Acquired Carotid-Jugular Fistula Secondary to a Pseudoaneurysm Following Carotid Endarterectomy.

Acquired arteriovenous fistulas involving the carotid artery are most frequently the result of trauma and iatrogenic causes such as central venous catheterisation. Occasionally, they may develop spontaneously due to erosion of an aneurysm into an adjacent vein. We report a rare case of an acquired carotid-jugular fistula secondary to a pseudoaneurysm that occurred four months following carotid endarterectomy.

Alternative access - Iliac artery angioplasty performed via left arm brachiocephalic fistula.

The majority of peripheral endovascular interventions are performed with access through the groin, followed by brachial and radial artery approaches. We describe a unique case of successful iliac artery endovascular intervention, performed via a left upper limb brachiocephalic fistula access site.

Proteomics of ischemia and reperfusion injuries in rabbit myocardium with and without intervention by an oxygen-free radical scavenger.

A brief period of ischemia followed by timely reperfusion may lead to prolonged, yet reversible, contractile dysfunction (myocardial stunning). Damage to the myocardium occurs not only during ischemia, but also during reperfusion, where a massive release of oxygen-free radicals (OFR) occurs. We have previously utilized 2-DE and MS to define 57 protein spot changes during brief ischemia/reperfusion (15 min ischemia, 60 min reperfusion; 15I/60R) injury in a rabbit model (White, M.

Modifications of myosin-regulatory light chain correlate with function of stunned myocardium.

The precise molecular basis for myocardial stunning remains unresolved, but protein damage within the myofibril is a likely mechanism. We used two-dimensional gel electrophoresis (2-DE) and mass spectrometry (MS) to identify protein modifications in stunned myocardium. In isolated, perfused rabbit hearts, low-flow ischemia (1 ml/min) and reperfusion resulted in impaired left-ventricular function (rate-pressure product (RPP) after 15-min ischemia: 65 +/- 5% pre-ischemia).

Duration of ischaemia determines matrix metalloproteinase-2 activation in the reperfused rabbit heart.

It has been hypothesised that activation of matrix metalloproteinase-2 (MMP-2) contributes to reversible myocardial dysfunction (stunning) following short-term ischaemia and reperfusion. Gelatin zymography was used to measure release of both pro-MMP-2 (72 kDa) and MMP-2 (62 kDa), into the coronary effluent from isolated, perfused rabbit hearts during 90 min aerobic perfusion (control), or low-flow ischaemia (15 or 60 min at 1 mL/min), followed by 60 min reperfusion. In controls, pro-MMP-2 was detected in the coronary effluent throughout the first 30 min of aerobic perfusion, but MMP-2 was not detected.