Rupture of an Abdominal Aortic Aneurysm in a Young Man with Marfan Syndrome.

Abdominal aortic aneurysms (AAAs) are very rare in Marfan syndrome. We present a case with a young nonsmoking and normotensive male with Marfan syndrome, who developed an infrarenal AAA that presented with rupture to the retroperitoneal cavity causing life-threatening bleeding shock. The patient had acute aortic surgery and survived. Five months before this incident, the patient had uneventful elective aortic root replacement (ad modum David) due to an enlarged aortic root. At that time, his abdominal aorta was assessed with a routine ultrasound scan that showed a normal-sized abdominal aorta. This documents that the aneurysm had evolved very rapidly despite young age and absence of risk factors.

A symptomatic pseudoaneurysm caused by stent fracture in the external iliac artery.

Pseudoaneurysms, as a result of endovascular stent fracture, are a rare yet important vascular surgery complication. A 64-year-old man presented with a painful mass in the left groin with accompanying critical ischemia of the left leg. Diagnostic angiography revealed a pseudoaneurysm caused by stent fracture in the left external iliac artery. The patient was treated with embolization of the left external iliac artery and ultimately above-the-knee amputation. Awareness of this uncommon complication is important due to its potential risk of severe disability.

Different mechanisms involved in liraglutide and glucagon-like peptide-1 vasodilatation in rat mesenteric small arteries.

BACKGROUND AND PURPOSE: Glucagon-like peptide-1 (GLP-1) is an incretin hormone that regulates insulin biosynthesis and secretion in a glucose-dependent manner and has been reported to induce vasodilatation. Here, we examined the possible vasorelaxant effect of GLP-1 and its underlying mechanisms. EXPERIMENTAL APPROACH: Rat mesenteric arteries (diameter ≈ 200-400 µm) and human s.c. arteries were mounted in microvascular myographs for isometric tension recordings. The effect of GLP-1 on vascular responses was examined under normoglycaemic conditions and at high glucose concentrations. KEY RESULTS: In rat mesenteric arteries and human s.c. arteries without branches, physiological concentrations (1-100 nM) of GLP-1(7-36) and liraglutide failed to cause relaxation or affect contractions evoked by electrical field stimulation. In contrast to GLP-1(7-36), liraglutide induced relaxations antagonized by the GLP-1 receptor antagonist, exendin-(9-39), in branched mesenteric arteries. In contrast to liraglutide, GLP-1 leftward shifted the concentration relaxation curves for bradykinin in s.c. arteries from patients with peripheral arterial disease, an effect resistant to exendin-(9-39). Under normoglycaemic conditions, neither GLP-1 nor liraglutide affected ACh relaxation in rat mesenteric arteries. In arteries exposed to 40 mM glucose, GLP-1, in contrast to liraglutide, potentiated ACh-induced relaxation by a mechanism that was not antagonized by exendin-(9-39). GLP-1 decreased superoxide levels measured with dihydroethidium in rat mesenteric arteries exposed to 40 mM glucose. CONCLUSIONS AND IMPLICATIONS: GLP-1 receptors are involved in the liraglutide-induced relaxation of branched arteries, under normoglycaemic conditions, while GLP-1 inhibition of vascular superoxide levels contributes to GLP-1 receptor-independent potentiation of endothelium-dependent vasodilatation in hyperglycaemia.

The "human visceral homunculus" to pain evoked in the oesophagus, stomach, duodenum and sigmoid colon.

The oesophagus, stomach, duodenum and sigmoid colon were electrically stimulated in 12 healthy volunteers with a thin nasal endoscope. The painful cortical evoked potentials (EPs) were recorded from 64 surface electrodes. The early EPs with latencies < 200 ms were studied and the corresponding dipole sources were calculated. The electrical current intensities needed to evoke pain were highest in the stomach and duodenum, compared to the other segments (F = 7.8; P < 0.001; post hoc analysis P < 0.05). The EP latencies after stimulation of the stomach and sigmoid colon were shorter compared with those to stimulation of the oesophagus and duodenum (all P values < 0.001). The EP amplitudes were higher to oesophagus stimulation (all P values < 0.001 except for the early positivity). The potential fields obtained after stimulation of the most distal segments (duodenum and sigmoid colon) were in general distributed more posteriorly compared to those recorded in the more proximal regions. The EP topographies to stimulation of all gut tracts were explained by a bilateral source in the second somatosensory (SII) area, by a dipole in the anterior cingulate cortex (ACC), and by a bilateral generator in the insular cortex. However, the position of the sources significantly changed depending on the stimulated gut tract. Moreover, while the SII and ACC sources were initially activated to oesophagus and stomach stimulation, the ACC and insular activities were the earliest ones after stimulation of the lower gut segments. The findings reflect differences in pathways and brain processing of visceral nociceptive inputs coming from either upper or lower gut and may improve our understanding of the brain-gut axis in health and disease.