TY - CHAP
T1 - Sex and gender aspects in antiarrhythmic therapy
AU - Kurokawa, Junko
AU - Kodama, Masami
AU - Furukawa, Tetsushi
AU - Clancy, Colleen E
PY - 2012
Y1 - 2012
N2 - Although cardiac arrhythmia had long been considered a predominantly male syndrome, it is now clear that arrhythmia is also a primary cause of mortality in women. Notably, the manifestation of specific arrhythmia syndromes appears to be gender specific. In particular, female sex is an independent risk factor for development of torsade de pointes (TdP) arrhythmias not only in congenital long QT syndromes but also in acquired long QT syndromes which occur as adverse effects of existing drugs. Males, on the other hand, are more likely to develop Brugada syndrome. Recent clinical and experimental studies suggest that these differences may stem from intrinsic sex differences in cardiac tissue. These include fundamental electrical differences resulting from variable ion channel expression and diverse sex hormonal regulation via long-term genomic and acute nongenomic pathways, and sex differences in drug responses and metabolisms. Undoubtedly, determining the effect of gender on cardiac function will be difficult and require sophisticated methodologies. However, gender differences underlying predilection to distinct arrhythmia syndromes must be revealed so that new therapeutic strategies that take gender into account can be applied to at-risk patients.
AB - Although cardiac arrhythmia had long been considered a predominantly male syndrome, it is now clear that arrhythmia is also a primary cause of mortality in women. Notably, the manifestation of specific arrhythmia syndromes appears to be gender specific. In particular, female sex is an independent risk factor for development of torsade de pointes (TdP) arrhythmias not only in congenital long QT syndromes but also in acquired long QT syndromes which occur as adverse effects of existing drugs. Males, on the other hand, are more likely to develop Brugada syndrome. Recent clinical and experimental studies suggest that these differences may stem from intrinsic sex differences in cardiac tissue. These include fundamental electrical differences resulting from variable ion channel expression and diverse sex hormonal regulation via long-term genomic and acute nongenomic pathways, and sex differences in drug responses and metabolisms. Undoubtedly, determining the effect of gender on cardiac function will be difficult and require sophisticated methodologies. However, gender differences underlying predilection to distinct arrhythmia syndromes must be revealed so that new therapeutic strategies that take gender into account can be applied to at-risk patients.
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U2 - 10.1007/978-3-642-30726-3_12
DO - 10.1007/978-3-642-30726-3_12
M3 - Chapter
C2 - 23027454
AN - SCOPUS:84868327387
SN - 9783642307256
VL - 214
T3 - Handbook of Experimental Pharmacology
SP - 237
EP - 263
BT - Handbook of Experimental Pharmacology
ER -