Ann Thorac Surg 2010;89:614-616. doi:10.1016/j.athoracsur.2009.07.047
© 2010 The Society of Thoracic Surgeons
Case Reports
Percutaneous Extracorporeal Membrane Oxygenation for Cardiogenic Shock Due to Acute Fulminant Myocarditis
Abdallah Fayssoil, MDa,*,
Olivier Nardi, MDa,
David Orlikowski, MDa,
Alain Combes, MDb,
Jean Chastre, MDb,
Djillali Annane, MD, PhDa
a Critical Care Medicine, Raymond Poincaré Hospital, Garches, France
b Critical Care Medicine, Pitié Salpêtrière Hospital, Paris, France
Accepted for publication July 10, 2009.
* Address correspondence to Dr Fayssoil, Critical Care Medicine, Raymond Poincaré Hospital, AP-HP, 104 Blvd Raymond Poincaré, 92380, Garches, France (Email: fayssoil2000{at}yahoo.fr).
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Abstract
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Percutaneous extracorporeal membrane oxygenation is an invasive technique that provides emergent circulatory support for patients with cardiogenic shock. We report a favorable outcome of an acute fulminant myocarditis in a 25-year-old myasthenia patient with cardiogenic shock supported by percutaneous extracorporeal membrane oxygenation.
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Introduction
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Clinical manifestations of myocarditis range from an asymptomatic state to a fulminant state characterized by cardiogenic shock, arrhythmias, and death. With aggressive management, including mechanical circulatory support, patients with cardiogenic shock secondary to acute fulminant myocarditis can recover [1]. We report a favorable outcome of an acute fulminant myocarditis in a 25-year-old myasthenia patient with cardiogenic shock supported by percutaneous extracorporeal membrane oxygenation (ECMO).
A 25-year-old man was referred to our unit for fever and erythematic skin. His past medical history was pertinent for myasthenia. He took daily pyridostigmine, azathioprine, and prednisone. On admission, the patient had a body temperature of 38.4°C, blood pressure of 115/48 mm Hg, heart rate of 112 beats per minute, and oxygen saturation of 99%. He complained of a cough and asthenia. Clinical examination disclosed normal pulmonary auscultation and normal cardiac auscultation. Laboratory results were as follows: white blood cells count (5,020 /mm3), hemoglobin (13g/dL), platelets (150,000/mm3), protein C reactive (218 mg/L), and creatinine (103 µmol/L). His chest roentgenogram was normal. The electrocardiography showed a sinus rhythm with ST normal repolarization. Two days after admission, his clinical situation became worse with both respiratory and hemodynamic failures. Echocardiography disclosed severe left ventricular dysfunction with left ventricular ejection fraction of 18%, a low cardiac output (cardiac output index, 1 L/min/m2), and elevated left ventricular filling pressure (flow velocity propagation, 26 cm/s). The indexed left ventricular end-diastolic diameter was 30 mm/m2; the systolic pulmonary artery pressure was 40 mm Hg; the maximal and minimal vena caval diameters were 24 mm and 20 mm, respectively. Immediately, the patient was intubated and vasopressor support (epinephrine) was instituted. Because of persistent hemodynamic failure, the patient was rapidly applied for percutaneous ECMO using right femoro-femoral cannulation. A cutaneous biopsy was performed and a nonspecific lymphocytic infiltrate was found. A myocardial biopsy was also performed and disclosed an inflammatory infiltrate. Immunologic and virologic studies were negative for antibodies to neutrophil cytoplasmic antigens, nuclear anti factor, hepatitis B virus, hepatitis C virus, herpes simplex virus 1 and 2, treponema pallidum hemagglutination assay, venereal disease research laboratory, cytomegalovirus, varicella-zoster virus, adenovirus, and human immunodeficiency virus. The evolution was favorable leading to the ablation of the extracorporeal membrane oxygenation on day 7. No immunosuppressive treatment was administrated. On day 7, a control echocardiography revealed a notable amelioration of the left ventricular systolic function (ie, 50%). The patient remained in excellent condition during follow-up, with complete cardiac recovery. The echocardiography after 1 year revealed normal left ventricular function (left ventricular systolic function, 56%), with normal kinetic motion and an indexed left ventricular end-diastolic diameter of 27 mm/m2.
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Comment
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We report a case of an acute fulminant myocarditis (AFM) in a 25-year-old patient with myasthenia. Acute myocarditis is defined as inflammation of the myocardium. An AFM is characterized by a brutal and distinct onset of severe congestive heart failure or cardiogenic shock [1, 2]. Endomyocardial biopsy (EMB) may be helpful for the diagnosis of myocarditis. The EMB has historically been the reference standard for the diagnosis of myocarditis [1]. However, because the inflammation of the myocardium may be patchy and missed, the sensitivity of EMB remains low. In this case report, the EMB disclosed an inflammatory infiltrate. Only two thirds of patients with typical clinical presentation of an AFM had positive biopsies in the study reported by Ducan and colleagues [3]. In the Myocarditis Multicentre Trial positive biopsies for myocarditis were found in only 10% of patients with suspected myocarditis [4]. Biopsy is reserved for patients with rapidly progressive cardiomyopathy refractory to conventional therapeutic management or with unexplained cardiomyopathy associated with progressive conduction system disease or for patients with life-threatening ventricular arrhythmias. The American College of Cardiology and the American Heart Association guidelines for the treatment of heart failure describe EMB as a class IIb recommendation [5]. In this case report, after considering the initial clinical presentation of viral prodrome within a few days prior to the onset of rapid hemodynamic compromise, the presence of inflammatory infiltrate in endomyocardial biopsies and the complete cardiac function recovery after aggressive treatment, AFM was diagnosed. During medical management, no immunosuppressive treatment was provided. Immunosuppression has not been shown to be effective as a routine treatment for acute myocarditis. No benefits of immunosuppressive treatment in myocarditis regarding mortality and ventricular function were found in the Myocarditis Multicentre Trial [4]. Supportive treatment is crucial in AFM and relies on positive inotropic drugs, vasopressors, and aggressive management. Indeed, despite the high risk of death during the acute phase, long-term survival of patients with AFM is excellent [1]. In a prospective study, McCarthy and colleagues [1] compared the outcomes of 15 patients with acute fulminant myocarditis and 132 patients with acute nonfulminant myocarditis. There were 93% of patients with AFM who survived 11 years after the diagnosis without the need for heart transplantation; whereas only 45% of patients with acute myocarditis were still living without heart transplantation [1]. A survival rate of 50% to 70% after implementation of mechanical support was reported by Acker [6]. These data support the need for circulatory mechanical support in AFM with cardiogenic shock. The use of ECMO is a well-established technique that provides emergent circulatory support to patients with cardiogenic shock [3]. Successful results have already been reported in the literature using percutaneous circulatory support for AFM [7]. Use of ECMO provides a bridge-to-recovery or decision regarding either heart transplantation or ventricular assist device. Moreover, in comparison with a ventricular assist device, ECMO is less costly, and a percutaneous approach is sufficient to provide circulatory support. This approach can be started within 30 minutes at the bedside. Also, a high survival rate has been reported with ECMO, compared with ventricular assist device [6]. Physiologically, ECMO reduces wall stress, decreases cytokine activation, and improves myocyte contractile function. However, the success of this procedure may be limited by complications like thromboembolic events. Furthermore, in patients with severe heart failure, the left ventricular decompression may be inadequate with ECMO because of the risk of edema and hemorrhage. Finally, ECMO treatment is limited to a period of 7 to 10 days.
In conclusion, in AFM with cardiogenic shock, ECMO remains an essential invasive rescue procedure to support patients, considering the heart can recover after the acute period.
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References
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- McCarthy 3rd RE, Boehmer JP, Hruban RH, et al. Long-term outcome of fulminant myocarditis as compared with acute (nonfulminant) myocarditis N Engl J Med 2000;342:690-695.[Medline]
- Cooper Jr LT. Myocarditis N Engl J Med 2009;360:1526-1538.[Medline]
- Duncan BW, Bohn DJ, Atz AM, French JW, Laussen PC, Wessel DL. Mechanical circulatory support for the treatment of children with acute fulminant myocarditis J Thorac Cardiovasc Surg 2001;122:440-448.[Abstract/Free Full Text]
- Mason JW, O'Connell JB, Herskowitz A, et al. A clinical trial of immunosuppressive therapy for myocarditis. The Myocarditis Treatment Trial Investigators. N Engl J Med 1995;333:269-275.[Medline]
- Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005 Guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing committee to update the 2001 guidelines for the evaluation and management of heart failure) Circulation 2005;112:e154-e235.[Free Full Text]
- Acker MA. Mechanical circulatory support for patients with acute fulminant myocarditis Ann Thorac Surg 2001;71:S73-S76.[Medline]
- Grundl PD, Miller SA, del Nido PJ, Beerman LB, Fuhrman BP. Successful treatment of acute myocarditis using extracorporeal membrane oxygenation Crit Care Med 1993;21:302-304.[Medline]
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Abstract
Introduction
