Matrix Gla protein (MGP) is an extracellular matrix protein with wide tissue distribution. It has been demonstrated that the expression of MGP is detected not only in the normal blood vessels but also calcified atherosclerotic plaques, and that MGP deficient mice develop extensive arterial calcification. MGP is thought to be a regulator of vascular calcification. A recent clinical study demonstrates the association between polymorphisms of the MGP gene and increased risk of myocardial infarction. However, there are no reports of the relationship between serum MGP levels and coronary artery calcification (CAC). We evaluated the severity of CAC using electron-beam computed tomography (EBCT), and measured serum MGP levels by enzyme-linked immunosorbent assay in 115 subjects with suspected coronary artery disease. CAC scores were correlated with traditional risk factors, such as age, gender, hyper-tension, diabetes, hyperlipidemia and smoking. The serum MGP levels were lower in patients with CAC than in those without CAC (p<0.001). As the severity of CAC increased, there was a significant decrease in serum MGP levels. Serum MGP levels (U/L) were 116.7 +/- 20.3, 104.9 +/- 19.2, 95.2 +/- 15.2 and 82.2 +/- 19.7, (medians 115.5, 105.0, 94.8, and 81.9) for the subjects with normal (CAC score=0), mild (CAC score=1 to 99), moderate (CAC score=100 to 400), and severe (CAC score >400) coronary calcification, respectively. We found that serum MGP levels are inversely correlated with the severity of CAC. These data suggest a possible role for MGP in the development of vascular calcification.

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A liver transplant was performed in a woman, aged 41 years, with advanced primary biliary cirrhosis. Prior to surgery, her investigations included a contrast-enhanced computed tomography (CT) scan of the abdomen. Good views were obtained of the splenic artery and no abnormalities were detected (Fig. 1). On the sixth day after surgery, she developed abdominal pain and became hypotensive. A repeat CT scan showed a splenic artery aneurysm, 1.8 cm in diameter, in the mid-portion of the splenic artery (Fig. 2). The aneurysm was surrounded by tissue with a density consistent with a blood clot (arrow). Angiography was performed and the aneurysm was treated by transcatheter coil embolization. Subsequent CT scans after 3 and 6 months showed that the size of the aneurysm was stable.Incidental splenic artery aneurysms can be found at angiography in approximately 1% of patients. Most of these aneurysms were located in the middle third (20%) and distal third (75%) of the splenic artery. Aneurysms are more common in women than in men, particularly those women who have had multiple pregnancies. The prevalence of splenic artery aneurysms in patients with cirrhosis varies widely in different studies but may be approximately 10%. Aneurysms are more common in patients with wide splenic arteries, suggesting a relationship between aneurysm formation and arterial flow. The above case records the development of a splenic artery aneurysm after liver transplantation. Seven similar cases have been reported previously, three with aneurysm rupture within 8 days of transplantation and four who developed aneurysms after months or years. Although reasons for the development of splenic artery aneurysms after transplantation remain unclear, one possible factor is an increase in splenic artery blood flow associated with a reduction in portal vein resistance. In general, the risk of rupture of splenic artery aneurysms is low but it is uncertain whether this also applies to aneurysms in the setting of cirrhosis and liver transplantation.

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