Rapid access carotid endarterectomy can be performed in the hyperacute period without a significant increase in procedural risks.

OBJECTIVES: The highest risk of recurrent stroke after suffering a transient ischaemic attack (TIA) or minor stroke is during the first 7-14 days. Contemporary guidelines recommend that carotid endarterectomy (CEA) should be performed within this time period, but there are concerns regarding (1) how this can be achieved logistically and (2) whether this policy is associated with a significant increase in procedural risks. DESIGN: This is a prospective, consecutive study of delays to surgery and 30-day outcomes in recently symptomatic patients who underwent CEA between 1 October 2008 and 15 June 2010 after the creation of a rapid access TIA service. RESULTS: A total of 109 symptomatic patients underwent CEA, 78% within 14 days of the index event and 90% within 14 days of referral. The median delay to surgery was 9 days from the index event and 4 days from referral. There were no perioperative deaths. Two strokes occurred (one intra-operative and one post-operative) to give a 30-day death/stroke rate of 1.83%. Patients undergoing CEA within 14 days of the index event incurred a death/stroke rate of 2.4% (2/84), increasing to 4.3% in patients undergoing surgery within 7 days (2/47). CONCLUSION: Service reconfigurations can lead to significant reductions in delays to treatment in patients with symptomatic carotid disease. CEA can be performed in the hyperacute period without significantly increasing the operative risk.

A single five minute period of rapid atrial pacing fails to limit infarct size in the in situ rabbit heart.

OBJECTIVE: Rapid pacing has been shown to precondition the dog heart against ischaemic dysrhythmia. The aim of this study was to determine whether rapid pacing could also limit infarct size. METHODS: Rabbits (n = 5) were rapidly paced via the left atrium at 420-480 beats.min-1. Five min of rapid pacing and 10 min of recovery in sinus rhythm were followed by 45 min of regional ischaemia and 120 min of reperfusion. Control rabbits (n = 9) were treated identically without prior rapid pacing. Infarct size was determined in both groups using tetrazolium and expressed as a percentage of the area at risk demarcated by fluorescent microspheres. In a separate series of experiments, rapidly paced Langendorff perfused rabbit hearts (n = 9) were used to determine coronary flow under perfusion conditions designed to simulate the in vivo situation during rapid pacing. RESULTS: Rapid pacing caused a fall in systolic pressure from 91.4(SEM 4.5) to 47.0(5.9) mm Hg (p < 0.01) and diastolic pressure from 67.2(2.9) to 23.6(3.2) mm Hg (p < 0.01). Both recovered within 30 s of cessation of pacing. During rapid pacing the action potential duration shortened from 192(13) to 128(5) ms (p = 0.01) and developed electrical alternans (n = 4). Following rapid pacing the ECG showed either ST depression or T wave inversion (n = 4). Despite these profound changes, rapid pacing did not reduce infarct size v control [52.7(4.6)% v 60.8(9.1)% of the area at risk, respectively]. The in vitro experiments estimated that rapid pacing would result in a reduction in coronary flow to 44% of that in sinus rhythm without a significant rise in lactate efflux. CONCLUSIONS: In our model, pretreatment with rapid pacing fails to reduce infarct size. The most likely reason for this is that rapid pacing at a rate of 480 beats.min-1 does not cause myocardial ischaemia of sufficient severity to trigger the preconditioning response.