Augmented hyperaemia and reduced tissue injury in response to ischaemia in subjects with the 34C > T variant of the AMPD1 gene

• Published in: European heart journal Vol. 28; no. 9; pp. 1085 - 1091
• Main Authors: Riksen, Niels P., Franke, Barbara, Oyen, Wim J.G., Borm, George F., van den Broek, Petra, Boerman, Otto C., Smits, Paul, Rongen, Gerard A.
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01.05.2007; Oxford Publishing Limited (England)
• Subjects: Adult; AMP Deaminase - genetics; Biological and medical sciences; Cardiology. Vascular system; Dipyridamole - pharmacology; Female; Forearm - blood supply; Humans; Hyperemia - genetics; Ligation; Male; Medical sciences; Reperfusion Injury - genetics; Vasodilator Agents - pharmacology; Ischaemia; Adenosine; Scintigraphy; genotype; Blood flow; Radionuclide study; Human; Typing; Injury; AMPD1 genotype; Cardiovascular disease; Genotype; Phlebology; Trauma; Response; Variant; Tissue; Microbiological investigation; Gene; Ischemia; Medical imagery; Genetics; Circulatory system; Lesion; Cardiology

Aims In patients with coronary artery disease, the 34C > T variant of the adenosine mono-phosphate deaminase gene (AMPD1), encoding a dysfunctional protein, predicts improved survival. We hypothesized that in subjects with this variant allele, ischaemia-induced intracellular adenosine formation i...