Homocysteine and coronary microcirculation: Is it a microvasculopathic agent?

Abstract

Recently, we read the paper of Yamashita et al. [1] with a great interest. In their study, they evaluated the effects of experimental hyperhomocysteinemia (oral methionine load) on coronary flow velocity reserve (CFR) in healthy individuals and the impact of addition of oral vitamin C to oral methionine load. They have measured CFR before and 4 h after administration of placebo, oral methionine and oral methionine+vitamin C. Experimentally induced hyperhomocysteinemia by oral methionine load has been reported to be associated with impaired CFR and this impairment has been shown to be reversed with vitamin C administration. Previously, Tawakol et al. [2] have investigated the effect of acute hyperhomocysteinemia on coronary microvascular dilator function and detected an impaired microvascular dilator function in subjects with acute hyperhomocysteinemia as a result of decreased nitric oxide bioavailability. In addition Coppola et al. [3] have shown that acute hyperhomocysteinaemia reduces CFR and pretreatment with antioxidant vitamin E and ascorbic acid has been detected to prevent the effects of hyperhomocysteinaemia, suggesting an oxidative mechanism. Besides, Ascione et al. [4] have also found a significant association between acute hyperhomocysteinemia and reduced CFR. All these studies have reported a significant negative correlation between postload homocysteine levels and CFR. CFR represents the regulatory ability of coronary microcirculation to increase its blood flow during hyperemic