BackgroundThere is ongoing debate regarding the efficacy of the radial artery (RA) as an aortocoronary conduit, with few solid data regarding long-term clinical results. We sought to determine if the use of the RA as the second arterial conduit, beside left internal thoracic artery (LITA), would improve long-term clinical outcome after CABG as compared to saphenous vein graft (SVG).MethodsBetween March 2001 and November 2003, 200 patients underwent isolated CABG and were randomized in 1:1 fashion to receive either LITA and RA grafts or LITA and SVGs. The primary end point was composite of cardiovascular mortality, non-fatal myocardial infarction and need for repeat myocardial revascularization (either surgical or percutaneous).ResultsThere was no significant difference in absolute survival, with 12 deaths in each group during the study period (log rank = 0.01, p = 0.979). There were 3 and 2 cardiac deaths in RA and SVG groups, respectively. There was no difference in long-term clinical outcome between the groups (log rank = 0.450, p = 0.509). Eleven patients in RA group had one or more non-fatal events; 7 patients suffered a myocardial infarction, 9 patients underwent percutaneous coronary angioplasty, and 1 patient required redo coronary surgery. Likewise, 13 patients in SVG group had non-fatal event; 7 patients had myocardial infarction, 13 patients had percutaneous coronary intervention and 3 patients required redo coronary surgery. Angiograms were performed in 23 patients in RA group (patency rate 92 %) and 24 in SVG group (patency rate 86 %) (p = 0.67).ConclusionIn this small randomised study our data indicate that there is no difference in the 8 year clinical outcomes in relatively young patients between those having a RA or a saphenous vein graft used as a second conduit, beside LITA, for surgical myocardial revascularisation.

Correcting chronic IMR with either repair or replacement produces a good mid-term survival rate (approximately 75%) for survivors in NYHA classes I and II. In our study, mortality rates for the MVP and MVR groups were similar, even though the repair group had a lower mean ejection fraction and a higher NYHA class before and after the operation. We therefore conclude that repair is superior to replacement in treating ischemic mitral insufficiency. A prospective randomized study is needed to better compare these 2 approaches.

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Background/Aims: Study elucidates and compares the mitochondrial bioenergetic-related molecular basis of sevoflurane and propofol cardioprotection during aortic valve replacement surgery due to aortic valve stenosis. Methods: Twenty-two patients were prospectively randomized in two groups regarding the anesthetic regime: sevoflurane and propofol. Hemodynamic parameters, biomarkers of cardiac injury and brain natriuretic peptide (BNP) were measured preoperatively and postoperatively. In tissue samples, taken from the interventricular septum, key mitochondrial molecules were determined by Western blot, real time PCR, as well as confocal microscopy and immunohisto- and immunocyto-chemical analysis. Results: The protein levels of cytochrome c oxidase and ATP synthase were higher in sevoflurane than in propofol group. Nevertheless, cytochrome c protein content was higher in propofol than sevoflurane receiving patients. Propofol group also showed higher protein level of connexin 43 (Cx43) than sevoflurane group. Besides, immunogold analysis showed its mitochondrial localization. The mRNA level of mtDNA and uncoupling protein (UCP2) were higher in propofol than sevoflurane patients, as well. On the other hand, there were no significant differences between groups in hemodynamic assessment, intensive care unit length of stay, troponin I and BNP level. Conclusions: Our data indicate that sevoflurane and propofol lead to cardiac protection via different mitochondrially related molecular mechanisms. It appears that sevoflurane acts regulating cytochrome c oxidase and ATP synthase, while the effects of propofol occur through regulation of cytochrome c, Cx43, mtDNA transcription and UCP2.