HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
Male, 72 years old. No known drug allergies. No toxic habits. Arterial hypertension of 10 years of evolution, in treatment with bisoprolol and enalapril. Altered basal glycaemia of 2 years of evolution, on dietary treatment. No known cardiological history. No other medical or surgical history of interest. Home treatment: bisoprolol 5 mg (two tablets every 24 h); ramipril 5 mg (1-0-0).

Present illness
He presented to his health centre with nausea and general malaise of two hours' duration. No palpitations or chest pain. No syncope. No evidence of heart failure. During his stay at the health centre, frequent episodes of incessant wide QRS tachycardia with rapid rates (200 bpm) were recorded on the monitor and he was transferred to hospital.

Physical examination
Blood pressure (BP) 120/70 mmHG, heart rate (HR) 80 bpm, oxygen saturation 100%. Good general condition. Normal skin and mucous membrane colouring. No jugular plethora. Cardiac auscultation: rhythmic heart tones, no murmurs. Pulmonary auscultation: preserved vesicular murmur.

Abdominal examination: soft, depressible, no megaliths, no pain, preserved peristaltic sounds. Extremities: no oedema, with preserved peripheral pulses.


COMPLEMENTARY TESTS
Baseline electrocardiogram (ECG): atrial fibrillation with controlled ventricular response. QRS of 120 ms, intraventricular conduction disorders. No signs of acute ischaemia. Presence of frequent ventricular extrasystoles (VE) with right ventricular outflow tract (RVOT) morphology. Electrocardiogram during tachycardia: wide QRS tachycardia, with morphology of complete left bundle branch block, left inferior axis, cycle 260 ms. Regular R-R. Prior to the onset of tachycardia we observed frequent right ventricular outflow tract extrasystoles with a different morphology to that of the tachycardia (R more prominent and positive in III). Laboratory tests on admission: haemoglobin 15.9 g/dl, leucocytes 5.20 10^3/μl, platelets 113.0 10^3/μl. Prothrombin time (PT) s 14.4. Quick's index 65%. INR 1.33. APTT (T. cephalin) s 47.1. Glucose 93 mg/dl, urea 22.0 mg/dl, creatinine 0.95 mg/dl, uric acid 5.1 mg/dl, albumin 4.3 g/dl, total protein 7.0 g/dl. Total cholesterol 148 mg/dl, HDL cholesterol 34.5 mg/dl, non-HDL cholesterol 113.5 mg/dl, LDL cholesterol 102.9 mg/dl, VLDL cholesterol 10.6 mg/dl, triglycerides 53.0 mg/dl, sodium 136 mm/l, potassium 4.0 mm/l, phosphorus 2.7 mg/dl, total bilirubin 0.98 mg/dl. GPT (ALT) 28.4 U/l, GOT (AST) 35.7 U/l, gamma GT 34.5 U/l, alkaline phosphatase 53.0 U/l, LDH 221.5 U/l, creatine kinase 288 U/l, glycosylated haemoglobin A1c (DCCT) 6.0%. Thyroid stimulating hormone 0.310 mIU/l, free T3 - free triiodothyronine 2.54 pg/ml, free T4 - free thyroxine 0.84 ng/dl. Myocardial damage markers (troponin I and CK-MB) were normal serially x 3. Chest X-ray: normal. Cardiothoracic index (CTI) within normal. Transthoracic echocardiogram (TTE) on admission: non-dilated left ventricle (LV) with moderate concentric hypertrophy. Moderate-severe ventricular dysfunction (LVEF 35% by Simpson biplane), global hypokinesia with worse anterior contractility. Slightly dilated left atrium. Structurally normal mitral valve with mild insufficiency. Aortic valve trivalve, sclerotic, normofunctioning. Normal tricuspid valve. Non-dilated right ventricle (RV) with good systolic function. No pericardial effusion. Transthoracic echocardiogram at one week: non-dilated LV with moderate concentric hypertrophy. Global systolic function preserved without contractility alterations. LVEF by Simpson BP 55%. Rest unchanged with respect to previous study. Coronary angiography: left vascular tree without lesions. Dominant right coronary artery (RCA), with lesion of doubtful significance in the middle third. After intravascular ultrasound (IVUS), 70% stenosis was found. Revascularisation: right coronary: direct drug-eluting stent implantation (Resolute Onix 4 x 12 mm) in the middle third. Good final angiographic result. Electrophysiological study (EEF): with right femoral venous access. There is evidence of atrial fibrillation (AF) with EV with left bundle branch block morphology (LBBB) ID axis with other advanced complexes and wide QRS presenting LBBB with axis II. A pathological HV of 80 msg is evident, which is difficult to maintain stable. High-dose aleudrine increased atrioventricular (AV) conduction to a HR of 120-130 without aberrant conduction. After TEE ruled out thrombi in the left atrium (LA), electrical cardioversion (ECV) was performed with a switch to SR with 200 J in biphasic mode. Aleudrine induced ventricular tachycardia in a fairly reproducible manner (periods without AV ratio 1x1, with AV dissociation with morphology equal to the clinical one [LBBB and with transition in V4-V5]), well tolerated and with a cycle of 260 msg. In the case of suspected branch-branch ventricular tachycardia (BRVT), attempts are made to obtain stable His, which is impossible using Josephson tetra, His tetra and deflectable decapolar. Neither is it possible to analyse pacing from the RA because of the large pacing artefact that prevents verification of the QRS morphology. However, we concluded that it was RRVT with other criteria: return cycle from RV apex of 0 and electrogram of right ventricular apex early on the onset of the QRS. Right bundle branch ablation was performed using a conventional 4 mm FJ catheter, which was achieved after three applications. The right bundle branch was found not to lead for 30 minutes. Subsequently, a DDDR Boston bicameral pacemaker was implanted.

CLINICAL EVOLUTION
With the diagnosis of probable ventricular tachycardia, treatment was started with beta-blockers and amiodarone, and he was admitted to the cardiology ward with telemetry. Forty-eight hours after admission, during his stay on the ward, a transthoracic echocardiogram was performed, showing the presence of severe global LV dysfunction, with worse contractility in the anterior territory, which recovered completely one week after admission. Coronary angiography was performed, which revealed an intermediate lesion in the mid-right coronary artery. Revascularisation with a drug-eluting stent was considered. Given the clinical presentation (no chest pain, no signs of acute ischaemia in the electrocardiogram and no elevation of myocardial damage markers), the presence of severe global ventricular dysfunction that recovered early after control of the arrhythmia was considered as dysfunction secondary to tachycardiomyopathy. Finally, an electrophysiological study was performed which documented, firstly, that it was a ventricular tachycardia (existence of VA dissociation) and subsequently, by means of manoeuvres, that it was a branch-branch ventricular tachycardia (electrogram of the right ventricular apex early on the start of the QRS) and, another fundamental fact, the return cycle was very short (10 ms) after the tachycardia was triggered from the RV apex. Right bundle branch ablation and DDD pacemaker implantation was performed (due to HV lengthening up to 100 ms). Once discharged, the patient's evolution has been excellent. No arrhythmic recurrences. Ejection fraction remained preserved. In addition, he was referred to neurology consultations to rule out the possibility of neuromuscular disease (due to its association with this type of tachycardia in patients without heart disease), and an electromyogram and genetic study were performed, which ruled out this possibility.

DIAGNOSIS
Branch-branch ventricular tachycardia (BRVT).
Tachycardiomyopathy. Preserved left ventricular function at discharge.
Intermediate lesion in the middle DC. Revascularisation by drug-eluting stent implantation.
Right bundle branch ablation. Implantation of DDDR Boston pacemaker.
