We present the case of a 49-year-old male patient with prosthetic mitral valve endocarditis associated with QT prolongation and torsades de pointes. He was asymptomatic until the end of January 2012, when he was admitted to our hospital emergency unit because of syncope, fever, and suspicion of endocarditis. Cardiologic evaluation was requested and the transthoracic (TTE) and transesophageal (TEE) echocardiograms revealed vegetations on the prosthetic mitral valve. All cultures were positive for methicillin-sensitive Staphylococcus aureus. The corrected QT (QTc) interval was markedly prolonged upon admission (QTc 540 ms). He experienced torsades de pointes (TdP) several times and he was recovered after bystander cardiopulmonary resuscitation. The clinical course and the long QTc interval with deep inverted T wave were completely normalized 4 weeks after. He continued on triple antibiotic therapy for 45 days with a good revolution. The clinical features and the possible mechanisms of QT prolongation (inflammation, infection) of this patient are discussed

A. Tounsi

L. Abid

M. Akrout

M. Hentati

S. Kammoun

Case Reports in Medicine

PubMed

Directory of Open Access Journals

QT Prolongation Complicated with Torsades de Pointes in Prosthetic Mitral Valve Endocarditis: A Case Report

We present the case of a 49-year-old male patient with prosthetic mitral valve endocarditis associated with QT prolongation and torsades de pointes. He was asymptomatic until the end of January 2012, when he was admitted to our hospital emergency unit because of syncope, fever, and suspicion of endocarditis. Cardiologic evaluation was requested and the transthoracic (TTE) and transesophageal (TEE) echocardiograms revealed vegetations on the prosthetic mitral valve. All cultures were positive for methicillin-sensitiveStaphylococcus aureus. The corrected QT (QTc) interval was markedly prolonged upon admission (QTc 540 ms). He experienced torsades de pointes (TdP) several times and he was recovered after bystander cardiopulmonary resuscitation. The clinical course and the long QTc interval with deep inverted T wave were completely normalized 4 weeks after. He continued on triple antibiotic therapy for 45 days with a good revolution. The clinical features and the possible mechanisms of QT prolongation (inflammation, infection) of this patient are discussed.</jats:p

Crossref

Hindawi Publishing CorporationCase Reports in MedicineVolume 2012, Article ID 574923, 4 pagesdoi:10.1155/2012/574923Case ReportQT Prolongation Complicated with Torsades de Pointes inProsthetic Mitral Valve Endocarditis: A Case ReportA. Tounsi, L. Abid, M. Akrout, M. Hentati, and S. KammounCardiology Department, Hedi Chaker University Hospital, Sfax 3029, TunisiaCorrespondence should be addressed to L. Abid, leilaabidt@yahoo.frReceived 2 August 2012; Revised 8 September 2012; Accepted 9 September 2012Academic Editor: Dianne L. AtkinsCopyright © 2012 A. Tounsi et al. This is an open access article distributed under the Creative Commons Attribution License,which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.We present the case of a 49-year-old male patient with prosthetic mitral valve endocarditis associated with QT prolongationand torsades de pointes. He was asymptomatic until the end of January 2012, when he was admitted to our hospital emergencyunit because of syncope, fever, and suspicion of endocarditis. Cardiologic evaluation was requested and the transthoracic (TTE)and transesophageal (TEE) echocardiograms revealed vegetations on the prosthetic mitral valve. All cultures were positive formethicillin-sensitive Staphylococcus aureus. The corrected QT (QTc) interval was markedly prolonged upon admission (QTc 540ms). He experienced torsades de pointes (TdP) several times and he was recovered after bystander cardiopulmonary resuscitation.The clinical course and the longQTc interval with deep inverted Twave were completely normalized 4 weeks after. He continued ontriple antibiotic therapy for 45 days with a good revolution. The clinical features and the possible mechanisms of QT prolongation(inflammation, infection) of this patient are discussed.1. IntroductionInfective endocarditis (IE) is lethal if not aggressivelytreated with antibiotics, combined or not with surgery.Developments in antibacterial therapy, clinical microbiology,cardiac imaging, and cardiac surgery have revolutionizedits diagnosis and prognosis. The classical fever of unknownorigin presentation represents a minority of IE cases today;thus, clinicians need to have a high index of suspicionin unusual presentations [1]. Torsade de pointe (TdP) isa devastating form of polymorphic ventricular arrhythmiaassociated with corrected QT (QTc) interval prolongation.A few cases of infective endocarditis-induced QTc prolonga-tion complicated by TdP have been reported. In this paperwe report a case of prosthetic mitral valve endocarditiscomplicated with QTc prolongation and recurrent TdP, andventricular fibrillation.2. Case ReportA 49-year-oldman was admitted to our hospital complainingof intermittent fever and syncope. He had prosthetic mitralvalve replacement in 1998.On physical examination the patient had a fever of38◦C. His blood pressure was 105/70mmHg. There wereno signs of heart failure. He had no signs of splinterhaemorrhages, skin nodules, enlarged lymph nodes, norhepatosplenomegaly. The electrocardiogram showed atrialfibrillation. The QT interval was markedly prolonged(Figure 1). His blood chemistry on admission showed anelevated C-reactive protein (CRP). His leukocyte count onadmission and throughout the hospital course was withinthe normal range. Serum potassium, magnesium, calcium,and thyroid function tests were within the normal range. Hehad no history of taking drugs that prolong the QT inter-val. Transthoracic echocardiography revealed a functioningprosthetic bileaflet mitral valve. The mean pressure gradientacross the mitral valve was 5. The left atrium was enlarged(62mm).Because of high clinical suspicion, transesophagealechocardiography (TEE) was done, which revealed vegeta-tion on the anterior mitral annulus (1.2∗ 0.5 cm) (Figure 2).A diagnosis of IE was made and an empirical antibioticregimen of vancomycin 2 g/day, gentamycin 160mg/day,and rifampicin 1200mg/day was started on the first day ofadmission. Cultures were positive for methicillin-sensitive2 Case Reports in MedicineFigure 1: The electrocardiogram showed atrial fibrillation. The QTinterval was markedly prolonged.Figure 2: Transesophageal echocardiography (TEE) revealed vege-tation on the anterior mitral annulus (1.2∗ 0.5 cm).Staphylococcus aureus. So the antibiotic regimen was changedto oxacillin (2 g∗ 6/day), rifampicin (600mg/day), andgentamycin (160mg/day).On the third day of admission, the patient lost conscious-ness, ceased spontaneous breathing, BP was unmeasurable,the SpO2 was 36%, and the ECG showed ventricularfibrillation. A direct current of 200 J was applied 3 timesusing a biphasic defibrillator. The ECG showed resolution ofthe ventricular fibrillation. However, shortly thereafter TdP-type polymorphic ventricular tachycardia was developed.Defibrillation was performed 3 times, and 1mg epinephrineand 100mg lidocaine were intravenously administered.Additionally, magnesium sulfate 2 g was given intravenouslyover 10min. The BP increased to 146/80mmHg and theSpO2 to 95%. The patient was moved to the intensivecare unit (ICU) with endotracheal intubation in a stablecondition. An ECG showed bradyarrhythmia, a HR of 48beats/min, QTc interval prolongation (610ms), and deepinverted T wave (Figure 3). Isoproterenol was continuouslyadministered intravenously at a rate of 3 µg/min. Then,a temporary pacemaker was inserted in the right ventri-cle apex via the right femoral vein. An echocardiogramshowed no remarkable change of left ventricular systolicfunction. The vital signs stabilized. All electrolytes werewithin normal limits including potassium (4.1mmol/L),magnesium (2.2mg/dL), and calcium (2.45mmol/L). Thepatient was moved to the general ward on the 3rd dayFigure 3: ECG showed bradyarrhythmia, a HR of 48 beats/min,QTc interval prolongation (610ms), and deep inverted T wave.without relapse of TdP. He did not have any recurrence ofarrhythmia and QTc was normalized to 390ms after day 30of antimicrobial therapy (Figure 4). He was clinically andhemodynamically stabilized. C-reactive protein decreasedto 13mg/L (Figure 5). He continued on twin antibiotictherapy for 45 days. The patient has remained symptom- andarythmia-free over a 6-month followup.3. DiscussionLong QT syndrome is an arrhythmogenic cardiovasculardisorder with prolongation of ventricular repolarization,including a QTc interval prolongation longer than 440msfor males or 460ms for females, and an abnormal T wave(broad, notched, small) that causes ventricular tachycardiasuch as TdP and ventricular fibrillation resulting in syncopeor sudden death [2]. Long QT syndrome has traditionallybeen categorized as either congenital or acquired. CongenitalLong QT syndrome is a heritable ion channel diseasedue to gene mutations of the transmembrane sodium orpotassium ion channel proteins. Acquired factors lead-ing to long QT syndrome include hypokalaemia, hypo-magnesaemia, hypocalcaemia marked bradycardia, cocaineabuse, organophosphorus compound poisoning, subarach-noid haemorrhage, stroke, myocardial ischaemia, protein-sparing fasting by using liquid protein diets, autonomicneuropathy, and human immunodeficiency virus disease[3]. Certain common antibiotics, such as erythromycin,appetite suppressants, and decongestants, may trigger dan-gerous heart rhythms. Antiarrhythmic drugs, calcium chan-nel blockers, psychiatric drugs, antihistamines, antimicro-bial and antimalarial drugs, serotonin agonists/antagonists,immunosuppressant, and antidiuretic hormones are capableof prolonging the QT interval [4].A clinical study on acute promyelocytic leukemia therapyby arsenic trioxide revealed that mild and moderate anaemiadid not aﬀect QTc and QTd [5]. Neither hypoproteinaemianor hyperbilirubinaemia correlated with a prolonged QTinterval [6]. However, patients with chronic renal diseasehave elongated a QT interval, which was further prolongedby dialysis therapy [7]. However, it has recently beensuggested that acquired Long QT syndrome is linked to asilent mutation in the gene that causes congenital long QTCase Reports in Medicine 3Figure 4: QTc was normalized to 390ms after day 30.70060050040030020010001 3 5 7 9 11 13 15 17 19 21QTc interval (ms)CRP (mg/dL)Creatin (µmol/L)Figure 5: Biological course: CRP: C-reactive protein, Creat:creatinine levels.syndrome [8]. Long QT syndrome can also be divided intoadrenergic- and pause-dependent types.Most acquired longQT syndrome is the pause-dependenttype that causes QTc interval prolongation and arrhythmiavia bradyarrhythmia or sinus pause.Transmural dispersion (i.e., significant diﬀerences inrepolarization in the various layers of the myocardium)is a feature of TdP and ventricular fibrillation in patientswith long QT syndrome [9, 10]. A decrease in the outwardpotassium ion current or an increase in the slow calcium ioninward current during repolarization resulting from muta-tion of the gene encoding the ion channel prolongs the actionpotential duration that leads to early after depolarization(EAD). In addition to the reentry mechanism, EAD andtransmural dispersion induce TdP [11]. The mechanismsunderlying QTc interval prolongation after conversion toa sinus rhythm are not clearly understood. In the presentpatient, a hereditary basis of long QT syndrome might bemissing as the familial history was scanty; however, a geneticscreening test was not conducted. Laboratory tests ruledout the possibility of hypomagnesaemia, hypocalcaemia, orhypokalaemia. Thus, predisposing factors for acquired longQT syndrome may include mitral valve regurgitation causedby infective endocarditis, renal failure, glomerulonephritis,bradyarrhythmia (atrial fibrillation with slow ventricularresponse), febrile infection [12], and medications, such asdiuretics, or antibiotics.Magnesium sulfate is the treatment of choice for TdPand lidocaine can also be used. Serum potassium should bechecked and maintained as a high normal level [13]. Tem-porary transvenous pacing is an eﬀective way of controllingTdP. Pacing is particularly eﬀective in pause-dependent longQT syndrome [14]. If all of these treatments are ineﬀective,defibrillator should be carried out. There are only 3 cases inthe literature reporting an infective endocarditis presentingwith long QT syndrome.Sayar et al. [15] reported a case of prosthetic mitral valveBrucella endocarditis complicated with torsades de pointesin a 58-year-old woman.Yuan et al. [16] reported a longQT syndrome in extensiveinfective endocarditis complicating hypertrophic obstructivecardiomyopathy in a 52-year-old female.Irie et al. [17] described a QT interval prolongation andtorsades de pointes induced by propofol and hypoalbumine-mia in a 70-year-old man presented with IE.This case is unusual in its presentation. The patienthad a markedly prolonged QTc interval, and associatedtorsades de pointes and ventricular fibrillation as presentingscenario, and surprisingly the QT interval normalized afterthe thirtieth day of appropriate medical therapy, coincidingwith the patient’s clinical and hemodynamic stabilization.4. ConclusionThis case exemplifies that TdP due to acquired long QTsyndrome is a serious and potentially fatal complication inIE. Multiple factors including antimicrobial drugs are at anincreased risk for the development of acquired long QTcsyndrome. Physicians should therefore always maintain ahigh degree of clinical suspicion for the presence of long QTsyndrome in patients with IE and should be aware of theQT-prolonging side eﬀects of drugs they prescribe for thesepatients.References[1] M. H. Crawford and D. T. Durack, “Clinical presentation ofinfective endocarditis,” Cardiology Clinics, vol. 21, no. 2, pp.159–166, 2003.[2] A. Garson Jr., M. Dick II, A. Fournier et al., “The long QTsyndrome in children: an international study of 287 patients,”Circulation, vol. 87, no. 6, pp. 1866–1872, 1993.[3] I. A. Khan, “Long QT syndrome: diagnosis and management,”American Heart Journal, vol. 143, no. 1, pp. 7–14, 2002.[4] Y. G. Yap and A. J. Camm, “Drug induced QT prolongationand torsades de pointes,” Heart, vol. 89, no. 11, pp. 1363–1372,2003.[5] J. Zhou, R. Meng, X. Li, C. Lu¨, S. Fan, and B. Yang, “The eﬀectof arsenic trioxide on QT interval prolongation during APL4 Case Reports in Medicinetherapy,” Chinese Medical Journal, vol. 116, no. 11, pp. 1764–1766, 2003.[6] C. M. Oakley, “Mitral valve palpitations,” Australian and NewZealand Journal of Medicine, vol. 22, no. 5, supplement, pp.562–565, 1992.[7] O. B. Familoni, C. O. Alebiosu, and O. E. Ayodele, “Eﬀects andoutcome of haemodialysis on QT intervals and QT dispersionin patients with chronic kidney disease,” CardiovascularJournal of South Africa, vol. 17, no. 1, pp. 19–23, 2006.[8] P. Chevalier, C. Rodriguez, L. Bontemps et al., “Non-invasivetesting of acquired long QT syndrome: evidence for multiplearrhythmogenic substrates,” Cardiovascular Research, vol. 50,no. 2, pp. 386–398, 2001.[9] F. G. Akar, G. X. Yan, C. Antzelevitch, and D. S. Rosenbaum,“Unique topographical distribution of M cells underliesreentrant mechanism of torsade de pointes in the long-QTsyndrome,” Circulation, vol. 105, no. 10, pp. 1247–1253, 2002.[10] C. Antzelevitch andW. Shimizu, “Cellular mechanisms under-lying the long QT syndrome,” Current Opinion in Cardiology,vol. 17, no. 1, pp. 43–51, 2002.[11] P. C. Viswanathan and Y. Rudy, “Cellular arrhythmogeniceﬀects of congenital and acquired long-QT syndrome in theheterogeneous myocardium,” Circulation, vol. 101, no. 10, pp.1192–1198, 2000.[12] J. Karjalainen and M. Viitasalo, “Fever and cardiac rhythm,”Archives of Internal Medicine, vol. 146, no. 6, pp. 1169–1171,1986.[13] J. Hasegawa, T. Takami, T. Kaneda et al., “Treatment of torsadede pointes with intravenous magnesium in idiopathic long QTsyndrome,” Japanese Circulation Journal, vol. 55, no. 11, pp.1057–1060, 1991.[14] B. N. Koo, O. C. Kang, K. B. Kim et al., “Anesthetic manage-ment of a patient with congenital long QT syndrome,” KoreanJournal of Anesthesiology, vol. 46, pp. 743–746, 2004.[15] N. Sayar, S. Terzi, H. Y. Yilmaz et al., “A case of prostheticmitral valve Brucella endocarditis complicated with torsadesde pointes,” Heart and Vessels, vol. 21, no. 5, pp. 331–333, 2006.[16] S. M. Yuan, E. Demosthenous, and V. Coman, “Long QTsyndrome in extensive infective endocarditis complicatinghypertrophic obstructive cardiomyopathy,” Kardiologia Polska,vol. 67, no. 1, pp. 53–57, 2009.[17] T. Irie, Y. Kaneko, T. Nakajima, A. Saito, and M. Kurabayashi,“QT interval prolongation and torsade de pointes induced bypropofol and hypoalbuminemia,” International Heart Journal,vol. 51, no. 5, pp. 365–366, 2010.Submit your manuscripts athttp://www.hindawi.comStem CellsInternationalHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014MEDIATORSINFLAMMATIONofHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Behavioural NeurologyEndocrinologyInternational Journal ofHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Disease MarkersHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014BioMed Research InternationalOncologyJournal ofHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Oxidative Medicine and Cellular LongevityHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014PPAR ResearchThe Scientific World JournalHindawi Publishing Corporation http://www.hindawi.com Volume 2014Immunology ResearchHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Journal ofObesityJournal ofHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014 Computational and  Mathematical Methods in MedicineOphthalmologyJournal ofHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Diabetes ResearchJournal ofHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Research and TreatmentAIDSHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Gastroenterology Research and PracticeHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Parkinson’s DiseaseEvidence-Based Complementary and Alternative MedicineVolume 2014Hindawi Publishing Corporationhttp://www.hindawi.com

A case of prosthetic mitral valve Brucella endocarditis complicated with torsades depointes,”HeartandVessels,vol.21,no.5,pp.331–333,2006.

Anesthetic management of a patient with congenital long QT syndrome,”

C.AntzelevitchandW.Shimizu,“Cellularmechanismsunderlying the long QT syndrome,” Current Opinion in Cardiology,

Cellular arrhythmogenic eﬀects of congenital and acquired long-QT syndrome in the heterogeneous myocardium,”

Clinical presentation of infective endocarditis,”

Eﬀects and outcome of haemodialysis on QT intervals and QT dispersion in patients with chronic kidney disease,”

Fever and cardiac rhythm,”

h e v a l i e r ,C .R o d r i g u e z ,L .B o n t e m p se ta l . ,“ N o n - i n v a s i v e testing of acquired long QT syndrome: evidence for multiple arrhythmogenic substrates,”

Long QT syndrome in extensive infective endocarditis complicating hypertrophicobstructivecardiomyopathy,”KardiologiaPolska,

Long QT syndrome: diagnosis and management,”

Mitral valve palpitations,” Australian and New Zealand

QT interval prolongation and torsade de pointes induced by propofol and hypoalbuminemia,”

T.Kaneda et al., “Treatment oftorsade depointeswithintravenousmagnesiuminidiopathiclongQT syndrome,”

The eﬀect of arsenic trioxide on

The long QT syndrome in children: an international study of 287 patients,”

Unique topographical distribution of M cells underlies reentrant mechanism of torsade de pointes in the long-QT syndrome,”

QT Prolongation Complicated with Torsades de Pointes in Prosthetic Mitral Valve Endocarditis: A Case Report

Abstract

Similar works

Full text

Available Versions

Directory of Open Access Journals

Crossref