Long term follow up results of sequential left internal thoracic artery grafts on severe left anterior descending artery disease

<p>Abstract</p> <p>Purpose</p> <p>Several alternative procedures have been proposed to achieve complete revascularization in the presence of diffuse left anterior descending coronary artery (LAD) disease. With the extensive use of internal thoracic artery grafts in coronary artery bypass procedures, sequential anastomosis of the left internal thoracic artery (LITA) to LAD has gained popularity in these challenging cases. The long term results of sequential LITA to LAD anstomosis were examined in this study.</p> <p>Patients and Methods</p> <p>In order to determine the long term results of the sequential revascularization of LAD by LITA graft, 41 out of 49 patients operated between January 2001 and December 2005 were selected for control coronary arteriography. The median period for control coronary arteriography was 64 months.</p> <p>Results</p> <p>Seventy five anastomoses were found to be fully patent (91,46%) among the 82 sequential LITA anastomoses (41 LITA grafts) on the LAD at a median follow-up period of 64 months (53 to 123 months). Among the 41 LITA grafts used for this purpose, 36 were found intact (complete patency of the proximal and distal anastomoses) (87,8%). Two LITA grafts (4 anastomoses) were found to be totally occluded (4,87%). The proximal anastomosis of the LITA graft was observed to be 90% stenotic in one patient (1,21%). In one patient tight stenosis of the distal anastomosis line was observed (1,21%), while in another patient 70% narrowing of LITA lumen after the proximal anastomosis was detected (1,21%).</p> <p>Conclusion</p> <p>We strongly beleive that sequential LITA grafting of LAD is a safe alternative in the presence of severe LAD disease to achieve complete revascularization of the anterior myocardium with patency rates not much differing from conventional single LITA to LAD anastomosis.</p

The effect of captopril on membrane bound enzymes in ischemia-reperfusion injury

There is substantial evidence that Na+K+/Mg2+ ATPase and Ca2+/Mg2+ ATPase enzymes would effect the membrane integrity. Forty guinea pig (n = 10 in each group) hearts were studied in an isolated Krebs-Henseleit solution perfused Langendorff cardiac model. The first group was utilized as the control group. Group 2 hearts were arrested with captopril (200 mu mol/l) added St Thomas Hospital Cardioplegic Solution (STHCS). Group 3 animals were pretreated with oral captopril (0.3 mg/kg/twice a day) for 10 days and then arrested with STHCS. Group 4 hearts were again pretreated with oral captopril (0.3 mg/kg/twice a day for 10 days) arrested with STHCS and reperfused with captopril added Krebs-Henseleit solution (200 mu mol/l). Hearts were subjected to normothermic global ischemia for 90 min and than were reperfused at 37 degrees C. When the treated groups were compared with control, best results were achived by group 4. The Na+K+ and Ca2+/Mg2+ ATPase levels increased from 466.38 +/- 5.99 to 564.13 +/- 7.77 and 884.69 +/- 9.13 to 1254.29 +/- 5.75 nmol Pi/mg/prot/h respectively (P < 0.05). These results suggest that captopril protects the membrane integrity and thus played a role at the recovery of depressed membrane bound Na+K+/Mg2+ ATPase and Ca-2 (+)/Mg2+ ATPase activity and also in ischemia-reperfusion injury. (C) 2000 The International Society for Cardiovascular Surgery. Published by Elsevier Science Ltd. All rights reserved

The effect of captopril on membrane bound enzymes in ischemia–reperfusion injury

There is substantial evidence that Na+K+/Mg2+ ATPase and Ca2+/Mg2+ ATPase enzymes would effect the membrane integrity. Forty guinea pig (n = 10 in each group) hearts were studied in an isolated Krebs-Henseleit solution perfused Langendorff cardiac model. The first group was utilized as the control group. Group 2 hearts were arrested with captopril (200 mu mol/l) added St Thomas Hospital Cardioplegic Solution (STHCS). Group 3 animals were pretreated with oral captopril (0.3 mg/kg/twice a day) for 10 days and then arrested with STHCS. Group 4 hearts were again pretreated with oral captopril (0.3 mg/kg/twice a day for 10 days) arrested with STHCS and reperfused with captopril added Krebs-Henseleit solution (200 mu mol/l). Hearts were subjected to normothermic global ischemia for 90 min and than were reperfused at 37 degrees C. When the treated groups were compared with control, best results were achived by group 4. The Na+K+ and Ca2+/Mg2+ ATPase levels increased from 466.38 +/- 5.99 to 564.13 +/- 7.77 and 884.69 +/- 9.13 to 1254.29 +/- 5.75 nmol Pi/mg/prot/h respectively (P < 0.05). These results suggest that captopril protects the membrane integrity and thus played a role at the recovery of depressed membrane bound Na+K+/Mg2+ ATPase and Ca-2 (+)/Mg2+ ATPase activity and also in ischemia-reperfusion injury. (C) 2000 The International Society for Cardiovascular Surgery. Published by Elsevier Science Ltd. All rights reserved

C677T mutation of methylenetetrahydrofolate reductase gene and serum homocysteine levels in Turkish patients with coronary artery disease

Elevated levels of homocysteine is a risk factor for coronary artery disease. The C677T transition in methylenetetrahydrofolate reductase (MTHFR) is associated with increased homocysteine levels in the general population. We analysed the association between the MTHFR C677T polymorphism and serum homocysteine concentrations in patients with coronary artery disease (CAD). Allele frequencies for the 'C' (wild-type) and 'T' alleles were 0.71 and 0.29 in CAD patients and 0.70 and 0.30 in controls, respectively. There was no difference in the distribution of MTHFR genotypes between patients with CAD and control subjects (p > 0.05). In the patient group, homocysteine levels were higher than controls but not significantly (13.99 +/- 7.44 vs. 11.77 +/- 5.18 mu mol l(-1); p > 0.05). Serum homocysteine concentration was significantly higher in the TT genotype with respect to CC and CT genotypes in both the control group (p < 0.01) and patient group (p < 0.01). Systolic and diastolic blood pressures in subjects with different MTHFR genotypes did not differ significantly. In conclusion, MTHFR C677T mutation was significantly related to hyperhomocysteinemia. In spite of the clear effect of the MTHFR polymorphism on elevated homocysteine levels, we did not observe any associations among the MTHFR genotypes with a the risk of CAD in the Turkish population. Copyright (c) 2005 John Wiley & Sons, Ltd

The protective effect of lisinopril on membrane-bound enzymes in myocardial preservation

A number of studies have reported that oxidant stress reduces the activity of isolated Na+ - K+ ATPase and Ca2+ ATPase which are known to affect the cell membrane integrity. The aim of the study is to determine whether the administration of lisinopril is able to protect the membrane-bound enzyme levels in isolated guinea pig hearts and also ascertain whether or not a relationship exists between oxygen free radicals and membrane bound Na+ - K+ ATPase and Ca2+ ATPase. Forty guinea pig hearts were studied in an isolated Krebs-Henseleit solution-perfused Langendorff cardiac model. In all groups cardioplegic: arrest was achieved by administering St. Thomas' Hospital cardioplegic solution (STHCS). Group 1 (control, n = 10) received only STHCS. Group 2 (n = 10) were arrested with lisinopril (1 mu mol 1(-1)) added STHCS, Group 3 (n = 10) were pretreated with oral lisinopril (0.2 mg kg(-1) twice a day) for 10 days and then arrested with STHCS. Group 4 were also pretreated with oral lisinopril (0.2 mg kg(-1) twice a day for 10 days), arrested with STHCS and reperfused with lisinopril added to Krebs-Henseleit solution (1 mu mol 1(-1)). Hearts were subjected to normothermic global ischaemia for 90 min and then reperfused at 37 degrees C. Pretreatment and addition of lisinopril in the reperfusion buffer improved the levels of membrane-bound enzymes. When the treated groups were compared with control hearts, the best results were achieved in group 4. The Na+ - K+ and Ca2+ ATPase levels increased from 466.38+/-5.99 to 560.12+/-18.02 and 884.69+/-9.13 to 1287.71+/-13.01 nmolPi mg(-1) protein h(-1) respectively (p < 0.05). These results suggest that lisinopril protects the cell membrane integrity and lessens free radical-induced oxidant stress. Copyright (C) 2000 John Wiley & Sons, Ltd

C677T mutation of methylenetetrahydrofolate reductase gene and serum homocysteine levels in Turkish patients with coronary artery disease

Elevated levels of homocysteine is a risk factor for coronary artery disease. The C677T transition in methylenetetrahydrofolate reductase (MTHFR) is associated with increased homocysteine levels in the general population. We analysed the association between the MTHFR C677T polymorphism and serum homocysteine concentrations in patients with coronary artery disease (CAD). Allele frequencies for the 'C' (wild-type) and 'T' alleles were 0.71 and 0.29 in CAD patients and 0.70 and 0.30 in controls, respectively. There was no difference in the distribution of MTHFR genotypes between patients with CAD and control subjects (p > 0.05). In the patient group, homocysteine levels were higher than controls but not significantly (13.99 +/- 7.44 vs. 11.77 +/- 5.18 mu mol l(-1); p > 0.05). Serum homocysteine concentration was significantly higher in the TT genotype with respect to CC and CT genotypes in both the control group (p < 0.01) and patient group (p < 0.01). Systolic and diastolic blood pressures in subjects with different MTHFR genotypes did not differ significantly. In conclusion, MTHFR C677T mutation was significantly related to hyperhomocysteinemia. In spite of the clear effect of the MTHFR polymorphism on elevated homocysteine levels, we did not observe any associations among the MTHFR genotypes with a the risk of CAD in the Turkish population. Copyright (c) 2005 John Wiley & Sons, Ltd