We present the case of a 55-year-old woman with giant cell myocarditis who experienced a rapid deterioration in her condition. As her heart failure progressed, she developed more ventricular ectopic beats, which culminated in a polymorphic ventricular tachycardia that did not improve despite immunosuppressive and antiarrhythmic therapy. Emergent biventricular assist device placement, however, did eliminate her arrhythmia

Raasch, Hannah

Simpson, Ross J.

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Texas Heart Institute Journal Biventricular Assist Device Terminates Polymorphic VT      719© 2012 by the Texas Heart ® Institute, HoustonBiventricular Assist Device Terminates Polymorphic Ventricular Tachycardiain Giant Cell MyocarditisWe present the case of a 55-year-old woman with giant cell myocarditis who experienced a rapid deterioration in her condition. As her heart failure progressed, she developed more ventricular ectopic beats, which culminated in a polymorphic ventricular tachycardia that did not improve despite immunosuppressive and antiarrhythmic therapy. Emergent biven-tricular assist device placement, however, did eliminate her arrhythmia. (Tex Heart Inst J 2012;39(5):719-21)G iant cell myocarditis (GCM) is a rare form of cardiomyopathy with a high mortality rate. In the largest GCM series published to date (63 patients),1 the rate of death or cardiac transplantation was 89%, with a median sur-vival of 5.5 months from the onset of symptoms to the time of death or transplan-tation. Patients with GCM manifest a diffuse, infiltrative disease process and often have conduction system abnormalities such as heart block, bundle branch block, and ventricular tachycardia (VT). We present the case of a patient, diagnosed with GCM, whose ventricular arrhythmias were refractory to medical management but resolved after mechanical circulatory support.Case ReportIn 2011, a previously healthy 55-year-old Caucasian woman came to her primary care provider with progressive shortness of breath and abdominal fullness. A chest radio-graph revealed pulmonary edema, and she was admitted to her local hospital. Her tro-ponin I level was elevated, at 3.62 µg/L. An electrocardiogram revealed sinus rhythm with an intraventricular conduction delay resembling a left bundle branch block (Fig. 1). Cardiac catheterization showed normal coronary arteries. An echocardiogram re-vealed severe left ventricular systolic dysfunction (ejection fraction, 0.25), moderate-ly decreased right ventricular function, and moderate-to-severe mitral regurgitation. She was treated with furosemide and nesiritide drips. Carvedilol and ramipril were also initiated. Her systolic blood pressure readings were between 70 and 90 mmHg, which made it difficult to accomplish diuresis and afterload reduction. She was transferred to a tertiary care facility for further management. In the subsequent days, her troponin levels remained elevated and she developed runs of asymp tomatic nonsustained VT. Her β-blocker and angiotensin-converting enzyme inhibitor were stopped due to hypotension, a Swan-Ganz catheter was placed, and milrinone and amiodarone drips were initiated. On a dosage of 0.1 µg/kg/min of mil-rinone, she had a Fick cardiac index of 1.4 L/min/m2, a pulmonary artery diastolic pressure of 30 mmHg, and a mixed venous oxygen saturation (SvO2) of 46%. Evaluation of her cardiomyopathy included thyroid function tests, serum and urine protein electrophoresis, an iron panel, and a general viral serology panel, all of which yielded results within normal limits. Her antinuclear antibody test was positive at 1:80, which prompted additional consideration of an autoimmune origin. Cardiac magnetic resonance imaging was ordered to evaluate for an infiltrative process, but she was not able to lie flat for the time required to complete the examination. The pa-tient was sent for cardiac biopsy, which subsequently provided the diagnosis of giant cell myocarditis (Fig. 2).CaseReportsHannah Raasch, MDRoss J. Simpson, Jr., MD, PhDKey words: Giant cells/pathology; heart-assist devices; myocarditis/com-plications/diagnosis/phys-iopathology; tachycardia, ventricular/etiology/physio-pathologyFrom: Division of Cardiology, University of North Caro lina at Chapel Hill, Chapel Hill, North Carolina 27599Address for reprints: Hannah Raasch, MD,  CB #7075, 6th Fl., Burnett-Womack Bldg., 99 Manning Dr., Chapel Hill, NC 27599E-mail:  hraasch@unch.unc.eduVolume 39, Number 5, 2012720      Biventricular Assist Device Terminates Polymorphic VT Immunosuppressive therapy was initiated with meth-ylprednisolone and cyclosporine. Several hours later, she experienced multiple episodes of VT, with rates ranging from 100 to 170 beats/min. An amiodarone infusion was re-initiated (after having been discontinued when her previous run of ventricular ectopic beats had sub-sided). By the next morning, the patient was in poly-morphic VT (Fig. 3), with a rate of approximately 140 beats/min. The tachycardia alternated between right and left axis and had varying forms of right bundle branch morphology. This rhythm was hemodynamical-ly tolerated: she was alert and communicating through-out the episodes, which lasted several minutes before abating and then recurring. Even though her milrinone was increased to 0.4 µg/kg/min, her SvO2 was 40%. The patient was emergently transported to the cardiac catheterization laboratory for placement of an intra- aortic balloon pump, which decreased, but did not eliminate, her ventricular ectopic arrhythmia. She was subsequent-ly sent for emergent placement of a CentriMag® Blood Pump (Thoratec Corporation; Pleasanton, Calif ) as a right and left ventricular assist device. After placement of the CentriMag, she had no further episodes of poly-morphic VT. She achieved hemodynamic stability and was placed on the cardiac transplantation list. Unfortu-nately, after 19 days of successful ventricular assist device support, she suffered a hemorrhagic stroke and care was subsequently withdrawn.DiscussionArrhythmias are common in heart failure, but VT in giant cell myocarditis is highly unusual, because it is rel-atively slow (155 beats/min on average, in a series of 5 patients) and does not necessarily result in hemodynam-ic compromise.2 Although left ventricular function is moderately to severely depressed, the left ventricle might be only mildly enlarged, which reflects the rapid course and limited time for remodeling in this aggressive dis-ease process.3 In a series of 9 patients with GCM,2 5 presented with sustained monomorphic VT and the re-maining 4 experienced monomorphic VT during their hospitalization. Our patient’s case is unusual in that she experienced polymorphic VT in addition to the monomorphic VT that is more commonly seen in GCM patients. Al-though the mechanism for polymorphic VT has not been specif ically explained, the underlying myocar-dial f ibrosis might result in multiple foci of triggered automaticity and early after-depolarization.4 In mono-morphic tachycardia, it has been suggested that the increased fibrosis and separated myocardial strands ob-served in histologic samples of inflammatory heart dis-ease might provide the substrate for the unidirectional block and reentry that sustains the arrhythmia.5 Our patient is also unusual in that her polymorphic VT was refractory to immunosuppressive and antiar-rhythmic therapy but did resolve once biventricular mechanical circulatory support was initiated. We con-sidered the addition of procainamide to the amioda-rone, but dual antiarrhythmic therapy was rejected due to our concern about worsening the conduction abnor-malities with multiple levels of blockade. Although ven-tricular assist device support often provides increased Fig. 1  The initial electrocardiogram reveals sinus rhythm, left-axis deviation, and a wide QRS that manifests an intraventricular conduction delay with the pattern of a left bundle branch block.Fig. 2  Photomicrograph at myocardial biopsy reveals multinucle-ated giant cells and myocytic necrosis consistent with giant cell myocarditis.Fig. 3  Despite immunosuppressive and antiarrhythmic therapy, this electrocardiogram shows nonsustained polymorphic ven-tricular tachycardia, with a rate of approximately 140 beats/min.Texas Heart Institute Journal Biventricular Assist Device Terminates Polymorphic VT      721hemodynamic stability, it does not routinely eliminate the occurrence of ventricular arrhythmias. In a series of 195 patients with left ventricular assist devices,6 36 had ventricular arrhythmias after implantation. In our patient, the mechanical off-loading of her right and left ventricles might have decreased wall stress, resulting in a decrease in triggered activity that originated from an underlying lymphocytic inflammatory infiltrate.References  1. Cooper LT Jr, Berry GJ, Shabetai R. Idiopathic giant-cell myocarditis--natural history and treatment. Multicenter Giant Cell Myocarditis Study Group Investigators. N Engl J Med 1997;336(26):1860-6.  2. Graner M, Lommi J, Kupari M, Raisanen-Sokolowski A, Toivonen L. Multiple forms of sustained monomorphic ven-tricular tachycardia as common presentation in giant-cell myocarditis. Heart 2007;93(1):119-21.  3. Lakdawala NK, Givertz MM. Dilated cardiomyopathy with conduction disease and arrhythmia. Circulation 2010;122(5): 527-34.  4. Antzelevitch C, Sicouri S. Clinical relevance of cardiac ar-rhythmias generated by afterdepolarizations. Role of M cells in the generation of U waves, triggered activity and torsade de pointes. J Am Coll Cardiol 1994;23(1):259-77.  5. Hsia HH, Marchlinski FE. Characterization of the electro-anatomic substrate for monomorphic ventricular tachycardia in patients with nonischemic cardiomyopathy. Pacing Clin Electrophysiol 2002;25(7):1114-27.  6. Genovese EA, Dew MA, Teuteberg JJ, Simon MA, Kay J, Siegenthaler MP, et al. Incidence and patterns of adverse event onset during the f irst 60 days after ventricular assist device implantation. Ann Thorac Surg 2009;88(4):1162-70.

Biventricular Assist Device Terminates Polymorphic Ventricular Tachycardia in Giant Cell Myocarditis

http://www.ncbi.nlm.nih.gov/pubmed/23109777

Biventricular Assist Device Terminates Polymorphic Ventricular Tachycardia in Giant Cell Myocarditis

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