Dual Percutaneous Mechanical Circulatory Support as a Bridge to Recovery in Fulminant Myocarditis

To the Editor: Fulminant myocarditis is a rare clinical manifestation of cardiac inflammation characterized by its distinct, rapid onset, and severe hemodynamic compromise. With appropriate management, often including mechanical support, the majority of patients will experience full recovery. To maintain adequate cardiac output in the acute setting, intraaortic balloon pump (IABP) is often insufficient, and additional support may be needed. We herein describe an alternative method using a combination of percutaneous mechanical circulatory support with both IABP and Impella 2.5 in a 21-year-old patient with fulminant myocarditis as a bridge to recovery. The Impella 2.5 is a catheter-mounted left ventricular assist device (LVAD), which is percutaneously inserted through the femoral artery. It provides mechanical hemodynamic support in patients with severe left ventricular dysfunction by aspirating blood from left ventricle through an inlet area near the tip in left ventricle and propelling it forward across the aortic valve into the systemic vasculature. Impella has been used in various clinical settings, including hemodynamic support during high-risk percutaneous coronary interventions, cardiogenic shock, etc.; however, the combined use of Impella and IABP is rare; only a few cases have been reported.1–3 We report a successful bridge to recovery of a patient with fulminant lymphocytic myocarditis using dual mechanical support with an Impella 2.5 percutaneous VAD in conjunction with an IABP. In a recent case, a 21-year-old previously healthy woman presented with a 3-day history of gastrointestinal symptoms and chest pain (informed consent was obtained from the patients.). Her initial assessment revealed hypotension (systolic blood pressure of 50 mm Hg), complete heart block with diffuse ST elevation on electrocardiogram, and nondilated left ventricle with severe biventricular dysfunction (left ventricular ejection fraction [LVEF] of 10%) on echocardiogram. Laboratory studies disclosed elevated troponin levels (12.79 ng/ml, normal <0.03 ng/ml) and evidence of multiorgan failure (Table 1). Coronary angiography demonstrated no coronary artery disease. An IABP, a right-heart catheter, and a transvenous pacemaker were placed. Milrinone was initiated at an infusion rate of 0.375 μg/kg/min, and the patient was transferred to a tertiary care center with a presumptive diagnosis of fulminant myocarditis.Table 1: Hemodynamic Measures, Laboratory, and Infusion Rate of Inotropes During Mechanical Circulatory SupportOn hospital arrival, the patient was alert and oriented. Her blood pressure was 72/56 (61) mm Hg, and she remained in complete heart block with an accelerated junctional rhythm at a rate of 90 bpm. Hemodynamic measures demonstrated elevated right and left heart pressures with low cardiac output (Table 1). Repeat echocardiography demonstrated severe biventricular systolic dysfunction with an LVEF of 30% and severe global hypokinesis but with a left ventricular internal dimension diastole of 3.3 cm. Dobutamine infusion of 3 μg/kg/min was added to her treatment. A right ventricular septal biopsy was performed, revealing a severe lymphocytic myocarditis with a predominant T-cell infiltration and absence of giant cells, granuloma, or eosinophils (Figure 1). Despite IABP and inotropic support, the patient's cardiac index and mixed venous saturation continued to deteriorate, and she suffered multiple episodes of nonsustained ventricular tachycardia, dyspnea, desaturation, and oliguria. The patient was brought to the cardiac catheterization laboratory where an Impella 2.5 was percutaneously placed by the left femoral artery (Figure 2). It was considered providing adequate support for her body surface area of 1.76 m2, and the flow was titrated up to a maximal support of 2.5 L/min. The IABP was left in place as a synergistic and backup support.Figure 1.: Endomyocardial biopsy demonstrating (A) (×4) severe diffusely inflammatory cell infiltrating the myocardium with multifocal moderate necrosis of myocardial fibers and (B) (×40) lymphocyte infiltration. C: Immunohistochemical staining demonstrating predominance of T-cell lymphocytes (CD 3).Figure 2.: Chest radiograph demonstrating Impella 2.5 (black arrow) and intraaortic balloon pump (white arrow) in position. Pulmonary edema is also noted.With both devices functioning, the patient's cardiac index rose from 1.5 to 2.0 L/min/m2 (Table 1). Over the next 48 hours, the patient developed hemolysis (LDH 6,779 unit/L, haptoglobin <10 mg/dL, and indirect bilirubin 2.2 mg/dL), thrombocytopenia, and mild hemorrhage from her nose and femoral sheath insertion sites, requiring blood transfusion (Table 1). Because of hemolysis and her improved hemodynamic status from myocardial recovery, the IABP was removed. Heparin dosing was titrated down to maintain the minimal anticoagulation necessary to support Impella 2.5 use. On day 4, she regained normal sinus rhythm with a rate of 70–80 bpm, and the transvenous pacemaker was removed. Because of significant clinical and hemodynamic improvement, the performance level of Impella was gradually lowered on day 4 of support, and the device was removed on day 7. Milrinone and dobutamine were successfully weaned off 3 and 10 days after device removal, respectively. The patient was discharged after 23 days of hospitalization with New York Heart Association (NYHA) class II symptoms. Her discharge medication included carvediol 6.25 mg oral twice a day and candesartan 8 mg oral daily. Six weeks after discharge, her symptoms had improved to NYHA class I, and repeat echocardiography revealed a LVEF of 45–50% with a mildly enlarged right ventricle and moderately impaired right ventricular systolic function. This case illustrates the opportunities and challenges of using percutaneous support devices in patients with fulminant myocarditis. Fulminant myocarditis is usually associated with favorable long-term outcomes with conventional therapies despite severe ventricular dysfunction and the frequent need for aggressive hemodynamic support in the acute phase; in fact, the survival rate has been reported to be 93% at 1 year with sustained recovery lasting over a decade. Therefore, the definitive diagnosis, by using all clinical, echocardiographic and histology finding, is crucial to determine the need and type of mechanical circulatory support. In our patient, her rapid hemodynamic instability, typical echocardiographic finding including nondilated left ventricle with high normal septal thickness, and diffuse lymphocytic infiltration with significant myocardial necrosis on histology finding are consistent with fulminant myocarditis. In patients refractory to medical treatment, mechanical circulatory support devices such as IABP and VADs are the treatment of choice to maintain end-organ perfusion and unload the ventricle during the acute phase. Traditionally, surgical LVAD is a mainstay mechanical circulatory support in the patients with fulminant myocarditis in whom IABP fails to provide adequate support. Impella 2.5 was developed out of a need for a less invasive approach compared with surgically implanted LVADs and higher support, up to 2.5 L/min estimated forward flow at its maximum rotation of 51,000 rpm,4 higher when compared with 20% increase in cardiac output from IABP,5 and possibly leads to greater left ventricular systolic function recovery in patients with cardiogenic shock.6 Previous publications reported seven cases using Impella (two cases using Impella 2.5 and five cases with the Impella 5.0) in fulminant myocarditis. Although Impella 5.0 requires the surgical cut down for insertion, Impella 2.5 can be inserted with 13-Fr femoral sheath. Impella was used as a bridge to recovery in three patients and a bridge to a surgical LVAD in one patient; in the other three cases, the patients did not survive. Of these seven cases, three patients had IABP before switching to Impella, and none of them had dual mechanical circulatory supports.7–11 The combined use of Impella and IABP was studied in a sheep model of acute myocardial infarction, showing a benefit of ventricular unloading from Impella and higher end-organ perfusion when use in conjunction with IABP.12 Therefore, the combined use of Impella and IABP offers maximum circulatory support compared with either the stand-alone support,12 thereby allowing myocardial recovery in acute fulminant myocarditis without the need for a surgically implanted LVAD. Additionally, if one device becomes dysfunctional, then the other device can provide at least some mechanical support. The combined use of IABP and Impella 2.5 is rare. There are three case reports of their combined use in the literature. There are two reported cases that involved patients with cardiogenic shock secondary to myocardial infarction, one with a favorable outcome and the other with a fatal outcome.1,2 In the third case, the outcome was favorable in a patient with profound nonischemic cardiogenic shock after cardiac arrest.3 To our knowledge, our patient is the first reported case using both IABP and Impella simultaneously for support in a patient with fulminant myocarditis. The correct positioning and functioning of Impella 2.5 is guided by a portable mobile console, connected to distal end of catheter, displaying invasive pressure with the actual revolution per minute of the pump. Despite the correct position and appropriate functioning of confirmed by echocardiogram and invasive pressure monitoring, the possible complications such as aortic insufficiency, valvular obstruction, endocardial suction, bleeding, and peripheral thrombosis should be closely monitored. Thrombocytopenia and hemolysis were observed in our case and believed to be secondary to high shear stress of the axial pump, especially when the device was used along with IABP. Therefore, hemolysis monitoring should be periodically performed in the patients who require high and prolonged support. Additionally, the Impella 2.5 is designed for left ventricular support and, similar to traditional VADs, should be used cautiously in patients with severe right ventricular failure. With the aid of invasive hemodynamic monitoring and optimization of the patient's volume status, we were able to manage our patient without the need for biventricular mechanical support. Our case illustrates that in current practice, patients with profound cardiogenic shock despite IABP support may have alternatives to surgical VAD placement. The combined use of IABP and Impella 2.5 support in our patient with fulminant lymphocytic myocarditis allowed a bridge to significant myocardial recovery and increased perfusion to the vital organs. As device-related complications may occur, careful monitoring and decisions regarding length of support are crucial. Tanyanan Tanawuttiwat Barry H. Trachtenberg Ray E. Hershberger Joshua M. Hare Mauricio G. Cohen Cardiovascular division, Department of Medicine University of Miami Miller School of Medicine Miami, Florida Ray E. Hershberger Joshua M.