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COVID 19 has so far found the only barrier in the use of mRNA and viral vector vaccines. Among the rare adverse effects related to mRNA vaccines is myocarditis (4.8 cases per million doses) a disease already found in COVID 19 infection but not in the safety studies of the vaccines. Males not older than 30 years (40% of the total), subjected to the second dose inoculation, are most affected. During our recent clinical practice there was a case of a patient with myocarditis, attributable to vaccination for COVID 19. It was a male, twenty–year–old, non–allergic smoker, subjected to second dose of Pfizer–BioNTech vaccine (BNT162b2). On the fifth day after the inoculation, the patient, already asthenic from the previous days, complained of an episode of oppressive chest pain, which lasted about 15 minutes, which returned, more intense the following night, associated with dyspnea, lasted for hours. When the patient went to the emergency room the pain was in regression and there was good hemodynamic compensation. EKG: sinus rhythm, slight diffuse ST segment elevation, more pronounced in the inferior–lateral leads, slight lowering of the P–R segment. Blood tests: troponin, CKMB and PCR increase, negativity of the molecular test for COVID 19. Echocardiography: normal left ventricle, non–dilated right sections, normokinetic right ventricle, normal valves, pericardial hyper–refraction without effusion, normal diastolic relaxation. In the suspicion of myocarditis, the patient was admitted to our intensive cardiological care. With the high–dose anti–inflammatory and beta–blocker therapy the pain gradually disappeared; never fever; EKG showed progressive ST segment improvement and T wave negativization. Never arrhythmic events. Negativity for all infections with common viral pathogens. MRI: hyperintensity (T2 STIR sequences and late enhancement) in the infero–lateral area. Patient discharged in therapy with lysine acetylsalicylate, to be reduced, associated with pantoprazole, and metoprolol and indicated for outpatient checks. In conclusion, the case presented reflects the scientific literature in the type of patient and in the favorable evolution of the disease.

A 65–year–old patient, hypertensive, dyslipidemic, strong smoker. He has heart disease with hypokinetic evolution EF 47%, mild MI. Negative Dipyridamole–stress echocardiography dated January 2008. Recently atrial fibrillation (AF) is found and anticoagulant therapy was started. Dyspnea and weight loss occurred in past two months. Detected keratinizing squamous pulmonary Ca with negative markers. This injury was judged to be inoperable, and the patient get indications for chemotherapy and radiotherapy. The patient also starts complaining of dyspnea and chest pain on exertion: Not serological modification, not ischemic ECG. Echocardiogram LVEF 47–50% highlights diffuse hypokinesia, regular valves. Ergometric test was not evaluable for ischemia. Coronary angiography shows stenosis of proximal and middle anterior interventricular coronary and non–critical lesions of circumflex and right coronary. Ecodobutamine test was positive for ischemia and arrhythmias (AF and wide QRS tachycardias in recovery phase), but negative for angor. The patient was treated with CT and IVA I – II. angioplasty Monitoring shows AF with high penetrance, wide QRS tachycardia runs and very short TVNS. ECG 1: During atrial tachycardia, show broad QRS conduction to BBSX alternating with narrow QRS with the same RR interval. ECG 2. show fusion between the wavefront conducted with narrow QRS and that with wide QRS. These are supraventricular arrhythmias that run along the atrioventricular nodal pathway (NAV) in the narrow QRS tracts and take an accessory pathway in the wide QRS run.The Mahaim fibers have decremental conductivities like the AV node, therefore high ventricular frequencies does not occur AF appeared during ecodobutamine, but some beats were conducted by an anomalous path in a discontinuous way); they are generally directed from the atrium or the NAV, towards another part of the right ventricular conduction system, with atrium wave or NAV – RB, therefore the early activation of the RB generates a widened QRS, with a LBB morphology. ECG 3 Re–entry on Mahaim pathway, ventricular activation widened through Mahaim fiber, which generate LBB morphology with retrograde atrial depolarization. In this case there is no reentry, but we have an atrial tachycardia conducted alternately on an accessory pathway and across the NAV. Given the patient‘s clinical problems and the total absence of symptoms, the patient remains asymptomatic during therapy with amiodarone and beta–blocker.