methodologically inaccurate studies, even if their biased results are replicated in different settings and by different authors, should not be the driving force in conducting randomized trials. The scientific evidence on the potential beneficial effects in new indications of existing drugs will need to be more carefully assessed before embarking on long and expensive unsubstantiated trials. Abbreviations: CABG coronary artery bypass surgery CHD coronary heart disease COPD chronic obstructive pulmonary disease GRPD General Research Practice Database HRT hormone replacement therapy ICS inhaled corticosteroids LABA long-acting beta(2)-agonist PTCA percutaneous transluminal coronary #selleck inhibitor keyword# angioplasty RCT randomized controlled trial WHI Women’s Health Initiative Footnotes
Conflict of interest: No potential conflict of interest relevant to this article was reported.
Sudden cardiac death Inhibitors,research,lifescience,medical caused by a ventricular arrhythmia is a disastrous event, especially when it occurs in young individuals. Among the five major arrhythmogenic Inhibitors,research,lifescience,medical disorders occurring in the absence of structural heart diseases is catecholaminergic polymorphic ventricular tachycardia (CPVT), which is a highly lethal form of inherited arrhythmogenic disease characterized by adrenergically mediated polymorphic ventricular tachycardia.1–4 In response to physical activity or emotional stress, this disease is characterized by episodes of syncope, seizures, or sudden death.1,2 CPVT was first described as a case report by Reid et Inhibitors,research,lifescience,medical al.5 who reported on a bidirectional ventricular tachycardia triggered by physical effort
and emotional stress in a 6-year-old girl (who survived a cardiac arrest) with no evidence of any structural heart disease. Later on, in 1978 and 1995, Coumel et al.6 and Leenhardt et al.7 reported a series of cases in familial as well Inhibitors,research,lifescience,medical as in sporadic forms of the arrhythmia and introduced the term catecholaminergic polymorphic ventricular tachycardia (CPVT) to refer to a disease characterized by adrenergically mediated bidirectional and/or polymorphic 3-mercaptopyruvate sulfurtransferase ventricular tachycardia in the absence of cardiac pathology. In 2001, Priori et al.8 and Lahat et al.9 identified mutations in the cardiac ryanodine receptor (RyR2) and cardiac calsequestrin (CASQ2) genes, respectively, underlying autosomal dominant and autosomal recessive forms of the disease. RyR2 is a cardiac Ca2+ release channel located on the sarcoplasmic reticulum (SR) membrane and has a key role in the process of calcium-induced calcium release (CICR) during the excitation–contraction (E–C) coupling.10,11 CASQ2 is a high-capacity, low-affinity Ca2+-binding protein, operating as a major Ca2+-buffering factor, and together with RyR2 forms the SR Ca2+ release unit.