DOCSLIB.ORG

Pulmonary Hypertension Versus Pulmonary Arterial

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Pulmonary Hypertension Versus Pulmonary Arterial 6/27/2019 PULMONARY HYPERTENSION VERSUS PULMONARY ARTERIAL HYPERTENSION WHAT’S THE DIFFERENCE? Angela Hatch, PA-C 1 DISCLOSURES • Consultant for Actelion Pharmaceuticals, providing consultation on patient perspective and barriers to disease recognition. 2 1 6/27/2019 PULMONARY HYPERTENSION A disease of hemodynamics. • Increased blood pressure in the pulmonary circulation • PH is defined as mean pulmonary artery pressure > 20 mmHg • Normal mean arterial pressure at rest is 14.0+3.3 mmHg • New definition as of March 2018 (published January 2019). 3 HISTORY OF THE WORLD SYMPOSIA ON PULMONARY HYPERTENSION (WSPH) 1st WSPH (1973) • Organized by WHO because of an epidemic of PAH cases due to aminorex (an anorexigen drug) • Achievements • Classification system of PH was created: Primary and Secondary Pulmonary Hypertension • Hemodynamic definition of the disease as a mean arterial pressure of > 25 mmHg was set 4 2 6/27/2019 WSPH (CONTINUED) 2nd WSPH (1998) • A decision was made to start an ongoing series of symposia, fueled by the development of 2 effective treatments: • Flolan (epoprostenol) • High dose CCBs in patients who respond to acute vasoreactivity testing • 5 group classification system was created “Primary and Secondary Pulmonary Hypertension” were abandoned 5 WSPH (CONTINUED) 3rd WSPH (2003) • Specific treatment algorithms were proposed because additional medications were available: • ERAs • Prostacyclins and prostanoids • PDE5 inhibitors • Soluble guanylate cyclase stimulators • Gene mutations had begun to be identified for familial PAH (BMPR2 mutation and others). • 5 classifications remained. 6 3 6/27/2019 WSPH (CONTINUED) 4th WSPH (2008) • Randomized control trial parameters were discussed and defined. • New management strategies again discussed, now including recommendations for treatment of mildly symptomatic patients. 5th WSPH (2013) • Findings and recommendations of 12 Worldwide Task Forces were presented 7 WSPH (CONTINUED) 6th WSPH (2018) – Findings published January 2019 • New definition of pulmonary hypertension was established lowering threshold for diagnosis from a mPAP > 25 mmHg to > 20 mmHg • Following patients should undergo more aggressive assessment and screening: • Congential heart disease (CHD) • Connective tissue disease (CTD) • HIV • Portopulmonary hypertension (POPH) 8 4 6/27/2019 WSPH (CONTINUED) 6th WSPH (continued) • Genetic counseling was recommended for all idiopathic, anorexiant and familial PAH patients and first generation asymptomatic family members. • Post-operative congenital heart disease patients throughout long-term cardiology follow up. • A definition of exercise-induced pulmonary hypertension was still not established. 9 13 TASK FORCES 1) Pathology and Pathobiology 8) New trial designs and potential 2) Genetics and genomics therapies for PAH 3) Pathophysiology 9) Chronic Thromboembolic Pulmonary Hypertension 4) Definitions and Diagnosis 10 & 11) PH due to left heart and lung 5) Epidemiology and registries diseases 6) Standard of care 12)Pediatric PH 7) Treatment Goals 13)Patients’ Perspectives • Defined success of therapy based on symptoms, exercise capacity, and RV function 10 5 6/27/2019 MODIFIED CLASSIFICATION OF PH 1. Pulmonary arterial hypertension (PAH) 3. PH due to lung disease and/or hypoxia 1.1 Idiopathic PAH (IPAH) 3.1 COPD 1.2 Heritable PAH (FPAH) 3.2 Interstitial lung disease 1.2.1 BMPR2 3.3 Other pulmonary diseases with mixed restrictive and 1.2.2 ALK1, ENG, SMAD9, CAV1, KCNK3 obstructive pattern 1.2.3 Unknown 3.4 Sleep-disordered breathing 1.3 Drug- and toxin-induced 3.5 Alveolar hypoventilation disorders 1.4 Associated with 3.6 Chronic exposure to high altitude 1.4.1 Connective tissue diseases 3.7 Developmental lung diseases 1.4.2 HIV infection 4. CTEPH 1.4.3 Portal hypertension 5. PH with unclear multifactorial mechanisms 1.4.4 Congenital heart disease 5.1 Hematological disorders: chronic hemolytic anemia, 1.4.5 Schistosomiasis myeloproliferative disorders, splenectomy Group 1’. Pulmonary veno-occlusive disease and/or pulmonary 5.2 Systemic disorders: sarcoidosis, pulmonary capillary hemangiomatosis Langerhans cell histiocytosis, lymphangioleiomyomatosis, Group 1”. Persistent pulmonary hypertension of the newborn neurofibromatosis, vasculitis PAH long-term responders to calcium channel blockers (2018) 5.3 Metabolic disorders: glycogen storage disease, 2. PH due to left heart disease Gaucher disease, thyroid disorders 2.1 LV systolic dysfunction 5.4 Others: tumoral obstruction, fibrosing mediastinitis, 2.2 LV diastolic dysfunction chronic renal failure, segmental PH 2.3 Valvular disease 2.4 Congenital / acquired left heart inflow / outflow obstruction 11 SO, WHERE’S THE PH REALLY AT? 12 6 6/27/2019 WHY IS PAH SO MUCH WORSE THAN PH? • It’s progressive and there is no reversing damage once it has occurred. The goal of treatment is directed at slowing it down. • There is not a cure and it’s considered terminal – the patient will either die from complete RV failure or require a lung transplant. • Average time from diagnosis to death based on registry findings: • 2.8 years without therapy. • 7 years on therapy. • Average time from lung transplant to death is 5.5 years. • Double lung transplant is required (possible heart and lung). 13 PAH VASCULAR DYSFUNCTION AND REMODELING 14 7 6/27/2019 PAH VASCULAR DYSFUNCTION AND REMODELING Plexiform Lesions https://www.youtube.com/watch?v=VCvBh41OyZs 15 The majority of cases are mixed class disease. (i.e., LV dysfunction and OSA) Over time, PH can cause PAH! 16 8 6/27/2019 PATHOGENESIS OF PAH: LESSONS FROM CANCER 17 HOW DOES PAH PRESENT CLINICALLY? • First symptom is dyspnea on exertion • Breathlessness without overt signs of heart and lung disease is concerning. • Are they always the one who is slower than everyone else? • Fatigue, often chronic and tends to worsen over time • Angina • Edema • Weakness • Lightheadedness and syncope • Tips: • PAH is nearly 4 times as prevalent in females than males, even in FPAH. • Look for hypoxia with exertion • 6MWT is part of the formal diagnostic protocol. • Shape-HF submaximal cardiopulmonary exercise testing provides more information. 18 9 6/27/2019 19 DIAGNOSIS OF PH • It starts with you….. • Incidental findings on EKG, Chest Xray, Echocardiogram • EKG: RVH, RAE, or right axis deviation. Normal EKG doesn’t exclude PH. • CXR, CT: Cardiomegaly with RV enlargement, enlarged pulmonary arteries, pulmonary venous congestion. • Echo: Elevated RVSP and RA pressures, RA and/or RV enlargement, tricuspid regurgitation. 20 10 6/27/2019 DEGREE OF PH BASED ON ECHO Jet of TR (RVSP = 4V2) RA pressure is calculated based on IVC diameter and inspiratory collapse. PASP = RVSP + RAP Tip: If you see a patient’s echo has normal LV systolic and diastolic function, but elevated RVSP you should start to be concerned about possible PAH or CTEPH. 21 22 11 6/27/2019 PAH IS A DISEASE OF RESISTANCE Progression of PVR on Catheterization A dilated RV with low pressures on echo is cause for concern. 23 PH TREATMENT • Early identification and treatment of pulmonary hypertension is advised because advanced disease is less responsive to therapy. • “Primary therapies” are directed at the underlying etiologies. • “Advanced therapies” are directed at the PH itself, rather than the underlying disease. • Only used in Group 1 PAH and Group 4 (CTEPH) • All patients with SpO2 of less than 90% should have oxygen therapy This is critical! • Other medications effective in all groups include the following when indicated: • Diuretics, digoxin, and exercise • Anticoagulation guidelines are unclear. It’s theorized that AC should be used in the following patient groups: • IPAH • FPAH • PAH due to anorexigens • CTEPH 24 12 6/27/2019 PH TREATMENT • Group 1 PAH • There are no effective primary therapies for Group 1 PAH • Oxygen therapy is indicated. Keep SpO2 >90% • CCB (less than 10% of patient’s are responders on RHC) and advanced therapies • Group 2 PH (left heart disease) treat the underlying disease • Group 3 (lung diseases) • Oxygen therapy is the only modality with a proven mortality benefit in this group • Again, treat the underlying disease • Group 4 PH (CTEPH) • Very specific recommendations from Task Force on CTEPH • Anticoagulation • Pulmonary endarterectomy (PEA) is the treatment of choice – don’t wait on this • Medical therapy for patients who aren’t surgical candidates or with residual PH s/p surgery • Group 5 PH • The occurrence of PH in this category is rare and treatment should be directed at the underlying disease 25 ADVANCED THERAPIES • Medication categories: • Calcium channel blockers (if patient shows acceptable vasoreactivity on testing) • Amlodipine, nifedipine, diltiazem • Phosphodiesterase 5 inhibitors • Sildenafil, tadalfil, and vardenafil • Endothelin receptor antagonists • Ambrisentan, macitentan, and bosentan • Prostacyclins/prostanoids • Soluble guanylate cyclase stimulants • Adempas (riociguat) • Increase the sensitivity of sGC to NO and directly stimulate the receptor to mimic the action of NO 26 13 6/27/2019 PROSTANOID DETAILS • Prostanoids – The big guns in PH. • Dilate the blood vessels in the lungs • Slow scarring and cell growth in pulmonary vasculature • Flolan (epoprostenol), Ventavis (iloprost), Remodulin (treprostinil) • Various forms of administration: SubQ and IV most common. • IV therapy is continuous infusion through a central line. • Inhaled variants require 4 times a day dosing. • Oral treprostinil (Orenitram) was approved in 2013 after having been declined by the FDA for approval on two previous
Load more

Recommended publications
  • Pulmonary Arteriopathy in Patients with Mild Pulmonary Valve Abnormality Without Pulmonary Hypertension Or Intracardiac Shunt Karam Obeid1*, Subeer K
    Original Scientific Article Journal of Structural Heart Disease, June 2018, Received: September 13, 2017 Volume 4, Issue 3:79-84 Accepted: September 27, 2017 Published online: June 2018 DOI: https://doi.org/10.12945/j.jshd.2018.040.18 Pulmonary Arteriopathy in Patients with Mild Pulmonary Valve Abnormality without Pulmonary Hypertension or Intracardiac Shunt Karam Obeid1*, Subeer K. Wadia, MD2, Gentian Lluri, MD, PhD2, Cherise Meyerson, MD3, Gregory A. Fishbein, MD3, Leigh C. Reardon, MD2, Jamil Aboulhosn, MD2 1 Department of Biological Sciences, Old Dominion University, Norfolk, Virginia, USA 2 Department of Internal Medicine, Ahmanson/UCLA Adult Congenital Heart Disease Center, Los Angeles, California, USA 3 Department of Pathology, Ronald Reagan/UCLA Medical Center, Los Angeles, California, USA Abstract benign course without episodes of dissection or rup- Background: The natural history of pulmonary artery ture despite 6/11 patients with PAA ≥ 5 cm. PA dilation aneurysms (PAA) without pulmonary hypertension, progresses slowly over time and does not appear to intracardiac shunt or significant pulmonary valvular cause secondary events. Echocardiography correlates disease has not been well studied. This study looks to well with magnetic resonance imaging and computed describe the outcome of a cohort of adults with PAA tomography and is useful in measuring PAA over time. without significant pulmonic regurgitation and steno- Copyright © 2018 Science International Corp. sis. Imaging modalities utilized to evaluate pulmonary artery (PA) size and valvular pathology are reviewed. Key Words Methods: Patients with PAA followed at the Ahmanson/ Pulmonary artery aneurysm • Pulmonary stenosis • UCLA Adult Congenital Heart Disease Center were in- Pulmonary hypertension • Aortic aneurysm cluded in this retrospective analysis.
    [Show full text]
  • Shovlin Wilmshurst and Jackson.Pdf
    Eur Respir Mon 2011; 54: 218–245. DOI: 10.1183/1025448x.10008410 Pulmonary arteriovenous malformations and other pulmonary aspects of hereditary haemorrhagic telangiectasia Claire L Shovlin, 1 2 Peter Wilmshurst 3 4 and James E. Jackson 5 1NHLI Cardiovascular Sciences, Imperial College, London, UK. 2Respiratory Medicine, 5Imaging, Hammersmith Hospital, Imperial College Healthcare NHS Trust, London UK. 3 Department of Cardiology, Royal Shrewsbury Hospital, UK; 4 University of Keele, UK Corresponding author: Dr Claire L. Shovlin PhD FRCP, HHTIC London, Respiratory Medicine, Hammersmith Hospital, Du Cane Rd, London, W12 0NN, UK. Phone (44) 208 383 4831; Fax (44) 208 383 1640; [email protected] CLS and JEJ acknowledge support from the NIHR Biomedical Research Centre Funding Scheme. The authors have no conflicts of interest to declare KEY WORDS: Contrast echocardiography, diving, hypoxaemia, pulmonary hypertension, stroke. 1 SUMMARY: Pulmonary arteriovenous malformations (PAVMs) are vascular structures that provide a direct capillary-free communication between the pulmonary and systemic circulations. The majority of patients have no PAVM-related symptoms, but are at risk of major complications that can be prevented by appropriate interventions. More than 90% of PAVMs occur as part of hereditary haemorrhagic telangiectasia (HHT), the genetic condition most commonly recognised by nosebleeds, anaemia due to chronic haemorrhage, and/or the presence of arteriovenous malformations in pulmonary, hepatic or cerebral circulations. Patients with HHT are also at higher risk of pulmonary hypertension and pulmonary embolic disease, management of which can be compounded by other aspects of their HHT. This chapter primarily addresses PAVMs and pulmonary HHT in the clinical setting, in order to improve patient care.
    [Show full text]
  • Hypertension and Cardiac Arrhythmias: a Consensus Document from The
    Europace (2017) 19, 891–911 CONSENSUS DOCUMENT doi:10.1093/europace/eux091 Hypertension and cardiac arrhythmias: a consensus document from the European Heart Rhythm Association (EHRA) and ESC Council on Hypertension, endorsed by the Heart Rhythm Society (HRS), Asia-Pacific Heart Rhythm Society (APHRS) and Sociedad Latinoamericana de Estimulacion Cardıaca y Electrofisiologıa (SOLEACE) Gregory Y.H. Lip1,2, Antonio Coca3, Thomas Kahan4,5, Giuseppe Boriani6, Antonis S. Manolis7, Michael Hecht Olsen8, Ali Oto9, Tatjana S. Potpara10, Jan Steffel11, Francisco Marın12,Marcio Jansen de Oliveira Figueiredo13, Giovanni de Simone14, Wendy S. Tzou15, Chern-En Chiang16, and Bryan Williams17 Reviewers: Gheorghe-Andrei Dan18, Bulent Gorenek19, Laurent Fauchier20, Irina Savelieva21, Robert Hatala22, Isabelle van Gelder23, Jana Brguljan-Hitij24, Serap Erdine25, Dragan Lovic26, Young-Hoon Kim27, Jorge Salinas-Arce28, Michael Field29 1Institute of Cardiovascular Sciences, University of Birmingham, UK; 2Aalborg Thrombosis Research Unit, Department of Clinical Medicine, Aalborg University, Aalborg, Denmark; 3Hypertension and Vascular Risk Unit, Department of Internal Medicine, Hospital Clınic (IDIBAPS), University of Barcelona, Barcelona, Spain; 4Karolinska Institutet Department of Clinical Sciences, Danderyd Hospital, Stockholm, Sweden; 5Department of Cardiology, Danderyd University Hospital Corp, Stockholm, Sweden; 6Cardiology Department, University of Modena and Reggio Emilia, Policlinico di Modena, Modena, Italy; 7Third Department of Cardiology, Athens
    [Show full text]
  • Risk for Systemic Embolization of Atrial Fibrillation Without Mitral Stenosis
    Risk for Systemic Embolization of Atrial Fibrillation Without Mitral Stenosis Henry S. Cabin, MD, K. Soni Clubb, BS, Cynthia Hall, MD, Robin A. Perlmutter, MPH, and Alvan R. Feinstein, MD trial fibrillation (AF) has often been associated The risk for systemic embolixation was studied in with systemic embolization.*-I’ In studies of ce- 272 patients wlthout mitral stenosis or prosthetic A rebrovascular events, 6 to 23% of strokes have valves who were referred to the echocardlography been attributed to cardiogenic emboli,8~12+13almost half laboratory with atrial fibrillation (AF). During a of which were in patients with AF.‘*Y’~Although it was mean follow-up perfod of 33 months (range <I to reportedly highest in patients with mitral stenosis and 83), 27 (10%) patients had a systemic embolic AF,3,4,15,16the risk of systemic embolization has also event, which was cerebral in 23 patients (85%) and been suggestively increased when AF occurred without peripheral in 4 (15%). In the analysis of individual mitral stenosis.4v’5T17The increasedrisk of embolization variables, the risk of embolixation was increased by has been reported in patients with AF alone* and in female sex, underlying heart disease and left atrial those with associatedcoronary artery disease,4thyro- she 14.0 cm, but not by age, hypertension or type toxicosis,* 8 systemic hypertensionl 9 or dilated left of AF (paroxysmal vs chronic). In multivariable atria.*O Patients with AF have seldom been followed, analysis, left atrial size 14.0 cm was the single however,to identify risk factors for subsequentsystemic strongest predkitor of htcreased risk for embolixa- embolization.
    [Show full text]
  • Blueprint Genetics Congenital Structural Heart Disease Panel
    Congenital Structural Heart Disease Panel Test code: CA1501 Is a 114 gene panel that includes assessment of non-coding variants. Is ideal for patients with congenital heart disease, particularly those with features of hereditary disorders. Is not ideal for patients suspected to have a ciliopathy or a rasopathy. For those patients, please consider our Primary Ciliary Dyskinesia Panel and our Noonan Syndrome Panel, respectively. About Congenital Structural Heart Disease There are many types of congenital heart disease (CHD) ranging from simple asymptomatic defects to complex defects with severe, life-threatening symptoms. CHDs are the most common type of birth defect and affect at least 8 out of every 1,000 newborns. Annually, more than 35,000 babies in the United States are born with CHDs. Many of these CHDs are simple conditions and need no treatment or are easily repaired. Some babies are born with complex CHD requiring special medical care. The diagnosis and treatment of complex CHDs has greatly improved over the past few decades. As a result, almost all children who have complex heart defects survive to adulthood and can live active, productive lives. However, many patients who have complex CHDs continue to need special heart care throughout their lives. In the United States, more than 1 million adults are living with congenital heart disease. Availability 4 weeks Gene Set Description Genes in the Congenital Structural Heart Disease Panel and their clinical significance Gene Associated phenotypes Inheritance ClinVar HGMD ABL1 Congenital
    [Show full text]
  • Subclinical Coronary Atherosclerosis in Patients Undergoing Catheter
    European Journal of Therapeutics DOI: 10.5152/eurjther.2020.20058 Original Research Subclinical Coronary Atherosclerosis in Patients Undergoing Catheter Ablation for Idiopathic Premature Ventricular Complexes Ahmet Hakan Ateş1 , Hikmet Yorgun1 , Uğur Canpolat1 , Muhammet Dural2 , Yusuf Ziya Şener1 , Metin Oksul1 , Sevilay Karahan3 , Kudret Aytemir1 1Department of Cardiology, Hacettepe University School of Medicine, Ankara, Turkey 2Department of Cardiology, Eskisehir Osmangazi University School of Medicine, Eskisehir, Turkey 3Department of Biostatistics, Hacettepe University School of Medicine, Ankara, Turkey ABSTRACT Objective: Idiopathic premature ventricular complexes (PVC) occur in the absence of clinically apparent structural heart disease (SHD) and are treated effectively with catheter ablation. We aimed to evaluate the association of PVC characteristics with subclinical coronary artery disease (CAD) during catheter ablation. Methods: A total of 116 patients (age: median 55 years; sex: 58.6% men), without SHD, in whom PVC ablation and coronary angiography had been performed simultaneously were enrolled. PVC localizations were categorized into 4 groups as; right ventricular outflow tract (RVOT), left ventricular outflow tract (LVOT), left ventricle (LV)-body, and right ventricle (RV)-body. PVC frequency was also classified as moderate (5,000–10,000 PVCs/day) and frequent (≥10,000 PVCs/day). Coronary artery stenoses were categorized as normal, non-critical (<50%), and critical (≥50%). Results: Co-incidental CAD was more frequent among
    [Show full text]
  • Relationship of Obstructive Sleep Apnoea Severity and Subclinical Systemic Atherosclerosis
    Early View Original article Relationship of obstructive sleep apnoea severity and subclinical systemic atherosclerosis Soriul Kim, Ki Yeol Lee, Nan Hee Kim, Robert D. Abbott, Cherry Kim, Seung Ku Lee, Seong Hwan Kim, Chol Shin Please cite this article as: Kim S, Lee KY, Kim NH, et al. Relationship of obstructive sleep apnoea severity and subclinical systemic atherosclerosis. Eur Respir J 2019; in press (https://doi.org/10.1183/13993003.00959-2019). This manuscript has recently been accepted for publication in the European Respiratory Journal. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Copyright ©ERS 2019 Original Research Title: Relationship of obstructive sleep apnoea severity and subclinical systemic atherosclerosis Authors: Soriul Kim1, Ki Yeol Lee2,*, Nan Hee Kim3, Robert D. Abbott1, Cherry Kim2, Seung Ku Lee1, Seong Hwan Kim4, Chol Shin1,5,* 1 Institute for Human Genomic Study, College of Medicine, Korea University, Seoul, Republic of Korea 2 Department of Radiology, Korea University Ansan Hospital, Ansan, Republic of Korea 3 Division of Endocrinology and Metabolism, Department of Internal Medicine, Korea University Ansan Hospital, Ansan, Republic of Korea 4 Division of Cardiology, Department of Internal Medicine, Korea University Ansan Hospital, Ansan, Republic of Korea 5 Division of Pulmonary Sleep and Critical Care Medicine, Department of Internal Medicine, Korea University Ansan Hospital, Ansan, Republic of Korea * To whom correspondence should be addressed. C. Shin (Corresponding author) Division of Respiratory and Critical Care, Department of Internal Medicine, Korea University Ansan Hospital #123, Jeokgeum-ro, Danwon-gu.
    [Show full text]
  • Structural Heart Disease
    Zurich Open Repository and Archive University of Zurich Main Library Strickhofstrasse 39 CH-8057 Zurich www.zora.uzh.ch Year: 2015 Treatment and clinical outcomes of transcatheter heart valve thrombosis Latib, Azeem ; Naganuma, Toru ; Abdel-Wahab, Mohamed ; Danenberg, Haim ; Cota, Linda ; Barbanti, Marco ; Baumgartner, Helmut ; Finkelstein, Ariel ; Legrand, Victor ; de Lezo, José Suárez ; Kefer, Joelle ; Messika-Zeitoun, David ; Richardt, Gert ; Stabile, Eugenio ; Kaleschke, Gerrit ; Vahanian, Alec ; Laborde, Jean-Claude ; Leon, Martin B ; Webb, John G ; Panoulas, Vasileios F ; Maisano, Francesco ; Alfieri, Ottavio ; Colombo, Antonio Abstract: BACKGROUND: Valve thrombosis has yet to be fully evaluated after transcatheter aortic valve implantation. This study aimed to report the prevalence, timing, and treatment of transcatheter heart valve (THV) thrombosis. METHODS AND RESULTS: THV thrombosis was defined as follows (1) THV dysfunction secondary to thrombosis diagnosed based on response to anticoagulation therapy, imaging modality or histopathology findings, or (2) mobile mass detected on THV suspicious of thrombus, irrespective of dysfunction and in absence of infection. Between January 2008 and September 2013, 26 (0.61%) THV thromboses were reported out of 4266 patients undergoing transcatheter aortic valve implantation in 12 centers. Of the 26 cases detected, 20 were detected in the Edwards Sapien/Sapien XT cohort and 6 in the Medtronic CoreValve cohort. In patients diagnosed with THV thrombosis, the median time to THV thrombosis post-transcatheter
    [Show full text]
  • The Structural Heart Disease Program 3 Alternative Treatments for Inoperable Or High-Risk Heart Patients
    Covenant Structural Heart Disease Program Guide The Structural Heart Disease Program 3 alternative treatments for inoperable or high-risk heart patients Do you or a loved one have Structural Heart Disease? Research shows that an estimated two million people in the U.S. are currently living with this complex heart condition. While most individuals can get surgery to help improve their heart condition, some patients may be considered inoperable or high-risk. As a result, they find themselves living in constant fear and exhaustion because they’ve been told that there’s nothing else they can do. But now there’s new hope for inoperable or high-risk heart patients. With the first and most comprehensive Structural Heart Disease Program in the Great Lakes Bay Region, Covenant Center for the Heart is leading with new, emerging options in minimally invasive treatments. So if you or a loved one have been told that you’re inoperable or high-risk, don’t lose heart. There are alternative treatment options available to help improve your heart condition and even more, your overall quality of life. The Structural Heart Program offers three non-invasive procedures for inoperable or high-risk heart patients. This guide will walk you through each alternative treatment, so you can talk with your doctor to determine if an option may be right for you. It’s easy to get lost in the medical terminology. We know you’re not a multi-syllable diagnosis with a catchy acronym. You’re a human being with things to do and a life to live.
    [Show full text]
  • Patient with Pulmonary Hypertension and Hepatic Encephalopathy Chit Wai Wong* Department of Medicine and Geriatrics, Caritas Medical Centre, Hong Kong
    ical C lin as Wong, J Clin Case Rep 2013, 3:2 C e f R o l e a p DOI: 10.4172/2165-7920.1000252 n o r r t u s o J Journal of Clinical Case Reports ISSN: 2165-7920 Case Report Open Access Hereditary Hemorrhagic Telangiectasia: Patient with Pulmonary Hypertension and Hepatic Encephalopathy Chit Wai Wong* Department of Medicine and Geriatrics, Caritas Medical Centre, Hong Kong Abstract Hereditary hemorrhagic telangiectasia (HHT) is usually under recognized. It is a rare genetic disorder characterized by telangiectasia and epistaxis. Visceral involvement by HHT is common but frequently asymptomatic and remains undiagnosed. However, once the visceral manifestation of the disease occurs, it can result in significant morbidity and mortality. This case report demonstrates the rare complications of pulmonary hypertension and hepatic encephalopathy in HHT. Case Report mmol/L) and glucose (5.9 mmol/L) showed no significant abnormality. Blood gas result (pH 7.43, pCO2 58.5 mmHg, pO2 61 mmHg, Bicarbonate A 78 year-old lady had diagnosis of hereditary hemorrhagic 40.2 mmol/L) showed no significant difference over the previously one telangiectasia (HHT). She had telangiectasia over mucosa of nasal year. However, there was elevated serum ammonia level to 54 μmol/L. septum, tongue and both forearm, and frequent recurrent epistaxis for Chest X-ray was clear and CT brain showed only old lacunar infarcts. more than 20 years. She had iron deficiency anemia and endoscopy She was managed as hepatic encephalopathy with lactulose and fleet in 2003 revealed multiple angiodysplasia in the stomach. Endoscopic enema.
    [Show full text]
  • Evaluation of Patients with Syncope in the Emergency Department: How to Adjust Pharmacological Therapy
    medicina Review Evaluation of Patients with Syncope in the Emergency Department: How to Adjust Pharmacological Therapy Martina Rafanelli *,†, Giuseppe Dario Testa †, Giulia Rivasi and Andrea Ungar Syncope Unit, Geriatric and Intensive Care Unit, University of Florence and Azienda Ospedaliero-Universitaria Careggi, Largo Brambilla 3, 50134 Florence, Italy; [email protected] (G.D.T.); giulia.rivasi@unifi.it (G.R.); aungar@unifi.it (A.U.) * Correspondence: martina.rafanelli@unifi.it; Tel.: +39-055-7949558 or +39-333-6022642 † Contributed equally to the paper. Abstract: The rate of syncope in the Emergency Department ranges between 0.9 and 1.7%. Syncope is mostly related to a underlying reflex or orthostatic mechanism. A bradycardic or a hypotensive phenotype, may be identified. The latter is the most common and could be constitutional or drug induced. Consequently, obtaining an accurate drug history is an important step of the initial assess- ment of syncope. As anti-hypertensive medication might be responsible for orthostatic hypotension, managing hypertension in patients with syncope requires finding an ideal balance between hypoten- sive and cardiovascular risks. The choice of anti-hypertensive molecule as well as the therapeutic regimen and dosage, influences the risk of syncope. Not only could anti-hypertensive drugs have a hypotensive effect but opioids and psychoactive medications may also be involved in the mechanism of syncope. Proper drug management could reduce syncope recurrences and their consequences. Citation: Rafanelli, M.; Testa, G.D.; Keywords: syncope; orthostatic hypotension; hypotensive phenotype; hypotensive susceptibility; Rivasi, G.; Ungar, A. Evaluation of pharmacological therapy; drugs Patients with Syncope in the Emergency Department: How to Adjust Pharmacological Therapy.
    [Show full text]
  • The Pediatric and Adult Interventional Cardiac Symposium (PICS/AICS) 22Nd Annual Meeting San Diego, California, September 4-7, 2019
    Meeting Abstracts Journal of Structural Heart Disease, August 2019, Published online: August 2019 Volume 5, Issue 4:75-205 DOI: https://doi.org/10.12945/j.jshd.2019.018.19 The Pediatric and Adult Interventional Cardiac Symposium (PICS/AICS) 22nd Annual Meeting San Diego, California, September 4-7, 2019 2. ENDOVASCULAR TREATMENT OF CRITICAL Patients with hypoplasia of the aorta and concomitant CHD COARCTATION OF THE AORTA (COA) IN NEWBORNS referred surgery. In presence of low pulmonary flow, and AND INFANTS absence or hypoplasia of the aorta, dilatation performed Elnur Imanov1,1, Sabina Hasanova2, Aysel Yusifli 1, Vasiliy urgently. After angioplasty pressure gradient decreased to Lazoryshynets3, Leman Rüstemzade2, Fuad Abdullayev4, 19 ±7 mm Hg; LVEF increased to 63 ± 7%. Farida Hajyeva2, Samir Mamedov2, Oleksandr Pliska 5 1 Health Ministry of Republic of Azerbaijanjan Education Group with endovascular treatment made an uneventful Therapeutic Clinic of Azerbaijan Medical University, Baku, recovery. 13 (68.4%) patients need surgery for re - CoA on Azerbaijan. 2Health Ministry of Republic of Azerbaijanjan 3 - 6 months after dilation. Education Therapeutic Clinic of Azerbaijan Medical University, Baku, Azerbaijan. 3Amosov National Institute of Cardiovascular Conclusion: In critic patients endovascular interven- Surgery, Kiev, Ukraine. 4Health Ministry of Republic of Azerbaijan tion should be preferred with good immediate results. Scientific Center of Surgery Named After M.A.Topchubashov Feasibility of angioplasty of CoA in newborns and infants Pediatric Cardiac Surgery and Neonatal Surgery center, Baku, with CoA remains controversial through a high rate of Azerbaijan. 5Dragomanov National Pedagogical University, Kiev, re-coarctation and re-interventions Ukraine 4. CARDIOVASCULAR DISEASE AND IT PREVENTION Background: Newborns and infants with CoA combined Purusharth Kumar Sharma with hypoplasia of the aorta, CHD, and Ductus dependent Jaipur Rajasthan India flow (DDF) referred to critical heart defects.
    [Show full text]