Kuo-Hung LIN,' MD. Chi-Tai Ku0.l MD, andchih-ta LIN,' MD
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1 Screw-n Atral Lead n a Sck Snus Syndrome Patent wth Anomalous Inferor Vena Cava Kuo-Hung LIN,' MD. Ch-Ta Ku0.l MD, andchh-ta LIN,' MD h%t?~% Anomalous nferor vena cava wthout ntracardac anomaly s an unusual condton. Heren, we report a 48-year-old female wth left-sded nferor vena cava and azygous contnuaton, accompaned by sck snus syndrome. Ths anomaly resulted n dfculty n mplantng a tradtonal hwk-on atral lead. Atral lead dslodgment occurred repeatedly soon after mplantng the pacemaker because of an anomalou zygous ven dranng nto the superor vena cava. makng a gant connecton wth the rght atrum, thus elmnatng the space of the atral appendage for lead lodgment. Fnally. we attempted to utlze a screw-n atral lead n ths patent and she s cumtly dong well. We therefore suggest that a screw-n atral lead should be taken nto account for such patents n order to obtan a stable fxaton. (Jpn Heart J 2001: 42: ) Key words: Screw-n atral lead, Anomalous nferor vena cava. Sck snus syndrome ANOMALOUS nferor vena cava s an unusual malformaton wth a frequency of about 1.3 percent of all venous malformatons." Ths anomaly of the nferor vena cava produces no symptoms by tself. However, t s often assocated wth some ntracardac anomales and rhythm dsorders.?." Heren, we report a patent wth an anomalous nferor vena cava and sck snus syndrome. Dffcultes were encountered n mplantng a permanent pacemaker probably because of an anomalous venous return. Implantaton of an AAIR permanent pacemaker wth a tradtonal hook-on atral lead was attempted huce but faled both tmes due to lead dslodgment. The pacemaker was later successfully mplanted wth a screw-n atral lead.! = I A 48-year-old female patent was well except for a 10-year hstory of asymptomatc bradycarda. She was admtted to our hosptal for progressve dyspnea, dzzness and near syncope for one month. On admsson, her blood pres- Fmm '!he Frst Cardorrvulu Dvson. Depanmmt olmedcm, Chann Gung Unrmr)l. md Chan~ gun^ Mcrnaal Holpml-Lnkou, Tawan. AM- lor cc-spmdmer: Ch-Tr Kuo. MD. C h q Gung Memoral Holptal. IW TunpHwa N Rd.. Tape. Tawan. Rarrrd Tor plblcalon [kccrnk I R.?Om. Revd md a-td May 14.?
2 640 LIN. ETAL Ipn Heart 1 septrmbr rorl, sure was mmhg wth a regular pulse rate of 35 beatslmn. A grade 216 ejecton systolc murmur was noted at the aortc area. An electrocardogram showed marked snus bradycarda. Holter showed a long snus pause >3 seconds. Chest x-rays revealed a normal heart sze wth an azygous knob on the rght margn of the cardac slhouette. Asymptomatc snus bradycarda and snus pause wth junctonal rhythm developed durng a treadmll exercse test. The echocardogram faled to show sgnfcant abnormaltes n the cardac chambers. Durng electrophysologc study, we found the excurson of the catheter n the area of the rght atrum was restrcted. Venography showed a left-sded nferor vena cava (Fgure IA) dranng nto an engorged azygous ven n the low thorax regon and then nto the superor vena cava. Of note, the connecton between the superor vena cava and rght atrum was dlated (Fgure 1B). The rght atral pressure was wthn normal range. Snus node recovery tme obtaned from an overdrve suppresson test was prolonged to 4.38 seconds akr rapd pacng at a pacng cycle length of 450 msec. AV node functon was normal. Intally, an AAlR pacemaker wth a tradtonal sterod elutng, tned, hook-on bpolar atral endocardal lead (CapSure Z cm; Medtronc; Mnneapols, MN) was mplanted va the left subclavan approach uneventfully on June 11, 1999 (Fgure 2A). However, lead dslodgment was noted soon thereafter when the surgeon was suturng the I.-I! I. Fkvm I A: Vmaemm (polrm-vnnm vew) sharng I kn-sfded nkrsr rrru cava. B: Venspa, (afnal vew) fmm an! mlargrd ygow nn lhmng tphl -cdg am" a-ncr af Lr lnwlour vwus pslhwa). Pcaw ~ ( hc c markedly dated cmrrslan aftkaqnorvctu uva nndrghl atrum ( d n mwrl.
3 \c, A? \.I I SICK SINUS SYNDROME WITH LEFT INFERIOR VENA CAVA 64 1 wound. The atral lead was then re-mplanted the same day. The atral-pacng threshold was 0.6 V, pacng mpedance was 844 ohms. and P wave ampltude was 3.2 mv upon ntal measurement. A generator was then connected, and the ECG showed normal sngle-chamber AAlR pacng. Unfortunately, recurrent lead dslodgment was observed the next day. Snce the atral lead dslodged twce, probably because of anomalous azygous ven dranage nto the superor vena cava makng a gant connecton wth the rght atrum, we decded to use a screw-n atral lead (CapSureFx cm: Medtronc) for better fxaton on June 14, 1999 (Fgure 2B). Atral pacng threshold was 0.8 V, pacng mpedance was 412 ohms, and the P wave ampltude was 2.6 mv. Computed tomography of the chest and abdomen showed the vscera n a normal poston except for a left-sded nferor vena cava dranng nto an azygous ven n the lower thorax, then onto the superor vena cava (Fgure 3A). Although ths s usually accompaned by another malformaton, there are no abnormaltes n the shape or number of the spleen. lver, and kdneys. The patent was dscharged several days later after an ECG showng approprate sngle-chamber AAlR pacng. Durng the follow-up perod, her pacemaker functon was adequate. A recent transesophageal echogram - revealed the atral lead s sttng securely at the shallow appendage (Fgure 38). Flun 1 A: A mdlaul hd-m I d was uud nn~ally 8: An mdocrrd.l mplanted. rsmr-nn sual kd w!hen lvcr
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5 ,.I 12 YO' SICKSINUS SYNDROME WITH LEFT INFERIOR VENA CAVA 643 catheterzaton. Embryologcally. the nferor vena cava orgnates from the fuson and alteraton of components of several dfferent prmtve venous pathways. Even though there may be some varants, bascally, there are two types. those wth azygous contnuaton and those wth hem-azygous contnuaton.'" Anomalous nferor vena cava wth azygous or hem-azygous contnuaton s best nterpreted as an nterrupton or falure of the fuson of the hepatc and prerenal segments of the nferor vena cava, combned wth the persstence of ether the rght lumbar azygous ven or the left lumbar hem-azygous ven. In our case, the. patent had a persstent left nferor vena cava wth dranage to the enlarged azygous ven and then onto the rght superor vena cava. Anomalous nferor vena cava s known to frequently accompany varous rhythm dsorders. However, only a few cases have been reported."' Kakura, et a16' suggested that the pacemaker cells do not dfferentate durng the process of development and produce hypoplastc snus nodes, resultng n sck snus syndrome. Congental abnormal systemc venous return, sucb as a persstent left superor vena cava dranng nto the coronary snus, has been mplcated n the dslodgment of the pacng electrode tp and resulted n pacemaker fal~re.'.~' In our case, dslodgment of the hook-on atral lead occurred repeatedly, most lkely due to the enlarged - superor vena cava-rght - atral connecton, whch mght - allevate the space of atral appendage for lead lodgment (Fgure 1B). Leads can be stablzed n the heart that s always beatng. The stablty of leads may depend on atral volume (relatve poston between the aurcle and the superor vena cava), or shape of the atral appendage. Consequently, we had to use a screw-n atral lead to overcome the problem. In concluson, placement of a tradtonal hook-on atral lead can be problematc n such patents. Thus, for better lead fxaton, we strongly recommend usng a screw-n atral lead for sck snus syndrome patents wth anomalous nferor vena cava. Ths dsease entty should be added to the ndcaton lst of an atral actve fxaton lead when t comes to mplantng a permanent pacemaker. I. Muclhrrnr GH, J. MuddG. Anomalous nl'vmscava. Am J Csrdlal I%>% Hsmlu AR. RodngwzEomrel A. Anmalous nferor vvls cnva wth q ~ acontnuaon. r hgh (snus vcmsur)amsl repral defmnd aleratons ofrnoamal h@rn. Am J Csrdol 1968; 21: van dm Hont RL. Goraman MS. Abnarmallk of anal depolarmnaron n nwaphrapstc nlermplon of nkror \ma cava. Br Hean J : An& RC. A h P. Buke B. Anomalous nf- vma esvs wm qgovr m~nlraron (nhhcparc nurrvpm of& nfmor vms cam). Thc Journal of Pedsncr 1961: Fuktuma J, H d lrh Y. er 01. A <car e n of solated lcvad wthout nwcvd ammaln arurated wth rcksnus ryndnme. Jpn Crc J 1993: 65: 245-W.
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