Introduction: Ventricular tachycardia is a life-threatening arrhythmia, which frequently appears in ischemic substrate.
Case presentation: A 64-year old man, hypertensive, diabetic, smoker, with a history of inferior myocardial infarction medically treated 16 years ago and atherosclerotic coronary disease with chronic occlusion of RCA and LAD stenosis, with elective PCI with stents, 10 and 5 years ago, was admitted for ventricular ta-chycardia with low hemodynamic tolerance. The pati-ent was intense symptomatic, accusing dyspnoea, pal-pitations, dizziness. The ECG shows sustained ventri-cular tachycardia, which converts at sinus rhythm with Q waves in inferior derivations, 1mm ST depression in V₄-V₆. Laboratory tests show no elevation in the markers for myocardial necrosis and no dyselectrolytemias.
Echocardiography shows moderate systolic dysfuncti-on with 37% ejection fraction of the left ventricle with akinetic and hypokinetic segments in the inferior, in-ferolateral walls and in the inferior interventricular septum, mild mitral regurgitation and no pericardial effusion. Considering the context, the ethology of the ventricular tachycardia was investigated through coro-narography, but no significant in-stent restenosis and no new lesion were found.
Particularities: During the hospitalisation, the pati-ent has multiple episodes of unsustained ventricular tachycardia and three episodes of monomorphic sus-tained ventricular tachycardia with low hemodynamic tolerance, which are converted to sinus rhythm with lidocaine. The patient receives beta-blocker and amio-darone and an internal cardiac defibrillator (ICD) was implanted as secondary prevention. After two months, the patient was admitted with electrical storm, with many episodes of palpitations, dyspnoea, dizziness and the ICD recorded 76 episodes of ventricular tachycar-dia in the last 3 days, stopped by the ATP- antitachycar-dia pacing. Ablation of the ventricular tachycardia was performed by applying radiofrequency on two areas of the fibrosis in the inferior wall. Before the ablation, VT monomorphic is induced by stimulation, producing hemodynamic instability, and is converted by overdri-ve, but after the ablation VT could not be induced. The evolution was favourable, and at 3 months follow-up, no VT was observed.
Conclusions: We present the case of a patient with car-diovascular risk factors and ischemic heart disease, and a recurrent life-threatening complication- sustained ventricular tachycardia, and for resolving the case complex interventional techniques were used. We emphasi-ze the importance of revascularization with PCI with stent in acute myocardial infarction with ST elevation, which could not be done at that time, in this case and that caused the large area of fibrosis. The ischemic sub-strate is a frequent cause of VT and the large fibrosis can have many arrhythmogenic areas, therefore the di-fficulty of the ablation procedure is higher.