Abstract <p>Abdominal aortic aneurysm (AAA) is often associated with vascular calcification, the calcium-phosphate crystal deposition in the aortic wall, which could impact aneurysm progression and/or stability. Tissue-nonspecific alkaline phosphatase (TNAP) hydrolyzes pyrophosphate—a natural inhibitor of calcification—thereby promoting calcium deposition. This study analyzes phosphatase activity and pyrophosphate dynamics in the plasma of AAA patients, randomly selected from the whole VIVA cohort, including controls (<i>n</i> = 48, aortic diameter in &lt; 30&#xa0;mm) and small AAA patients (<i>n</i> = 96, aortic diameter 30–55&#xa0;mm), which were stratified by growth rate (low &lt; 2&#xa0;mm/year or high &gt; 2&#xa0;mm/year, <i>n</i> = 48 in each group), initially adjusted by aortic diameter. The phosphatase activity was assessed at physiological (7.4) and optimal (10.5) pH levels. Phosphatase activity was significantly higher in AAA patients at physiological pH, a pattern absent at optimal pH, suggesting disease-specific alterations. Small AAA patients showed notably higher phosphatase activity and pyrophosphate hydrolysis than controls at physiological pH. An inverse correlation was also observed between phosphatase activity and aortic growth rate.</p> Key messages <p><UnorderedList Mark="Bullet"> <ItemContent> <p>Increased alkaline phosphatase activity was detected in heparin-plasma samples from patients with abdominal aortic aneurysm at physiological pH (7.4), but not under optimal experimental conditions (pH 10.5), suggesting a disease-related effect that may reflect processes occurring in vivo.</p> </ItemContent> <ItemContent> <p>Concentrations of tissue-nonspecific alkaline phosphatase in heparin-plasma samples remained unchanged, despite increased hydrolysis of pyrophosphate, a key inhibitor of vascular calcification.</p> </ItemContent> <ItemContent> <p>Pyrophosphate hydrolysis in heparin-plasma samples correlated inversely with aortic growth rate in abdominal aortic aneurysm patients.</p> </ItemContent> </UnorderedList></p>

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Inverse correlation between plasma pyrophosphate hydrolysis and early growth of abdominal aortic aneurysm: a pilot study

  • Ricardo Villa-Bellosta,
  • Jes S. Lindholt,
  • Jose Luis Martin-Ventura

摘要

Abstract

Abdominal aortic aneurysm (AAA) is often associated with vascular calcification, the calcium-phosphate crystal deposition in the aortic wall, which could impact aneurysm progression and/or stability. Tissue-nonspecific alkaline phosphatase (TNAP) hydrolyzes pyrophosphate—a natural inhibitor of calcification—thereby promoting calcium deposition. This study analyzes phosphatase activity and pyrophosphate dynamics in the plasma of AAA patients, randomly selected from the whole VIVA cohort, including controls (n = 48, aortic diameter in < 30 mm) and small AAA patients (n = 96, aortic diameter 30–55 mm), which were stratified by growth rate (low < 2 mm/year or high > 2 mm/year, n = 48 in each group), initially adjusted by aortic diameter. The phosphatase activity was assessed at physiological (7.4) and optimal (10.5) pH levels. Phosphatase activity was significantly higher in AAA patients at physiological pH, a pattern absent at optimal pH, suggesting disease-specific alterations. Small AAA patients showed notably higher phosphatase activity and pyrophosphate hydrolysis than controls at physiological pH. An inverse correlation was also observed between phosphatase activity and aortic growth rate.

Key messages

Increased alkaline phosphatase activity was detected in heparin-plasma samples from patients with abdominal aortic aneurysm at physiological pH (7.4), but not under optimal experimental conditions (pH 10.5), suggesting a disease-related effect that may reflect processes occurring in vivo.

Concentrations of tissue-nonspecific alkaline phosphatase in heparin-plasma samples remained unchanged, despite increased hydrolysis of pyrophosphate, a key inhibitor of vascular calcification.

Pyrophosphate hydrolysis in heparin-plasma samples correlated inversely with aortic growth rate in abdominal aortic aneurysm patients.