Myocarditis is a broad term with various definitions and subtypes. In the 2013 position paper by the European Society of Cardiology (ESC), myocarditis is defined on the basis of histological, immunological, and immunohistochemical criteria [3]. This involves an array of investigations such as serological investigations (troponin, white cell count, C-reactive protein), an electrocardiogram, echocardiogram, and cardiac magnetic resonance imaging. However, the gold standard is EMB contributing towards a definite histological diagnosis [3,4,5]. Despite this recommendation, an EMB is usually limited to life-threatening situations or when the diagnosis is unclear. This is likely secondary to the risks involved, together with the decreasing availability of trained staff and equipment, as well as the increasing availability of CMR [6]. A statement paper by the American Heart Association recommends limiting the use of EMB to cases of an unexplained cardiomyopathy complicated by high degrees of block, ventricular arrhythmias, inotrope requirement, or failure to respond to medical treatment. If these are not present, then a CMR would suffice for the diagnosis [7]. In our case, an EMB was recommended based on both above guidelines and it was indeed essential as it provided a definite diagnosis while excluding other important differentials which may have required tailored therapy. A more recent expert consensus statement published in 2020 describes myocarditis with associated advanced AVB and LV impairment as complicated acute myocarditis, in keeping with our case [8]. In cases of fulminant myocarditis, LV impairment leads to cardiogenic shock requiring inotropic or mechanical circulatory support by definition, which was not required in our case [9].

The EMB reported a diagnosis of lymphocytic myocarditis which is characterised by CD3+ T lymphocyte and CD68+ macrophage infiltrates leading to myocyte inflammation and necrosis of varying degrees [5, 8]. The cause of the myocarditis in our case was assumed to be viral given the patient’s prodrome; however, there was no detected viral genome on polymerase chain reaction of the EMB. Having said this, a causative virus is only found in 30 to 40% of viral-induced lymphocytic myocarditis [10]. The results of autoimmune and toxic screens were normal, therefore excluding these factors in our case.

High-grade AVB is an uncommon finding in patients with acute lymphocytic myocarditis [2]. Varying degrees of AVB may occur in acute myocarditis due to ongoing inflammation resulting in myocardial interstitial oedema involving the conduction system [11]. As early as 1992, Morgera et al. [12] reported an incidence of 15.5% in active myocarditis. However, a more recent large observational study of 31,760 patients with myocarditis reported an incidence of high-grade AVB to be only 1.1% [1]. Given the rarity of high-grade AVB in myocarditis patients, other causes of AVB must be excluded. This may include cardiomyopathies (hypertrophic cardiomyopathy, other myocarditis types), electrolyte imbalances, hormonal deficiencies (such as hypothyroidism), and drug related [13]. All these differentials were sufficiently excluded on the basis of the adequate history taking, blood investigations, and the EMB. Indeed, AVB is more common in other types of myocarditis such as Lyme carditis, giant cell myocarditis, and sarcoiditic myocarditis. This complication has been reported in approximately 20–50% of these cases and indeed contributes significantly to an increased morbidity and mortality [10, 14, 15]. Apart from the higher incidence of AVB in these conditions, another early study noted that a pacemaker was required in 60% of cases with giant cell myocarditis, while only 8.3% of AVB in lymphocytic myocarditis required a pacemaker [16]. Permanent pacemaker insertion is rarely required in lymphocytic myocarditis with only a handful of cases reported [17,18,19]. A permanent pacemaker was inserted on presentation in our case due to several reasons. Firstly, it provided atrio-ventricular synchrony which helped stabilise the patient’s condition. This synchrony is not possible with a single lead temporary pacemaker. Furthermore, the outcome of the CHB is difficult to predict in cases of complicated acute myocarditis. It may take days to weeks to resolve and may possibly re-emerge once thought to be resolved. Indeed, monitoring the rhythm closely in the acute and subacute stages is essential. This may be done on ambulatory ECG monitoring or recordings from the pacemaker device as was done in our case. Early fibrosis of the myocardium in published cases seemingly played an important role in persistent high degree AVB and pacemaker dependence [18]. Therefore, CMR and EMB may aid in the decision for requirement of a permanent pacemaker based on fibrotic changes and a high degree of late gadolinium enhancement on CMR. In our case, the patient's AVB completely resolved in conjunction with CMR results (no late gadolinium enhancement or fibrosis), indicating a good prognosis.

Heart failure in acute myocarditis may lead to cardiogenic shock, hence the importance of guideline-directed heart failure treatment to assist in the myocardium recovery [20]. Inotropic and mechanical circulatory support may be required in cases of fulminant myocarditis [9]. In our case, inotropic support was not required and the patient’s LV recovered after a few weeks of anti-heart failure treatment.