HISTORY, CURRENT DISEASE AND PHYSICAL EXAMINATION
57-year-old patient with CVRF and a history of anterior and apical AMI in 1997 with surgical revascularisation with VSF-DA and VSF-CD bypass. The patient was being monitored by the Cardiology department with CF NYHA I-II. After observing NSVT on Holter monitoring, it was decided to perform EPS with induction of polymorphic VT. A programmed single-chamber ICD was implanted in 2003 with a therapy zone starting at 200 bpm. In the last control echocardiogram: severely dilated LV, with severely depressed systolic function (25%) and anteroseptal and apical akinesia.
Given the presence of LVEF < 35 %, CF NYHA II, QRS 160 ms (BRD+HBAS) with adequate medical treatment, it was decided to upgrade to ICD with cardiac resynchronisation therapy (ICD-CRT) on an outpatient basis.
The patient was admitted to our department for the procedure. The procedure was carried out with implantation of a tetrapolar electrode in the left lateral vein (very difficult access due to the ostimum valve in the coronary sinus) and an electrode in the right atrial appendage. Programming optimisation was performed and DDDR 45 was finally programmed, Biv +30 ms with 3-shell ring pacing, resulting in a stimulated QRS of 128 ms.
A few hours after implantation, the patient presented sustained monomorphic ventricular tachycardia at 160 bpm with inferior axis and QS morphology in precordial leads with good haemodynamic tolerance. Treatment was started with amioradone and intravenous beta-blocker, reprogramming the device to therapy from 140 bpm (previously programmed from 200 bpm). An attempt was made at ATP and after sedation with midazolam and etomidate, two attempts were made at internal CV with ICD and two more attempts with external defibrillator which were not effective. Finally, it was during anaesthetic induction with propofol that the patient reverted to sinus rhythm.

Physical examination: BP 110/57 mmHg, HR 160 bpm, T 36.4 oC, baseline SatO2 95%. Patient conscious and oriented, normohydrated and normal colour. Mild tachypnoea. Cardiac auscultation: rhythmic heart sounds without murmurs. Pulmonary auscultation: normoventilation. Abdomen soft, depressible, not painful on palpation, no masses or megaliths palpable. Peristalsis preserved. Jugular ingurgitation, hepatojugular reflux. No oedema in the lower extremities or signs of DVT.

COMPLEMENTARY TESTS
Transthoracic echocardiogram: LV severely dilated (LVEDD 74 mm). Severely depressed LVEF (estimated by Simpson 25%). Akinesia with septal and apical hyperenhancement with an impression of eschar. Atria of normal size. MV: mild calcification of the posterior mitral annulus with mild MR. VAo: trivalva with mild sclerosis of the sigmoid valve without restricting its opening. RV of normal size and function. Mild TR with RV-AD gradient of 25 mmHg. IVC not dilated with normal inspiratory collapse.
Stimulated PAPs of 30 mmHg. No pericardial effusion.
Chest X-ray: cardiomegaly. No signs of acute HF. DAITRC electrodes in normal position.


ECG: wide QRS tachycardia 160 bpm with inferior axis and QS morphology in precordial leads suggestive of VT of apical anterior origin.
Blood tests: cardiac markers: TnI 0.09, myoglobin 160, ProBNP 2400.
Biochemistry: glycaemia 139 mg/dL, creatinine 0.97 mg/dL, Na 135 mEq/l, Cl 98 mEq/l, K 4.1 mEq/l, Ca 9.2 mg/dL. Mg 2 mEq/l. Normal thyroid function with TSH 4.7 and T4 0.88.
Haemogram: leucocytes 8,800/mL with 77 % neutrophils. Hb 13.4 g/dl, platelets 225,000/mcL. Coagulation: normal.

EVOLUTION
After the patient went into sinus rhythm, he was admitted to the Coronary Unit for monitoring and treatment. The case was discussed with the Arrhythmia Unit of our hospital and VT ablation was decided. Using the CARTO 3 navigation system, an anatomical reconstruction and LV voltage mapping was performed, identifying a dense anteroseptal and apical scar with late potentials (LP) at its edges. The pacemapping was very similar to the clinical VT. It is noteworthy after different radiological projections that this area was close to the location of ring 3 of the LV pacing electrode, which was programmed with ring 3-shell pacing. The LPs were abolished by radiofrequency (RF) application. Subsequently, pacing manoeuvres were performed from RV and LV, without tachycardia induction.
Finally, LV bipolar pacing was reprogrammed from ring 1-2 (area furthest from the scar). Based on these data, it was concluded that we were dealing with a possible case of proarrhythmia after cardiac resynchronisation.
The patient was discharged from hospital, stable and asymptomatic with no new arrhythmic events. He is being monitored by the Arrhythmia Unit and the Heart Failure Unit of our Department.

DIAGNOSIS
Sustained monomorphic ventricular tachycardia possibly induced after cardiac resynchronisation therapy in a patient with ischaemic dilated cardiomyopathy with severely depressed systolic function.
Radiofrequency ablation of ischaemic VT substrate.
