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Bilateral axillary arterial cannulation for selective cerebral perfusion might minimize cerebral embolic complications during surgery on the ascending aorta and aortic arch. From March 2002 through February 2004, bilateral axillary arterial perfusion was applied in 12 consecutive patients (mean age, 61.3 years). Operative procedures were total arch replacement in 8 patients, hemiarch replacement in 1, and ascending aorta replacement in 3. Antegrade selective cerebral perfusion was established through vascular grafts anastomosed to the bilateral axillary arteries and a perfusion catheter placed directly into the left carotid artery. Bilateral axillary arterial perfusion through the grafts was successful in all patients. There were no early or late deaths and no incidence of neurologic deficit. There were no complications related to cannulation of the axillary arteries. Bleeding, temporary renal failure, acute respiratory distress syndrome, and graft infection occurred in one patient each; all recovered from these complications. Bilateral axillary arterial perfusion is feasible and effective for brain protection during surgery on the ascending aorta and aortic arch.

We examined influences of a blocker (glibenclamide) and an opener (nicorandil) of the ATP-sensitive potassium (KATP) channel on extracellular K concentration [( K+]e), as well as the myocardial function and metabolites during global ischemia and reperfusion in Langendorff-perfused rat heart preparation. In control hearts, [K+]e began to rise 20 s after the onset of ischemia up to an initial peak (8.3 +/- 0.3 mM) at 2.5 +/- 0.7 min, then fell to 6.0 +/- 0.8 mM after 8.2 +/- 0.7 min, and then rose progressively to 14.6 +/- 0.8 mM at the end of 30 min of ischemia. Glibenclamide (50 microM) reduced the initial peak of [K+]e to 7.2 +/- 0.3 mM (P less than 0.01), and nicorandil (200 microM) increased it to 9.4 +/- 0.6 mM (P less than 0.01). There were no significant differences in [K+]e values among all groups at the end of ischemia. During ischemia, nicorandil decreased the time to mechanical arrest from 1.9 +/- 0.1 min to 1.5 +/- 0.1 min, whereas it was increased by glibenclamide to 2.7 +/- 0.4 min. In control hearts, the time to onset of ischemic contracture was 14.7 +/- 1.8 min. Nicorandil delayed onset of contracture and glibenclamide accelerated it. Thus we have confirmed that some part of the early increase in [K+]e during ischemia is attributable to K+ efflux through the KATP channel in our model, and opening of the KATP channel may contribute to a rapid reduction of the contractility of the ischemic myocardium that subsequently protects the myocardium against further ischemic injury.

This report describes 2 cases of a type A acute aortic dissection combined with myocardial infarction caused by a retrograde dissection into the left main trunk of the coronary artery. Successful surgical treatments, including the replacement of the ascending aorta, aortic valve resuspension and coronary artery bypass grafting, were performed in both patients, and they recovered well from cardiogenic shock. However, left ventricular function of both patients remained depressed postoperatively, which limited their quality of life. Because no definite method for salvaging infarcted myocardium has yet been established, either more timely surgery or the preoperative placement of a perfusion catheter in the left main coronary artery is mandatory.