Abstract Introduction Ventricular arrhythmias (VA) represent a common complication of myocardial infarction (MI). Typically, they occur in two scenarios: during acute MI, related to ongoing ischemia, as ventricular tachycardia (VT) or ventricular fibrillation (VF), or in the context of a late phase of MI, related to the presence of a scar, as monomorphic VT (mVT). Despite the above, their occurrence may be atypical. Clinical Case 55–year–old man affected by obesity, diabetes and hypertension, admitted to our department for subacute MI. Coronarography showed three–vessel disease with indication for surgical revascularization. Thirty hours after admission, in absence of symptoms, occurrence of cardiovascular arrest due to mVT, which degenerated into VF. After resuscitation, ECG and Echo findings did not change compared to those observed at admission, excluding the presence of current ischemia. A blood gas analysis excluded dysionias. Few minutes later, arrhythmic recurrence of mVT degenerated into VF. This was refractory to electrical and antiarrhythmic therapy and stopped only after percutaneous left stellate ganglion block (LSGB) and deep sedation. Then, emergency surgical revascularization was performed. In the early postoperative days, during weaning attempts from sedation and ECMO support, that had become necessary due to hemodynamic instability after surgery, numerous recurrences of mVT, regressed only after deepening of sedation, multiple external shocks, antiarrhythmic polytherapy, and LSGB. A new coronarography documented patency of coronary artery bypass grafts. On 6th postoperative day, discontinuation of deep sedation and weaning from circulatory support without recurrence of VA. The patient was discharged from the intensive care unit and started on a rehabilitation pathway. Conclusions mVTs are commonly related to the presence of a scar, formed late after MI, or to the context of ongoing ischemia in acute MI. However, it should be remembered that even during the subacute phase of MI, arrhythmic instability might still occur. The responsible mechanisms are not completely known but it can be assumed that, even in the absence of a new ischemic event, the process of scar maturation may have led to a transient proarrhythmic substrate, responsible for the arrhythmic storm. Further studies are needed to clarify the mechanisms of arrhythmogenesis in the subacute phase of MI.