Introduction: Myocarditis is usually difficult to diagnose considering the complex clinical presentation and that myocardial biopsies are not commonly performed. The incidence of this disease is not well established due to same reasons. The majority of the epide-miological data results from autopsies. Approximately, 20-30% of cases evolve into DCM and have a poor prognosis.
„The Global Burden of Myocarditis” task force from 2010 revealed that men are more commonly affected and develop more severe forms compared to women. The risk of death or heart transplant is of 27% according to an Italian study and varies between 19.2% and 22% according to various studies from Germany. Myocarditis is the cause of 15% of cardiac deaths and 9.9% of sudden cardiac deaths. The TIMIC trial showed a decrease of mean LVEF in patients with inflammatory cardiomyopathy from 27.6% to 19.5% in a 6 months period.
The coexistence of coronary heart disease and inflammatory cardiomyopathy leads to a poor prognosis as diagnosis is delayed.
Case presentation: A 49 years old man, smoker (30 packs-year), non-drinker presented for a cardiologic evaluation. He complained of SOB on moderate exer-tion and impaired effort capacity that developed sud-denly about two years ago, two weeks after an acute infectious episode (pneumonia).
The physical examination revealed intermittent ar-rhythmic heart sounds, a systolic murmur of mitral regurgitation, with no pulmonary or systemic stasis, BP=110/60 mmHg, HR=80 bpm.
The laboratory findings showed an NT-proBNP of 1300 pg/ml and hypertriglyceridemia. ECG: sinus rhythm, QRS axis at 0 degrees, negative T waves in DI, aVL, V5-V6.
The echocardiography described a dilated LV with severely impaired LVEF (25%), severe diastolic dys-function, global hypokinesis, global longitudinal strain 10%, mild mitral regurgitation, dilated RV, mild tricus-pid regurgitation, no pulmonary hypertension.
Considering the clinical presentation and the echo-cardiography results, we recommended a cardiac MRI that showed findings consistent with cardiomyopathy secondary to myocarditis- enlarged LV indexed volu-mes, severely impaired LVEF (21%), myocardial fibrosis secondary to myocarditis, RV with severely impai-red systolic function, moderate mitral and tricuspid regurgitation, mild aortic regurgitation.
The Holter ECG monitoring revealed a maximum HR of 127 bpm, minimum HR of 54 bpm and 11330 supraventricular premature complexes, the majority of them isolated and 324 isolated ventricular premature complexes of 2 different morphologies.
As the symptoms were not corresponding to the se-verity of the disease (LVEF severely impaired) we decided to do an exercise stress testing for the classification of the cardiac insufficiency and for the evaluation of inducible ischemia. The test was stopped at the beginning of phase 2 for physical exhaustion and showed a 1-1.5 ST segment depression in DII, DIII, aVF, V6 and numerous PACs – couplets and triplets; the patient achieved 30% of predicted METs (severely impaired effort capacity) and did not accuse chest pain.
We proposed that the patient underwent a coronary angiography as recommended by the European guide-lines and found a severe distal stenosis of the LMS that involved the origin of the LAD and LCx, a 95% calci-fied stenosis of the second segment of the LAD and the origin of the 1st septal branch and a 90% calcified, pro-ximal stenosis of LCx.
Considering the fibrotic lesions described by the MRI a more extensive investigation was needed to es-tablish the myocardial viability. The myocardial per-fusion scintigraphy showed viable myocardium in all LV segments, a dilated LV with small perfusion de-fects (<10%), TDV=286 ml, TSV=220 ml, LVEF=23-25%, global hypokinesis, and apical hypokinesis with a dyskinetic tendency.
The Heart Team took into account the severity of the ischemic lesions and the severely impaired LVEF and recommended PCI, but the patient refused so he recei-ved optimal medical treatment. He had no complaints at follow-up appointments.
Case particularities: The particularity of this case con-sists of the complex etiology of the dilated cardiomyopathy. The clinical presentation and MRI findings are consistent for cardiomyopathy secondary to myocarditis. On the other hand, the extensive coronary lesions remained silent, possibly due the subsequent reduction of the myocardial mass in the context of inflammation. Hence, in this case, we cannot quantify in what proportion the myocardial fibrosis was secondary to myocarditis and how much was due to ischemia.
Conclusion: To conclude, the diagnosis of myocardi-tis should not limit the extent of investigations and the role of cardiac MRI must be further studied. The dia-gnostic utility of the cardiac MRI is well established, but the prognostic role of it is not yet confirmed by ran-domized trials. Although there is at least one study that claims that the cardiac MRI can be used as an alternati-ve to invasive investigations in patients with DCM, this claim has not been yet confirmed.