We describe the case of a patient implanted with a DeBakey left ventricular assist device (LVAD) as bridge to transplant who survived 7 h of ventricular fibrillation. He was successfully converted into a stable sinus rhyth

Lachat, Mario L.

Salzberg, Sacha P.

Turina, Marko I.

Zünd, Gregor

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Case reportLeft ventricular assist device (LVAD) enables survival during 7 hof sustained ventricular fibrillationSacha P. Salzberg*, Mario L. Lachat, Gregor Zu¨nd, Marko I. TurinaDepartment of Cardiovascular Surgery, University Hospital Zurich, Zurich, SwitzerlandReceived 12 March 2004; received in revised form 30 April 2004; accepted 3 May 2004; Available online 7 June 2004AbstractWe describe the case of a patient implanted with a DeBakey left ventricular assist device (LVAD) as bridge to transplant who survived 7 hof ventricular fibrillation. He was successfully converted into a stable sinus rhythm.q 2004 Elsevier B.V. All rights reserved.Keywords: LVAD; Arrhythmia; Ventricular fibrillation; Survival1. BackgroundVentricular fibrillation (VF) is a pulseless arrhythmia inwhich chaotic electrical activity causes absence of ven-tricular contraction with immediate loss of cardiac output.The subsequent hypo-perfusion creates global tissueischaemia; brain and myocardium are most susceptibleorgans and it may lead to irreparable damage and death ifnot treated immediately [1]. VF is the primary cause ofsudden cardiac death in the world. Regular cardiac activitycan be restored with mechanical resuscitation or externalDC defibrillation. The most important determinant ofsurvival in VF is rapid defibrillation [2]. American HeartAssociation Guidelines 2000 conference recommends thatearly defibrillation be available throughout all hospital andoutpatient medical facilities [3].With the rising incidence of congestive heart failure(CHF) due to the aging population, mechanical circulatorysupport pose themselves as interesting adjuvant therapeuticoption. According to the REMATCH study [4], the use ofleft ventricular assist devices (LVAD) resulted in over twicethe survival rate and an improved quality of life, incomparison to optimal medical management. Since 1988researchers from the Baylor College of Medicine (Houston,TX) with engineers from NASA have developed theDeBakey LVAD (MicroMed Inc.) [5]. This implantablecontinuous flow blood pump creates a maximal flow of.10 l/min, providing relief to the sick heart by taking overpart of the pumping action [5]. As this LVAD has beenavailable in our centre since October 1999, we haveevaluated this new device in 17 patients.We report the experience of one patient with acontinuous flow LVAD surviving sustained and documen-ted VF for nearly 7 h.2. Case reportA 61-year-old male suffering from a terminal heartfailure (NYHA class III–IV) and a left ventricular ejectionfraction of ,25% with two previous cardiac surgeries,namely mechanical aortic valve replacement in 1987 andimplantation of a biventricular pacemaker in late 2001 ispresented. For a few months cardiac function has beengetting worse, and the patient felt a significant decrease ofquality of life. As ultimate treatment this patient wasselected for heart transplantation (HTX).Based on our experience with mechanical supportsystems, and the actual trend in the treatment of chronicheart failure, an LVAD was indicated; this patient wasenrolled in our bridge to heart transplantation study andreceived an LVAD [5,6] as bridge to heart transplantation.This LVAD is a fully implantable miniaturised bloodpump used in patients suffering from terminal heart failure[7]. It creates a constant flow (may exceed 10 l/min) andprovides supportive pump action for the sick heart.European Journal of Cardio-thoracic Surgery 26 (2004) 444–446www.elsevier.com/locate/ejcts1010-7940/$ - see front matter q 2004 Elsevier B.V. All rights reserved.doi:10.1016/j.ejcts.2004.05.010* Corresponding author. Address: Department of Cardiothoracic Surgery,1190 Fifth Avenue, Box 1028, New York, NY 10029, USA. Tel.: þ1-212-659-1360; fax: þ1-212-659-6818.E-mail address: sacha.salzberg@msnyuhealth.org (S.P. Salzberg).In the course of a multicentre study, we have successfullyimplanted 17 patients. Eight have been successfully bridgedto HTX, 8 deaths occurred, 6 among 8 emergent implants and2 among 7 elective procedures. As mortality of transplan-tation candidates on waiting lists is high and with theincreased survival after HTX, LVAD are considered a safeand efficient bridging tool in the setting of terminal heartfailure [4].The patient was implanted successfully, successfullyweaned from the respirator on the second post-operative dayand transferred to the regular ward after 4 days. The rest ofhis stay in the hospital was uneventful. He was released intoa specialised cardiac rehabilitation facility after 4 weeks.Patients on LVAD support are discharged as soon aspossible into a cardiac rehabilitation centre. They come toour centre once a week for a thorough check-up by our HTXteam. In this case all visits were satisfactory. Pulmonaryvascular resistance (PVR) decreases; increased exercise andregression of plasma b-type natriuretic peptide (BNP) wereall stigmata of regressing heart failure. The patient himselfdescribed his physical state as a rebirth and was goodspirited toward his upcoming HTX. The anticoagulationregimen of all our LVAD patients consists of onlyacetylsalicylic acid 100 mg/day and warfarin with an aimINR of 1.5–2.5.Eighteen days after discharge (73 days of LVADsupport), we received a call from the rehabilitation centre,informing us that the patient was taken ill while on a longwalk during a hot summer day in the mountains. He hadsuffered a sudden onset of light-headedness, nausea and coldsweats, no collapse or loss of consciousness was noted.After a short rest on a bench and a cold beverage, thesymptoms improved and he was bought back to the centre.An ECG was immediately done showing what initially wasinterpreted as atrial flutter activity with irregular pacemakeractivity. Immediate treatment was initiated (intravenoussaline and bolus of 300 mg Amiodarone) while the transferto our centre was organised.On arrival at our hospital this oligosymptomatic patientwas walking about the hospital ward as if nothing happened.Physical examination showed turgescent jugular veins andabsence of heart sounds, the pump making its normalturbine like noise. Precordial ECG, however, showed VFwith irregular pacemaker activity. The patient was rapidlytransferred to the ICU. Pacemaker memory function(MedTronic InSync III, with automatic diagnosis system)yielded very surprising information, the onset of VFhappened 6 h prior the onset of symptoms. Pressure curvesdisplayed on the clinical data acquiring system (CDAS) ofthe LVAD and on the ICU monitoring screens werecompletely flat, attesting to the absence of left ventricularejection (Fig. 1). Absence of flow through the aortic valveand impactment of the right ventricle on the left weredocumented by echography (Fig. 2). The INR was 2.7 andpotassium was found at 4 mmol/l. Heart enzymes had risensignificantly (Troponin T 5.88 mg/l, CK tot. 712 U/l,CK-Mb act. 71 U/l, Myoglobin 278 mg/l). After intravenoussedation (propofol and fentanyl) and bolus of 5000 IE heparinwe proceeded to electroconvert the patient. Three attemptswith A/P external defibrillation (360 J) and intravenouslidocaine were necessary to restore regular sequential pacedheart rhythm. Restored left ventricular ejection and flowthrough the aortic valve were observed on echocardiography,cardiovascular monitoring and on the display of the CDAS.The patient regained consciousness a few minutes later with astable cardiac rhythm requiring no pharmacological support.Laboratory values showed a normalisation ofcardiac enzymes after 5 days (Troponin T 1.61 mg/l, CKtot. 73 U/l, CK-Mb act. 11 U/l, Myoglobin 88 mg/l).Twelve hours after defibrillation the patient developedsevere neurological symptoms. A cerebral CT-scan showeda massive frontal intra-cerebral haemorrhage. Upon this allanticoagulation was stopped. The patient never recuperatedfrom this neurological event and the LVAD was turned of14 of ICU treatment.3. CommentVery few reports describing survival after sustained VFexist in the literature, VF being lethal if not treatedimmediately [8,9].Fig. 1. ICU monitoring before electro conversion.Fig. 2. Trans thoracic echocardiography (during VF) shows acceleratedflow through compressed left ventricle with dilated right ventricle.S.P. Salzberg et al. / European Journal of Cardio-thoracic Surgery 26 (2004) 444–446 445This LVAD provides assistance for the failing heart. Inthis report we illustrate the role of this small device creatingsufficient blood flow to allow viable end-organ functioneven with absence of left ventricular ejection.The mechanisms causing VF are well known. Generallythe aetiology is cardiac (dilatative or ischaemic cardiomyo-pathy) or metabolic. We believe that hypo-kaliemia inducedthrough the diuretic action of furosemide combined with anexcess of physical exercise under extreme conditions(altitude, heat, sun) caused this arrhythmia. The patienthaving an underlying cardiomyophathy known to causearrhythmia, this VF was probably precipitated by thehypokaliemia.By survival and recuperation of efficient cardiac activityafter such a long period of VF, the normalisation of cardiacenzymes (CK, Myoglobin, Troponin T) provide insightinto the physiological consequences of VF. The flow(2.5–3.4 l/min) provided by the LVAD, was sufficient toavoid irreversible ischaemic cardiac damage. In contrast tothe maximum flow capacity of this device (.10 l/min) theturbine was functioning in a low speed mode (only8500 rpm—maximum 15,000 rpm). This shows the inten-sity of necessary flow to effectively replace cardiac output.The physiological mechanism allowing a sustainedeffective pulmonary circulation in the absence of leftventricular ejection is due to two factors: the increase incentral venous pressure and the negative pressure at theinflow-tract generated by the turbine in this micro-axialpump. The blood is passively moved through the lungs,suctioned by the turbine and propelled into the aorta. In thiscase this was enough to allow sufficient oxygenation andend organ perfusion for survival.This report demonstrates the efficacy of the LVAD notonly as circulatory support but also as effective substitute inabsence of any cardiac activity.Bleeding is the most frequent complication of mechan-ical support systems (MCS). But the medical managementof terminal heart failure very often includes oral antic-oagulation and platelet inhibition of any kind. In this case,retrospectively one could consider that the IV bolus ofheparin (standard protocol for electro conversion) may havelead to the neurological outcome. We also believe that it isfurther necessary to study the precise effects of heparin,continuous flow and the brain blood barrier, all this inthe setting of long-term support periods which destinationtherapy patients will undergo.Furthermore the question now may arise as to theartificial heart. If left ventricular assistance is sufficient forlife support, additional fully implantable devices replacingthe heart will not be necessary, adding implantableautomatic defibrillators would be enough for long-termassistance. Further studies are being conducted in this field,and we hope that our experience will be a valuable brick inthe fight against heart failure.References[1] Al-Khatib SM, Granger CB, Huang Y, Lee KL, Califf RM, SimoonsML, Armstrong PW, Van de Werf F, White HD, Simes RJ, MoliternoDJ, Topol EJ, Harrington RA. Sustained ventricular arrhythmias amongpatients with acute coronary syndromes with no ST-segment elevation:incidence, predictors, and outcomes. Circulation 2002;106:309–12.[2] Angelos MG, Menegazzi JJ, Callaway CW. Bench to bedside:resuscitation from prolonged ventricular fibrillation. Acad EmergMed 2001;8:909–24.[3] Shuster M, Tang A. Advanced cardiovascular life support Guidelines2000: pharmacological changes to the treatment of ventricularfibrillation/pulseless ventricular tachycardia. Can J Cardiol 2001;17:1022–5.[4] Rose EA, Gelijns AC, Moskowitz AJ, Heitjan DF, Stevenson LW,Dembitsky W, Long JW, Ascheim DD, Tierney AR, Levitan RG,Watson JT, Meier P, Ronan NS, Shapiro PA, Lazar RM, Miller LW,Gupta L, Frazier OH, Desvigne-Nickens P, Oz MC, Poirier VL. Long-term mechanical left ventricular assistance for end-stage heart failure.N Engl J Med 2001;345:1435–43.[5] Noon GP, Morley DL, Irwin S, Abdelsayed SV, Benkowski RJ, LynchBE. Clinical experience with the MicroMed DeBakey ventricular assistdevice. Ann Thorac Surg 2001;71:S133–8. Discussion S144–6.[6] Frazier OH. The development of an implantable, portable, electricallypowered left ventricular assist device. Semin Thorac Cardiovasc Surg1994;6:181–7.[7] Cohn JN. Mortality as an endpoint for cardiac failure therapy. J CardFail 1995;1:191–4.[8] Lewis CT, Graham TR, Marrinan MT, Chalmers JA, Colvin MP,Withington PS, Coumbe A. The use of an implantable left ventricularassist device following irreversible ventricular fibrillation secondary tomassive myocardial infarction. Eur J Cardiothorac Surg 1990;4:54–6.[9] McGinley AM, Matthews AS, Graham TR. Use of an implantable leftventricular assist device for irreversible ventricular fibrillationsecondary to massive myocardial infarction—a case study. IntensiveCare Nurs 1990;6:138–49.S.P. Salzberg et al. / European Journal of Cardio-thoracic Surgery 26 (2004) 444–446446

Left ventricular assist device (LVAD) enables survival during 7 h of sustained ventricular fibrillation

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