations. In the present study we evaluated whether diltiazem could ameliorate or reverse the disease phenotype in cells and in vivo in Mybpc3-targeted knock-in (KI) mouse model of HCM...
January 15, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28089740/early-remodeling-of-repolarizing-k-currents-in-the-%C3%AE-mhc-403-mouse-model-of-familial-hypertrophic-cardiomyopathy
#5
Rocco Hueneke, Adam Adenwala, Rebecca L Mellor, Jonathan G Seidman, Christine E Seidman, Jeanne M Nerbonne
Familial hypertrophic cardiomyopathy (HCM), linked to mutations in myosin, myosin-binding proteins and other sarcolemmal proteins, is associated with increased risk of life threatening ventricular arrhythmias, and a number of animal models have been developed to facilitate analysis of disease progression and mechanisms. In the experiments here, we use the αMHC(403/+) mouse line in which one αMHC allele harbors a common HCM mutation (in βMHC, Arg403 Gln). Here, we demonstrate marked prolongation of QT intervals in young adult (10-12week) male αMHC(403/+) mice, well in advance of the onset of measurable left ventricular hypertrophy...
January 12, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28073646/hypertrophic-cardiomyopathy-without-ventricular-hypertrophy-usefulness-of-genetic-and-pathological-study-in-preventing-sudden-death
#6
Federico Segura-Villalobos, Ana Isabel Hernández-Guerra, Fernando Wanguemert-Pérez, Juan Carlos Rodríguez-Pérez, Haridian Mendoza-Lemes, Roberto Barriales-Villa
No abstract text is available yet for this article.
January 7, 2017: Revista Española de Cardiología
https://www.readbyqxmd.com/read/28072930/left-ventricular-outflow-tract-obstruction-be-prepared
#7
J S Evans, S J Huang, A S McLean, M Nalos
The current trend to treat hypotension in critically ill patients is to place a greater emphasis on inotropic support and less on fluid resuscitation in order to limit the potential harm from fluid overload. This combination may trigger left ventricular outflow tract obstruction (LVOTO) in susceptible patients. Although LVOTO is classically described in patients with hypertrophic cardiomyopathy it has been reported in other conditions including septic shock, apical ballooning syndrome, myocardial infarction, respiratory failure, and post valvular surgery...
January 2017: Anaesthesia and Intensive Care
https://www.readbyqxmd.com/read/28069318/right-ventricular-hypertrophy-systolic-function-and-disease-severity-in-anderson-fabry-disease-an-echocardiographic-study
#8
Francesca Graziani, Marianna Laurito, Maurizio Pieroni, Faustino Pennestrì, Gaetano Antonio Lanza, Valentina Coluccia, Antonia Camporeale, Daniela Pedicino, Elena Verrecchia, Raffaele Manna, Filippo Crea
BACKGROUND: Right ventricular (RV) involvement has been described in Anderson-Fabry disease (AFD), especially in patients with established Fabry cardiomyopathy (FC). However, few and controversial data on RV systolic function are available, and there are no specific tissue Doppler studies. METHODS: Detailed echocardiographic examinations were performed in 45 patients with AFD. FC, defined as maximal left ventricular wall thickness ≥ 15 mm, was present in 12...
January 6, 2017: Journal of the American Society of Echocardiography
https://www.readbyqxmd.com/read/28069158/systolic-myocardial-volume-gain-in-dilated-hypertrophied-and-normal-heart-cmr-study
#9
Ł Mazurkiewicz, E Orłowska-Baranowska, J Petryka, M Śpiewak, M Gawor, B Miłosz-Wieczorek, K Werys, Ł A Małek, M Marczak, J Grzybowski
AIM: To investigate changes in myocardial tissue volume during the cardiac cycle to verify the hypothesis of non-compressibility of the myocardium in healthy individuals (HI) as well as in patients with hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), and aortic stenosis (AS). MATERIALS AND METHODS: The study group included 30 HI, and patients with HCM (n=110), DCM (n=89), and AS (n=78). Left ventricular (LV) function, end-diastolic, and end-systolic volumes were calculated based on cardiac magnetic resonance imaging (CMR) for all participants...
January 6, 2017: Clinical Radiology
https://www.readbyqxmd.com/read/28065693/inhibition-of-mir-208b-improves-cardiac-function-in-titin-based-dilated-cardiomyopathy
#10
Qifeng Zhou, Sonja Schötterl, Daniel Backes, Eva Brunner, Julia Kelley Hahn, Elena Ionesi, Parwez Aidery, Carsten Sticht, Siegfried Labeit, Reinhard Kandolf, Meinrad Gawaz, Michael Gramlich
BACKGROUND: Dilated cardiomyopathy (DCM) is the result of maladaptive cardiac remodeling, which involves microRNA regulation. In turn, microRNAs can contribute to the remodeling process by post-transcriptional modulation of gene expression networks. The exact role of microRNAs in the pathogenesis of DCM is largely unknown. Here, we used an inducible DCM mouse model that carries a human truncation mutation in the sarcomeric protein titin to dissect microRNA pathways in DCM development...
December 28, 2016: International Journal of Cardiology
https://www.readbyqxmd.com/read/28065448/left-ventricular-dyssynchrony-and-2d-and-3d-global-longitudinal-strain-for-differentiating-physiological-and-pathological-left-ventricular-hypertrophy
#11
Julien Ternacle, Camille Bremont, Thomas d'Humieres, Laureline Faivre, Huy Long Doan, Romain Gallet, Leopold Oliver, Jean-Luc Dubois-Randé, Pascal Lim
BACKGROUND: Diagnosis of hypertrophic cardiomyopathy (HCM) in athletes can be challenging. AIMS: To ascertain parameters that differentiate patients with HCM from athletes with moderate left ventricular (LV) hypertrophy (LVH 13-15mm). METHODS: We retrospectively included 100 men: 50 elite rugby players (25 with moderate LVH and 25 with no LVH), 25 patients with HCM and moderate LVH and 25 controls. LV dyssynchrony was defined as the standard deviation of time to peak 2D longitudinal strain (16-segment model) and global strain components were computed from two- (2D) and three-dimensional (3D) speckle tracking...
January 3, 2017: Archives of Cardiovascular Diseases
https://www.readbyqxmd.com/read/28034463/glucose-transporters-in-healthy-heart-and-in-cardiac-disease
#12
REVIEW
Leszek Szablewski
Heart consumes more energy than any other organ. It can utilize various metabolic substrates as a source of energy. The primary substrates are free fatty acids, especially long-chain fatty acids and glucose. The lipid bilayer of plasmalemma is impermeable for glucose. Therefore, glucose transport across the plasma membrane is mediated via glucose transporters. In human, cardiac cells are expressed as 2 families of glucose transporters: GLUTs and SGLTs. These transport proteins are GLUT1, GLUT3, GLUT8, GLUT10, GLUT11, GLUT12 and SGLT1...
December 21, 2016: International Journal of Cardiology
https://www.readbyqxmd.com/read/28031684/myectomy-like-extended-alcohol-septal-ablation-for-hypertrophic-obstructive-cardiomyopathy
#13
Denisa Jahnlová, Pavol Tomašov, Josef Veselka
Currently, two therapeutic options are available for patients with drug-resistant obstructive hypertrophic cardiomyopathy. While there is a tendency in extended myectomy to perform a larger septal reduction to eliminate left ventricular outflow tract gradient more effectively, there has been a trend in recent years toward using lower dosages of alcohol during alcohol septal ablation (ASA) to reduce the risk of arrhythmic complications. We report a case of a symptomatic patient with severe septal hypertrophy who underwent an extended ASA of three septal branches...
December 2016: International Journal of Angiology: Official Publication of the International College of Angiology, Inc
https://www.readbyqxmd.com/read/28018818/surgical-myectomy-after-failed-ablation-for-hypertrophic-obstructive-cardiomyopathy
#14
Ioannis Bougioukas, Uta Hoppe, Bernhard Danner, Friedrich A Schoendube
Background Hypertrophic cardiomyopathy is a genetic disease of the myocardial sarcolemma characterized by left ventricular hypertrophy. When obstruction to the left ventricular outflow tract is present and symptoms are refractory to medication, surgical myectomy or alcohol septal ablation is indicated. Case Description We report a case of a patient presented for myectomy due to recurrence only 1 year after alcohol ablation. Interesting findings were a firm subaortic membrane and a direct insertion of the papillary muscle into the mitral valve...
December 2016: Thoracic and Cardiovascular Surgeon Reports
https://www.readbyqxmd.com/read/28013283/delayed-and-decreased-lv-untwist-and-unstrain-rate-in-mutation-carriers-for-hypertrophic-cardiomyopathy
#15
Floris Kauer, Bas M van Dalen, Michelle Michels, Arend F L Schinkel, Wim B Vletter, Marjon van Slegtenhorst, Osama I I Soliman, Marcel L Geleijnse
BACKGROUND: The echocardiographic focus to detect abnormalities in genetically hypertrophic cardiomyopathy (HCM) affected subjects without left ventricular (LV) hypertrophy (G+/LVH-) has been on diastolic abnormalities in transmitral flow and longitudinal myocardial function with tissue Doppler imaging. The aim of this study was to assess diastolic LV unstrain and untwist. METHODS AND RESULTS: Forty-one consecutive genotyped family members of HCM patients (mean age 37 ± 11 years, 16 men) and 41 age- and gender-matched healthy volunteers underwent speckle-tracking echocardiography to measure untwist and unstrain...
December 24, 2016: European Heart Journal Cardiovascular Imaging
https://www.readbyqxmd.com/read/28009297/integrative-analysis-of-prkag2-cardiomyopathy-ips-and-microtissue-models-identifies-ampk-as-a-regulator-of-metabolism-survival-and-fibrosis
#16
J Travis Hinson, Anant Chopra, Andre Lowe, Calvin C Sheng, Rajat M Gupta, Rajarajan Kuppusamy, John O'Sullivan, Glenn Rowe, Hiroko Wakimoto, Joshua Gorham, Kehan Zhang, Kiran Musunuru, Robert E Gerszten, Sean M Wu, Christopher S Chen, Jonathan G Seidman, Christine E Seidman
AMP-activated protein kinase (AMPK) is a metabolic enzyme that can be activated by nutrient stress or genetic mutations. Missense mutations in the regulatory subunit, PRKAG2, activate AMPK and cause left ventricular hypertrophy, glycogen accumulation, and ventricular pre-excitation. Using human iPS cell models combined with three-dimensional cardiac microtissues, we show that activating PRKAG2 mutations increase microtissue twitch force by enhancing myocyte survival. Integrating RNA sequencing with metabolomics, PRKAG2 mutations that activate AMPK remodeled global metabolism by regulating RNA transcripts to favor glycogen storage and oxidative metabolism instead of glycolysis...
December 20, 2016: Cell Reports
https://www.readbyqxmd.com/read/28005231/life-long-tailoring-of-management-for-patients-with-hypertrophic-cardiomyopathy-awareness-and-decision-making-in-changing-scenarios
#17
M Michels, I Olivotto, F W Asselbergs, J van der Velden
Hypertrophic cardiomyopathy (HCM) is the most common genetic heart disease, characterised by complex pathophysiology and extensive genetic and clinical heterogeneity. In most patients, HCM is caused by mutations in cardiac sarcomere protein genes and inherited as an autosomal dominant trait. The clinical phenotype ranges from severe presentations at a young age to lack of left ventricular hypertrophy in genotype-positive individuals. No preventative treatment is available as the sequence and causality of the pathomechanisms that initiate and exacerbate HCM are unknown...
December 22, 2016: Netherlands Heart Journal
https://www.readbyqxmd.com/read/28003350/blood-gene-signatures-of-chagas-disease-cardiomyopathy-with-or-without-ventricular-dysfunction
#18
Ludmila Rodrigues Pinto Ferreira, Frederico Moraes Ferreira, Helder Imoto Nakaya, Xutao Deng, Darlan da Silva Cândido, Lea Campos de Oliveira, Jean-Noel Billaud, Marion C Lanteri, Vagner Oliveira-Carvalho Rigaud, Mark Seielstad, Jorge Kalil, Fabio Fernandes, Antônio Luiz P Ribeiro, Ester Cerdeira Sabino, Edecio Cunha-Neto
Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, affects 7 million people in endemic Latin America. About 30% of infected patients will develop chronic Chagas disease cardiomyopathy (CCC), an inflammatory cardiomyopathy characterized by hypertrophy, fibrosis and myocarditis. Further studies are necessary to understand the molecular mechanisms of disease progression. Transcriptome analysis has been increasingly used to identify molecular changes associated with disease outcomes. We thus assessed the whole-blood transcriptome of Chagas disease patients...
December 21, 2016: Journal of Infectious Diseases
https://www.readbyqxmd.com/read/28002430/a-novel-hras-mutation-independently-contributes-to-left-ventricular-hypertrophy-in-a-family-with-a-known-myh7-mutation
#19
Maria Elena Sana, Lawrence A Quilliam, Andrea Spitaleri, Laura Pezzoli, Daniela Marchetti, Chiara Lodrini, Elisabetta Candiago, Anna Rita Lincesso, Paolo Ferrazzi, Maria Iascone
Several genetic conditions can lead to left ventricular hypertrophy (LVH). Among them, hypertrophic cardiomyopathy (HCM), caused by mutations in sarcomere genes, is the most common inherited cardiac disease. Instead, RASopathies, a rare class of disorders characterized by neuro-cardio-facial-cutaneous abnormalities and sometimes presenting with LVH, are caused by mutations in the RAS-MAPK pathway. We report on a 62-years-old male who presented isolated severe obstructive LVH but did not carry the sarcomere mutation previously identified in his affected relatives...
2016: PloS One
https://www.readbyqxmd.com/read/27995696/prevention-of-the-development-of-heart-failure-with-preserved-ejection-fraction-by-the-phosphodiesterase-5a-inhibitor-vardenafil-in-rats-with-type-2-diabetes
#20
Csaba Mátyás, Balázs T Németh, Attila Oláh, Marianna Török, Mihály Ruppert, Dalma Kellermayer, Bálint A Barta, Gábor Szabó, Gábor Kökény, Eszter M Horváth, Beáta Bódi, Zoltán Papp, Béla Merkely, Tamás Radovits
AIMS: Heart failure with preserved ejection fraction (HFpEF) has a great epidemiological burden. The pathophysiological role of cyclic guanosine monophosphate (cGMP) signalling has been intensively investigated in HFpEF. Elevated levels of cGMP have been shown to exert cardioprotective effects in various cardiovascular diseases, including diabetic cardiomyopathy. We investigated the effect of long-term preventive application of the phosphodiesterase-5A (PDE5A) inhibitor vardenafil in diabetic cardiomyopathy-associated HFpEF...
December 19, 2016: European Journal of Heart Failure
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