Decision making in a presumptive case of STEMI-like myocarditis

Abstract

In youngmales, differential diagnosis during chest pain is not always easy. When ECG findings suggest a cardiac origin of such symptoms, myo-pericarditis is usually themost likely hypothesis, beingmore common than Acute Coronary Syndromes (ACS) in the first decades of life [1]. In the presence of ST segment elevation, Troponin release and ventricular wall motion abnormalities, the diagnosis can be challenging, though. In the young a lowcoronary risk profile and atypical symptoms seldom support a working diagnosis of Coronary Heart Disease (CHD), and, therefore, urgent coronary angiography is not recommended routinely, although cases of early ACS are not so rare. In October 2014 a 26-year-old man was admitted to our ICCU for chest pain, started 2 h earlier, radiating to the left shoulder and changing with position. The young man used to practice sports regularly and adhere to a hyperprotein diet. No history of traditional cardiovascular risk factor was present, excluding cigarette smoke. Two weeks before a selflimiting fever had occurred. Family history was negative for cardiovascular diseases. At presentation a 12-leads ECG was registered, showing concave ST segment elevation in V1–V5 without reciprocal ST segment depression, and negative asymmetric Twaves in inferior leads (Fig. 1). A blood sample collected 30 min earlier showed no increase in troponin levels, 13,000white blood cells/mm3 and high C-reactive protein levels. Echocardiography revealed a mild systolic dysfunction with a mild hypokinesia of anterior mid-septal and periapical segments, without pericardial effusion. During the acquisition of the images, the patient became more diaphoretic and chest pain tended to increase. Albeit the initial hypothesis of a STEMI-like myocarditis, in the raising clinical suspicion of an ACS the patient was pre-treated with aspirin, a loading dose of prasugrel and unfractionated heparin, and referred to the cath lab for an urgent coronary angiography, which showed a proximal occlusion of Left Anterior Descending Artery (LAD)with a high thrombotic load (Fig. 2), treatedwith thrombus aspiration followed by coronary angioplasty and drug-eluting stent placement on the underlying coronary plaque, accounting for around 80% of the LAD lumen, achieving a TIMI 3 flow. The patient was post-treated with abciximab bolus plus infusion. No other coronary lesionswere detected. During hospital stay, coagulation factors' analysis unveiled a moderate reduction in the activity of Protein C and Protein S, while the use of multiple antiplatelet agents in the acute and post-acute phases didn't allow the performance of platelet functionality tests. Genetic characterization is still ongoing. CHD is known to be one of the main causes of hospital admission in Western Countries, and acute coronary syndromes are the leading cause of death in this context. Though AcuteMyocardial Infarction is rather infrequent in the young, in the Global Registry of Acute Coronary Events (GRACE) Study 6.3% of ACS occurred in this sub-population [2], and the same datawere confirmed in several registries [3]. Clinical presentation of ACS in this context is often atypical, and a low-cardiovascularrisk profile makes the diagnosis of CAD even more unlikely, given a higher incidence ofmyocardial inflammatory diseases in the same population. One of the electrocardiographic markers which has been deemed to be able to discriminate amyocarditis froma STEMI is ST segment elevation without reciprocal ST depression [4], but sensitivity and specificity of such sign are not well established, and its poor diagnostic performance arises the risk of a missed diagnosis, as shown by our case. On the other hand, segmental abnormalities of left ventricular wall motion are not peculiar of ACS, given the possibility of a spotty distribution ofmyocarditis impairing segmental and global ventricularmotion [5,6]. All these overlapping features create a gra