Fulminant myocarditis is an inflammation of the myocardium, which is caused by viral, bacterial, or protozoal infections, drug toxicity, or immunological reaction [1]. Fulminant myocarditis is characterized by acute onset with severe hemodynamic deterioration. Diagnosis of fulminant myocarditis in the early stages of the disease may be difficult. It may be initially misdiagnosed as septic shock, in which myocardial dysfunction and mild troponin I elevation are commonly seen [1, 2]. Fulminant myocarditis is different from acute myocarditis in its clinical features [1, 3]. Fulminant myocarditis was diagnosed on the basis of clinical features at presentation, including the presence of severe hemodynamic compromise, rapid onset of symptoms, and fever. On the other hand, acute myocarditis usually shows less severe hemodynamic compromise and did not have these features [3, 4].
There is no specific treatment for fulminant myocarditis. Thus, treatment remains supportive. Physicians suspecting fulminant myocarditis must be prepared to use therapeutic options, such as mechanical circulatory support, prior to occurrence of severe organ failure [1, 5, 6]. With appropriate treatment, fulminant myocarditis is commonly reversible within a few days and is associated with better long-term prognosis than acute myocarditis [3].
Mechanical circulatory support in myocarditis is used for maintenance of cardiac output and organ perfusion, and to minimize the need for inotropic support until myocardial recovery. There are several methods for mechanical circulatory support. These include the intra-aortic balloon pump, non-pulsatile extracorporeal life support, and pulsatile extracorporeal life support, such as T-PLS, which we used for our cases, and ventricular assist devices.
A non-pulsatile pump has advantages over a pulsatile pump in that it maintains regular blood pressure with less hemolysis during total extracorporeal circulation. However, it does not maintain higher pulse pressure or mean blood pressure than the pulsatile pump [7–9], which probably results in less tissue perfusion [10].
T-PLS has an actuator and two blood sacs, and the reciprocating actuator pushes on the blood sacs alternatively, causing pulsatile flow (Figure 2). The T-PLS system has an effective pulsatility in hemodynamic energy and provides a beneficial effect on the coronary arteries in terms of blood flow, flow velocity, and resistance, and also provides better tissue perfusion than the non-pulsatile pump [10, 11]. Compared to other pulsatile pumps with different pulse generating mechanisms, the dual sac structure of T-PLS can effectively reduce high membrane oxygenator inlet pressure, and, thus, reduce hemolysis [7, 8, 12, 13].
T-PLS is not synchronized with native heart beat. When it is used in severe heart failure patient where there is very low pulsatility from the heart, no synchronization is required. When the heart is recovered and makes higher pulsatility, T-PLS rate is weaned down so that it does not eject too strongly when the heart ejects.
As proven by previous studies, T-PLS can improve coronary and other tissue perfusion with less hemolysis [7, 8, 12], and those advantages are essential for treatment of fulminant myocarditis; therefore, we think that T-PLS is one of the most suitable treatment options for fulminant myocarditis.