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THIS ISSUE:

- Pulmonary hypertension: prevalence and mortality in the Armadale echocardiology cohort.

- Exercise training for pumonary hypertension: another prescription to write?.

- REVEAL: a contemporary US pulmonary arterial hypertension registry.

- Classification of pulmonary hypertension.

- and 14 other PHT publications


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1. Cardiology. 2012 Jul 3;122(2):101-102. [Epub ahead of prin
Unfavourable Effect of Pulmonary Arterial Dilatation in Pulmonary Hypertension.
Tamura YSukegawa HOno TSano MFukuda K.
Source
Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.
Abstract
No abstract available.
Copyright © 2012 S. Karger AG, Basel.
  PMID: 22760090 [PubMed - as supplied by publisher]
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2. J Pak Med Assoc. 2012 Apr;62(4):388-91.
Inhaled iloprost in the treatment of pulmonary hypertension in very low birth weight infants: a report of two cases.
Gokce IKahveci HTurkyilmaz ZAdakli BZeybek C.
Source
Department of Paediatrics, Erzurum District Training and Research Hospital, Erzurum, Turkey.
Abstract
We treated 2 very low birth weight (VLBW) infants with respiratory distress syndrome suffering from refractory hypoxic respiratory failure complicated with severe pulmonary hypertension with inhaled iloprost. The first infant was an 800 gram male and the second case was a 920 gram female. Echocardiography revealed a right to left shunt through patent duct in the first case; suprasystemic pulmonary arterial pressure was estimated by using tricuspid regurgitation of moderate severity in the second case. Inhaled iloprost was started in those infants when conventional therapies including the administration of exogenous surfactant and high-frequency oscillatory ventilation failed. After the commencement of therapy, the clinical condition of the infants improved dramatically. Pulmonary arterial pressure returned to normal levels within five days. We suggest that inhaled iloprost may be helpful by improving oxygenation and reducing the need for aggressive mechanical ventilation in some cases of severe hypoxaemic respiratory failure in VLBW infants.
  PMID: 22755287 [PubMed - in process]
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3. Hypertension. 2012 Jul 2. [Epub ahead of print]
Genistein, a Soy Phytoestrogen, Reverses Severe Pulmonary Hypertension and Prevents Right Heart Failure in Rats.
Matori HUmar SNadadur RDSharma SPartow-Navid RAfkhami MAmjedi MEghbali M.
Source
Department of Anesthesiology, Division of Molecular Medicine, Cardiovascular Research Laboratories, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA; Department of Pathology, University of Southern California, Los Angeles, CA.
Abstract
Pretreatment with a phytoestrogen genistein has been shown to attenuate the development of pulmonary hypertension (PH). Because PH is not always diagnosed early, we examined whether genistein could also reverse preexisting established PH and prevent associated right heart failure (RHF). PH was induced in male rats by 60 mg/kg of monocrotaline. After 21 days, when PH was well established, rats received daily injection of genistein (1 mg/kg per day) for 10 days or were left untreated to develop RHF by day 30. Effects of genistein on human pulmonary artery smooth muscle cell and endothelial cell proliferation and neonatal rat ventricular myocyte hypertrophy were assessed in vitro. Severe PH was evident 21 days after monocrotaline, as peak systolic right ventricular pressure increased to 66.35±1.03 mm Hg and right ventricular ejection fraction reduced to 41.99±1.27%. PH progressed to RHF by day 30 (right ventricular pressure, 72.41±1.87 mm Hg; RV ejection fraction, 29.25±0.88%), and mortality was ≈75% in RHF rats. Genistein therapy resulted in significant improvement in lung and heart function as right ventricular pressure was significantly reduced to 43.34±4.08 mm Hg and right ventricular ejection fraction was fully restored to 65.67±1.08% similar to control. Genistein reversed PH-induced pulmonary vascular remodeling in vivo and inhibited human pulmonary artery smooth muscle cell proliferation by ≈50% in vitro likely through estrogen receptor-β. Genistein also reversed right ventricular hypertrophy (right ventricular hypertrophy index, 0.35±0.029 versus 0.70±0.080 in RHF), inhibited neonatal rat ventricular myocyte hypertrophy, and restored PH-induced loss of capillaries in the right ventricle. These improvements in cardiopulmonary function and structure resulted in 100% survival by day 30. Genistein restored PH-induced downregulation of estrogen receptor-β expression in the right ventricle and lung. In conclusion, genistein therapy not only rescues preexisting severe PH but also prevents the progression of severe PH to RHF.
  PMID: 22753213 [PubMed - as supplied by publisher]
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4. Pulm Pharmacol Ther. 2012 Jun 27. [Epub ahead of print]
Regulation of GPCR-mediated smooth muscle contraction: Implications for asthma and pulmonary hypertension.
Wright DBTripathi SSikarwar ASantosh KTPerez-Zoghbi JOjo OOIrechukwu NWard JPSchaafsma D.
Source
Department of Asthma, Allergy, and Lung Biology, King's College, London, United Kingdom.
Abstract
Contractile G-protein-coupled receptors (GPCRs) have emerged as key regulators of smooth muscle contraction, both under healthy and diseased conditions. This brief review will discuss some key topics and novel insights regarding GPCR-mediated airway and vascular smooth muscle contraction as discussed at the 7th International Young Investigators' Symposium on Smooth Muscle (2011, Winnipeg, Manitoba, Canada) and will in particular focus on processes driving Ca(2+)-mobilization and -sensitization.
Copyright © 2012 Elsevier Ltd. All rights reserved.
  PMID: 22750270 [PubMed - as supplied by publisher]
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5. Heart Fail Clin. 2012 Jul;8(3):xxi-xxii.
Pulmonary hypertension.
Murali SBenza RL.
Source
Cardiovascular Institute, Allegheny General Hospital, 320 East North Avenue, Pittsburgh, PA 15212, USA.
  PMID: 22748910 [PubMed - in process]
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6. Heart Fail Clin. 2012 Jul;8(3):485-95.
Exercise-induced pulmonary hypertension.
Bossone ENaeije R.
Source
Division of Cardiology, Cava de'Tirreni-Amalfi Coast Hospital, Salerno, Italy; Department of Cardiology and Cardiac Surgery, University Hospital "Scuola Medica Salernitana", Salerno, Italy; Department of Cardiology and Cardiac Surgery, IRCCS Policlinico San Donato, Milan, Italy.
Abstract
Exercise stress tests of the pulmonary circulation show promise for the detection of early or latent pulmonary vascular disease and may help us understand the clinical evolution and effects of treatments in patients with established disease. Exercise stresses the pulmonary circulation through increases in cardiac output and left atrial pressure. Recent studies have shown that exercise-induced increase in pulmonary artery pressure is associated with dyspnea-fatigue symptomatology, validating the notion of exercise-induced pulmonary hypertension. Exercise in established pulmonary hypertension has no diagnostic relevance, but may help in the understanding of changes in functional state and the effects of therapies.
Copyright © 2012 Elsevier Inc. All rights reserved.
  PMID: 22748908 [PubMed - in process]
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7. Heart Fail Clin. 2012 Jul;8(3):475-83.
Chronic thromboembolic pulmonary hypertension.
Moraca RJKanwar M.
Source
Department of Thoracic and Cardiovascular Surgery, Gerald McGinnis Cardiovascular Institute, Allegheny General Hospital, 320 East North Avenue, Pittsburgh, PA 15212, USA.
Abstract
Chronic thromboembolic pulmonary hypertension (CTEPH) is a potentially life-threatening condition characterized by obstruction of pulmonary arterial vasculature by acute or recurrent thromboemboli with subsequent organization, leading to progressive pulmonary hypertension and right heart failure. Until relatively recently, CTEPH was a diagnosis made primarily at autopsy, but advances made in diagnostic modalities and surgical pulmonary endarterectomy techniques have made this disease treatable and even potentially curable. Although published guidelines are available, in the absence of randomized controlled trials regarding CTEPH there is a lack of standardization, and treatment options have to be individualized.
Copyright © 2012 Elsevier Inc. All rights reserved.
  PMID: 22748907 [PubMed - in process]
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8. Heart Fail Clin. 2012 Jul;8(3):461-74.
Pulmonary hypertension in parenchymal lung disease.
Ruggiero RMBartolome STorres F.
Source
Division of Pulmonary and Critical Care Medicine, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8550, USA.
Abstract
The pathophysiology of pulmonary hypertension (PH) in parenchymal lung diseases is partially related to hypoxic pulmonary vasoconstriction. PH treatment is controversial for these patients. This article focuses on group III PH, namely PH attributable to lung diseases and/or hypoxia. Group III includes chronic obstructive pulmonary disease and interstitial lung diseases, the most common parenchymal lung diseases associated with PH. It also includes sleep-disordered breathing and hypoventilation from any cause. Other parenchymal lung diseases associated with PH, namely sarcoidosis and systemic vasculitides (group V), are discussed. The data describing PH in specific parenchymal diseases are reviewed.
Published by Elsevier Inc.
  PMID: 22748906 [PubMed - in process]
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9. Heart Fail Clin. 2012 Jul;8(3):447-59. Epub 2012 May 18.
Pulmonary hypertension associated with left-sided heart disease.
Barnett CFDe Marco T.
Source
Division of Cardiology, University of California, San Francisco, San Francisco General Hospital, 1001 Potrero Avenue, San Francisco, CA 94110, USA.
Abstract
Pulmonary hypertension (PH) is characterized hemodynamically by significantly elevated pulmonary artery pressure, which if sustained can result in clinical deterioration due to progressive right-sided heart failure and death. Establishing the etiology of PH in a patient before treatment is imperative. Effective evidence-based therapeutic agents for treating PH have been developed. However, appropriately powered, randomized trials in PH associated with left-sided heart failure are sparse, and those that have been performed have shown no benefit or harm. An improved understanding of the pathophysiology, definition, and development of new therapies for treating PH associated with left-sided heart failure is urgently needed.
Copyright © 2012. Published by Elsevier Inc.
  PMID: 22748905 [PubMed - in process]
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10. Heart Fail Clin. 2012 Jul;8(3):427-45.
Congenital heart disease and pulmonary hypertension.
Gupta VTonelli ARKrasuski RA.
Source
Department of Internal Medicine, The Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA; Department of Medicine, The Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA.
Abstract
Many patients with congenital heart disease and systemic-to-pulmonary shunts develop pulmonary arterial hypertension (PAH), particularly if the cardiac defect is left unrepaired. A persistent increase in pulmonary blood flow may lead to obstructive arteriopathy and increased pulmonary vascular resistance, a condition that can lead to reversal of shunt and cyanosis (Eisenmenger syndrome). Cardiac catheterization is crucial to confirm diagnosis and facilitate treatment. Bosentan is the only medication to date to be compared with placebo in a randomized controlled trial specifically targeting congenital heart disease-associated PAH. Lung transplantation with repair of the cardiac defect or combined heart-lung transplantation is reserved for recalcitrant cases.
Copyright © 2012 Elsevier Inc. All rights reserved.
  PMID: 22748904 [PubMed - in process]
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11. Heart Fail Clin. 2012 Jul;8(3):403-12.
Right ventricular remodeling in pulmonary hypertension.
Franco V.
Source
Department of Cardiovascular Disease, Pulmonary Hypertension and Adult Congential Heart Disease Program, Advanced Heart Failure and Transplantation Program, The Ohio State University, 473 West 12th Avenue, Columbus, OH 43210, USA.
Abstract
The right ventricle (RV) is in charge of pumping blood to the lungs for oxygenation. Pulmonary arterial hypertension (PAH) is characterized by high pulmonary vascular resistance and vascular remodeling, which results in a striking increase in RV afterload and subsequent failure. There is still unexploited potential for therapies that directly target the RV with the aim of supporting and protecting the right side of the heart, striving to prolong survival in patients with PAH.
Copyright © 2012 Elsevier Inc. All rights reserved.
  PMID: 22748902 [PubMed - in process]
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12. Heart Fail Clin. 2012 Jul;8(3):331-52.
Diagnostic dilemmas in pulmonary hypertension.
Frantz RPMcGoon MD.
Source
Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, 200 1st Street Southwest, Rochester, MN 55905, USA.
Abstract
Dilemmas persist in the screening, assessment, and follow-up of patients with pulmonary hypertension, relating to issues of whom and how to screen, how to resolve ambiguities in the clinical classification of patients with multiple potential substrates of pulmonary vascular disease, how to interpret test results, how to integrate multiple clinical parameters into a global diagnosis, how to use ambiguous test results, how to determine disease severity and prognosis, and how to monitor patients on treatment. This article describes how to incorporate available information into the diagnostic process, and where lack of concrete data should impose caution in patient management.
Copyright © 2012 Elsevier Inc. All rights reserved.
  PMID: 22748898 [PubMed - in process]
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13. Heart Fail Clin. 2012 Jul;8(3):301-17.
Classification of pulmonary hypertension.
McGlothlin D.
Source
Division of Cardiology, UCSF Medical Center, 505 Parnassus Avenue, Box 0124, San Francisco, CA 94143-0124, USA.
Abstract
Pulmonary hypertension (PH) can develop in association with many different diseases and risk factors, and its presence is nearly always associated with reduced survival. The prognosis and management of PH is largely dependent upon its underlying etiology and severity of disease. The combination of clinical and hemodynamic classifications of PH provides a framework for the diagnostic evaluation of PH to establish a final clinical diagnosis that guides therapy. As our understanding of the different pathologic mechanisms that underlie the syndrome of PH evolves, so too will the classification and treatment of PH.
Copyright © 2012 Elsevier Inc. All rights reserved.
  PMID: 22748896 [PubMed - in process]
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14. Eur Respir Rev. 2012 Mar 1;21(123):40-7. doi: 10.1183/09059180.00009011.
How to detect disease progression in pulmonary arterial hypertension.
Vachiéry JLYerly PHuez S.
Source
Dept. of Cardiology, CUB Hôpital Erasme, Brussels, Belgium. jvachier@ulb.ac.be
Abstract
Pulmonary arterial hypertension (PAH) is a rapidly progressive disease, ultimately leading to right heart failure and death. Accumulating evidence indicates that intervention early in disease progression results in better outcomes than delaying treatment. In this review we will discuss the assessments and strategies that can be used to monitor disease progression and guide clinical management. Many tools, such as symptoms, functional classification, exercise capacity, haemodynamic measures, findings on cardiac imaging and levels of biomarkers, have shown to be prognostic for survival both at diagnosis and during treatment. However, attempts to define goal thresholds have produced a variety of results. Several groups have developed risk calculators to estimate individual patients' mortality risk, but the accuracy of these tools across different patient populations remains unknown. What is clear is the importance of regularly assessing a range of parameters and then tailoring treatment goals to each patient. In addition, the use of a multidisciplinary team approach is crucial in order to support patients through all aspects of managing their condition. There is still an urgent need for prospective collaborative initiatives to assess novel goals and improve treatment strategies that would allow physicians to personalise and optimise clinical management for their patients with PAH.
  PMID: 22379173 [PubMed - indexed for MEDLINE]
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15. Eur Respir Rev. 2012 Mar 1;21(123):8-18. doi: 10.1183/09059180.00008211.
REVEAL: a contemporary US pulmonary arterial hypertension registry.
McGoon MDMiller DP.
Source
Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN, # ICON Late Phase and Outcomes Research, San Francisco, CA, USA.
  PMID: 22379169 [PubMed - indexed for MEDLINE]
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16. Eur J Appl Physiol. 2012 Apr;112(4):1285-94. Epub 2011 Jul 23.
Effects of epoprostenol and sildenafil on right ventricular function in hypoxic volunteers: a tissue Doppler imaging study.
Pavelescu ANaeije R.
Source
Department of Pathophysiology, Faculty of Medicine of the Université Libre de Bruxelles, Brussels, Belgium.
Abstract
Sildenafil and epoprostenol are effective therapies in pulmonary arterial hypertension (PAH). Both drugs increase cardiac output, which has been in part attributed to improved right ventricular (RV) contractility. We therefore used tissue Doppler imaging (TDI) to test whether sildenafil and epoprostenol might differently affect RV function in normal subjects before and after induction of acute hypoxic pulmonary hypertension. Ten healthy volunteers underwent this randomized, double-blind, placebo-controlled cross-over study. Echocardiographic measurements were obtained 60 min after the intake of a placebo or 50 mg sildenafil or under 8 ng/kg/min iv epoprostenol, in normoxia or after 60 min of hypoxic breathing (FIO(2) of 0.12). Right ventricular systolic function was assessed by systolic strain (ε), strain rate (SR), isovolumic contraction acceleration (IVA) and tricuspid annulus plane systolic excursion (TAPSE), and diastolic function by tricuspid annulus E/A ratio and isovolumic relaxation time related to RR interval (IRT/RR). Pulmonary artery pressure was calculated from the acceleration time of pulmonary flow and cardiac output from the left ventricular outflow tract flow-velocity. Hypoxia increased pulmonary vascular resistance (PVR) by 78%, did not affect indices of RV systolic function, decreased E/A and increased IRT/RR. Epoprostenol more than sildenafil increased cardiac output, apical ε and TAPSE, the latter in proportion to decreased PVR. In addition, apical SR was increased only by epoprostenol. None of the drugs affected IVA, basal SR, E/A and IRT/RR. These results are not suggestive of intrinsic positive inotropic effects of either sildenafil or epoprostenol at maximal doses tolerated by normal subjects.
  PMID: 21785860 [PubMed - indexed for MEDLINE]
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17. Eur Respir J. 2012 Jul;40(1):7-8.
Exercise training for pulmonary hypertension: another prescription to write?
Rubin LJ.
Source
School of Medicine, University of California, San Diego, 9300 Campus Point Dr, M/C 7372, La Jolla, CA 92037, USA. E-mail:ljrubin@ucsd.edu.
  PMID: 22753832 [PubMed - in process]
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18. Heart. 2012 Jul 3. [Epub ahead of print]
Pulmonary hypertension: prevalence and mortality in the Armadale echocardiography cohort.
Strange GPlayford DStewart SDeague JANelson HKent AGabbay E.
Source
Victoria, Australia.
Abstract
BACKGROUND:
Pulmonary hypertension (PHT) lacks community prevalence and outcome data.
OBJECTIVE:
To characterise minimum 'indicative' prevalences and mortality data for all forms of PHT in a selected population with an elevated estimated pulmonary artery systolic pressure (ePASP) on echocardiography.
DESIGN:
Observational cohort study.
SETTING:
Residents of Armadale and the surrounding region in Western Australia (population 165 450) referred to our unit for transthoracic echocardiography between January 2003 and December 2009.
RESULTS:
Overall, 10 314 individuals (6.2% of the surrounding population) had 15 633 echo studies performed. Of these, 3320 patients (32%) had insufficient TR to ePASP and 936 individuals (9.1%, 95% CI 8.6% to 9.7%) had PHT, defined as, ePASP>40 mm Hg. The minimum 'indicative' prevalence for all forms of PHT is 326 cases/100 000 inhabitants of the local population, with left heart disease-associated PHT being the commonest cause (250 cases/100 000). 15 cases of pulmonary arterial hypertension/100 000 inhabitants were identified and an additional 144 individuals (15%) with no identified cause for their PHT. The mean time to death for those with ePASP >40 mm Hg, calculated from the first recorded ePASP, was 4.1 years (95% CI 3.9 to 4.3). PHT increased mortality whatever the underlying cause, but patients with PHT from left heart disease had the worst prognosis and those with idiopathic pulmonary arterial hypertension receiving disease-specific treatment the best prognosis. Risk of death increased with PHT severity: severe pulmonary hypertension shortened the lifespan by an average of 1.1 years compared with mild pulmonary hypertension.
CONCLUSIONS:
In this cohort, PHT was common and deadly. Left heart disease was the most common cause and had the worst prognosis and treated pulmonary arterial hypertension had the best prognosis.
Free Article
  PMID: 22760869 [PubMed - as supplied by publisher]
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