School of Life Sciences， Faculty of Sciences， Queensland University of Technology， 2 George Street， GPO Box 2434， Brisbane， Queensland 4001， Australia.

    Current concepts in drug therapy for cardiovascular diseases often attempt drug treatment of large patient populations as only one group， irrespective of the potential for individual， genetically based differences in drug response. It is well recognized that most cardiovascular medications exhibit wide inter-patient variability in their efficacy and toxicity. Pharmacogenetics is the study of the influence of genetic factors in the individual variation in drug response， whereas pharmacogenomics is a more global definition and entails the study of the entire spectrum (network) of genes and their contribution to variability in drug efficacy and toxicity using genome-wide approaches Pharmacogenomic analysis can identify disease susceptibility genes representing potential new drug targets and focus effective therapy on smaller patient subpopulations which although demonstrating the same disease phenotype are characterized by distinct genetic profiles. 

    Evidence is accumulating to indicate that responses to cardiovascular drugs are at least partly under genetic control. Pharmacogenetics mostly relies on associations between a specific genetic marker like single nucleotide polymorphisms (SNPs)， either alone or arranged in a specific linear order on a certain chromosomal region (haplotypes)， and a particular response to drugs. Numerous genes， in particular those encoding PhasA I and II drug metabolizing enzymes (e.g. CYPs and UGTs)， drug transporters (e.g. MDR1 and MRPs) and drug targets (e.g. ADRB1-3)， have been identified to play a role in response to many cardiovascular drugs.  Recently， for instance， associations have been reported between specific alleles of the CYP2C9 gene and the blood clotting response to warfarin. Several SNPs in NR1I2 (PXR) gene leads to altered clearance of nifedipine.

    Ethnicity is an important variable contributing to inter-individual variability in response to cardiovascular drugs. The frequency of functional SNPs varies widely between ethnic groups and the Asian population is no exception to this. However， most of the current literature is concerned with polymorphisms in Caucasians and African-Americans， whereas the data in Asian populations are scant. In recent years， we have investigated the polymorphisms in a number of genes encoding Phase I and II drug metabolizing enzymes including CYP1A1， CYP3A4， CYP3A5， GSTM1， GSTP1， NAT2， NR1I2 (PXR)， UGT1A1 and TPMT and MDR1 in Chinese population. Significant differences in the frequencies of common alleles encoding these proteins have been observed between Chinese and other ethnic groups. As such， dose requirements of certain cardiovascular drugs may not be optimal for our population and a second look at the factors responsible for this difference is necessary.

    Thus far， most pharmacogenetic studies have been limited to a priori selected candidate genes due to restricted genotyping and analytical capacities. Thanks to the large number of SNPs now available in the public domain through the SNP Consortium and the newly developed technologies (high throughput genotyping， bioinformatics software)， it is now possible to interrogate more than 200，000 SNPs distributed over the entire human genome. All of this will lead to novel approaches in drug discovery， individualized dosing of cardiovascular medications， and new insights into cardiovascular disease susceptibility and prevention.