Minimally Invasive Aortic Valve Replacement on Minimally Invasive Extracorporeal Circulation: Going beyond Aesthetics.

We present our multidisciplinary and multistep strategy in patients undergoing minimally invasive aortic valve replacement (mAVR) on minimally invasive extracorporeal circulation (MiECC) compared with control groups of a single strategy and conventional techniques. This cohort study included high-risk patients (Society of Thoracic Surgeons [STS] risk score >8%) undergoing aortic valve surgery under different strategies during the period from January 2017 until March 2019. Patients were matched for age, gender, body mass index, and STS score: group 1 (MiAVR) based on a minimally invasive technique with J-mini-sternotomy, rapid deployment valve (RDV), and type IV customized MiECC; group 2 (control-mAVR) consisted of minimally invasive technique with only J mini-sternotomy and RDV on a conventional extracorporeal system; group 3 (control-MiECC): full sternotomy and type IV customized MiECC; and group 4 (control): full sternotomy on a conventional extracorporeal system. The MiAVR group had significantly less duration of x-clamp time (35.4 ± 11 minutes), postoperative respiratory support (4.1 ± 1 hour), postoperative hemorrhage (250 ± 50 mL), and intensive care unit stay (1 ± .5 days) than the control-conventional (group 4) group. Seventy-six percent of patients did not receive any blood products in MiAVR (p = .025 vs. group 4). Incidence of atrial fibrillation (8%) and low cardiac output (14%) in MiAVR were significantly better than control. Critics of minimally invasive techniques sustain that potential advantages are offset by a longer cross-clamp and cardiopulmonary bypass duration, which may translate into inferior clinical outcomes. We advocate that our multidisciplinary approach supported by multiple technologies may be associated with faster recovery and superior outcomes than conventional minimally/conventional techniques.

Different effects of PPARA, PPARG and ApoE SNPs on serum lipids in patients with coronary heart disease based on the presence of diabetes.

BACKGROUND: The aim of this study was to investigate the individual or combined effects of PPARA-L162V, PPARG-C161T and APOE polymorphisms on hyperlipidemia in coronary heart disease (CHD) patients. METHODS: Our study included 223 patients with CHD (103 with type 2 diabetes (T2DM), 120 without diabetes) and 101 controls. All genotypes were determined by PCR-RFLP technique. RESULTS: Genotypic and allelic distributions of PPARA-L162V polymorphism were similar between study and control groups (p>0.05). The serum total-cholesterol (TC) and LDL-cholesterol (LDL-C) levels were higher in PPARA-V162 allele carriers in non-diabetic CHD patients (p=0.007 and p=0.038, respectively). The increasing effect of the PPARA-V162 allele on serum TC and LDL-C levels was weakened with the presence of PPARG-161T allele in the non-diabetic CHD patients. The ApoE4-PPARA-V162 allelic combination of the ApoE/PPARA genes was found to be more frequent in diabetic CHD patients independent of serum lipids (p=0.035). CONCLUSIONS: The PPARA V162 allele has an increasing effect on TC and LDL-C levels and this effect was reduced by carrying PPARG T161 allele in non-diabetic CHD patients. On the other hand, the V162 allele may be associated with an increased risk of CHD in diabetic CHD patients due to the presence of ApoE4 allele independent of serum lipids. We suggest that the PPARA L162V polymorphism may have diverse effects on serum lipids and CHD risk depends on the presence of T2DM.

Investigation of polymorphic variants of PPARD and APOE genes in Turkish coronary heart disease patients.

The aim of this study was to determine the role of polymorphic variants of apolipoprotein E (APOE) and peroxisome proliferator-activated receptor delta (PPARD) genes in the development of coronary heart disease (CHD), and the PPARD and APOE gene-gene interaction in a Turkish population. This study was carried out using a sample of 223 patients with CHD (103 with diabetes and 120 without diabetes) and 101 controls. PPARD +294T/C and APOE genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism technique. The PPARD and APOE genotype distributions were the same between study groups (p>0.05). In the nondiabetic CHD patients, the PPARD +294 C allele showed higher serum low-density lipoprotein cholesterol (LDL-C) level than the common +294 TT homozygote genotype (3.83 ± 1.01 vs. 3.33 ± 1.14, p=0.015). In addition, a significant association between APOE 4 and PPARD +294 C alleles was detected based on their effects on LDL-C in the nondiabetic CHD patients (+294 C/APOE4: 4.43 ± 0.88 vs. +294 TT/nonAPOE 4: 3.48 ± 1.09, p = 0.009). This association indicated the interaction of two genes on plasma LDL-C levels ascended in the order +294 T<+294 T-APOE 4<+294 C27. In addition, the CHD patients who were +294 C allele carriers had a 2.48-fold higher risk of LVH than subjects homozygous for the T allele. An increasing effect of the PPARD +294 C allele was shown on serum LDL-C levels in nondiabetic CHD patients. In addition, the results suggested that the +294 C allele might be associated with an increased LVH risk especially in male CHD patients. Furthermore, gene-gene interaction between the PPARD +294T/C and the APOE polymorphisms was observed regarding LDL-C concentrations.

Associations of receptor for advanced glycation end products -374 T/A and Gly82 Ser and peroxisome proliferator-activated receptor gamma Pro12Ala polymorphisms in Turkish coronary artery disease patients.

AIM: The aim of the present study was to investigate the individual and combined effects of receptor for advanced glycation end products (RAGE) -374T/A, RAGE Gly82Ser, and peroxisome proliferator-activated receptor gamma (PPAR-γ) Pro12Ala polymorphisms on the development of coronary artery disease (CAD). MATERIALS AND METHODS: This study was carried out in 87 patients with CAD and 52 CAD-free healthy controls. Polymerase chain reaction, restriction fragment length polymorphism, and agarose gel electrophoresis techniques were used to determine RAGE -374T/A, RAGE Gly82 Ser, and PPAR-γ Pro12 Ala. RESULTS: Individual allele and genotype frequencies of RAGE -374T/A, RAGE Gly82Ser, and PPAR-γ Pro12Ala polymorphisms were not significantly different between study groups. However, compared with the control group, wild-type T allele frequency was found to be higher in patients with diabetes (p=0.009). To investigate the combined effects of RAGE and PPAR polymorphisms, haplotype analysis was elevated and there was no statistical difference between the haplotypes of RAGE Gly82Ser with RAGE-374T/A or PPAR Pro12Ala. However, the frequency of RAGE-374T/PPAR12Ala haplotype was found to be higher in both the patient group (p=0.024) and in patients without diabetes (p=0.037). CONCLUSION: The results of the present study demonstrated that possessing the A allele of RAGE -374T/A polymorphism by diabetic CAD patients and possessing the-374T/Ala12 haplotype of RAGE -374T/A and PPAR-γ Pro12 Ala polymorphisms by the patients group were the most important risk factors for CAD.

The LOX-1 3'UTR188CT polymorphism and coronary artery disease in Turkish patients.

In coronary artery disease (CAD), a potentially reversible factor leading to cardiac death is left ventricular hypertrophy (LVH). The 3'untranslated region (3'UTR) 188CT polymorphism of lectin-like oxidized low-density lipoproteins receptor-1 (LOX-1) gene has been associated with an increased risk for CAD. We aim to investigate, in a Turkish population, whether 3'UTR188CT variation could affect the development of LVH in CAD patients. In a population-based case-control study, we compared 83 cases with CAD and 99 healthy controls for this polymorphism. The LOX-1 3'UTR188CT genotypes were determined by PCR-RFLP technique. LOX-1 3'UTR188 TT genotype was associated with significantly increased systolic blood pressure (P = 0.047) and risk of LVH (P = 0.014, OR: 3.541) when compared with the C allele carriers. In addition, the TT genotype was positively associated with decreased levels of HDL-cholesterol in the control subjects (P = 0.031) and increased levels of VLDL-C in the patient group (P = 0.009). The LOX-1 3'UTR188CT gene polymorphism may predispose to the development of LVH in CAD patients, dependent on blood pressure.

Effects of the PPARG P12A and C161T gene variants on serum lipids in coronary heart disease patients with and without Type 2 diabetes.

We investigated whether PPAR-γ2 gene polymorphisms are associated with serum lipids and the occurrence of coronary heart disease (CHD) prospectively characterised for the presence or absence of Type 2 diabetes in a Turkish population. Our study included 202 patients with CHD (102 with diabetes, 100 without diabetes) and 105 controls. PPARγ genotypes were determined by PCR-RFLP technique. The PPARγ-C161T CC homozygote genotype was associated with significantly increased CHD risk when compared with the T allele carriers (CT+TT) in CHD patients with diabetes (OR:1.951, 95%CI: 1.115-3.415, P = 0.019), whereas PPARγ-P12A polymorphism was not associated with CHD risk (P > 0.05). Serum HDL-C levels were significantly lower in controls with the P12A heterozygote when compared with the P12P homozygote (P = 0.002). In the CHD patients with diabetes, CT heterozygote genotype showed higher serum triglyceride than the CC homozygote genotype (CT:2.42 ± 1.89 vs. CC:1.61 ± 0.21, P = 0.015). Our findings shows the association of these two polymorphisms with serum triglyceride levels, which was increased in the order of P12P-CC < P12P-CT < P12A-CC < P12A-CT in the CHD patients with diabetes. Furthermore, we observed that the increasing effects of the CT genotype on serum triglyceride levels could be modified by PPARγ P12A polymorphism (P12A-CT:2.30 ± 1.75 vs. P12P-CC:1.79 ± 1.14, P = 0.028). We suggested that homozygote CC genotype of the PPARγ C161T polymorphism might be associated with an increased CHD risk especially in patients with diabetes. We observed that the C161T CT heterozygote genotype shows an unfavorable effect on serum lipid profile in CHD patients with diabetes and this effect was weaken with the presence of P12P homozygote genotype.

MMP2 gene polymorphisms and MMP2 mRNA levels in patients with superficial varices of lower extremities.

BACKGROUND: Although superficial varices of lower extremities with high morbidity are common, their etiology has not been elucidated yet. Previously, it was thought that venous hypertension was responsible for such cases by causing valvular insufficiency, but recent findings indicate that the changes in the venous wall structure might be main initiating factors. Matrix metalloproteinase enzyme-2 (MMP2) is one of the enzymes known to have functions in remodelling of the extracellular matrix mainly in vascular structures. MATERIALS AND METHODS: We studied two functional gene polymorphisms in -735 and -1306 regions of matrix metalloproteinase enzyme-2 (MMP2) gene, and their effects on mRNA expression of MMP2. We used a previously defined (PCR-RFLP) method for polymorphism analyses. RESULTS: CC genotype and C allele for MMP2 -735 gene region were more common in the control group and there was no significant difference between groups for MMP2 - 1306 gene polymorphisms. MMP2 mRNA levels were higher in the group that had both varices and coronary artery disease (CAD). CONCLUSION: There was no significant effect of MMP2 polymorphisms on mRNA expression. As MMP2 mRNA levels were higher in varices patients with CAD compared to the CAD only and varices only groups, it is necessary to make advanced researches to elucidate the relationship between CAD and varices.

Effects of myeloperoxidase -463 G/A gene polymorphism and plasma levels on coronary artery disease.

Myeloperoxidase is a lysosomal enzyme of polymorphonuclear leucocytes that contributes to inflammatory responses. In previous studies it was shown that MPO was synthesized in atherosclerotic lesions responsible of lipoprotein oxidations. We aimed to determine the MPO -463 G/A gene polymorphism distribution in Turkish population and evaluate the effects of it on myeloperoxidase levels. There were 100 myocardial infarct patients and 100 healthy control subjects in our study. MPO polymorphism was studied by using PCR-RFLP technique and MPO levels were measured by ELISA. It was shown that MPO levels were increasing in patients after myocardial infarct event but there were no effect of MPO -463 G/A polymorphism on MPO levels. It was also found that serum total cholesterol and LDL-cholesterol levels and smoking was contributing factors in increments of MPO enzymes. We observed that MPO levels were increased in CAD but there were no effect of MPO -463 G/A polymorphism on MPO levels.

Is LOX-1 K167N polymorphism protective for coronary artery disease?

BACKGROUND: Human lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1, OLR1) has been identified as a cell surface endocytosis receptor for oxidized low-density lipoprotein (oxLDL) on vascular endothelial cells. OxLDLs are avidly ingested by macrophages, resulting in foam cell formation. OxLDLs are also involved in inducing smooth muscle cell migration, proliferation and transformation. A single nucleotide polymorphism K167N (G501C) of the LOX-1 gene results in an amino acid dimorphism (Lys/Asn) at residue 167. Replacement of this Lys residue causes reduced binding and internalization of oxLDL. The purpose of this study was to investigate the effect of the LOX-1 K167N gene polymorphism in Turkish patients with coronary artery disease (CAD). MATERIALS AND METHODS: K167N polymorphism were studied in 91 patients with CAD and 72 healthy controls by the PCR-RFLP method. RESULTS: The frequencies of the KK genotype and the K allele were higher in the CAD group than the controls (p<0.05), while the frequency of the NN genotype was higher in the control group than in the CAD group (p<0.05). It was observed that the decreased CAD risk in patients who had the N allele was reversed by male sex (OR: 0.400 -->0.481) and smoking (OR: 0.400 -->0.949). Although male sex and smoking were lower than other cardiovascular risk factors in patients with the N allele they were higher than other cardiovascular risk factors in patients with the K allele. CONCLUSION: Male sex and smoking decrease the protective effects of the N allele. The adverse effects of the K allele on the CAD risk resulting from the K167N polymorphism appear to be independent of other cardiovascular risk factors.

Thromboelastography-based transfusion algorithm reduces blood product use after elective CABG: a prospective randomized study.

OBJECTIVE: Bleeding and allogeneic transfusion remain constant problems in cardiac surgical procedures. In this study, we aimed to test the role of a routine thromboelastography (TEG)-based algorithm on bleeding and transfusions in patients undergoing elective coronary artery bypass grafting (CABG). METHODS: Patients (n = 224) undergoing elective CABG with cardiopulmonary bypass were prospectively randomized into two groups according to transfusion strategy: in group 1 (clinician-directed transfusion, n = 110) need for blood transfusion was based on clinician's discretion and standard coagulation tests and in group 2 (TEG algorithm group, n = 114) kaolin-activated (k) TEG-based algorithm-guided perioperative transfusion management. Transfusion, blood loss, and outcome data were recorded. RESULTS: There were no differences in consumption of packed cell units, blood loss, re-exploration for bleeding, and early clinical outcome between the groups. Patients in the TEG group had significantly lower median units of fresh frozen plasma and platelets compared with the other group (p = 0.001). The median number of total allogeneic units transfused (packed cells and blood products) was significantly reduced in the TEG group compared with the other group (median 2, range 1-3 units vs. median 3, range 2-4 units, respectively, p = 0.001). The need for tranexamic acid was significantly diminished in the TEG group compared with the other group (10.3% vs. 19%, respectively, p = 0.007). CONCLUSION: Our results show that routine use of a kTEG-guided algorithm reduces the consumption of blood products in patients undergoing elective CABG. Adopting such an algorithm into routine management of these patients may help to improve clinical outcome and reduce the potential risks of transfusion-related complications and total costs after CABG.

APE1 and XRCC3 polymorphisms and myocardial infarction.

BACKGROUND: In most cells, DNA is regularly damaged by mutagens. Different DNA repair mechanisms operate on specific types of damaged DNA. When DNA damage resulting from free radicals is not repaired, it might lead to deteriorated gene expression, the development of a number of diseases such as cancer, diabetes, vascular diseases, and aging. In the present study, APE1 and XRCC3 gene polymorphisms were investigated in patients with myocardial infarction. MATERIALS AND METHODS: Forty-five first time elective coronary artery bypass grafting (CABG) patients with cardiopulmonary bypass (CPB) and 40 healthy individuals were studied. Gene polymorphisms were determined by a polymerase chain reaction-restriction fragment length polymorphism method. RESULTS: For the APE1 gene, the AG genotype was significantly higher in the patient group than in the control group. The patient group had significantly more G carriers but there was no statistically significant difference between patient and control groups the A allele. The XRCC3 TT genotype was found to be significantly more frequent in the patient group than it was in the control group. CONCLUSION: The results of our study suggested that the XRCC3 gene TT genotype and the APE1 gene AG genotype might increase the risk of myocardial infarcts.

Investigation of ABCA1 C69T and G-191C polymorphisms in coronary artery disease.

BACKGROUND: Defects of lipoprotein metabolism are common risk factors for coronary artery disease. The ATP binding cassette transporter 1 (ABCA1) plays an important role in carrying cholesterol from peripheral tissues to the liver. The role of ABCA1 C69T and G-191C gene polymorphisms on plasma lipid levels of patients with coronary artery disease was investigated. PATIENTS AND METHODS: Seventy-seven patients with coronary artery disease and fifty healthy controls were studied. Gene polymorphisms were determined by polymerase chain reaction-restriction fragment length polymorphism method. RESULTS: No differences in the distribution of C69T and G-191C polymorphisms were observed in the study groups. Plasma triacylglycerol and VLDL-cholesterol levels were shown to be higher in the patient group with the C69T CC genotype compared to these patients with the CT genotype. The C69T polymorphism was associated with HDL-cholesterol levels, which insignificantly increased in the order of the CC>CT>TT genotypes in our study. No association was found between G-191C genotype and lipid levels. CONCLUSION: The results of our study suggested that polymorphisms of ABCA1 C69T polymorphism may be associated with plasma triacylglycerol and VLDL-cholesterol levels in coronary artery patients.

[Thromboelastography and its use in cardiac surgery]. / Tromboelastografi ve kalp cerrahisinde kullanimi.

Thromboelastography is an alternative method to conventional coagulation tests for the general evaluation of hemostatic system. Cardiac surgery with cardiopulmonary bypass is accomplished by complex alterations of hemostasis, including acquired dysfunction of platelets, consumption coagulopathy and increased fibrinolysis. Despite major advances in blood conservation methods and perioperative care of the patients, transfusion rates in cardiac surgery remain high. Thromboelastography has an ability to assess almost all components of haemostatic system globally. Currently, thromboelastography is used with standard coagulation tests to decrease the microvascular bleeding and homologous blood transfusion in cardiac surgery with cardiopulmonary bypass. In this review, we aimed to discuss thromboelastography technology and its usage in cardiac surgery.

Effect of Ala16Val genetic polymorphism of MnSOD on antioxidant capacity and inflammatory response in open heart surgery.

BACKGROUND: Ischemia-reperfusion injury and inflammation in cardiac surgical patients involves complex humoral and cellular interactions. We investigated the effect of genetic polymorphism of manganase superoxide dismutase (MnSOD) a natural antioxidant, on cytokine release and manganesuperoxide dismutase in patients undergoing coronary artery bypass grafting (CABG) with cardiopulmonary bypass (CPB). PATIENTS AND METHODS: Forty-two patients undergoing elective CABG with CPB were included in the study. MnSOD polymorphism was performed by polymerase chain reaction (PCR). Levels of interleukin-6 and mangane superoxide dismutase (MnSOD) were measured by enzyme linked immunoabsorbent assay (ELISA). RESULTS: Baseline IL-6 did not differ between patients with different MnSOD genotypes. Postoperatively IL-6 levels were significantly higher in all patients but more significantly in V(VV+AV) carriers (p=0.003). The wild-type AA genotype had the highest preoperative (p<0.05) and postoperative IL-6 level. The MnSOD VV genotype was associated with significantly lower preoperative MnSOD levels compared to the AA carriers (p<0.05). CONCLUSION: These data demonstrate that MnSOD Ala16Val polymorphism influences IL-6 production and baseline MnSOD activity, suggesting that preoperative MnSOD concentration plays a role in cytokine release.

The effect of NQO1 polymorphism on the inflammatory response in cardiopulmonary bypass.

Cardiopulmonary bypass (CPB) has been associated with systemic inflammatory response syndrome (SIRS). Endothelial dysfunction related to non-laminar flow during CPB is known to play a key role in this complex pathology. Antioxidant response element (ARE) dependent NAD(P)H:quinone oxidoreductase 1 (NQO1) promoter is a regulatory element involved in the anti-inflammatory mechanism in vasculature exposed to non-laminar flow. Mutation of the NQO1 could represent a novel anti-inflammatory effect in CPB. The goal of this study was to demonstrate whether genetic variants of NQO1 affect cytokine release after CPB. Eighteen patients who underwent standard coronary artery bypass grafting (CABG) operation were included in the study. Genotyping for NQO1 was performed. Serum Interleukin-6 (IL-6) levels were measured before induction, during CPB after declamping the aorta, and 24 h after operation. Clinical data were collected respectively. Seven patients were NQO1 T carriers and 11 patients were NQO1 T non-carriers. During CPB, IL-6 concentrations were increased in NQO1 T carriers compared to T non-carriers (p = 0.038). Although ventilation times and blood loss were higher in T carriers these were not statistically significant. Patients with NQO1 T carriers showed significantly higher IL-6 levels during CPB. Non-laminar flow during CPB may diminish the transcriptional activation of the NQO1 in T carriers. Preoperative determination of this novel anti-inflammatory mechanism could be useful to improve operative outcome in CPB.

Genetic polymorphisms contribute to acute kidney injury after coronary artery bypass grafting.

BACKGROUND: Acute kidney injury is one of the most serious complications after cardiac surgery. Genetic polymorphisms are reported to be associated with postoperative renal impairment. The aim of this study was to investigate the relationship between selected gene polymorphisms and acute kidney injury after cardiac surgery. METHODS: Two hundred forty-eight elective coronary artery bypass grafting procedure patients were enrolled in the study. Angiotensin-converting enzyme (ACE) II, ID, and DD, apolipoprotein E (APO E), and angiotensin II type 1 receptor (AGTR1) A1166C genotypes were detected by polymerase chain reaction. Plasma levels of ACE were analyzed by enzyme-linked immunosorbent assay. Acute kidney injury after cardiac surgery was graded according to the RIFLE (risk, injury, failure, loss, and end-stage kidney disease) classification. RESULTS: In our study, 21.8% of patients had acute renal impairment after cardiac surgery. Among the 54 patients with acute kidney injury, ACE D allele frequency was 0.620. The plasma levels of ACE were significantly higher in the D allele carriers (P = .018). Three of the 54 patients with acute kidney injury were APO E epsilon 4 allele carriers (P = .002). AGTR1 C allele carriers constituted 46% of all patients with postoperative acute kidney injury. There was no statistically significant difference between A allele homozygotes and C allele carriers with respect to postoperative renal dysfunction (P > .05). CONCLUSIONS: The present findings support the hypothesis that ACE I/D and APO E gene polymorphisms may play a role in the development of acute kidney injury after cardiac surgery. However, AGTR1 does not have a unique association with postoperative renal impairment.

Presence of lipoprotein lipase S447X stop codon affects the magnitude of interleukin 8 release after cardiac surgery with cardiopulmonary bypass.

OBJECTIVE: Current data suggest that individual genetic predisposition may influence the magnitude of cytokine response and the degree of organ dysfunction after cardiopulmonary bypass. Lipoprotein lipase S447X polymorphism has been shown to be protective against atherosclerosis. The aim of the study was to investigate the effect of lipoprotein lipase S447X polymorphism on cytokine release and early outcome after cardiopulmonary bypass. METHODS: Forty patients who underwent coronary artery bypass grafting with cardiopulmonary bypass were included. Genotyping for lipoprotein lipase S447X polymorphism was performed by polymerase chain reaction. Levels of interleukins 6 and 8 were measured before induction and 6, 24, and 72 hours after operation by enzyme-linked immunosorbent assay. Clinical data were collected prospectively. Daily assessment of organ dysfunction was done according to the cardiac surgery scoring (CASUS) system. RESULTS: The allele frequency of lipoprotein lipase S447X stop codon was 17.5%. S447X carriers revealed significantly lower interleukin 8 levels at the sixth and 24th postoperative hours than the noncarrier group (P = .005 and P = .041, respectively). Patients in the S447X carrier group had significantly shorter ventilation times than the noncarrier group (P = .048). Also, the S447X carrier group revealed significantly lower postoperative 6-hour lactate levels, operative day, and postoperative day 1 organ dysfunction scores than the other group (P = .001, .005 and .002, respectively). CONCLUSION: Lipoprotein lipase S447X stop codon mutation is associated with lower levels of interleukin 8 after coronary artery bypass grafting. Identification of high-risk patients for cardiopulmonary bypass-related systemic inflammation by detecting lipoprotein lipase S447X stop codon polymorphism may improve early postoperative outcome, especially in patients with limited organ reserves.

Effect of a low molecular weight heparin molecule, dalteparin, on cellular apoptosis and inflammatory process in an incisional wound-healing model.

PURPOSE: In this study we aimed to test the effect of a low molecular weight heparin molecule, namely dalteparin, on the inflammation and cellular apoptosis in an incisional wound-healing model in rats. METHODS: Eighteen male Sprague-Dawley rats were randomly assigned to three groups (n = 6 for each group). Two full-thickness skin incisions were made over cervical and lumbar regions of all rats. Group 1 (sham group) received no treatment, group 2 (control group) received 0.01 ml/g saline subcutaneously 12 h two times daily from 0 to 10th postoperative day, and group 3 (dalteparin group): received 1 IU/g dalteparin subcutaneously two times daily from 0 to 10th postoperative day. A histological evaluation was done by light microscopy. Apoptosis was detected immunohistochemically by anti-poly (ADP-ribose) polymerase p85 fragment pAb. RESULTS: The early inflammatory response and related tissue edema were depressed on day 3 in the dalteparin group when compared with those in the other groups (P < 0.05). Fibroblast proliferation was also depressed on day 10 in the dalteparin group compared to the others (P < 0.05). Furthermore, increased apoptosis was detected in the dalteparin group both on day 3 and day 10. CONCLUSION: Our results showed that dalteparin may adversely affect the incisional wound healing by suppressing the early inflammatory process and increasing cellular apoptosis; however, further studies are warranted to confirm the results.

Coronary artery bypass grafting in idiopathic myelofibrosis: a case report.

The concomitant presence of myeloproliferative disorders and the need for coronary artery bypass surgery is a surgical dilemma. Thrombosis and hemorrhage can cause difficult problems and might require different approaches during and after surgery. We report a patient who had idiopathic myelofibrosis and underwent a successful coronary artery bypass surgery.