Recovery from myocarditis is a multiphasic process where clinical improvement often precedes structural healing, requiring phenotype-specific surveillance and careful follow-up.
Recovery after myocarditis is a complex, multiphasic process requiring phenotype-specific surveillance, as clinical improvement often precedes structural healing.
Myocarditis is one of the most varied syndromes seen in cardiovascular medicine, being diagnosed as a self-limited inflammatory injury with rapid resolution of symptoms, to fulminant cardiogenic shock, malignant arrhythmias and chronic inflammatory cardiomyopathy, as well as significant progression to dilated cardiomyopathy. Because of this, the term "recovery" after myocarditis cannot be defined in terms of one endpoint. A patient may have a good clinical status at the time of evaluation, yet still have residual myocardial scarring on cardiac magnetic resonance (CMR); cardiac biomarkers may resolve before a return to exercise tolerance; the patient may have returned to normal left ventricular ejection fraction (LVEF), yet the risk of arrhythmias in specific phenotypes still exists. This review paper will examine recovery from myocarditis as a multiphasic process comprising clinical improvement, normalization of ventricular function, electrical stability, structural healing, exercise tolerance, and long-term absence of heart failure or recurrent inflammatory events. The majority of patients with uncomplicated acute myocarditis will have a positive short-term clinical outcome according to published research and guidelines from multiple national and international cardiology and medical societies until 2026. However, many patients will have findings of residual abnormalities demonstrated through follow-up imaging studies. These include findings of late gadolinium enhancement (LGE) on CMR in most patients. Prognosis associated with myocarditis is not solely determined by diagnosis; other factors that influence prognosis include presentation phenotype, degree of left ventricular dysfunction, presence of malignant arrhythmias, known histologic subtype of myocarditis (when known), the burden of residual scarring, and the distribution of residual scarring in the ventricles. Fulminant myocarditis patients should receive special attention, as although there is a high rate of early mortality, surviving fulminant myocarditis patients often have impressive improvements in left ventricular function when there is rapid delivery of mechanical support and access to specialised care. Pediatric patients with myocarditis and patients with accusations of myocarditis following vaccination routinely have good medium-term clinical outcomes, but there is a very important concept that has been demonstrated to be true by these 2 groups of patients: that clinical improvement often precedes the resolution of the morbidly altered anatomic structure of the patients. Currently, there has been a move towards the use of phenotype-specific surveillance instead of the generic post-myocarditis strategy. However, early reassessments, repeat echocardiography, selective repeated CMR, ambulatory rhythm monitoring, and a carefully staged return to exercise remain the key components for the management of patients following myocarditis. Patients who exhibit symptoms, decreased LVEF, a significant degree of or septal LGE, ventricular arrhythmias, conduction disorders, autoimmune or biopsy-proven aggressive forms, and genetic predisposition should be followed closely. How residual inflammation and residual scar should be interpreted and how and when management should be altered based on the presence of LGE, and whether the use of imaging-guided recovery pathways can improve long-term outcomes, is the focus of future research investigations.
Bennani et al. (Mon,) conducted a review in Myocarditis. Recovery from myocarditis is a multiphasic process where clinical improvement often precedes structural healing, requiring phenotype-specific surveillance and careful follow-up.