Pulmonary valve endocarditis.
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Cardiac Surgical Procedures↗
Biomedical subjects
C Selim Isbir
Publications and source records attributed to C Selim Isbir.
Coronary artery bypass surgery in patients with severe left ventricular dysfunction.
OBJECTIVE: The role of coronary artery bypass grafting (CABG) in patients with severe left ventricular dysfunction was evaluated. METHODS: Two hundred and twelve patients (152 men, 60 women; age 35 to 82, mean 55) with ejection fraction (EF) of less than 30% underwent CABG between January 1996 and February 2001 by a single surgeon (SA). They compromised of 12% of 1759 patients operated on in this period. EF ranged from 17% to 30% (mean 25%). Preoperatively 68% had congestive heart failure and 72% had severe angina (CCS 3 or 4). A left main lesion was found in 26% of the cases. The mean number of grafts was 3.18 per patient. The left internal mammary artery (LIMA) was used on 107 patients (50.4%). Preoperative intraaortic balloon pump (IABP) was used on 32 patients (15%). Endarterectomy was performed on 53 patients (25%). The patients were followed for up to 58 months (mean 28.7). RESULTS: Twelve patients died in hospital (5.6%). Survival was 94%, 87%, 80% and 73% at 1, 2, 3 and 4 years respectively. Among the preoperative variables survival was negatively affected by chronic renal failure, older age, congestive heart failure, elevated pulmonary artery pressure and recent myocardial infarction, by means of multivariate analysis. Preoperative IABP support improved the operative mortality significantly (P=0.002). Use of LIMA did not have any influence on survival. CONCLUSION: CABG on patients with poor left ventricular function: (1). Can be performed with an acceptable mortality. (2). Mid term results are encouraging. (3). Preoperative IABP support improves the chance of survival.
Adult↗
Ischemic preconditioning and nicotinamide in spinal cord protection in an experimental model of transient aortic occlusion.
OBJECTIVES: Spinal cord injury is a devastating complication after aortic surgery. The aim of the present study is to examine the effects of ischemic preconditioning (IPC) and nicotinamide containing perfusate in transient aortic occlusion in the rat. METHODS: Thirty-two male Spraque-Dawley rats under general anesthesia were randomly assigned to four groups (n=8 in each group). The infrarenal aortas were clamped for 45 min. Groups were as follows: Group 1, undergoing occlusion but receiving no treatment. Group 2, had 5 min of IPC before occlusion. Group 3, received nicotinamide (0.2 ml/l) during the transient occlusion. Group 4, received combined IPC (5 min) and nicotinamide infusion during the transient occlusion. The rats were then allowed for recovery and were tested for their neurological status. All animals were sacrificed at the end of the 48 h and spinal cords also examined histologically. Anti- poly (ADP-ribose) polymerase p85 fragment pAb was used as an immunohistochemical marker for detection of apoptosis. RESULTS: In 24 h paraplegia represented as grade 0 and 1 occurred in six animals in Group 1 and two animals in Groups 2 and 3 and one in Group 4. In 48 h six animals in Group 1 and only one animal in Groups 2 and 3 showed a paraplegia. The incidence of neurologic deficit was significantly reduced in animals who had IPC and nicotinamide infusion (P<0.05). At 48 h, combined IPC and nicotinamide showed a significant benefit compared to nicotinamide but not to the IPC alone. Histologic examination of the spinal cords revealed that a neuronal necrosis contributes to acute spinal cord degeneration after a period of aortic occlusion and both nicotinamide and IPC have protective effects against neuronal necrosis. No difference was found among the groups. CONCLUSIONS: Both IPC and nicotinamide are beneficial in protection against neurological damage in transient aortic occlusion. IPC alone as expected is significantly beneficial both at 24 and 48 h compared to controls. At 24 h combined nicotinamide and IPC show significant benefit compared to only nicotinamide, but this difference is not maintained at 48 h.
Animals↗
The Effect Of Enalapril Maleat In Ischemia Reperfusion Injury: Possible Role of Membrane Bound Enzymes.
The present study evaluates the protective effect of enalapril maleat on myocardial ischemia-reperfusion injury. Membrane bound enzymes; Na(+)K(+)/Mg(2+) ATPase and Ca(2+)/Mg(2+) ATPase are known to regulate the membrane integrity. We hypothesized that if we could protect the cell membrane in ischemia-reperfusion period, we might have a chance to augment contractility. Thirty-two Guinea pig hearts were studied in an isolated Krebs-Henseleit solution-perfused Langendorff cardiac model. In Group 1, control hearts (n = 8) were arrested with St. Thomas Cardioplegic Solution (STHCS) alone. In Group 2 (n = 8), animals were pretreated with oral enalapril maleat (0.2mg/kg/daily) for ten days and arrested with STHCS. In Group 3, (n = 8) the hearts were arrested with enalapril maleat- (1 µmol/L) added STHCS. In Group 4 (n = 8), the hearts were again pretreated with oral enalapril maleat for ten days and then reperfused with enalapril maleat-added Krebs-Henseleit solution. Hearts were subjected to normothermic global ischemia for 90 minutes and then were reperfused at 37 degrees C. The study groups showed better recovery of left ventricular systolic function. In terms of biochemical determinations, best results were achieved at Group 4. The Na(+)K(+) ATPase and Ca(2+) ATPase levels were measured at 466.38 +/- 5.99 to 545.23 +/- 8.79, and 884.69 +/- 9.13 to 1254.34 +/- 1.56, respectively (p < 0.05). Based on these results, it can be concluded that enalapril maleat protects the membrane integrity and thus plays a role in restoring the contractility in ischemia-reperfusion injury. </hea
Journal Article↗
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 Ca(2+) 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 Ca(2+) 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 (l micromol l(-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 (l micromol l(-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 Ca(2+) 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.
Angiotensin-Converting Enzyme Inhibitors↗