Abstract 18437: Women and Ischemic Heart Disease: Which Role for Katp Channels?

Abstract

Background: In the last decades, scientists have been studying the pathophysiology of ischemic heart disease (IHD) in women. In fact, as it is well known, in women IHD differs in term of pathogenesis, symptoms and prognosis. Different risk factors and mechanisms of disease may be at work in women. Genetic polymorphisms (SNP) for coronary ion channels may be involved in IHD susceptibility. In particular, the SNP rs5215 for Kir6.2 subunit of ATP-dependent potassium (KATP) channels has been proposed as a protective factor in IHD susceptibility, mostly in women. Aim and methods: To confirm the preliminary encouraging results on the protective role SNP rs5215_GG in IHD susceptibility for women, we enrolled 460 consecutive patients (144 women) with an indication to undergo coronary angiography for suspected ischemic heart disease, performing intracoronary functional tests in patients showing anatomically normal arteries to evaluate coronary microvascular function. We analyzed SNPs relative to the Kir6.2 subunit of KATP channels. Results: Among 460 patients, 330 presented with CAD (72 women), 68 with microvascular dysfunction (39 women) and 62 with anatomically and functionally normal coronary arteries (33 women). The SNP rs5215_GG was found to be more frequent in women compared to men (21/144 -14.6%, vs. 36/316 -11.3%; p=0.36). In particular, rs5215_GG was more frequent in ladies with anatomically and functionally normal coronary arteries compared with women presenting CAD (9/33 -27.2% vs. 7/72 -9.7%; p=0.037), whereas there was no difference between men in normal and CAD groups. Discussion and conclusion: Our data validate the hypothesis that rs5215_GG could reduce susceptibility to IHD in women, since it is more frequent in ladies presenting anatomically and functionally normal coronary arteries. The results suggest that KATP channels with rs5215_GG could be protective against IHD. Our data endorse the prospect of associations between SNP encoding coronary ion channels and IHD, validating the idea that ion channels play in coronary homeostasis and that their polymorphisms act in IHD genesis.