DISCUSSION
In our case, the patient with typical ECG of Wellens syndrome unluckily had severe and diffuse stenosis of 95% proximal LAD and significant stenosis of 80-90% proximal LCx and 80% proximal MR. The treatment included DAPT, enoxaparin, angiotensin-converting enzyme inhibitors, dobutamine, and insulin human (rDNA) along with primary PCI for the culprit lesion in LAD according to the ECG of Wellens syndrome, the patient was being followed up at the cardiac intensive care unit room. On the second day after PCI, the cardiac arrest occurred spontaneously due to ventricular tachycardia which was successfully managed by cardiac defibrillations and amiodarone. Despite that, in the next day, the episodes of VTs continued to occur and the patient was diagnosed with cardiac ES which was controlled by the addition of another antiarrhythmic drug called lidocaine with 1mg/kg for the bolus dose and 1mg/min for continuous infusion dose in different vein, along with the continuous dose of amiodarone at 0.5mg/min. The ECG was back with sinus rhythm and the patient was stable hemodynamically and immediately transferred to the catheterization room in order to perform PCI for the LCx and the MR. After PCI for LCx and MR artery, the patient did not show any arrhythmias in the ECG and the clinical examination was progressively better without chest pain and shortness of breath. However, the ejection fraction did not show any improvement. He was treated with DAPT (81 mg Aspirin and 75 mg Clopidogrel), high-dose of Rosuvastatin at 40mg, 5 mg of Perindopril, and 25mg of Spinorolactone, low-dose of Bisoprolol at 1.25mg, 2000 mg of Metformin and 10 mg of Dapagliflozin. We intended to perform an Implantable Cardioverter-defibrillator (ICD) to prevent sudden cardiac death. However, after 3 months of following up on the above treatment, the patient was stable with sinus rhythm and the cardiac function was improved to 48%, therefore, we decided not to do so and keep following up with the patient with the treatment.
Herein according to the joint EHRA, ACCA, and EAPCI task force in 2014  and 2017 AHA/ACC/HRS guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death, patients with the acute coronary syndrome, presenting with the condition of incomplete revascularization as mentioned in our case with the significant stenosis of LCx and MR besides the culprit lesion in LAD, are at increased risk for the development of arrhythmia.16, 17 Currently, there has been a lack of larger trials comparing the benefit from complete revascularization and incomplete revascularization. Generally, it is recommended that non-culprit lesion revascularization should be performed by a staged percutaneous coronary intervention in order to achieve complete revascularization. Therefore, after the successful PCI of the culprit lesion, it is advisable to treat other lesions in the duration of hospitalization.18
In addition, we believe that if one antiarrhythmic drug could not control the rhythm, the additional one in a different group should be considered. We suppose that intravenous infusion of amiodarone and lidocaine in different veins should be considered as an option for controlling ventricular arrhythmias along with the control of electrolytes, analgesics, and sedatives.