Introduction: Fulminant myocarditis represents the myocardial inflammation subtype with a severe onset and rapidly progressive course, characterized by dramatically clinical scenarios, with hemodynamic collapse, resulting in cardiogenic shock, life-threatening arrhythmias, or sudden cardiac death. The fulminant presentation of myocarditis is linked to a high mortality rate, early diagnosis and adequate treatment repre-senting essential factors influencing the prognosis.

Case presentation: We report the case of a 21 year-old male patient, regular smoker, with no relevant family history of heart diseases, admitted to our department for clinical manifestations, serum parameters and electrocardiographic features suggestive of acute ST-ele-vation myocardial infarction (STEMI) of the inferior, posterior, and lateral walls, class I according to Killip classification. Since timely primary percutaneous coronary intervention was not available, the patient received reperfusion therapy with fibrinolysis in the regional medical hospital. Blood tests showed important leukocytosis, neutrophilia, and inflammatory syndrome, with negative procalcitonin and toxicological tests. The patient did not display symptoms suggestive of infection prior to hospital admission. An urgent coronary angiography was performed. However, all major coronary arteries were normal, except for important vasospasm in the proximal and paraostial segments of the right coronary artery, improved by intraprocedu-ral nitroglycerin administration. The patient’s clinical condition deteriorated to the extent of developing cardiogenic shock. He was admitted in the Intensive Care Unit for circulatory support, and received pharmaco-logical therapy with inotropes and vasopressors. The echocardiography demonstrated severe left ventricular systolic dysfunction, with an ejection fraction (EF) of 10%, global severe hypokinesis, a slightly dilated left ventricle, and a moderately severe mitral regurgitati-on. The patient’s clinical condition ameliorated, with improvement of hemodynamic status. Vasopressor therapy was weaned off. 7 days after hospital admissi-on, the echocardiographic parameters improved (left ventricular function recovered, with an EF of 40%). After remission of hemodynamic instability, 10 days from the acute cardiac pathology onset, the patient un-derwent cardiac magnetic resonance (CMR) imaging scan, which demonstrated mildly reduced left ventri-cular ejection fraction (EF of 55,95%), with normal left ventricular volumes, and normal right ventricular function. T2-weighted sequences did not describe left ventricular myocardial edema features, except for the distal portion of left ventricular papillary muscles. Late Gadolinium Enhancement (LGE) imaging did not de-monstrate pattern of delayed left ventricular myocardi-al enhancement. Fulminant myocarditis was suspected on the basis of rapidly progressive clinical course, with cardio-vascular collapse, in patient with pronounced vasospasm and accelerated remission of cardiac dysfunction under supportive care, in the absence of di-agnostic CMR tissue characterization criteria for myo-carditis (Lake Louise Criteria), and the standardized histologic criteria obtained by endomyocardial biopsy.

Particularities: 30 days from disease onset, CMR assessment did not demonstrate deterioration of left ventricular systolic function, or cardiac chamber en-largement. Morphologically, no areas of inflammatory and fibrotic left ventricular myocardial insults were recorded. However, LGE acquisitions depicted evidence of persisting focal late enhancement in the cranial segment of left ventricular papillary muscles. The initial therapeutic management of a young patient, with fulminant myocarditis mimicking signs and symptoms of acute myocardial ischemia, was the standardized STEMI therapy. The particularity of this clinical case is represented by the association of fulmi-nant myocarditis and coronary vasospasm, the latter depicted as a secondary pathophysiological process, complicating the early stages of fulminant myocarditis. Furthermore, the long-term prognosis of a survivor of an episode of fulminant myocarditis, complicated with cardiogenic shock, with rapid recovery in contractile function, remains a question mark. An imagistic pecu-liarity emphasized by the CMR exam, is represented by the area of initial edema and secondary focal fibrosis, localized in the cranial segment of the papillary muscles, as unique morphological sign of late myocardial damage, in the context of cardiogenic shock. The clinical course of fulminant myocarditis is in the majority of cases fatal, with high in-hospital mortality (50% reported in the literature). Early diagnosis and therapeutic management of fulminant myocarditis remain a challenge in clinical practice, especially when its manifestation closely mimics acute ST-elevation myo-cardial infarction.