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1 , urw>, ry1ry, 160 Medcal Educaton CME Artcle Electrocardographcal case J wave and presyncope n a mddle-aged woman Namboodr N, Bohora S, Dora S K, Tharakan J A t- R rla j1 4 y 7 ", 1»), e7 e MOM!l, m ` " :r;%-{ya!);? 71 P M dle >`lll, L;r- l +~ E t! } ; 1} n ñwltïhn,lal ü ll?,«erg, B llf, :l1f1 1+,r, : da, r ryyl{pìy ` t, [A { j;;;ìttlg141rj ; j l le {n ì; llllt!`lfl a - 7/e m11 1;, lllll lll ;; AEe`` ºn6re lû&jll í lßlllal uoll : " : lyl1r:71,` lrlr1:;,wlllllllüt tc: :? dll el 1RESllgfjNSJ1D111AfML Mu d ryy1:1 rltl3ltg: CC65 r1:1 C, : llllülll tn^ + a NL 1 aah,er Nb_,: jggup lr[r; aläuftül1lt11 mll! `s Nell -g- ;, BM, ìì Ç t l1131mm -l -, : l ü ; Ykr ; : rye{1 1l hllrj;} l FY91M1wfLr1NA gagggump `;_ le:, 1 ì,: :1: v 1,,,a ; 4,: ll a l 3:E: l no - ;- a ; :ü 1r! }r (1 H e 1 Y [ r,t ] +; `ü: Fg 112 -lead ECG at admsson lnlll r, s jltllle t;, [ s, :a : ssl í :-V Department of Cardology, Sree Chtra Trunal nsttute for Medcal Scences and Technology, Trvandrum, Kerala , nda CLNCAL PRESENTATON A 46 -year-old woman wth a hstory of hypertenson for the last 12 years, presented to us wth three epsodes of presyncope n the prevous two days Clncal examnaton was normal The 12 -lead electrocardogram (ECG) was done (Fg 1) What does the ntal ECG show? What s your dagnoss? Namboodr N, DM Assstant Professor Bohora S, DM Assstant Professor Dora SK, DM Professor Tharakan JA, DM Professor Correspondence to: Dr K K Narayanan Namboodr Tel: (91) Fax: (91)

2 a 2b Fg 2 (a) Lateral and (b) antero-posteror radographs of the skull show tny punched -out lesons, producng a so-called salt - and -pepper appearance ECG NTERPRETATON The ECG showed snus rhythm, relatvely -short QT nterval (QTc of 340 msec) wth shortenng predomnantly nvolvng the ST segment, and promnent J -waves n nferor leads (Fg1) Decreased T -wave ampltude 1 wth promnent U -waves n lead and mdprecordal leads were also noted Electrocardographcal J -waves have been descrbed wth hypotherma, hypercalcaema, Brugada syndrome, subarachnod haemorrhage and vasospastc angna DAGNOSS The presence of relatvely shortened QTc, J -waves and normal clncal condton made us to look for possble hypercalcaema n ths patent CLNCAL COURSE There was no documented brady- or tachyarrhythma Bochemcal evaluaton revealed serum calcum of 174 mg/dl, phosphorus of 23 mg/dl and alkalne phosphatase of 533 U/ml She was evaluated for hypercalcaema wth a provsonal dagnoss of prmary hyperparathyrodsm Radographcal evaluaton revealed a salt -and -pepper appearance of the skull (Fgs 2a-b) and subperosteal resorpton of phalanges (Fg 3) Ultrasonography of the neck showed adenoma of the rght upper parathyrod gland Parathyrod scntgraphy wth Tc -99m Tc-MB showed ncreased actvty n the rght upper parathyrod gland, whch perssted n the late mages She was managed wth salne duress followed by electve parathyrodectomy Per- and postoperatve perods were uneventful The ECG became normal wth the dsappearance of J -waves after treatment for hypercalcaema (Fg 4) She was asymptomatc at sx months follow-up Fg 3 Antero-posteror radograph of the hand shows subperosteal resorpton of dgtal tufts and phalanges

3 ^ É, ;+, 162 whz x " : : Y " u--, - -V -, dh !!!!! 1 a -y 0 :: : --w - :":, Fg 4 ECG, after correcton of hypercalcaema (Ca2 82 mg/dl, shows normal QTc and no J -waves DSCUSSON The presence of J -waves (Osborne waves) n hypercalcaema has rarely been reported(1-6) J -waves were descrbed wth hypotherma, Brugada syndrome and, more uncommonly, wth subarachnod haemorrhage and vasospastc angna Our case was unque n that the presentng symptom was presyncope, rather than systemc symptoms often seen wth prmary hyperparathyrodsm We assume the cause of presyncope n our case to be transent ventrcular arrhythmas However, no tachy- or bradyarrhythma could be documented n the hosptal Calcum levels came down to 104 mg% wthn 24 hours of admsson and the patent dd not have recurrence of symptoms afterwards The electrophysologcal bass of the J -wave s controversal Yan and Antzelevtch suggested a heterogeneous dstrbuton of a transent outward current -medated spke -and -dome morphology of the acton potental across the ventrcular wall as the cellular mechansm of the electrocardographcal J -wave() An accentuaton of the spke -and -dome morphology of the epcardal, but not endocardal acton potental, was shown to provde a voltage gradent that manfests as a J -wave or elevated J -pont n the ECG n hypercalcaema, ths s thought to be due to an ncreased net outward current durng the early phases of the acton potental, possbly due to an ncrease n calcum -actvated chlorde current and a decrease n c ($) The presence of a promnent transent outward current (to) n the epcardum has been shown to senstse tssue to the effects of hgh calcumm Apart from ths phase 2 re-entry, delayed after -depolarsaton -nduced trggered actvty n hypercalcaema also contrbute to the development of electrcal nhomogenety n the ventrcle, and thus leadng to the geness of ventrcular arrhythmas Apart from the Osborne wave, electrocardographcal changes assocated wth hypercalcaema nclude a relatvely shortened QT nterval, manly shortenng the ST segment component of t Decreased T -wave ampltude, T -wave notchng and T -wave nverson are also observed n severe hypercalcaema Wth ncreasng levels of serum calcum, a hgh take-off of the ST segment n leads V1 and V2, smulatng acute myocardal schaema, has also been descrbed(9-11) After t was descrbed ntally by Kraus n 1920,(1) J -wave n hypercalcaema was reported n a few cases n humans«-0 Proper recognton of ths abnormal ECG fndng and evaluaton elmnated further cardac evaluaton to nvestgate the cause of presyncope n our patent Ths case s beng reported to hghlght the assocaton of J -waves wth hypercalcaema and ts uncommon presentaton as presyncope ABSTRACT A 46 -year -old woman presented wth three epsodes of presyncope n the prevous two days Electrocardogram (ECG) showed snus rhythm, relatvely short QT nterval (QTc of 340 msec) and promnent J -waves n the nferor leads Bochemcal evaluaton revealed serum calcum of 174 mg/dl, phosphorus of 23 mg/dl and alkalne phosphatase of 533 U/ml She was managed wth salne duress followed by electve

4 163 parathyrodectomy ECG became normal wth the dsappearance of J -waves after correcton of hypercalcaema She was asymptomatc at sx months of follow-up The presence of J -waves (Osborne waves) n hypercalcaema has rarely been reported Keywords: hypercalcaema, hyperparathyrodsm, J -wave Sngapore Med J 2008; 49(2): REFERENCES 1 Kraus F Ueber de Wrkung des Kalzums auf den Kreslauf Deutsch Med Wochenschr 1920; 46: Srdharan MR, Horan LG Electrocardographc J wave of hypercalcema Am J Cardol 1984; 54: Netelenbos JC, VerheugtFW, de Rjk SH Hypercalcema and J waves Am J Cardol 1987; 59:724 4 Jenkns JK, Best TR, Ncks SA, et al Mlk -alkal syndrome wth a serum calcum level of 22 mg/dl and J waves on the ECG South Med J 1987; 80: Otero J, Lenhan DJ The "normothermc" Osborn wave nduced by severe hypercalcema Tex Heart nst J 2000; 27: TopsakalR,SaglamH,ArncH,EryolNK,CetnSElectrocardographc J wave as a result of hypercalcema aggravated by thazde duretcs n a case of prmary hyperparathyrodsm Jpn Heart J 2003; 44: Yan GX, Antzelevtch C Cellular bass for the electrocardographc J wave Crculaton 1996; 93: D Dego JM, Antzelevtch C Hgh [Ca2+]o-nduced electrcal heterogenety and extrasystolc actvty n solated canne ventrcular epcardum Phase 2 reentry Crculaton 1994; 89: NshSP,BarbagelataNA,AtarS,BrnbaumY,TueroEHypercalcema- nduc ed ST -segment elevaton mmckng acute myocardal nfarcton J Electrocardol 2006; 39: Turban S, Klckap M, Klnc S ST segment elevaton mmckng acute myocardal nfarcton n hypercalcema Heart 2005; 91: Ashzawa N, Arakawa S, Kode Y, et al Hypercalcema due to vtamn D ntoxcaton wth clncal features mmckng acute myocardal nfarcton ntern Med 2003; 42:340-4

5 164 SNGAPORE MEDCAL COUNCL CATEGORY 3B CME PROGRAMME Multple Choce Questons (Code SMJ 20082A) Queston 1 Electocardographcal J -waves are seen n: (a) Subarachnod haemorrhage (b) Vaso spastc angna (c) Long QT syndrome (d) Brugada syndrome True False Queston 2 Electrocardographcal changes assocated wth hypercalcaema nclude: (a) "hgh take off of ST segment" (b) Shortened QTc (c) Osborne wave (d) T -wave alternans Queston 3 The mechansm by whch hypercalcaema result n ventrcular arrhythmas nclude: (a) Phase 2 re-entry (b) Delayed after repolarsaton (c) Trggered actvty (d) ncreased automatcty Queston 4 Radologcal features of hyperparathyrodsm nclude: (a) Subpero steal resorpton (b) Osteoscleross (c) "Salt and pepper" appearance of the skull (d) Delayed epphy seal fuson Queston 5 The true statement on dagnoss and management of hyperparathyrodsm nclude: (a) Salne duress s used n acute emergency (b) Emergency parathyrodectomy s lfe-savng (c) ECG changes revert after a few days of correcton of hypercalcaema (d) Parathyrod scntgraphc scan s useful n localsaton of the adenoma Doctors partculars: Name n full: MCR number: Emal address: Specalty: SUBMSSON NSTRUCTONS: (1) Log on at the SM webste: wwwsmaorgsg/cme/smj and select the approprate set of questons (2) Select your answers and provde your name, emal address and MCR number Clck on "Submt answers" to submt RESULTS: (1) Answers wll be publshed n the SMJ Aprl 2008 ssue (2) The MCR numbers of successful canddates wll be posted onlne at wwwsmaorgsg/cme/smj by 15 Aprl 2008 (3) All onlne submssons wll receve an automatc emal acknowledgment (4) Passng mark s 60% No mark wll be deducted for ncorrect answers (5) The SMJ edtoral offce wll submt the lst of successful canddates to the Sngapore Medcal Councl Deadlne for submsson: (February 2008 SMJ 3B CME programme): 12 noon, 25 March 2008