Www.asecho.org



#ASECaseCompetition “I may have tugged a little too hard”: A Case of Traumatic Tricuspid Valve Injury following Pacemaker Lead ExtractionAuthorsBonita A. Anderson ACS, DMU(Cardiac), MApplSc, Natalie F. Edwards ACS, MCardiacUltrasound, Darryl J. Burstow MBBS, FRACP, Gregory M. Scalia MBBS, FRACP.From The Prince Charles Hospital, Echocardiography Laboratory, Cardiac Sciences Unit, Brisbane, Australia.KeywordsTraumatic tricuspid rupture, Severe tricuspid regurgitation, Hepatic venous systolic flow reversalHighlights 3-5 bullet points, max 128 characters (1 tweet)TTE has an important role in identifying potential causes of heart failure symptoms and in the detection of complications post interventional procedures.Traumatic TV rupture is an uncommon but recognized complication post PPM lead extraction.Doppler profiles of the TR jet and hepatic venous signals assist in determining the hemodynamic severity of TR.Tweet: Don’t tug too hard or you may get more than your bargained for! An echocardiographic case of traumatic tricuspid valve injury following pacemaker lead extraction. #ASECaseCompetition #ASE2019 @ASE360 @JournalASEcho #CASECVI #echofirstIntroduction (200 words or less)Tricuspid regurgitation (TR) is commonly seen in patients with pacemaker leads inserted into the right ventricle (RV). In these cases, pacemaker-induced TR may occur due to pacing lead impingement which prevents complete coaptation of the tricuspid valve (TV) leaflets during systole, lead entanglement within the supporting apparatus, lead adherence to the TV, or perforation of a TV leaflet [1,2]. TR following pacemaker lead extraction is less frequently encountered and may occur when there are fibrotic attachments between the tricuspid leaflet tissue and the ventricular pacing leads [3-5]. However, severe TR requiring surgery is not common [6]. We report on a case of traumatic TV injury following permanent pacemaker (PPM) lead extraction which resulted in severe TR necessitating TV replacement.Case presentation A 70-year-old male was referred to our institution for a PPM extraction due to infection. Two decades ago, the patient had a dual chamber PPM implanted for chronic, slow atrial fibrillation (AF). He had a recent generator change due to increased lead impedance. The patient noticed a small blister over the PPM site a few days after this procedure. The site was swollen and tender. The patient had a good appetite and felt generally well. He had no sweats and no fever. Prior to the generator change, the patient was very active walking 3-4 kilometers per day. There was also a history of ischemic heart disease requiring a prior percutaneous coronary intervention (2010) and subsequent coronary artery bypass grafts (2015). Other relevant history included type II diabetes mellitus, gastro-esophageal reflux disease, and hyperlipidemia.The PPM was extracted and replaced with a Medtronic MicraTM MC1VR01 Leadless device into the right ventricular outflow tract (Figure 1). Following the procedure, the patient’s hemoglobin dropped from 144 g/L to 99 g/L and he developed orthostatic hypotension (114/60 mm Hg while lying to 94/54 mm Hg when sitting). The patient felt weak and dizzy and was New York Heart Association (NYHA) class III. On examination, he was afebrile, oxygen saturations were at 98%, pulse rate was 60 beats/minute, heart sounds were dual with a systolic murmur, the chest was clear, the liver was pulsatile, and examination of the jugular venous pulse revealed giant V waves. A transthoracic echocardiogram (TTE) was requested to exclude a pericardial effusion and to exclude significant TR post PPM lead extraction.The TTE showed a normal left ventricular size with mildly impaired systolic function (ejection fraction of 42%). Dyssynchronous interventricular septal motion was present consistent with paced rhythm. RV size was markedly increased (6.5 cm at the base and 4.8 cm at mid cavity) with mildly impaired systolic function and preserved annular motion. Artifacts arising from the leadless pacing device were noted within the RV cavity. Both the left and right atria were marked dilated (48 mL/m2 and 62 mL/m2, respectively). The anterior tricuspid valve leaflet (atvl) and associated subvalvular apparatus appeared flail, prolapsing into the right atrium (RA) during systole (Figure 2 and Video 1). On color Doppler imaging (CDI), the TR jet was visually unimpressive due to the ‘wide-open’ nature of the severe TR jet (Video 2). The continuous-wave Doppler (CWD) profile of the TR jet showed features consistent with severe TR (Figure 3). This included (1) a strong CWD TR signal, (2) a low TR velocity, and a V cut-off sign [7,8]. Hepatic venous examination showed marked systolic flow reversal on CDI, color M-mode (CMM) and pulsed-wave Doppler (PWD) which is also consistent with severe TR (Video 3 and Figure 4). The patient was referred for cardiothoracic surgery for a tricuspid valve repair or replacement. The pre-operative two-dimensional (2D) and three-dimensional (3D) transesophageal echocardiography confirmed the TTE findings of a flail atvl involving the subvalvular apparatus (Videos 4 and 5). The surgical findings included avulsion of the anterior papillary muscle off the RV wall with a large flail segment involving almost the whole atvl with multiple leaflet perforations as well as multiple ruptured chordae on the atvl. The TV was considered unrepairable; hence, the anterior leaflet was excised along with the papillary muscle attached to it (Figure 5) and the posterior and septal leaflets were left alone. A 31 mm Mosaic tissue prosthetic was then sutured in place. The patient had an unremarkable post-operative course and was discharged two weeks following surgery. DiscussionThe incidence of traumatic TV injury complicating extraction of RV pacemaker leads is reported as 3.5% to 12% [5]. In many reported cases, injury is usually identified immediately after lead extraction with partial avulsion of TV tissue being visible on the tip of the extracted lead [9]. However, TV injury may also be suspected when patients presents with heart failure symptoms. TTE is extremely valuable in determining the cause of heart failure as well as in the detection of new TV damage. In this case, traumatic TV injury was evident on the 2D examination by the appearance of a flail atvl along with supporting apparatus. Thus, based on the 2D appearance of the TV severe TR is expected. However, in this case with no pulmonary hypertension and a large TR orifice, the pressure differential between the RA and RV is small resulting in little or no aliasing of the TR jet. As a result, this low turbulence, low velocity jet may be visually unimpressive on CDI. For this reason, a lower Nyquist may need to be used to enhance the detection of the TR jet. On the CWD trace of the TR jet, the intensity, velocity and contour of the TR jet are consistent with severe TR. The intensity or density of the CWD signal is proportional to the number of red blood cells travelling within the regurgitant jet; therefore, the greater the regurgitation, the denser the regurgitant CWD signal. The TR jet also reflects the pressure difference between the RV and the RA during systole. With very severe TR, the peak TR velocity is often low (2 m/sec) reflecting the near equalization between the RV and RA systolic pressures [7]. Furthermore, the contour of the TR signal may become triangular when there is severe TR and an associated marked elevation in the RA v-wave pressure; this results in a decline in the pressure difference between the RV and RA in mid-to-late systole. This ‘triangular’ appearance of the TR signal is also referred to as the ‘V cut-off’ sign. Evaluation of hepatic venous flow is helpful in verifying severe TR. Normally, there is systolic forward flow into the hepatic veins. With severe TR, systolic flow reversal (SFR) occurs. Recognition of SFR is most commonly identified on the PWD trace. SFR can also be appreciated on CDI and on color M-mode. While SFR is a very specific sign of severe TR, other conditions may result in SFR especially when there is atrial contraction against a closed TV as in the case of paced rhythms, atrioventricular dissociation and atrial arrythmias [10,11]. In this patient, the rhythm was paced and there was underlying AF. Despite this, the consistent appearance of SFR over respiration is most consistent with severe TR rather than paced rhythm or AF.ConclusionThis case demonstrates an uncommon complication of PPM lead extraction resulting in traumatic TV injury and acute severe TR. The severity of TR on CDI was underwhelming despite the clear 2D indication that severe TR must be present. Supportive findings of severe TR were evidenced by the strong intensity of the TR jet and the presence of the V cut-off sign on the CWD signal as well as hepatic venous systolic flow reversal exhibited on color Doppler imaging, color M-mode and pulsed-wave Doppler traces.References[1] Lin G, Nishimura RA, Connolly HM, Dearani JA, Sundt TM 3rd, Hayes DL. Severe symptomatic tricuspid valve regurgitation due to permanent pacemaker or implantable cardioverter-defibrillator leads. J Am Coll Cardiol. 2005 May 17;45(10):1672-5.[2] Al-Mohaissen MA, Chan KL. Prevalence and mechanism of tricuspid regurgitation following implantation of endocardial leads for pacemaker or cardioverter-defibrillator. J Am Soc Echocardiogr. 2012 Mar;25(3):245-52. [3] Park SJ, Gentry JL 3rd, Varma N, Wazni O, Tarakji KG, Mehta A, Mick S, Grimm R, Wilkoff BL. Transvenous Extraction of Pacemaker and Defibrillator Leads and the Risk?of?Tricuspid Valve Regurgitation. JACC Clin Electrophysiol. 2018 Nov;4(11):1421-1428. [4] Coffey JO, Sager SJ, Gangireddy S, Levine A, Viles-Gonzalez JF, Fischer A. The impact of transvenous lead extraction on tricuspid valve function. Pacing Clin Electrophysiol. 2014 Jan;37(1):19-24. [5] Birgersdotter-Green U, Dawood FZ. Transvenous Extraction of Pacemaker and Defibrillator Leads and the Risk?of?Tricuspid Valve Regurgitation. JACC Clin Electrophysiol. 2018 Nov;4(11):1429-1430. [6] Franceschi F, Thuny F, Giorgi R, Sanaa I, Peyrouse E, Assouan X, Prév?t S, Bastard E, Habib G, Deharo JC. Incidence, risk factors, and outcome of traumatic tricuspid regurgitation after percutaneous ventricular lead removal. J Am Coll Cardiol. 2009 Jun 9;53(23):2168-74. [7] Zoghbi WA, Adams D, Bonow RO, Enriquez-Sarano M, Foster E, Grayburn PA, Hahn RT, Han Y, Hung J, Lang RM, Little SH, Shah DJ, Shernan S, Thavendiranathan P, Thomas JD, Weissman NJ. Recommendations for Noninvasive Evaluation of Native Valvular Regurgitation: A Report from the American Society of Echocardiography Developed in Collaboration with the Society for Cardiovascular Magnetic Resonance. J Am Soc Echocardiogr. 2017 Apr;30(4):303-371. [8] Hahn RT, Thomas JD, Khalique OK, Cavalcante JL, Praz F, Zoghbi WA. Imaging Assessment of Tricuspid?Regurgitation?Severity. JACC: Cardiovascular Imaging Mar 2019, 12 (3) 469-490[9] Assayag P, Thuaire C, Benamer H, Sebbah J, Leport C, Brochet E. Partial rupture of the tricuspid valve after extraction of permanent pacemaker leads: detection by transesophageal echocardiography. Pacing Clin Electrophysiol. 1999 Jun;22(6 Pt 1):971-4.[10] Shaikh AY, Meyer TE, Robotis DA, Aurigemma GP, Tighe DA. Systolic pulmonary and hepatic vein flow reversal due to pacemaker-induced retrograde ventriculoatrial conduction. Echocardiography. 2013 Mar;30(3):E61-3. [11] Fadel BM, Mohty D, Husain A, Alassas K, Echahidi N, Dahdouh Z, Di Salvo G. Spectral Doppler of the Hepatic Veins in Rate, Rhythm, and Conduction Disorders. Echocardiography. 2016 Jan;33(1):136-40.Figure/Video legendsFigure 1 (A) Chest X-ray prior to extraction showing the pacemaker and pacing leads within the right heart chambers. (B) Fluoroscopy image showing the Medtronic MicraTM Leadless pacemaker device immediately following implantation. (C) The chest X-ray post PPM replacement showing the position of the leadless device within the right ventricular outflow tract.Figure 2 (A) Parasternal long axis view of right ventricular inflow and (B) apical 4-chamber view show a whip-like mobility of the flail anterior tricuspid valve leaflet and subvalvular apparatus (arrows). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. Figure 3 Continuous-wave Doppler of the tricuspid regurgitant (TR) jet demonstrates a peak TR velocity of 1.2 m/sec and a V cut-off sign (arrows) which is consistent with a marked increase in the right atrial V-wave pressure with ventricular systole. Figure 4 (A) Hepatic venous color M-mode trace and (B) hepatic venous pulsed-wave Doppler trace show marked systolic (S) flow reversal into the hepatic vein which is consistent with severe tricuspid regurgitation (TR). Figure 5 Surgical specimen of the damaged anterior tricuspid valve leaflet and the associated avulsed papillary muscle.Video 1 (A) Parasternal long axis view of right ventricular inflow and (B) apical 4-chamber view show a flail anterior tricuspid valve leaflet and subvalvular apparatus. Video 2 (A) Color Doppler parasternal long axis view of right ventricular inflow and (B) color Doppler apical 4-chamber view show severe tricuspid regurgitation. Video 3 Hepatic venous color Doppler imaging shows marked systolic flow reversal (red color) into the hepatic vein, consistent with severe tricuspid regurgitation (TR).Video 4 (A) Two-dimensional transesophageal echocardiographic images confirm the presence of a flail anterior tricuspid valve leaflet and the ‘torn off’ anterior papillary muscle. (B) Color Doppler imaging confirms the presence of severe, ‘wide-open’ tricuspid regurgitation.Video 5 Three-dimensional transesophageal echocardiographic images from an en-face right atrial perspective (left) and from the right ventricular (right) perspective showing the flail anterior tricuspid valve leaflet (atvl) and the ‘torn off’ anterior papillary muscle prolapsing into the right atrium. ptvl, posterior tricuspid valve leaflet; stvl, septal tricuspid valve leaflet. ................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download