HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
The patient is a 65-year-old man with no medical history of interest except for dyslipidaemia controlled by means of hygienic-dietary measures. Non-smoker and moderate drinker. He leads an active life, independent in terms of ADLs.
He reports a clinical history of approximately one month of moderate exertion dyspnoea together with episodes of palpitations and chest pain in the last two weeks. The previous night she had presented incessant palpitations and consulted her primary care physician.
On arrival at the outpatient clinic, an ECG was performed showing a regular tachycardia with wide QRS at 180lpm. The patient was haemodynamically stable with a slight feeling of dizziness.
The patient was transferred to hospital and an amiodarone infusion was started, but was not effective in reverting to sinus rhythm. The patient began to become hypotensive and a CVE at 100J was performed, leaving in SR after shock.
On arrival at the Emergency Department, the patient was stable, somewhat hypotensive, with an unremarkable physical examination, with no signs of HF on examination, and reported to be asymptomatic at that time.

COMPLEMENTARY TESTS
Outpatient ECG: regular tachycardia with wide QRS at 180lpm, BRDHH image with concordance in precordial and inferior axis ECG on arrival at the ED: sinus rhythm at about 65lpm, axis at -30o, BAV 1st degree (PR 280 msg), narrow QRS, abundant VE of different morphologies, some of the same morphology as VT but others of different ventricular focus.
CBC on admission: arterial ABE: PO2 140.0 mmHg [75-95], PCO2 33.0 mmHg [35-45], pH 7.350 [7.350-7.450], bicarbonate (HCO3) 18.2 mmol/l [21-26], lactate 18.0 mg/dl [4.5-19.8 ]. Biochemistry: glucose 181 mg/dl [70-110], urea 59 mg/dl [10-50], creatinine 1.53 mg/dl [.40-1.20], albumin 4.38 g/dl [3.50-5.50], total bilirubin 1.47 mg/dl [0-1.2], GPT 154 U/L [5-41], CK 214 U/L [0-195], troponin T 142 ng/l [0-14], total calcium 9.78 mg/dl [8.40-10.40], sodium 141.0 mmol/l [135-145], potassium 3.94 mmol/l [3.50-5.10], C-reactive protein 0.33 mg/dl [0-.50], HbA1c 5.9%. HRF: haemoglobin 16.6 g/dl [14.1-18], platelets 260 10^3/μL [135-450 ], leucocytes * 13.0 10^3/μL [4.5-11 ] (neutrophils 73.8 %, lymphocytes 18.5 %). Coagulation: prothrombin index 95 % [65-120], INR 1.03, APTT 33.6 sg [25-40], functional fibrinogen 324 mg/dL [200-450].
Enzyme curve: CK 182 U/L, troponin T 157 ng/L.
Other analytical determinations: lipidogram: total cholesterol 206 mg/dL, HDL 61 mg/dL, triglycerides 203 mg/dL. Iron metabolism: iron 93 μg/dl [59-158], ferritin 223 ng/ml [30-400]. Immunological study: ANAs, PR3-ANCA, MPO-ANCA antibodies negative. Normal thyroid hormones: TSH 1.29 μU/ml [0.27-4.20], free T4 14.8 pmol/l [10.3-26.0]. Enzymes: ACE 31 U/L [10-50]. Negative serologies for CMV, enterovirus, parvovirus, HCV, HIV, Trypanosoma cruzi.
Transthoracic echocardiogram: left ventricle not dilated, slightly hypertrophic and with good overall systolic function but at the limit of normality (LVEF 54%). Doubtful hypokinesia in the lower basal segment. No valvulopathies.
Right chambers not dilated and with good function. Mild PHT.
Coronary angio-CT: coronary network without significant lesions
CMR: LV slightly dilated with mildly depressed global function.
Hypokinesia of the basal medial inferior aspect. EF: 50%. In the Stir potentiated sequences an area of oedema was visualised in basal septal segments. In the early enhancement sequences, enhancement was visualised in the segments in which late enhancement was identified. In the late enhancement sequences: intramyocardial enhancement with transmural areas in basal septal segments, subepicardial enhancement in medial lower basal segments and extending with subendocardial enhancement to the inferolateral basal segment.
Electrophysiological study: sustained monomorphic ventricular tachycardia.
Substrate ablation with RDF. ICD implantation is indicated. The patient arrived at the study in sinus rhythm at 55 bpm with first-degree AVB and narrow QRS. The procedure was performed under sedation with propofol and ultiva and with the Navex-precision system. The left ventricle was mapped with the ablation catheter obtaining an anatomy and voltage map showing a single area of low voltage in the lateral area of the mitral annulus, where pacemapping reproduced the morphology of the tachycardia. Induction of clinical VT is attempted but not achieved at baseline. After iv. isoproterenol, clinical VT is induced and RDF is applied to the lateral aspect of the mitral annulus where early potential and good prior pacemapping is obtained.
During application, VT changes morphology and accelerates to a ventricular flutter that requires an electric shock for its termination. It is decided to continue with substrate ablation by administering a corona of lesions around the previous area in the mitral annulus.

EVOLUTION
In the case of the patient in question, given that he had remained stable at all times, showed no signs of heart failure and remained asymptomatic, it was decided to admit him to the ward with telemetry and treatment was started with beta-blockers (bisoprolol 2.5 mg, 1-0-1).
Given that most VTs occur in the context of ischaemic heart disease, it seems reasonable that this was the first possibility to rule out, despite the fact that neither the clinical, analytical nor echocardiographic data corresponded to ischaemic heart disease. As this was a patient with few CVRFs, it was decided to perform a coronary angio-CT scan. This showed a coronary network with no significant lesions.
Therefore, this cause was ruled out as a possible diagnosis.
To complete the study, a cardiac magnetic resonance (CMR) was scheduled.
The findings could be related to myocarditis as a first possibility due to its frequency, but these enhancements are described in other less probable entities, such as sarcoidosis or Chagas disease.
The possibility of sarcoidosis was considered, since the patient had a long RP and AVBs are quite frequent in this entity. This possibility was also ruled out since, although there are few cases of cardiac sarcoidosis without systemic involvement, there were no mediastinal adenopathies, restrictive signs or myocardial thickening to further support this diagnosis.
Acute myocarditis was therefore the first possibility.
During admission, the patient remained in sinus rhythm at all times with HR around 60-75 bpm, with increasingly infrequent VT, but even after a week in hospital, there were still bouts of non-sustained monomorphic VT, self-limited almost daily, with a maximum duration of about 20 seconds, with haemodynamic repercussions in some cases, for which reason amiodarone was associated without reducing the number of daily events.
In view of this situation, it was decided to ablate the VT substrate. In the electrophysiological study, during radiofrequency application, the VT changes morphology and accelerates to a ventricular flutter that requires an electric shock for its termination. It is decided to continue with substrate ablation by administering a lesion corona around the previous area in the mitral annulus. The reproducibility of post-ablation VT was not tested for fear of replaying the ventricular flutter and implantation of a bicameral ICD was indicated.
A couple of days later the ICD was implanted without complications and the patient was discharged.
The patient is currently asymptomatic and is being treated with beta-blockers (bisoprolol 5 mg, 1-0-1). Periodic follow-up is carried out in electrophysiology consultations and control of the device by remote monitoring. So far, 5 months after the episode presented, no arrhythmia requiring ICD discharge has been recorded, with only a few asymptomatic and self-limited episodes of NSTEVM.

DIAGNOSIS
Sustained ventricular tachycardia in the context of probable acute myocarditis.
