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Ann Thorac Surg 1999;68:2220-2224
© 1999 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Rescue for acute myocarditis with shock by extracorporeal membrane oxygenation

Yih-Sharng Chen, MDa, Ming-Jiuh Wang, MD, PhDb, Nai-Kuan Chou, MDa, Yin-Yi Han, MDa, Ing-Sh Chiu, MD, PhDa, Fang-Yue Lin, MD, PhDa, Shu-Hsun Chu, MDa, Wen-Je Ko, MDa

a Division of Cardiovascular Surgery, Department of Surgery National Taiwan University Hospital, Taipei, Taiwan
b Department of Anesthesiology, National Taiwan University Hospital, Taipei, Taiwan

Address reprint requests to Dr Ko, Department of Surgery, National Taiwan University Hospital, 7 Chung-Shan S. Rd, Taipei 100, Taiwan


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 References
 
Background. Acute myocarditis (AM) complicated with refractory cardiogenic shock carries a very high mortality. We report our experience in treating these patients, who were rescued by extracorporeal membrane oxygenation (ECMO) and intravenous immunoglobulin.

Methods. Over a 5-year period, 5 patients with AM were rescued with ECMO in our hospital. Femoral venoarterial ECMO was performed in 4 patients, and right atrium-left atrium-aorta ECMO in the other 1 due to ventricular dysfunction. Hemofiltration was applied to 3 patients. Marked elevated creatine kinase, its MB form, and troponin T (TnT) were found before ECMO.

Results. All the patients could be weaned off the ECMO after 140.0 ± 57.7 hours of ECMO support. One patient died of multiple organ failure 10 days later after removal of ECMO, resulting in a 20% mortality. Renal function returned to normal in all survivors. The 4 survivors were discharged uneventfully in 23.3 ± 8.3 days and resumed functional class I status. The TnT level declined to the low level within 3 days (slope -4.94 ± 1.18 ng/mL/day), and might be an indicator of good recovery of myocardium.

Conclusions. ECMO can provide an effective and simple treatment for critical AM with a satisfactory result and reduce the possibility of progressive cardiomyopathy.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 References
 
Acute myocarditis (AM) is an acute nonischemic inflammatory or immunologic response of the myocardium with various unknown causes. The course of AM is very diverse, and it is sometimes difficult to make an early diagnosis and treatment. Therefore, acute cardiopulmonary collapse may develop soon after the diagnosis.

Management of acute heart failure for AM includes sodium restriction, digitalis, diuretic, vasodilator, more aggressive use of inotropics, and intraaortic balloon pumping (IABP), especially in those with profound shock. Immunosuppressive therapy [1, 2] was also tried to resolve or shorten the course and rescue the deterioration. However, it usually cannot take effect in time to reverse or prevent circulatory collapse. For some critical patients who have difficulty in maintaining the hemodynamic status, extracorporeal membrane oxygenation (ECMO) [3, 4] and mechanical ventricular assist device (VAD) [5–7] might be alternative choices available. The AM patients successfully rescued by ECMO were sporadically reported before [3, 4], but only few series had been reported [8].

We report the result of our series in treating AM with cardiogenic shock by ECMO, and demonstrate troponin T (TnT) trend as a possible indictor for predicting the recovery of the myocardium and weaning of ECMO.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 References
 
Between July 1994 and July 1998, 5 patients (2 males and 3 females) with mean age of 15.4 ± 9.3 years (range 6 to 29 years) were treated with ECMO as mechanical support for cardiogenic shock due to AM. All of them were diagnosed with AM before and received maximal medical therapy, including high-dose catecholamine, diuretic, vasodilator, and ventilator support. Severe low-output syndrome, shock, oliguria, and disturbed consciousness persisted in all despite these treatments. They were transferred to our hospital under ventilator for mechanical support (Table 1).


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  		Table 1. Patient Data and Results

 
Pre-ECMO status
All had flu-like symptoms for 3 days to 1 week before hemodynamic collapse. Over 20 µg/kg/min dopamine and dobutamine was used in all patients before ECMO rescue. Also, epinephrine was infused in 2 of them (0.2 µg/kg/min), isoprotenolol in 1 (0.15 µg/kg/min), norepinephrine in 1, and milrinone in 1 (0.5 µg/kg/min). Two patients needed a temporary pacemaker due to atrioventricular block (AVB). Ventricular tachycardia occurred in 1. IABP was used in 1 patient before ECMO. Anuria for at least 6 hours occurred in all patients under these treatments. Three of them had been receiving continuous arteriovenous or venovenous hemofiltration (CAVH or CVVH) before ECMO rescue.

ECMO management
Cannulation
All patients except 1 were cannulated via femoral vessels with a CARMEDA cannula (Medtronic Inc, Anaheim, CA). The exceptional 1 was a 6-year-old girl with body weight below 20 kg (patient 5), who was cannulated through right internal jugular vein and right common carotid artery due to the small caliber of femoral vessels.

Another 6-year-old boy (patient 3), initially supported by femoral venoarterial ECMO, was changed from femoral ECMO to right atrium-left atrium-aorta (RA-LA-Ao) ECMO due to the insufficient flow and progressive distension of the left heart. Two right-angle venous cannulas (DLP; Medtronic, Grand Rapids, MI) were placed at appendage and midportion of RA for right heart decompression, and one 20-French right-angle venous cannula at LA dome for left heart decompression. The aortic route was made of an 8-mm Vascutek (SulzerMedica, Renfrewshire, Scotland) vascular graft anastomosed to the aorta and then connected to the 24-French straight aortic cannula (Argyle, St. Louis, MO) (Fig 1). The idea of the design was derived from that of VAD. Multiple drainage cannula at the heart allowed adequate decompression of the heart, and graft anastomosed to the aorta provided a more secure and flexible way for the placement of aortic cannulas, making primary skin closure of sternotomy wounds possible.



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  		Fig 1. Design of arterial line in ECMO. A vascular graft was anastomosed to the aorta, and then connected to an arterial cannula for more flexible and secure positioning of the outlet of ECMO.

 
Circuit and priming
The ECMO circuit had heparin-bonded CARMEDA bioactive surface system (Medtronic Inc, Anaheim, CA). We did not have bridging tubes between arterial and venous lines, thus, it is unnecessary to release the clamp intermittently at the bridging tube. This made the system simpler and saved manpower. But the bridging tube was reconnected to the circuit when the ECMO weaning was attempted. There was online blood oxygen saturation monitoring (BioTrend, Medtronic Inc.) in arterial and venous lines.

ECMO was primed with normal saline and heparin 2 U/mL, and was prewarmed up to 37°C. However, the ECMO in patient 5 was primed with blood, normal saline, and heparin 2 U/mL because of her lower body weight.

Flow and anticoagulation
Heparin 100 U/kg was given to the patient immediately before cannulation, and heparin 2 U/mL was added to the priming solution. Low-dose heparin was infused to keep activated clotting time (ACT) around 160 to 180 seconds. ACT was adjusted to 220 s during the period of weaning.

The pump flow started initially at 50 to 70 cc/kg/min, and the dosages of catecholamine were gradually tapered. If the myocardium was proved to improve by echocardiography, reduction of the pump flow and increase of the catecholamine were tried.

Immunoglobulin
In this series, 2 g/kg of immunoglobulin (Gamimune N; Bayer Corp., Elkhart, IN) was given to each patient according to the protocol that McNamara and associates recommended [2].

Change of ECMO
The whole circuit was changed, including pump head, oxygenator, and tubing system, when there was severe plasma leakage from oxygenator or deterioration of oxygenation function of ECMO (PaO2 < 150 mm Hg under the sweep gas flow of FiO2 = 1.0).

Other support
IABP was used in 2 adult cases as well (patients 1 and 4), and the IABP was removed soon after the discontinuation of ECMO.

Weaning
The major criteria in weaning was hemodynamic status, such as blood pressure, urine output, tissue perfusion, and catecholamine dosage during the period of the weaning. When repeated echocardiography revealed improvement of myocardial contractility as well as the TnT level, the ECMO weaning was tried. Usually, the weaning was first tried 3 days later when dopamine and dobutamine were tapered below 10 µg/kg/min and milrinone below 0.5 µg/kg/min. The weaning is discontinued when a high dosage of catecholamine (over 10 µg/kg/min dopamine and dobutamine) is necessary, and the second trial of weaning is restarted the next day. In this series, the weaning was tried twice only in patient 5, and the others were weaned off successfully the first time.

Cardiac evaluation and data collection
The blood urea nitrogen, creatinine, creatine kinase (CK), creatine kinase MB form (CK-MB), aspartate aminotransferase (AST), and TnT level were collected every day during the ECMO running period. Echocardiography was also performed every day to evaluate the ventricular function. TnT was determined by an enzyme-linked one-step sandwich immunoassay with streptavidin technology on the ES-300 immunochemical analyzer (Cardiac T ELISA Troponin T; Boehringer Mannheim Corp, Indianapolis, IN). Serology studies for possible viral origin, including Coxsakie virus, Ebstein-Barr virus (EBV), cytomegalovirus (CMV), enterovirus, herpes simplex virus, and parainfluenza virus, were done. Myocardial biopsy was performed in 3 cases.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 References
 
Pre-ECMO data
The pre-ECMO CK was 16,522.2 ± 13,120.7 U/L, CK-MB 339.4 ± 250.5 U/L, AST 4,317.6 ± 2,986.3 IU/L, and TnT 21.3 ± 5.7 ng/mL. All patients had anuria for at least 6 hours and needed ventilator support. The echocardiography showed severe impaired left ventricular (LV) ejection fraction (21.9% ± 7.7%). Pre-ECMO data revealed at least a two-organ system dysfunction, including ventilator-dependence, disturbed consciousness, severe heart injury, renal failure, and even impending death.

ECMO course and results
The duration of ECMO support was 140.0 ± 57.7 h. All could be weaned from ECMO (100%) without any neurological or peripheral vascular complication. One patient had received IABP support before the ECMO use, and IABP could be removed as well a few hours later after the ECMO weaning. One 6-year-old girl (patient 5), who needed a pacemaker for AVB, died of multiple organ failure 10 days later after removal of the ECMO, resulting in 20% mortality. This girl had a complicated ECMO course for 8 days. The intravenous pacemaker was dislodged at the third day of ECMO, which needed another epicardial pacemaker emergently via subxyphoid incision at bedside due to marked bradycardia. Unfortunately, reexploration was needed 2 days later because of cardiac tamponade caused by substernal oozing from the previous wound. However, ECMO was weaned off at the eighth day without any neurological sequel under dopamine 10 µg/kg/min, milrinone 0.3 µg/kg/min, and inhaled nitric oxide. But the renal failure persisted after removal of the ECMO, which needed CVVH. Unfortunately, multiple organ failure and sepsis developed gradually in spite of the recovery of the heart.

Three patients, who had received hemofiltration before the ECMO rescue, needed CVVH for an additional 15 to 21 days after removal of the ECMO because of persistent renal dysfunction. Two of them recovered renal function completely without any sequel. The third was the girl who died of multiple organ failure.

The average duration of ventilator support was 12.8 ± 6.9 days for the whole series, and 8.5 ± 1.5 days for the survivors. The four survivors were discharged routinely in 23.3 ± 8.3 days and resumed functional class I status with follow-up of 37.2 ± 10.3 months. Echocardiography during follow-up showed improved LV ejection fraction (from 21.9% ± 7.7% to 65.6% ± 9.7%, p < 0.05). It is worth mentioning that these 4 survivors did not develop progressive heart failure leading to cardiomyopathy during the follow-up period, even though the grave clinical manifestation occurred during the AM episode.

The serology results revealed that only 2 patients (patients 2 and 3) had significant elevated antibody titers for EBV and enterovirus type 70. Other patients did not have any abnormal serology finding.

Three patients received endomyocardial biopsy, which was confirmed by the diagnosis of AM by pathological finding.


   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
References
 
High mortality around 50% to 75% was reported in AM patients with abrupt-onset, progressive congestive heart failure, including pulmonary vascular congestion and cardiac index less than 2.1 L/min/m2 [9–11]. Several therapies were tried in AM with variable results, including immunoglobulin [2], steroid and cyclosporine, prednisolone and azathioprine [12], mechanical support [3–7, 13], and even heart transplantation [14].

Mechanical circulatory support provides a reasonable treatment for acute circulatory collapse in AM, which may be reversible. Three mechanical supports at present are available: IABP, VAD, and ECMO. IABP can only provide limited additional cardiac output, which usually is not adequate for the critical situation, and is not suitable for all sizes of patients as well. VAD implantation is expensive and time consuming, and not always available for adolescent and infant group patients. Besides, it also needs cardiopulmonary bypass for VAD setup and removal. Furthermore, the decision of choice of left VAD or biventricular VAD in the acute deteriorated patients may be difficult, because the right ventricular function is hard to evaluate in the emergent situation. It is also difficult to decide when to remove VAD because the VAD cannot be temporally turned off for several hours to evaluate the heart function due to the complication of clot formation.

For those patients who fail IABP support, ECMO immediately provides adequate perfusion to all organs no matter how poor the lung condition is. It can be set up within 30 min at bedside and can take over the functions of both ventricles and lungs. Furthermore, it can support the failing heart up to 40 days in our hospital and is easy to be removed at bedside in the intensive care unit. It also allows several hours to days to try weaning ECMO if the bridging tube is added to the circuit. It is reasonable to choose ECMO to treat AM with shock that usually improved within 2 weeks.

However, decompression of the left ventricle is unpredictable in standard ECMO, and elevated LV end diastolic pressure (LVEDP) may complicate the ECMO course [15]. Therefore, left ventricle contractility must be carefully monitored by echocardiography daily after ECMO use for early detection of global hypokinesia and distention. Decompression of LV had been attempted by different methods, including special cannula across tricuspid and pulmonary valves [16], and transjugular technique to cannulate the LA [17]. In our series, biatrial cannulation via sternotomy provided the best flow potential and much better decompression of the LA. Adding a vascular graft to the ascending aorta (Fig 1) can prevent the possible problem of dislodgment of the aortic cannula during the prolonged ECMO running. Besides, it provides a more flexible way to accommodate the multiple cannulas in the mediastinum, and allows primary sternal closure.

The surviving 4 patients recovered their ventricular function completely and remained in function class I status during the follow-up period up to 37 months, in spite of their critical conditions in the acute phase of myocarditis. It means that fulminant AM can be completely reversible without leading to cardiomyopathy after its recovery from the acute phase, if ECMO can be provided in time and long enough for the recovery of myocardium. The TnT level also provides an indicator to predict the recovery of the stunned myocardium. Previous studies showed that TnT was an indicator of myocardial damage [18–20], and the failure of TnT level to decline within 72 h was associated with complicated postoperative courses [20]. Our study found that the marked elevated TnT level (all above 10 ng/mL) was correlated to the critical clinical condition before the ECMO setup, but the level rapidly declined after the ECMO setup (Fig 2), which corresponded to the clinical course. Similar results were reported in critical patients [20] and thoracic surgery patients [21, 22]. The TnT curve of the nonsurvivor (patient 5) showed another elevated peak of TnT at the eighth day after the ECMO, which might be due to the tamponade episode caused by sternal oozing. The unstable ECMO flow and hemodynamic instability caused the secondary myocardial damage. The slope of TnT decline in 72 hours was demonstrated to be -4.94 ± 1.18 ng/mL/day in this group (Fig 2). In summary, the TnT trend may be an indicator of the recovery of myocarditis. The similar slope of TnT decline may be an indictor for recovery.



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  		Fig 2. Slope of TnT level for individual patient. (x-axis). The day of ECMO. (y-axis) TnT level (ng/mL). The rapid decline of TnT in 72 h means recovery of myocardium with a similar slope: -4.94 ± 1.18 ng/mL/day.

 
There were several reports regarding the analysis of the risk factors and determinants for cardiac surgical ECMO [9, 23], but no specific biochemical markers were identified to predict the results of ECMO for cardiac patients. In our study, there was a similar slope of decline level in TnT in 72 hours in those who could be weaned off from ECMO no matter what the renal function. Although we did not have any TnT data regarding the AM patients who were rescued by ECMO but could not be weaned from ECMO, the TnT level in the successfully rescued group could rapidly decline in 3 days whether there was renal insufficiency or not. It means that the trend of the TnT decline provides a more specific guide to evaluate the myocardial recovery and estimate the timing of weaning of the ECMO. This study, to our knowledge, may be the first report regarding the relationship among TnT, myocarditis, and ECMO.

Limitations of this study included the small group number, and no control group. It is very difficult to get a control group due to ethics, various manifestation of AM, and rapid deterioration of the clinical condition of this group of patients.

Conclusions
The survivors in this study resumed all their cardiac function completely after 37 months of follow-up despite the catastrophic episode during the acute phase. ECMO is a reasonable, easy, and effective way for rescuing acute myocarditis with cardiogenic shock. TnT provides a good indicator for recovery of AM and ECMO weaning. We think ECMO and immunoglobulin could be the first choice of rescue treatment instead of VAD for those patients who suffered AM with cardiogenic shock.


   Acknowledgments
 
We thank Dr Chih-Hsiang Chan for his talented artistic drawing, and the ECMO team in National Taiwan University for caring for these patients.


   References
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 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

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Accepted for publication May 24, 1999.




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