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Heart failure (HF) is an epidemic in healthcare worldwide, including Asia. It appears that HF will become more serious in the near future, with the epidemiological transition and ageing of the population. However, in contrast to Western countries, information on HF epidemiology is still limited in Asia, particularly in South Asia. In this review, we will briefly summarize available information regarding the current and future burden of HF in Asia, which indicates the importance of both primary prevention of underlying diseases of HF and secondary prevention, including management of ischaemic HF, HF with preserved EF, and HF in the elderly. [ABSTRACT FROM AUTHOR]

Heart failure (HF) is a global epidemic in health care and a leading cause of mortality and morbidity worldwide. In Asian countries, causes of mortality and morbidity have shifted or have been shifting from infectious diseases and/or nutritional deficiencies to lifestyle-related diseases, such as cardiovascular disease, cancers and diabetes, in conjunction with the transition from developing to developed countries during the past decades (so-called "the epidemiologic transition"). Because the effect of this epidemiologic transition varies among countries, the etiology, prevalence, management and outcomes of HF also differ among the countries. Thus, we need to assemble and comprehensively analyze the available evidence to date for daily HF practice in Asia and to systematically conduct future epidemiologic approaches to establishing appropriate prevention programs against the burden of HF in Asia. This review article will briefly update the epidemiology of HF in Asia.

Myocardial infarction is a common disease and among the leading causes of death in the world. We previously reported association of variants in LGALS2, encoding galectin-2, with myocardial infarction susceptibility in a case-control association study in a Japanese population. Here we identify BRAP (BRCA1-associated protein) as a galectin-2-binding protein. We report an association of SNPs in BRAP with myocardial infarction risk in a large Japanese cohort (P = 3.0 x 10(-18), OR = 1.48, 2,475 cases and 2,778 controls), with replication in additional Japanese and Taiwanese cohorts (P = 4.4 x 10(-6), 862 cases and 1,113 controls and P = 4.7 x 10(-3), 349 cases and 994 controls, respectively). BRAP expression was observed in smooth muscle cells (SMCs) and macrophages in human atherosclerotic lesions. BRAP knockdown by siRNA using cultured coronary endothelial cells suppressed activation of NF-kappaB, a central mediator of inflammation.