DOCSLIB.ORG

Pericarditis & Myocarditis

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

Carditis: Inside and Out Derek Brown, MD SAUSHEC Military EMS & Disaster Medicine Fellow Pericarditis Bruce Blaus https://commons.wikimedia.org/wiki/File:Pericarditis.png Pericarditis 0.1% of Hospitalized Patients 5% of ED Patients with non-ACS CP 80-90% Viral Complications: 21% Patients 18% recurrence 3-5% tamponade 2% constrictive pericarditis Pericarditis Not ACS Not Tamponade Not Myocarditis Pericarditis ECG James Heilman, MD https://commons.wikimedia.org/wiki/File:PericarditisMyocarditis.jpg Pericarditis STEMI Tamponade Pericarditis vs Myocarditis Pericarditis – 70% cases Myopericarditis – 25% cases Perimyocarditis – 5% cases Troponin Elevation: Ventricular Arrhythmias Heart Failure Reduced LVEF High Risk Features Fever >38°C (100.4° F) Subacute Course (several days – weeks) Cardiac Tamponade Large Pericardial Effusion (end-diastole Echo-free space >20mm) Immunosuppression / Immunocompromised Anticoagulation Use Trauma Failure of NSAID and/or Colchicine Elevated Troponin Myocarditis Variable Presentation: Viral Illness Cardiogenic Shock 41 – 89% Viral Prodrome Enterovirus, Adenovirus, Parvo B19, HHV 6 Severe Myocarditis 5yr Survival: 56% Pediatric: 90% with 80% requiring ICU care Myocarditis Presentation Pediatric Series: Key Features: 45% Chest Pain - EKG Changes of Myocardial 28% Resp. Distress Injury 27% GI Sx - Rise in Troponin 16% Poor Perfusion - Arrhythmia 41% Viral Prodrome - New/Unexplained Cardiac Dysfxn - Tachycardia Out-Of-Proportion Emergency Management Pediatric Series: 45% Significant Arrhythmia Frank Gaillard https://commons.wikimedia.org/wiki/File:AP_portable_CXR_of_a_patient_in_acu te_pulmonary_oedema.jpg Cardiogenic Shock Broad Differential Inotropes Mechanis Effect Adverse m Trial of IV Fluid Dobutamine Inodilator ↑Contract ↓SVR Hypotension Milrinone Inodilator ↑Contract ↓SVR Hypotension Inotropes Dopamine Mixed ↑Contract ↑↓SVR Arrhythmia, ↑ Mortality Norepinephrine Inopressor ↑Contract ↑SVR Positive Pressure Epinephrine Inopressor ↑Contract ↑SVR Tachycardia, Arrhythmia & Invasive Ventilation Mechanical Circulatory Support Regional Care System References: Baselet B, Rombouts C, Benotmane AM, Baatout S, Aerts A. Cardiovascular diseases related to ionizing radiation: The risk of low-dose exposure (Review). International Journal of Molecular Medicine. 2016;38(6):1623-1641. doi:10.3892/ijmm.2016.2777. Bergmann, K. R., Kharbanda, A., & Haveman, L. (2015). Myocarditis And Pericarditis In The Pediatric Patient: Validated Management Strategies. Pediatric emergency medicine practice, 12(7), 1-23. Davies, P., & Maconochie, I. (2009). The relationship between body temperature, heart rate and respiratory rate in children. Emergency Medicine Journal, 26(9), 641-643. De Backer, D., et al. (2010). Comparison of dopamine and norepinephrine in the treatment of shock. New England Journal of Medicine, 362(9), 779-789. Ghelani, S. J., et al. (2012). Demographics, trends, and outcomes in pediatric acute myocarditis in the United States, 2006 to 2011. Circulation: Cardiovascular Quality and Outcomes, 5(5), 622- 627. Grogan, M., et al. (1995). Long-term outcome of patients with biopsy-proved myocarditis: comparison with idiopathic dilated cardiomyopathy. Journal of the American College of Cardiology, 26(1), 80-84. Imazio, M., et al. (2003). Cardiac troponin I in acute pericarditis. Journal of the American College of Cardiology, 42(12), 2144-2148. Imazio, M., et al. (2004). Day-hospital treatment of acute pericarditis: a management program for outpatient therapy. Journal of the American College of Cardiology, 43(6), 1042-1046. Imazio, M., et al. (2007). Indicators of poor prognosis of acute pericarditis. Circulation, 115(21), 2739-2744. Kytö, V., Sipilä, J., & Rautava, P. (2014). Clinical Profile and Influences on Outcomes in Patients Hospitalized for Acute Pericarditis CLINICAL PERSPECTIVE. Circulation, 130(18), 1601-1606. - 5% hosp pts Levy, B., Perez, P., Perny, J., Thivilier, C., & Gerard, A. (2011). Comparison of norepinephrine-dobutamine to epinephrine for hemodynamics, lactate metabolism, and organ function variables in cardiogenic shock. A prospective, randomized pilot study. Critical care medicine, 39(3), 450-455. Mason JW, O'Connell JB, Herskowitz A, et al. A clinical trial of immunosuppressive therapy for myocarditis. The Myocarditis Treatment Trial Investigators. N Engl J Med 1995; 333:269. O’Connell, J. B., & Topol, E. J. (1998). Diagnosis and medical treatment of inflammatory cardiomyopathy. Topol et al. Cardiovascular Medicine. Philadelphia: Lipincott-Raven. Rossello, X., et al. (2014). New electrocardiographic criteria to differentiate acute pericarditis and myocardial infarction. The American journal of medicine, 127(3), 233-239. van Diepen, S., Katz, J. N., Albert, N. M., Henry, T. D., Jacobs, A. K., Kapur, N. K., ... & Thiele, H. (2017). Contemporary management of cardiogenic shock: a scientific statement from the American Heart Association. Circulation, 136(16), e232-e268..
Recommended publications
  • Guidelines on the Diagnosis and Management of Pericardial

    Guidelines on the Diagnosis and Management of Pericardial

    European Heart Journal (2004) Ã, 1–28 ESC Guidelines Guidelines on the Diagnosis and Management of Pericardial Diseases Full Text The Task Force on the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology Task Force members, Bernhard Maisch, Chairperson* (Germany), Petar M. Seferovic (Serbia and Montenegro), Arsen D. Ristic (Serbia and Montenegro), Raimund Erbel (Germany), Reiner Rienmuller€ (Austria), Yehuda Adler (Israel), Witold Z. Tomkowski (Poland), Gaetano Thiene (Italy), Magdi H. Yacoub (UK) ESC Committee for Practice Guidelines (CPG), Silvia G. Priori (Chairperson) (Italy), Maria Angeles Alonso Garcia (Spain), Jean-Jacques Blanc (France), Andrzej Budaj (Poland), Martin Cowie (UK), Veronica Dean (France), Jaap Deckers (The Netherlands), Enrique Fernandez Burgos (Spain), John Lekakis (Greece), Bertil Lindahl (Sweden), Gianfranco Mazzotta (Italy), Joa~o Morais (Portugal), Ali Oto (Turkey), Otto A. Smiseth (Norway) Document Reviewers, Gianfranco Mazzotta, CPG Review Coordinator (Italy), Jean Acar (France), Eloisa Arbustini (Italy), Anton E. Becker (The Netherlands), Giacomo Chiaranda (Italy), Yonathan Hasin (Israel), Rolf Jenni (Switzerland), Werner Klein (Austria), Irene Lang (Austria), Thomas F. Luscher€ (Switzerland), Fausto J. Pinto (Portugal), Ralph Shabetai (USA), Maarten L. Simoons (The Netherlands), Jordi Soler Soler (Spain), David H. Spodick (USA) Table of contents Constrictive pericarditis . 9 Pericardial cysts . 13 Preamble . 2 Specific forms of pericarditis . 13 Introduction. 2 Viral pericarditis . 13 Aetiology and classification of pericardial disease. 2 Bacterial pericarditis . 14 Pericardial syndromes . ..................... 2 Tuberculous pericarditis . 14 Congenital defects of the pericardium . 2 Pericarditis in renal failure . 16 Acute pericarditis . 2 Autoreactive pericarditis and pericardial Chronic pericarditis . 6 involvement in systemic autoimmune Recurrent pericarditis . 6 diseases . 16 Pericardial effusion and cardiac tamponade .
  • Myocarditis and Cardiomyopathy

    Myocarditis and Cardiomyopathy

    CE: Tripti; HCO/330310; Total nos of Pages: 6; HCO 330310 REVIEW CURRENT OPINION Myocarditis and cardiomyopathy Jonathan Buggey and Chantal A. ElAmm Purpose of review The aim of this study is to summarize the literature describing the pathogenesis, diagnosis and management of cardiomyopathy related to myocarditis. Recent findings Myocarditis has a variety of causes and a heterogeneous clinical presentation with potentially life- threatening complications. About one-third of patients will develop a dilated cardiomyopathy and the pathogenesis is a multiphase, mutlicompartment process that involves immune activation, including innate immune system triggered proinflammatory cytokines and autoantibodies. In recent years, diagnosis has been aided by advancements in cardiac MRI, and in particular T1 and T2 mapping sequences. In certain clinical situations, endomyocardial biopsy (EMB) should be performed, with consideration of left ventricular sampling, for an accurate diagnosis that may aid treatment and prognostication. Summary Although overall myocarditis accounts for a minority of cardiomyopathy and heart failure presentations, the clinical presentation is variable and the pathophysiology of myocardial damage is unique. Cardiac MRI has significantly improved diagnostic abilities, but endomyocardial biopsy remains the gold standard. However, current treatment strategies are still focused on routine heart failure pharmacotherapies and supportive care or cardiac transplantation/mechanical support for those with end-stage heart failure. Keywords cardiac MRI, cardiomyopathy, endomyocardial biopsy, myocarditis INTRODUCTION prevalence seen in children and young adults aged Myocarditis refers to inflammation of the myocar- 20–30 years [1]. dium and may be caused by infectious agents, systemic diseases, drugs and toxins, with viral infec- CAUSE tions remaining the most common cause in the developed countries [1].
  • ICD-10-CM Documentation and Coding Best Practices

    ICD-10-CM Documentation and Coding Best Practices

    ICD-10-CM Documentation and Coding Best Practices Cardiomyopathy Cardiomyopathy refers to diseases of the heart muscle, which can become enlarged, thick or rigid. In rare cases, cardiac muscle tissue can be replaced with scar tissue. As the condition worsens, the heart becomes weaker and less able to pump blood through the body or to maintain a normal electrical rhythm. Causes Risk factors that can increase the possibility of developing cardiomyopathy include: coronary artery disease, a history of heart attack (s), viral infections that cause heart inflammation, long-term hypertension or alcoholism, obesity, and diabetes to name a few. However, in most cases the exact cause is usually unknown (called primary or idiopathic cardiomyopathy). Symptoms Some patients will never have symptoms; others will not develop them until later in the disease. Symptoms can include: • Fatigue • Shortness of b reath or trouble breathing (dyspnea) • Dizziness, lightheadedness or fainting • Swelling in the ankles, feet, legs, abdomen and neck veins Treatment Treatment depends on the type of cardiomyopathy, the severity of symptoms, and the patient’s age and overall health. • Lifestyle changes can help manage condition(s) that may be causing cardiomyopathy. Recommendations include: o Consuming a heart healthy diet, engaging in physical activity, losing excess weight, giving up smoking, avoiding alcohol and illegal drugs, getting enough sleep, and reducing stress • Medicines may be p rescribed to: o Lower blood pressure (ACE inhibitors, angiotensin II receptor blo ckers, beta blockers, calcium channel blockers ) o Slow the heart rate (beta blockers, calcium channel blockers, digoxin) o Prevent arrhythmias (antiarrhythmics) o Remove excess fluid and sodium (diuretics) o Prevent blood clots (anticoagulants) • Alcohol septal ablation • Surgery o Septal myectomy – option for severe cases of obstructive hypertrophic cardiomyopathy Surgically implanted devices o .
  • Myocarditis, Pericarditis and Other Pericardial Diseases

    Myocarditis, Pericarditis and Other Pericardial Diseases

    Heart 2000;84:449–454 Diagnosis is easiest during epidemics of cox- GENERAL CARDIOLOGY sackie infections but diYcult in isolated cases. Heart: first published as 10.1136/heart.84.4.449 on 1 October 2000. Downloaded from These are not seen by cardiologists unless they develop arrhythmia, collapse or suVer chest Myocarditis, pericarditis and other pain, the majority being dealt with in the primary care system. pericardial diseases Acute onset of chest pain is usual and may mimic myocardial infarction or be associated 449 Celia M Oakley with pericarditis. Arrhythmias or conduction Imperial College School of Medicine, Hammersmith Hospital, disturbances may be life threatening despite London, UK only mild focal injury, whereas more wide- spread inflammation is necessary before car- diac dysfunction is suYcient to cause symp- his article discusses the diagnosis and toms. management of myocarditis and peri- Tcarditis (both acute and recurrent), as Investigations well as other pericardial diseases. The ECG may show sinus tachycardia, focal or generalised abnormality, ST segment eleva- tion, fascicular blocks or atrioventricular con- Myocarditis duction disturbances. Although the ECG abnormalities are non-specific, the ECG has Myocarditis is the term used to indicate acute the virtue of drawing attention to the heart and infective, toxic or autoimmune inflammation of leading to echocardiographic and other investi- the heart. Reversible toxic myocarditis occurs gations. Echocardiography may reveal segmen- in diphtheria and sometimes in infective endo-
  • Constrictive Pericarditis Causing Ventricular Tachycardia.Pdf

    Constrictive Pericarditis Causing Ventricular Tachycardia.Pdf

    EP CASE REPORT ....................................................................................................................................................... A visually striking calcific band causing monomorphic ventricular tachycardia as a first presentation of constrictive pericarditis Kian Sabzevari 1*, Eva Sammut2, and Palash Barman1 1Bristol Heart Institute, UH Bristol NHS Trust UK, UK; and 2Bristol Heart Institute, UH Bristol NHS Trust UK & University of Bristol, UK * Corresponding author. Tel: 447794900287; fax: 441173425926. E-mail address: [email protected] Introduction Constrictive pericarditis (CP) is a rare condition caused by thickening and stiffening of the pericar- dium manifesting in dia- stolic dysfunction and enhanced interventricu- lar dependence. In the developed world, most cases are idiopathic or are associated with pre- vious cardiac surgery or irradiation. Tuberculosis remains a leading cause in developing areas.1 Most commonly, CP presents with symptoms of heart failure and chest discomfort. Atrial arrhythmias have been described as a rare pre- sentation, but arrhyth- mias of ventricular origin have not been reported. Figure 1 (A) The 12 lead electrocardiogram during sustained ventricular tachycardia is shown; (B and C) Case report Different projections of three-dimensional reconstructions of cardiac computed tomography demonstrating a A 49-year-old man with a striking band of calcification around the annulus; (D) Carto 3DVR mapping—the left hand panel (i) demonstrates a background of diabetes, sinus beat with late potentials at the point of ablation in the coronary sinus, the right hand panel (iii) shows the hypertension, and hyper- pacemap with a 89% match to the clinical tachycardia [matching the morphology seen on 12 lead ECG (A)], and cholesterolaemia and a the middle panel (ii) displays the three-dimensional voltage map.
  • An Uncommon Clinical Presentation of Relapsing Dilated Cardiomyopathy with Identification of Sequence Variations in MYNPC3, KCNH2 and Mitochondrial Trna Cysteine M

    An Uncommon Clinical Presentation of Relapsing Dilated Cardiomyopathy with Identification of Sequence Variations in MYNPC3, KCNH2 and Mitochondrial Trna Cysteine M

    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by George Washington University: Health Sciences Research Commons (HSRC) Himmelfarb Health Sciences Library, The George Washington University Health Sciences Research Commons Pediatrics Faculty Publications Pediatrics 6-2015 An uncommon clinical presentation of relapsing dilated cardiomyopathy with identification of sequence variations in MYNPC3, KCNH2 and mitochondrial tRNA cysteine M. J. Guillen Sacoto Kimberly A. Chapman George Washington University D. Heath M. B. Seprish Dina Zand George Washington University Follow this and additional works at: http://hsrc.himmelfarb.gwu.edu/smhs_peds_facpubs Part of the Pediatrics Commons Recommended Citation Guillen Sacoto, M.J., Chapman, K.A., Heath, D., Seprish, M.B., Zand, D.J. (2015). An uncommon clinical presentation of relapsing dilated cardiomyopathy with identification of sequence variations in MYNPC3, KCNH2 and mitochondrial tRNA cysteine. Molecular Genetics and Metabolism Reports, 3, 47-54. doi:10.1016/j.ymgmr.2015.03.007 This Journal Article is brought to you for free and open access by the Pediatrics at Health Sciences Research Commons. It has been accepted for inclusion in Pediatrics Faculty Publications by an authorized administrator of Health Sciences Research Commons. For more information, please contact [email protected]. Molecular Genetics and Metabolism Reports 3 (2015) 47–54 Contents lists available at ScienceDirect Molecular Genetics and Metabolism Reports journal homepage: http://www.journals.elsevier.com/molecular-genetics-and- metabolism-reports/ Case Report An uncommon clinical presentation of relapsing dilated cardiomyopathy with identification of sequence variations in MYNPC3, KCNH2 and mitochondrial tRNA cysteine Maria J. Guillen Sacoto a,1, Kimberly A.
  • Pericardial Disease and Other Acquired Heart Diseases

    Pericardial Disease and Other Acquired Heart Diseases

    Royal Brompton & Harefield NHS Foundation Trust Pericardial disease and other acquired heart diseases Sylvia Krupickova Exam oriented Echocardiography course, 4th November 2016 Normal Pericardium: 2 layers – fibrous - serous – visceral and parietal layer 2 pericardial sinuses – (not continuous with one another): • Transverse sinus – between in front aorta and pulmonary artery and posterior vena cava superior • Oblique sinus - posterior to the heart, with the vena cava inferior on the right side and left pulmonary veins on the left side Normal pericardium is not seen usually on normal echocardiogram, neither the pericardial fluid Acute Pericarditis: • How big is the effusion? (always measure in diastole) • Where is it? (appears first behind the LV) • Is it causing haemodynamic compromise? Small effusion – <10mm, black space posterior to the heart in parasternal short and long axis views, seen only in systole Moderate – 10-20 mm, more than 25 ml in adult, echo free space is all around the heart throughout the cardiac cycle Large – >20 mm, swinging motion of the heart in the pericardial cavity Pericardiocentesis Constrictive pericarditis Constriction of LV filling by pericardium Restriction versus Constriction: Restrictive cardiomyopathy Impaired relaxation of LV Constriction versus Restriction Both have affected left ventricular filling Constriction E´ velocity is normal as there is no impediment to relaxation of the left ventricle. Restriction E´ velocity is low (less than 5 cm/s) due to impaired filling of the ventricle (impaired relaxation)
  • Case Report: Cytarabine-Induced Pericarditis and Pericardial Effusion Rino Sato, MD and Robert Park, MD

    Case Report: Cytarabine-Induced Pericarditis and Pericardial Effusion Rino Sato, MD and Robert Park, MD

    HEMATOLOGY & ONCOLOGY Case Report: Cytarabine-Induced Pericarditis and Pericardial Effusion Rino Sato, MD and Robert Park, MD INTRODUCTION for inpatient chemotherapy, and demonstrated mild global left ventricular dysfunction with ejection fraction Cytarabine (cytosine arabinoside, Ara-C) is an antime- of 40%. The cardiomyopathy was attributed to his tabolite analogue of cytidine that is used as a chemo- underlying hypertension or sleep apnea, and not therapeutic agent for the treatment of acute myelogenous coronary artery disease based on a normal coronary leukemia and lymphocytic leukemias1 . The most computed tomography (CT) angiogram. The patient common side effects of this therapy include myelosup- was started on induction therapy with high-dose pression, pancytopenia, hepatotoxicity, gastrointestinal cytarabine therapy at 3g/m2 every twelve hours without ulceration with bleeding, and pulmonary infiltrates2. an anthracycline agent such as doxorubicin. Cardio-pulmonary complications of cytarabine therapy are uncommon, but include supraventricular and On day 5 of cytarabine therapy, the patient developed ventricular arrhythmias, sinus bradycardia, and recurrent non-radiating sharp chest pain that worsened with heart failure2, 3. Occasionally, patients may develop inspiration and palpation. He had no cough or sputum pericarditis leading to pericardial tamponade, which can production. His cardiac exam revealed a tri-phasic, be fatal. We report a case of cytarabine-induced high-pitched friction rub best heard over the left lower pericarditis and pericardial effusion to increase awareness sternal border. He was normotensive, did not have pulsus about this serious side effect of cytarabine and review paradoxus, and had minimally distended jugular veins. the current literature. An electrocardiogram revealed widespread concave ST-elevation and PR-depression in the limb leads (I, II, III, CASE PRESENTATION avF) and precordial leads (V5-V6) concerning for acute pericarditis (Figure 1).
  • COVID 19 Vaccine for Adolescents. Concern About Myocarditis and Pericarditis

    COVID 19 Vaccine for Adolescents. Concern About Myocarditis and Pericarditis

    Opinion COVID 19 Vaccine for Adolescents. Concern about Myocarditis and Pericarditis Giuseppe Calcaterra 1, Jawahar Lal Mehta 2 , Cesare de Gregorio 3 , Gianfranco Butera 4, Paola Neroni 5, Vassilios Fanos 5 and Pier Paolo Bassareo 6,* 1 Department of Cardiology, Postgraduate Medical School of Cardiology, University of Palermo, 90127 Palermo, Italy; [email protected] 2 Department of Medicine, University of Arkansas for Medical Sciences and the Veterans Affairs Medical Center, Little Rock, AR 72205, USA; [email protected] 3 Department of Clinical and Experimental Medicine, University of Messina, 98125 Messina, Italy; [email protected] 4 Cardiology, Cardiac Surgery, and Heart Lung Transplantation Department, ERN, GUAR HEART, Bambino Gesu’ Hospital and Research Institute, IRCCS Rome, 00165 Rome, Italy; [email protected] 5 Neonatal Intensive Care Unit, Department of Surgical Sciences, Policlinico Universitario di Monserrato, University of Cagliari, 09042 Monserrato, Italy; [email protected] (P.N.); [email protected] (V.F.) 6 Department of Cardiology, Mater Misericordiae University Hospital and Our Lady’s Children’s Hospital Crumlin, University College of Dublin, School of Medicine, D07R2WY Dublin, Ireland * Correspondence: [email protected]; Tel.: +353-1409-6083 Abstract: The alarming onset of some cases of myocarditis and pericarditis following the adminis- tration of Pfizer–BioNTech and Moderna COVID-19 mRNA-based vaccines in adolescent males has recently been highlighted. All occurred after the second dose of the vaccine. Fortunately, none of Citation: Calcaterra, G.; Mehta, J.L.; patients were critically ill and each was discharged home. Owing to the possible link between these de Gregorio, C.; Butera, G.; Neroni, P.; cases and vaccine administration, the US and European health regulators decided to continue to Fanos, V.; Bassareo, P.P.
  • Acute Non-Specific Pericarditis R

    Acute Non-Specific Pericarditis R

    Postgrad Med J: first published as 10.1136/pgmj.43.502.534 on 1 August 1967. Downloaded from Postgrad. med. J. (August 1967) 43, 534-538. CURRENT SURVEY Acute non-specific pericarditis R. G. GOLD * M.B., B.S., M.RA.C.P., M.R.C.P. Senior Registrar, Cardiac Department, Brompton Hospital, London, S.W.3 Incidence neck, to either flank and frequently through to the Acute non-specific pericarditis (acute benign back. Occasionally pain is experienced on swallow- pericarditis; acute idiopathic pericarditis) has been ing (McGuire et al., 1954) and this was the pre- recognized for over 100 years (Christian, 1951). In senting symptom in one of our own patients. Mild 1942 Barnes & Burchell described fourteen cases attacks of premonitory chest pain may occur up to of the condition and since then several series of 4 weeks before the main onset of symptoms cases have been published (Krook, 1954; Scherl, (Martin, 1966). Malaise is very common, and is 1956; Swan, 1960; Martin, 1966; Logue & often severe and accompanied by listlessness and Wendkos, 1948). depression. The latter symptom is especially com- Until recently Swan's (1960) series of fourteen mon in patients suffering multiple relapses or patients was the largest collection of cases in this prolonged attacks, but is only partly related to the country. In 1966 Martin was able to collect most length of the illness and fluctuates markedly from of his nineteen cases within 1 year in a 550-bed day to day with the patient's general condition. hospital. The disease is thus by no means rare and Tachycardia occurs in almost every patient at warrants greater attention than has previously some stage of the illness.
  • Coxsackievirus B Detection in Cases of Myocarditis, Myopericarditis, Pericarditis and Dilated Cardiomyopathy in Hospitalized Patients

    Coxsackievirus B Detection in Cases of Myocarditis, Myopericarditis, Pericarditis and Dilated Cardiomyopathy in Hospitalized Patients

    MOLECULAR MEDICINE REPORTS 10: 2811-2818, 2014 Coxsackievirus B detection in cases of myocarditis, myopericarditis, pericarditis and dilated cardiomyopathy in hospitalized patients IMED GAALOUL1-3*, SAMIRA RIABI1*, RAFIK HARRATH1, TIMOTHY HUNTER2, KHALDOUN B. HAMDA4, ASSIA B. GHZALA5, SALLY HUBER3 and MAHJOUB AOUNI1 1Laboratory of Transmissible Diseases LR99‑ES27, Faculty of Pharmacy, Monastir 5000, Tunisia; 2DNA Microarray Facility, 305 Health Science Research Facility, University of Vermont; 3Department of Pathology, University of Vermont, Burlington, VT 05405, USA; 4Department of Cardiology, University Hospital Fattouma Bourguiba, Monastir 5000; 5Department of Cardiology, University Hospitals Farhat Hached and Sahloul, Sousse 4054, Tunisia Received November 9, 2013; Accepted May 21, 2014 DOI: 10.3892/mmr.2014.2578 Abstract. Coxsackieviruses B (CV-B) are known as the most Introduction common viral cause of human heart infections. The aim of the present study was to assess the potential role of CV-B in the Cardiovascular infections include a group of entities involving etiology of infectious heart disease in hospitalized patients. the heart wall, such as myocarditis, dilated cardiomyopathy The present study is based on blood, pericardial fluid and heart and pericarditis. These processes are associated with high biopsies from 102 patients and 100 control subjects. All of the morbidity and mortality. Although early diagnosis is essential samples were examined for the detection of specific enteroviral for adequate patient management and leads to improved prog- genome using the reverse transcription polymerase chain reac- nosis, the clinical manifestations are often non specific (1). tion (RT-PCR) and sequence analysis. Immunohistochemical Myocarditis is clinically and pathologically defined as investigations for the detection of the enteroviral capsid an inflammation of the heart muscle.
  • Etiopathogenesis of Arrhythmogenic Right Ventricular Cardiomyopathy

    Etiopathogenesis of Arrhythmogenic Right Ventricular Cardiomyopathy

    J Hum Genet (2005) 50:375–381 DOI 10.1007/s10038-005-0273-5 MINIREVIEW Maithili V.N. Dokuparti Æ Pranathi Rao Pamuru Bhavesh Thakkar Æ Reena R. Tanjore Æ Pratibha Nallari Etiopathogenesis of arrhythmogenic right ventricular cardiomyopathy Received: 19 May 2005 / Accepted: 20 June 2005 / Published online: 12 August 2005 Ó The Japan Society of Human Genetics and Springer-Verlag 2005 Abstract Arrhythmogenic right ventricular cardiomy- TGFb-3 for ARVC1 and the role of all these three genes opathy (ARVC) is characterised by progressive fibro- (plakoglobin, desmoplakin and plakophilin) in cardiac fatty replacement of right ventricular myocardium. morphogenesis indicate some kind of signal-transducing Earlier studies described ARVC as non-inflammatory, pathway disruption in the condition. The finding that non-coronary disorder associated with arrhythmias, ARVC as a milder form of Uhl’s anomaly indicates heart failure and sudden death due to functional exclu- similar ontogeny for the condition. Further, discovery of sion of the right ventricle. Molecular genetic studies have apoptotic cells in the autopsy of the right ventricular identified nine different loci associated with ARVC; myocardium of ARVC patients does indicate a common accordingly each locus is implicated for each type of pathway for different types of ARVCs, which is more ARVC (ARVC1–ARVC9). So far five genes have been specific for the right ventricular myocardium involving identified as containing pathogenic mutations for desmosomal plaque proteins, growth factors and Ca2+ ARVC. Though mutations in each of the gene/s indicate receptors. disruption of different pathways leading to the condi- tion, the exact pathogenesis of the condition is still Keywords Etiopathogenesis Æ ARVC Æ Desmosomes Æ obscure.