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[PMID]: 29524864
[Au] Autor:Lo Gullo A; Rodríguez-Carrio J; Aragona CO; Dattilo G; Zito C; Suárez A; Loddo S; Atteritano M; Saitta A; Mandraffino G
[Ad] Address:Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
[Ti] Title:Subclinical impairment of myocardial and endothelial functionality in very early psoriatic and rheumatoid arthritis patients: Association with vitamin D and inflammation.
[So] Source:Atherosclerosis;271:214-222, 2018 Mar 02.
[Is] ISSN:1879-1484
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:BACKGROUND AND AIMS: Cardiovascular (CV) morbidity is increased in inflammatory joint diseases (IJD), as rheumatoid (RA) and psoriatic arthritis (PsA). Whereas increased prevalence of subclinical atherosclerosis has been reported in these conditions, whether an early myocardial functionality is also impaired remains unknown. The aim of this study was to evaluate the myocardial functionality by speckle-tracking echocardiography (STE) in recent onset RA and PsA patients and its potential associations with the levels of circulating CD34  cells, vitamin D, and with disease activity. METHODS: STE was used to assess the myocardial functionality in patients with very early RA (n = 41) and PsA (n = 35) without traditional CV risk factors, and 58 matched healthy controls (HC). Global longitudinal and circumferential strain (GLS and GCS) was estimated. Pulse wave velocity (PWV) and carotid intima-media thickness (cIMT) were measured as surrogate markers of atherosclerosis. Circulating CD34  counts were evaluated by flow cytometry and vitamin D levels were quantified by HPLC. Disease activity was assessed by Disease Activity Score-28 (DAS28). RESULTS: RA patients exhibited impaired GLS and GCS (both p < 0.001) as compared to HC, GLS being also altered in PsA (p = 0.020 vs. HC). DAS28 was correlated to GLS (r = 0.908, p < 0.001) and GCS (r = 0.868, p < 0.001) in RA, these findings being confirmed by multivariate regression analyses adjusted for confounders and Principal Component Analyses. GLS and GCS were impaired in PsA patients with high disease activity as compared to HC, and GLS was found to be a predictor of cIMT in this condition. On the other hand, vitamin D was negatively associated with cIMT in HC (r = -0.308, p = 0.026) but not in PsA or RA, although decreased levels were observed (both p < 0.001). Vitamin D was an independent predictor of decreased CD34  levels in PsA and RA. CD34  counts negatively correlated DAS28, GLS and GCS in RA. CONCLUSIONS: Subclinical myocardial dysfunction is observed in IJD patients with preserved left-ventricular function and without traditional CV risk factors. Subclinical myocardial dysfunction was found to be a very early event in IJD. Disease activity was the main predictor of myocardial strain impairment. Interestingly, myocardial function was altered and associated with cIMT also in PsA patients with high disease activity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 165373 MEDLINE  
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[PMID]: 29438721
[Au] Autor:Jentzer JC; Anavekar NS; Mankad SV; White RD; Kashani KB; Barsness GW; Rabinstein AA; Pislaru SV
[Ad] Address:Department of Cardiovascular Medicine, Mayo Clinic, 200 First Street SW, Rochester MN 55905, United states; Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester MN 55905, United states. Electronic address: jentzer.jacob@mayo.e
[Ti] Title:Changes in left ventricular systolic and diastolic function on serial echocardiography after out-of-hospital cardiac arrest.
[So] Source:Resuscitation;126:1-6, 2018 Feb 10.
[Is] ISSN:1873-1570
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:AIM: Reversible myocardial dysfunction is common after out-of-hospital cardiac arrest (OHCA). The aim of this study was to determine if changes on serial transthoracic echocardiography (TTE) can predict long-term mortality in OHCA subjects. METHODS: This is a single-center historical cohort study of OHCA subjects undergoing targeted temperature management who received >1 TTE during hospitalization. Two-dimensional and Doppler parameters of systolic and diastolic function were compared between paired TTE. Univariate analysis was used to determine associations between TTE parameters and all-cause mortality. RESULTS: Fifty-nine patients were included; mean age was 59.4 ±â€¯11.2 years (75% male). Initial rhythm was shockable in 90%. Initial TTE was done a median of 10.4 h after admission and repeat TTE was done 5.7 ±â€¯4.1 days later. Between TTE studies, there were significant increases in left ventricular ejection fraction (LVEF, from 32% to 43%), cardiac output, stroke volume, and other Doppler-derived hemodynamic parameters, while systemic vascular resistance decreased (all p < 0.001). Systolic function and hemodynamic parameters on initial TTE were not associated with follow-up mortality. Patients who died during follow-up (n = 16, 27%) had smaller increases in LVEF and cardiac output-derived hemodynamic parameters than long-term survivors (p < 0.05). CONCLUSIONS: Significant changes in systolic function and hemodynamic parameters occur on serial Doppler TTE after OHCA, consistent with reversible post-arrest myocardial dysfunction. The magnitude of those changes is greater in long-term survivors, emphasizing that the degree of recovery from post-arrest myocardial dysfunction may be more important than its initial severity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 165373 MEDLINE  
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[PMID]: 29523920
[Au] Autor:Altit G; Bhombal S; Van Meurs K; Tacy TA
[Ad] Address:Division of Neonatology, Department of Pediatrics, McGill University - Montreal Children's Hospital, 1001 Decarie, Montreal, QC, H4A 3J1, Canada. Gabriel.altit@mail.mcgill.ca.
[Ti] Title:Diminished Cardiac Performance and Left Ventricular Dimensions in Neonates with Congenital Diaphragmatic Hernia.
[So] Source:Pediatr Cardiol;, 2018 Mar 09.
[Is] ISSN:1432-1971
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Newborns with congenital diaphragmatic hernia (CDH) have varying degrees of pulmonary hypoplasia and pulmonary hypertension (PH), and there is limited evidence that cardiac dysfunction is present. We sought to study early neonatal biventricular function and performance in these patients by reviewing early post-natal echocardiography (ECHO) measurements and comparing them to normal term newborns. METHODS: Retrospective case-control study reviewing clinical and ECHO data on term newborns with CDH and normal controls born between 2009 and 2016. Patients were excluded if major anomalies, genetic syndromes, or no ECHO available. PH was assessed by ductal shunting and tricuspid regurgitant jet velocity. Speckle-tracking echocardiography was used to assess myocardial deformation using velocity vector imaging. RESULTS: Forty-four patients with CDH and 18 age-matched controls were analyzed. Pulmonary pressures were significantly higher in the CDH cohort (systolic pulmonary arterial pressure to systolic blood pressure of 103 ± 13 vs. 78 ± 29%, p = 0.0001). CDH patients had decreased RV fractional area change (FAC - 28.6 ± 11.1 vs. 36.2 ± 9.6%, p = 0.02), tricuspid annular plane of systolic excursion (TAPSE-5.6 ± 1.6 vs. 8.6 ± 1.6 mm, p = 0.0001), and RV outflow tract stroke distance (8.6 ± 2.7 vs. 14.0 ± 4.5 cm, p = 0.0001) compared with controls. The left ventricular (LV) ejection fraction was similar in both groups, but CDH patients had a decreased LV end-diastolic volume by Simpson's rule (2.7 ± 1.0 vs. 5.0 ± 1.8 mL, p = 0.0001) and LVOT stroke distance (9.7 ± 3.4 vs. 12.6 ± 3.6 cm, p = 0.004). Biventricular global longitudinal strain (GLS) was markedly decreased in the CDH population compared to controls (RV-GLS: - 9.0 ± 5.3 vs. - 19.5 ± 1.4%, p = 0.0001; LV GLS: - 13.2 ± 5.8 vs. - 20.8 ± 3.5%, p = 0.0001). CONCLUSION: CDH newborns have evidence of biventricular dysfunction and decreased cardiac output. Abnormal function may be a factor in the non-response to pulmonary arterial vasodilators in CDH patients. A two-pronged management strategy aimed at improving cardiac function, as well as reducing pulmonary artery pressure in CDH newborns, may be warranted.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1007/s00246-018-1850-7

  4 / 165373 MEDLINE  
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[PMID]: 29523919
[Au] Autor:Iwasawa S; Uyeda T; Saito M; Ishii T; Inage A; Hamamichi Y; Yazaki S; Yoshikawa T
[Ad] Address:Department of Pediatric Cardiology, Sakakibara Heart Institute, 3-16-1 Asahi-cho, Fuchu, Tokyo, 183-0003, Japan. shinya.iwasawa.r3@dc.tohoku.ac.jp.
[Ti] Title:Efficacy and Safety of Low-Dose Amiodarone Therapy for Tachyarrhythmia in Congenital Heart Disease.
[So] Source:Pediatr Cardiol;, 2018 Mar 09.
[Is] ISSN:1432-1971
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Amiodarone (AMD) is a class III anti-arrhythmic drug that is highly effective for tachyarrhythmia treatment. AMD is widely used in adults with congenital heart disease (CHD); however, higher doses of AMD (> 200 mg/day) can cause various non-cardiac side effects. The purpose of this study was to assess the efficacy, safety, and adverse events of low-dose AMD (≤ 200 mg/day) for tachyarrhythmia in patients with CHD. We retrospectively studied 80 patients with CHD and tachyarrhythmia who received oral low-dose AMD (≤ 200 mg/day) from January 2004 to March 2016. Low-dose AMD therapy was used to treat supraventricular tachycardia (SVT) in 51 patients and ventricular tachycardia (VT) in 29 patients. After a mean follow-up of 2.9 years for SVT and 3.2 years for VT, 36% and 65% of the patients with SVT and VT, respectively, were free from a first tachyarrhythmia recurrence for 3 years. The incidence of AMD-induced side effects was 23%, and all these cases consisted of thyroid dysfunction. Low-dose AMD was effective for the treatment of tachyarrhythmia in patients with CHD and had a relatively low incidence of side effects. These findings suggest that low-dose AMD is useful and effective for decreasing the frequency of tachyarrhythmia in patients with CHD and has a low incidence of side effects.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1007/s00246-018-1853-4

  5 / 165373 MEDLINE  
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[PMID]: 29481819
[Au] Autor:Shinde AV; Su Y; Palanski BA; Fujikura K; Garcia MJ; Frangogiannis NG
[Ad] Address:The Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), Albert Einstein College of Medicine, Bronx, NY, United States.
[Ti] Title:Pharmacologic inhibition of the enzymatic effects of tissue transglutaminase reduces cardiac fibrosis and attenuates cardiomyocyte hypertrophy following pressure overload.
[So] Source:J Mol Cell Cardiol;117:36-48, 2018 Mar 01.
[Is] ISSN:1095-8584
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Tissue transglutaminase (tTG) is a multifunctional protein with a wide range of enzymatic and non-enzymatic functions. We have recently demonstrated that tTG expression is upregulated in the pressure-overloaded myocardium and exerts fibrogenic actions promoting diastolic dysfunction, while preventing chamber dilation. Our current investigation dissects the in vivo and in vitro roles of the enzymatic effects of tTG on fibrotic remodeling in pressure-overloaded myocardium. Using a mouse model of transverse aortic constriction, we demonstrated perivascular and interstitial tTG activation in the remodeling pressure-overloaded heart. tTG inhibition through administration of the selective small molecule tTG inhibitor ERW1041E attenuated left ventricular diastolic dysfunction and reduced cardiomyocyte hypertrophy and interstitial fibrosis in the pressure-overloaded heart, without affecting chamber dimensions and ejection fraction. In vivo, tTG inhibition markedly reduced myocardial collagen mRNA and protein levels and attenuated transcription of fibrosis-associated genes. In contrast, addition of exogenous recombinant tTG to fibroblast-populated collagen pads had no significant effects on collagen transcription, and instead increased synthesis of matrix metalloproteinase (MMP)3 and tissue inhibitor of metalloproteinases (TIMP)1 through transamidase-independent actions. However, enzymatic effects of matrix-bound tTG increased the thickness of pericellular collagen in fibroblast-populated pads. tTG exerts distinct enzymatic and non-enzymatic functions in the remodeling pressure-overloaded heart. The enzymatic effects of tTG are fibrogenic and promote diastolic dysfunction, but do not directly modulate the pro-fibrotic transcriptional program of fibroblasts. Targeting transamidase-dependent actions of tTG may be a promising therapeutic strategy in patients with heart failure and fibrosis-associated diastolic dysfunction.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  6 / 165373 MEDLINE  
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[PMID]: 29452157
[Au] Autor:Kampourakis T; Ponnam S; Irving M
[Ad] Address:Randall Centre for Cell and Molecular Biophysics, British Heart Foundation Centre of Research Excellence, King's College London, London SE1 1UL, United Kingdom. Electronic address: thomas.kampourakis@kcl.ac.uk.
[Ti] Title:Hypertrophic cardiomyopathy mutation R58Q in the myosin regulatory light chain perturbs thick filament-based regulation in cardiac muscle.
[So] Source:J Mol Cell Cardiol;117:72-81, 2018 Feb 13.
[Is] ISSN:1095-8584
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Hypertrophic cardiomyopathy (HCM) is frequently linked to mutations in the protein components of the myosin-containing thick filaments leading to contractile dysfunction and ultimately heart failure. However, the molecular structure-function relationships that underlie these pathological effects remain largely obscure. Here we chose an example mutation (R58Q) in the myosin regulatory light chain (RLC) that is associated with a severe HCM phenotype and combined the results from a wide range of in vitro and in situ structural and functional studies on isolated protein components, myofibrils and ventricular trabeculae to create an extensive map of structure-function relationships. The results can be understood in terms of a unifying hypothesis that illuminates both the effects of the mutation and physiological signaling pathways. R58Q promotes an OFF state of the thick filaments that reduces the number of myosin head domains that are available for actin interaction and ATP utilization. Moreover this mutation uncouples two aspects of length-dependent activation (LDA), the cellular basis of the Frank-Starling relation that couples cardiac output to venous return; R58Q reduces maximum calcium-activated force with no significant effect on myofilament calcium sensitivity. Finally, phosphorylation of R58Q-RLC to levels that may be relevant both physiologically and pathologically restores the regulatory state of the thick filament and the effect of sarcomere length on maximum calcium-activated force and thick filament structure, as well as increasing calcium sensitivity. We conclude that perturbation of thick filament-based regulation may be a common mechanism in the etiology of missense mutation-associated HCM, and that this signaling pathway offers a promising target for the development of novel therapeutics.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  7 / 165373 MEDLINE  
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[PMID]: 29447158
[Au] Autor:Ahmad A; Sattar MA; Azam M; Khan SA; Bhatt O; Johns EJ
[Ad] Address:School of Pharmaceutical Sciences, Universiti Sains Malaysia, Penang, Malaysia.
[Ti] Title:Interaction between nitric oxide and renal α1-adrenoreceptors mediated vasoconstriction in rats with left ventricular hypertrophyin Wistar Kyoto rats.
[So] Source:PLoS One;13(2):e0189386, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Left ventricular hypertrophy (LVH) is associated with decreased responsiveness of renal α1-adrenoreceptors subtypes to adrenergic agonists. Nitric oxide donors are known to have antihypertrophic effects however their impact on responsiveness of renal α1-adrenoreceptors subtypes is unknown. This study investigated the impact of nitric oxide (NO) and its potential interaction with the responsiveness of renal α1-adrenoreceptors subtypes to adrenergic stimulation in rats with left ventricular hypertrophy (LVH). This study also explored the impact of NO donor on CSE expression in normal and LVH kidney. LVH was induced using isoprenaline and caffeine in drinking water for 2 weeks while NO donor (L-arginine, 1.25g/Lin drinking water) was given for 5 weeks. Intrarenal noradrenaline, phenylephrine and methoxamine responses were determined in the absence and presence of selective α1-adrenoceptor antagonists, 5- methylurapidil (5-MeU), chloroethylclonidine (CeC) and BMY 7378. Renal cortical endothelial nitric oxide synthase mRNA was upregulated 7 fold while that of cystathione γ lyase was unaltered in the NO treated LVH rats (LVH-NO) group compared to LVH group. The responsiveness of renal α1A, α1B and α1D-adrenoceptors in the low dose and high dose phases of 5-MeU, CEC and BMY7378 to adrenergic agonists was increased along with cGMP in the kidney of LVH-NO group. These findings suggest that exogenous NO precursor up-regulated the renal eNOS/NO/cGMP pathway in LVH rats and resulted in augmented α1A, α1B and α1D adrenoreceptors responsiveness to the adrenergic agonists. There is a positive interaction between H2S and NO production in normal animals but this interaction appears absent in LVH animals.
[Mh] MeSH terms primary: Hypertrophy, Left Ventricular/physiopathology
Nitric Oxide/physiology
Receptors, Adrenergic, alpha-1/physiology
Vasoconstriction/physiology
[Mh] MeSH terms secundary: Animals
Rats
Rats, Inbred WKY
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Receptors, Adrenergic, alpha-1); 31C4KY9ESH (Nitric Oxide)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180216
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189386

  8 / 165373 MEDLINE  
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[PMID]: 29439144
[Au] Autor:Zhu Z; Li S
[Ad] Address:Department of Radiology, Cangzhou Central Hospital, Cangzhou 061001, Hebei Province, China.
[Ti] Title:Coronary computed tomography angiography detection of short- and long-term outcomes after heart valve surgery with high risk cardiovascular patients.
[So] Source:Biosci Rep;38(2), 2018 Apr 27.
[Is] ISSN:1573-4935
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Coronary computed tomography angiography (CCTA) is a promising alternative technique to detect significant coronary artery lesions in high-risk cardiovascular patients with left ventricular dysfunction (left ventricular ejection fractions < 40%) referred for elective valve surgery, while little research about the use of CCTA to detect the outcomes of heart valve surgery was performed. Forty-six consecutive high-risk cardiovascular patients with the New York Heart Association (NYHA) classification were retrospectively studied. Immediate, 10-week, 20-week, and 40-week outcomes after heart valve surgery were assessed with CCTA. Patients' average age at the time of surgery was 73 years, with the majority being male (54.35%). Among the CCTA parameters detected after 10, 20, and 40 weeks after heart valve surgery, only segment involvement score (SIS) did reach statistical significance when compared with baseline levels. The cumulative mortality rate at 10, 20, and 40 weeks were 19.56%, 30.43%, and 39.13% respectively. It can be seen that the early death is mainly due to complications, and with the time-lapse of surgery, the impact of complications on death is gradually eliminated. CCTA might be a useful tool to detect the outcomes of short- and long-term outcomes after heart valve surgery with high risk cardiovascular patients, and SIS level is associated with the short- and long-term outcomes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review

  9 / 165373 MEDLINE  
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[PMID]: 29377922
[Au] Autor:Sage M; Nadeau M; Forand-Choinière C; Mousseau J; Vandamme J; Berger C; Tremblay-Roy JS; Tissier R; Micheau P; Fortin-Pellerin É
[Ad] Address:Department of Pediatrics and Department of Pharmacology and Physiology, Université de Sherbrooke, Sherbrooke, Québec, Canada.
[Ti] Title:Assessing the impacts of total liquid ventilation on left ventricular diastolic function in a model of neonatal respiratory distress syndrome.
[So] Source:PLoS One;13(1):e0191885, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Filling the lung with dense liquid perfluorocarbons during total liquid ventilation (TLV) might compress the myocardium, a plausible explanation for the instability occasionally reported with this technique. Our objective is to assess the impacts of TLV on the cardiovascular system, particularly left ventricular diastolic function, in an ovine model of neonatal respiratory distress syndrome. METHOD: Eight newborns lambs, 3.0 ± 0.4 days (3.2 ± 0.3kg) were used in this crossover experimental study. Animals were intubated, anesthetized and paralyzed. Catheters were inserted in the femoral and pulmonary arteries. A high-fidelity pressure catheter was inserted into the left ventricle. Surfactant deficiency was induced by repeated lung lavages with normal saline. TLV was then conducted for 2 hours using a liquid ventilator prototype. Thoracic echocardiography and cardiac output assessment by thermodilution were performed before and during TLV. RESULTS: Left ventricular end diastolic pressure (LVEDP) (9.3 ± 2.1 vs. 9.2 ± 2.4mmHg, p = 0.89) and dimension (1.90 ± 0.09 vs. 1.86 ± 0.12cm, p = 0.72), negative dP/dt (-2589 ± 691 vs. -3115 ± 866mmHg/s, p = 0.50) and cardiac output (436 ± 28 vs. 481 ± 59ml/kg/min, p = 0.26) were not affected by TLV initiation. Left ventricular relaxation time constant (tau) slightly increased from 21.5 ± 3.3 to 24.9 ± 3.7ms (p = 0.03). Mean arterial systemic (48 ± 6 vs. 53 ± 7mmHg, p = 0.38) and pulmonary pressures (31.3 ± 2.5 vs. 30.4 ± 2.3mmHg, p = 0.61) were stable. As expected, the inspiratory phase of liquid cycling exhibited a small but significant effect on most variables (i.e. central venous pressure +2.6 ± 0.5mmHg, p = 0.001; LVEDP +1.18 ± 0.12mmHg, p<0.001). CONCLUSIONS: TLV was well tolerated in our neonatal lamb model of severe respiratory distress syndrome and had limited impact on left ventricle diastolic function when compared to conventional mechanical ventilation.
[Mh] MeSH terms primary: Diastole
Disease Models, Animal
Liquid Ventilation/methods
Respiratory Distress Syndrome, Newborn/therapy
Ventricular Function, Left
[Mh] MeSH terms secundary: Animals
Animals, Newborn
Fluorocarbons/pharmacokinetics
Respiratory Distress Syndrome, Newborn/physiopathology
Sheep
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Fluorocarbons); Q1D0Q7R4D9 (perflubron)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180130
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191885

  10 / 165373 MEDLINE  
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[PMID]: 29263174
[Au] Autor:Chan SY; Rubin LJ
[Ad] Address:Center for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, Blood, and Vascular Medicine Institute, Division of Cardiology, Dept of Medicine, University of Pittsburgh School of Medicine and University of Pittsburgh Medical Center, Pittsburgh, PA, USA chansy@pitt.edu.
[Ti] Title:Metabolic dysfunction in pulmonary hypertension: from basic science to clinical practice.
[So] Source:Eur Respir Rev;26(146), 2017 Dec 31.
[Is] ISSN:1600-0617
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Pulmonary hypertension (PH) is an often-fatal vascular disease of unclear molecular origins. The pulmonary vascular remodelling which occurs in PH is characterised by elevated vasomotor tone and a pro-proliferative state, ultimately leading to right ventricular dysfunction and heart failure. Guided in many respects by prior evidence from cancer biology, recent investigations have identified metabolic aberrations as crucial components of the disease process in both the pulmonary vessels and the right ventricle. Given the need for improved diagnostic and therapeutic options for PH, the development or repurposing of metabolic tracers and medications could provide an effective avenue for preventing or even reversing disease progression. In this review, we describe the metabolic mechanisms that are known to be dysregulated in PH; we explore the advancing diagnostic testing and imaging modalities that are being developed to improve diagnostic capability for this disease; and we discuss emerging drugs for PH which target these metabolic pathways.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1712
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process


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