Our data demonstrated that early application of IABP in the treatment of FM restores hemodynamic stability via unloading of the left ventricle, improves left ventricular function, shortens hospital stay, and improves survival. The findings advocate for early application of IABP in treatment of patients with FM and hemodynamic instability and/or arrhythmias.
The presentation of FM varies from cardiogenic shock to sudden death, while the complications include fatal arrhythmias, atrioventricular (AV) blocks, congestive heart failure, cardiac tamponade, acute renal failure, respiratory dysfunction, and multisystem organ failure. The diagnosis of FM in commonly based on comprehensive considerations of patients’ medical history, clinical manifestations, and accessory examinations15, 16. Patients who presented with a new onset of acute and severe heart failure, typically following a bout of viral infection, requiring parenteral inotropic or mechanical circulatory support are diagnosed as FM 5. The most common cause of FM is considered to be enteroviral infection, such as coxsackievirus. New causes of FM, including H1N1 influenza and drug-related eosinophilic myocarditis 17, 18 have emerged as the prevalence of enteroviral infection has waned.
The risk of in-hospital death was reduced by 29.5% in patients who received IABPs as compared to those who did not. In addition, the use of IABP significantly decreased the dose of vasoactive drugs, including norepinephrine and dopamine. The latter drugs may be detrimental in patients with FM 10, 11. Overall, the consensus is to minimize the use of vasoactive drugs in the treatment of FM 8. Despite the lower doses of norepinephrine and dopamine in patients with FM, hemodynamic indices were more stable inpatients with IABP than those without, indicating a beneficial effect of IABP in restoration of hemodynamic in FM patients.
Cardiac function improved after 24 hours of IABP application, as evidenced by a notable increase in echocardiographic LVEF from 37.5–45.4%, indicating that mechanical life support unloaded and enhanced the working efficiency of the heart. Although the LVEF was similar in both groups before discharge, application of IABP was associated with a higher and an earlier improvement in LVEF, an important determinant of survival in patients with FM 19. The use of IABPs had no significant effect on cTnI and BNP levels in FM patients.
FM is an excessive inflammatory response process in the heart mostly due to a viral infection, which causes acute-onset severe heart failure 20, 21. Although viral infection is the cause of most cases, over-activated immune responses and inflammatory cascades are the key pathogenic mechanisms for the initiation and development of FM 9, 22–24. Unlike the irreversible death of the myocardium that occurs in ischemic heart disease, inflammatory response-induced myocardial injury is in part a reversible pathological process 9. Thus, the pathophysiology of fulminant myocarditis involves direct myocardial injury caused by viral pathogens and indirect injury caused by the overwhelming immunologic responses and acute inflammatory shock 9. Therefore, temporary mechanical circulatory support to unload the heart could lead to a better outcome as the inflammation gradually subsides.
In summary, our data suggest that early IABP implantation reduced in-hospital mortality in patients with FM. It also improved hemodynamic instability and attenuated cardiac dysfunction. Our data suggest that patients with FM should receive IABP support as early as possible, unless it is contraindicated.