Pharmacogenetics in Cardiovascular Disorders: An Update on the Principal Drugs
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Pharmacogenetics in Cardiovascular Disorders: An Update on the Principal Drugs Irene M. Predazzi • Ruggiero Mango • Giuseppe D. Norata • Nicola Di Daniele Domenico Sergi • Francesco Romeo • Giuseppe Novelli
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Ó Springer International Publishing Switzerland 2013
Abstract In the coming years, genomics will impact clinical practice in multiple ways. However, one of the most important applications will be in the determination of the best treatments in personalized medicine. This is, in fact, one of the fields in which genetic variants have already been most successful and useful to clinicians. Here, we briefly review the current state of the art on pharmacogenomics and its applications to modern cardiovascular medicine.
1 Introduction It has been known for centuries that individuals respond differently to environmental stimuli, including drugs. In Classical Greece, Pythagoras already understood how fava beans can be poisonous to certain individuals, causing hemolytic anemia. This observation was the first recognition
I. M. Predazzi (&) Center for Human Genetics research, Vanderbilt University School of Medicine, Vanderbilt University Medical Center, 511 Light Hall, 2215 Garland Avenue, Nashville, TN 37232, USA e-mail: [email protected] I. M. Predazzi R. Mango G. Novelli (&) Department of Biomedicine and Prevention, Tor Vergata University of Rome, Rome, Italy e-mail: [email protected] R. Mango N. Di Daniele D. Sergi F. Romeo Department of System Medicine, Tor Vergata University of Rome, Rome, Italy G. D. Norata Department of Pharmacological Sciences, Universita` degli Studi di Milano, Milan, Italy
of toxin hemolytic anemia and for this reason the rule ‘‘be far from the consumption of fava beans’’ was part of Pythagorean’s doctors’ consultations [1]. In the 1940s, different observations regarding both favism and malaria led to the identification of mutations in the glucose-6-phosphate dehydrogenase encoding gene as the etiologic agent of such hemolytic anemia [1, 2]. In the beginning of the 19th century, Archibald Garrod hypothesized and demonstrated that alkaptonuria is not a disease, rather an alternative course of metabolism, caused by chemical individuality and recurring in interbred families, therefore suggesting a genetic etiology to this phenotype [3]. In 1957, a report in the Journal of the American Medical Association on drug reactions stated that emerging data suggested that genetic traits or enzyme deficiencies could be the underlying cause of the pathogenesis of hyper-susceptibility and hypo-susceptibility to drugs [4]. Two years
G. D. Norata Center for the Study of Atherosclerosis, Bassini Hospital, Cinisello Balsamo, Italy G. D. Norata The Blizard Institute Centre for Diabetes, Barts and The London School of Medicine & Dentistry, Queen Mary, University of London, London, UK G. Novelli FBF Hospital San Pietro, Rome, Italy G. Novelli ANVUR, National Agency for Evaluation of Universities and Research Institute, Rome, Italy
I. M. Predazzi et al.
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