In spite of the available clinical and electrocardiographic criteria for the differential diagnosis of wide QRS complex tachycardias, distinguishing orthodromic supraventricular tachycardias is still a challenge. We present a case of a 63-year old patient admitted in our clinic after experiencing two episodes of syncope. Echocardiography showed left ventricular hypertrophy, grade 1 diastolic dysfunction and left atrial enlargement. A Holter monitoring revealed episodes of atrial fibrillation and paroxysmal narrow QRS tachycardia alternating with wide QRS tachycardia (170-180 bpm). During an electrophysiology study we induced self-limiting orthodromic supraventricular tachycardias with narrow and left bundle branch block patterns. Retrograde mapping near the mitral annulus identified a concealed accessory posteroseptal by-pass tract which was successfully ablated. After the procedure the patient developed atrial flutter and atrial fibrillation with rapid ventricular response (196 beats per minute) with a 3.9 s post-tachycardia pause. The patient underwent implantation of a cardiac pacemaker which allowed us to start antiarrhythmic treatment with amiodarone. This case shows that occult accessory posteroseptal by-pass tracts can have a late-onset presentation in a 63-year old male and explains why latent rhythm disturbances require a step-by-step medical approach.

Brugada syndrome can induce malignant ventricular arrhythmias in the absence of structural heart disease. The hallmark of the condition is the ''coved'' (type I) or ''saddle-back'' (types II and III) ST segment elevation in the right precordial leads. The definite diagnosis requires the documentation of the type I morphology. The electrocardiographic pattern is often dynamic, but it can be unmasked by sodium channel blockers such as flecainide. We report the case of a 33-year old male, with family history significant for sudden cardiac death, who underwent successful cardio-pulmonary resuscitation for ventricular fibrillation-associated cardiac arrest. The 12 lead electrocardiogram performed after the resuscitation maneuvers showed intermittent type 1 Brugada pattern. General physical examination and routine laboratory evaluation were unremarkable. A repeated electrocardiogram revealed sinus tachycardia with right bundle branch block. We performed a flecainide challenge test which reproduced the initial coved-type ST segment elevation in V1 and V2. We decided to implant a ventricular single chamber cardioverter-defibrillator with one therapeutical window for ventricular fibrillation (at 300 ms), high energy shocks without antitachycardia pacing. The device was successful in preventing another episode of ventricular fibrillation just 2 days after the procedure. Implantable cardioverter-defibrillators are the most effective secondary prophylaxis therapeutic options for individuals with Brugada Syndrome, but they subject the patient to complications related to device implantation and inappropriate shocks.