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Homocysteine impairs coronary microvascular dilator function in humans

Ahmed Tawakol, MD^*,*, Marc A. Forgione, MD, Markus Stuehlinger, MD^||, Nathaniel M. Alpert, MD, John P. Cooke, MD, PhD, FACC^||, Joseph Loscalzo, MD, PhD, FACC, Alan J. Fischman, MD, PhD, Mark A. Creager, MD, FACC and Henry Gewirtz, MD^*

^* Departments of Medicine (Cardiac Unit), Massachusetts General Hospital, Boston, Massachusetts, USA
Department of Radiology and Nuclear Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA
Department of Medicine (Cardiovascular Division), Brigham and Women’s Hospital, Boston, Massachusetts, USA
Department of Medicine, Boston University Medical Center, Boston, Massachusetts, USA
^|| Department of Medicine, Stanford University Medical Center, Stanford, California, USA

View larger version (16K): [in a new window]   Figure 1 (A) Effect of acute hyperhomocysteinemia on the myocardial blood flow (MBF) response to adenosine. This figure depicts MBF at rest and during infusion of low and high dose adenosine, after placebo and during methionine-induced hyperhomocysteinemia (METH). The adenosine dose response curve is significantly impaired during methionine vs. placebo (p < 0.05, ANOVA). (B) Acute hyperhomocysteinemia impairs the coronary microvascular dilator response to adenosine. This figure depicts the MBF response to the low and high doses of adenosine. The coronary microvascular dilator response to low dose adenosine was significantly blunted during METH (p < 0.05). In contrast, the microvascular dilator response to high dose adenosine was unaffected.

View larger version (19K): [in a new window]   Figure 2 (A) Effect of nitric oxide inhibition on the myocardial blood flow (MBF) response to adenosine. This figure depicts the MBF at rest and during low and high dose adenosine infusions, after placebo and during infusion of the nitric oxide synthase inhibitor, NG-monomethyl-l-arginine (l-NMMA). The adenosine dose response curve is significantly impaired during l-NMMA vs. placebo (p < 0.05, analysis of variance [ANOVA]). While nitric oxide inhibition significantly reduced MBF to low-dose adenosine, the MBF response to high dose adenosine was unaffected. (B) Effect of nitric oxide inhibition on the myocardial conductance response to adenosine. This figure depicts the myocardial conductance (G) at rest and during low and high dose adenosine infusions, after placebo and during infusion of the nitric oxide synthase inhibitor, l-NMMA. The adenosine dose response curve is significantly impaired during l-NMMA versus placebo (p < 0.05, ANOVA). Nitric oxide inhibition significantly reduced conductance to both low- and high-dose adenosine.