Unstable carotid plaques exhibit raised matrix metalloproteinase-8 activity.

BACKGROUND: The fibrous cap of atherosclerotic plaques is composed predominantly of type I and III collagen. Unstable carotid plaques are characterized by rupture of their cap, leading to thromboembolism and stroke. The proteolytic mechanisms causing plaque disruption are undefined, but the collagenolytic matrix metalloproteinase (MMP) -1, -8, and -13 may be implicated. The aim of this study was to quantify the concentrations of these collagenases in carotid plaques and to determine their relationship to markers of plaque instability. METHODS AND RESULTS: Atherosclerotic plaques were collected from 159 patients undergoing carotid endarterectomy. The presence and timing of carotid territory symptoms were ascertained. Preoperative embolization was recorded by transcranial Doppler. Each plaque was assessed for histological features of instability. Plaque MMP concentrations were quantified with ELISA. Significantly higher concentrations of active MMP-8 were observed in the plaques of symptomatic patients (20.5 versus 11.4 ng/g; P=0.0002), in plaques of emboli-positive patients (22.7 versus 13.5 ng/g; P=0.0037), and in those plaques showing histological evidence of rupture (20.8 versus 14.7 ng/g; P=0.0036). No differences were seen in the levels of MMP-1 and MMP-13. Immunohistochemistry, in situ hybridization, and colocalization studies confirmed the presence of MMP-8 protein and mRNA within the plaque, which colocalized with macrophages. CONCLUSIONS: These data suggest that the active form of MMP-8 may be partly responsible for degradation of the collagen cap of atherosclerotic plaques. This enzyme represents an attractive target for drug therapy aimed at stabilizing vulnerable plaques.

Elevation in plasma MMP-9 following carotid endarterectomy is associated with particulate cerebral embolisation.

OBJECTIVES: To study plasma MMP-9 levels before and after carotid endarterectomy (CEA). DESIGN: Observational study. METHODS: Pre-operative (morning of surgery) and post-operative (48 h) plasma samples were obtained from 75 consecutive patients undergoing CEA. MMP-9 concentrations were quantified using ELISA. Transcranial Doppler monitoring was performed on each patient to detect particulate embolisation during the dissection phase of the CEA, until the application of carotid clamps. RESULTS: The median post-operative plasma MMP-9 level of emboli-positive patients was significantly higher than their median pre-operative value (14.9 ng/ml vs. 8.8 ng/ml; p=0.038). However, no significant difference was seen in the plasma MMP-9 level of emboli-negative patients (7.7 ng/ml vs. 7.1 ng/ml; p=0.364). A greater rise was seen in the median plasma MMP-9 levels of those patients suffering >2 emboli (from 3.4 to 19.3 ng/ml; p=0.041) than those patients suffering 1 or 2 emboli (from 10.1 to 12.8 ng/ml; p=0.340). CONCLUSIONS: Plasma MMP-9 only rises after CEA in patients with evidence of embolisation. This increase is more pronounced in those with high numbers of emboli. These data suggest that the increase in MMP-9 is due to cerebral damage caused by embolisation.

Laparoscopic reduction of incarcerated Meckel's diverticulum following abdominal hysterectomy.

BACKGROUND: Laparoscopic techniques are increasingly being utilized to diagnose and successfully manage intestinal obstruction. CASE REPORT: We describe a patient who presented with intestinal obstruction following a recent abdominal hysterectomy. The obstruction was caused by entrapment of a segment of small bowel containing a Meckel's diverticulum within a pouch formed by the peritoneal layer following mass closure of the abdominal wound. DISCUSSION: We discuss the literature on the abdominal wound closure technique. The role of laparoscopy in dealing with intestinal obstruction is reviewed briefly. We have also summarized the management of an incidental Meckel's diverticulum found at laparoscopy.