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More than 90% of sudden cardiac deaths (SCD) occur in patients with a known or previously unrecognised pre-existing coronary artery disease (CAD) or cardiomyopathy. It has become evident that SCD occurs, with sufficient frequency, in patients with an apparently normal heart, and ventricular fibrillation (VF) may represent the first clinical sign of structural heart disease that becomes manifest, only several years later, among survivors. Different causes of SCD have been documented, mainly by genetic screening and a more accurate clinical evaluation of the group of patients suffering from so-called idiopathic VF (IVF) [1–26]. Brugada syndrome [1, 5, 10, 14–16, 21–25] has been clearly shown to be one of the most frequent causes of SCD in this context, and should be differentiated from other clinical conditions or cardiac diseases [7, 13, 19, 20, 22, 26]. The purpose of the present article is: (1) to clarify the ionic alterations and electrophysiological mechanisms, underlying Brugada syndrome; (2) to verify the importance of triggering factors detected by ECG and clinical events; (3) discuss the long-term outcomes of Brugada syndrome patients and their family members.

Atrial fibrillation (AF) in both the paroxysmal and persistent atrial forms has been documented both in normal hearts without signs of demonstrable cardiac disease [1–67] and, since 1990, also in some professional and competitive athletes, by Furlanello et al. [4–17, 68–73], Maron and Mitchell [11], Fenici et al. [41] Zeppilli [42], and Naccarella and Brachetti [20, 67]. A useful classification from the diagnostic and therapeutic points of view is the following: 1. Lone vagal AF associated with severe sinus bradycardia and cardiac pauses [19,20,29,30,33–38] 2. Lone sympathetic AF induced only by strenuous physical activity or exercise test or psychological stress. [24,36–38] 3. A mixture of 1 and 2 [19,20,24] 4. AF associated with supraventricular tachycardia (RSVT) [20–27] 5. AF associated with Wolff-Parkinson-Write (WPW) syndrome or cardiac pre-excitation syndromes [21–27,32] 6. “Familial ”lone AF [29–31,43–49]