Risk factors for midterm cardiac function deterioration after valve replacement surgery in patients with rheumatic mitral stenosis.

BACKGROUND: A symptomatic reduction in left ventricular ejection fraction (LVEF) is the main reason for postoperative heart failure after valve replacement surgery. However, postoperative heart failure occurs in patients with normal preoperative LVEF. Therefore, we examined clinical and echocardiographic data of patients with rheumatic heart disease to determine additional risk factors for low LVEF in the postoperative period. METHODS AND RESULTS: Ninety-seven patients with rheumatic heart disease (RHD) who underwent mitral valve replacement for severe mitral valve stenosis were included retrospectively in this study. All patients had normal LVEF before surgery. Patients were divided into 2 groups based on postoperative LVEF 6 months after surgery. Groups A had normal postoperative LVEF (82 cases, 84.5%), and group B had low postoperative LVEF (15 cases, 15.5%). Clinical and electrocardiographic data were collected to determine risk factors for deterioration in cardiac function. Multivariate analysis revealed that preoperative low systolic peak velocities at the lateral tricuspid annulus (St) and no or mild aortic stenosis were independent risk factors for cardiac deterioration in patients with normal preoperative LVEF. Individuals with preoperative St ≤ 4.8 cm/s were more likely to develop lower LVEF at follow-up (χ(2) = 7.54; P = .006; odds ratio 5.03, 95% confidence interval 1.31-20.82). All 15 patients who had normal preoperative LVEF but abnormal postoperative LVEF had no or only mild aortic valve stenosis. CONCLUSIONS: Decreased right ventricular function and no or mild aortic stenosis were independent risk factors for low LVEF at follow-up in patients with RHD who had normal preoperative LVEF. The velocity of the tricuspid valve ring should be included in preoperative evaluations to improve the accuracy of postsurgical prognosis and clinical decision making.

[The anatomy features and surgical significance of the pulmonary circuits of pulmonary atresia with ventricular septal defect and major aortopulmonary collateral arteries].

OBJECTIVES: To analyze the anatomy features of the pulmonary circuits in the patients with pulmonary atresia (PA) with ventricular septal defect (VSD) and major aortopulmonary collateral arteries (MAPCA), and discuss the clinical significance. METHODS: From April 2002 to June 2010, the anatomy features of pulmonary circuits in 33 patients with PA/VSD/MAPCA were examined and analyzed. There were 21 male and 12 female patients. The age ranged from 11 months to 29 years. The anatomic types of PA/VSD included group B for 22 cases, group C for 11 cases. Thirty-one patients of them underwent 33 operative procedures. The operations included aorta-pulmonary shunt in 8 cases, one stage unifocalization with VSD open in 2 cases, complete repair in 23 cases. RESULTS: Twenty-nine (87.9%) patients had native pulmonary arteries, 6 of them were normal size and 23 were hypoplastic size. Four patients (12.1%) had no native pulmonary arteries. The postoperative oxygen saturation of the patients undergone shunt and one stage unifocalization was increased to 83% to 90%. There was one early death after complete repair because of multiorgan function failure. There were 4 cases of severe low cardiac output and 3 cases of respiratory function failure. Sixteen patients after complete repair were followed up more than one year. The postoperative right ventricular pressure was 41 to 99 mmHg (1 mmHg = 0.133 kPa). The ejection fraction value was more than 50% in 14 patients and less than 50% in 2 patients. Two patients had medium pulmonary insufficiency. CONCLUSIONS: An individualized approach based on the anatomy of the pulmonary circuits permits achievement in the patients with PA/VSD/MAPCA. The surgical strategy for PA/VSD/MAPCA mainly depends on the anatomy features of native pulmonary arteries, confluent pulmonary arteries and MAPCA.

Interaction of Adiponectin Genotypes and Insulin Resistance on the Occurrence of Taiwanese Metabolic Syndrome.

BACKGROUNDS: Adiponectin (apM1) may affect insulin sensitivity, and tumor necrosis factor (TNF-α) can inhibit the binding of insulin and insulin receptors. However, whether apM1 and TNF-α genes influence the development of metabolic syndrome (MetS) preceded by insulin resistance is unclear. The current study examines the interactions between the apM1 +45 genotypes, TNF-α -308 genotypes, and insulin resistance on the occurrence of MetS. METHODS: A total of 329 community residents were recruited, and their personal characteristics were collected. Waist circumference and biochemical markers were examined for determining MetS. Genotypes were identified by the polymerase chain reaction. RESULTS: After adjusting for the confounding effects, compared to apM1 +45 GG and GT genotypes carriers with HOMR-IR less than 2.0, those carriers with HOMA-IR greater than 2.0 had an increased MetS risk (OR = 4.35, 95% CI 2.14-8.85). Further, apM1 +45 TT carriers with HOMA-IR greater than 2.0 experienced a higher MetS risk (OR = 5.91, 95% CI 2.78-12.54). A significant interaction of the apM1 +45 genotype and insulin resistance on the MetS development was observed (P = 0.04). CONCLUSION: Our data suggested that apM1 +45 genotypes might modify the effect of insulin resistance on the development of Taiwanese MetS.

Myocardial ischaemic and diazoxide preconditioning both increase PGC-1alpha and reduce mitochondrial damage.

OBJECTIVES: Pretreatment with diazoxide, a mitochondrial ATP-sensitive potassium channel (mito KATP) opener, was found to protect the rat heart against ischaemia-reperfusion (I/R) injury by mimicking ischaemic preconditioning (IPC). However, the protection mechanisms have not been fully clarified yet.We hypothesize that molecular regulation of mitochondrial energetics is integral to this cardioprotective programme. We explored the involvement of peroxisome proliferator-activated receptor gamma coactivator-1-1alpha (PGC-1alpha) in the effect of IPC and diazoxide preconditioning (DPC) with regard to its role in protection against I/R injury. METHODS: 30 Wistar rats were used to establish the Langendorff isolated perfused heart model. Rats were randomly divided into 5 groups, 6 in each group: (1) the I/R group: after 30 min of equilibration perfusion, the heart was subjected to 30 min of ischaemia and 1 h of reperfusion; (2) the IPC group: after 10 min of equilibration perfusion, the heart was subjected to two times 5 min ischaemia and 5 min of reperfusion, followed by 30 min of ischaemia and 1 h of reperfusion; (3) the DPC group: after 10 min of equilibration perfusion, the heart was given two times a K-H perfusion solution containing diazoxide (100 micromol/l) for 5 min then a non-diazoxide K-H perfusion solution for 5 min, followed by 30 min of ischaemia and 1 h of reperfusion; (4) a blank control group: an equal amount of saline was used instead of diazoxide. The perfusion procedure was the same as in the DPC group; (5) the dimethyl sulfoxide (DMSO) group: DMSO was applied instead of diazoxide, and the perfusion procedure was the same as in the DPC group. Cardiac apex muscle was cut for frozen section. Immunohistochemistry staining of PGC-1alpha was performed and average absorbance was calculated. An electron microscope was used for Flameng scoring of the myocardial mitochondria. RESULTS: The average absorbance values of PGC-1alpha were: I/R group (3.88 +/- 1.72), IPC group (10.94 +/- 5.23), DPC group (8.40 +/- 3.64), blank control group (3.55 +/- 1.56) and DMSO group (4.16 +/- 0.52), respectively. The expression of PGC- 1alpha was significantly increased in the IPC and DPC groups and the differences were statistically significant compared to the I/R, blank control and DMSO groups, i.e., P < 0.01 for IPC group and P < 0.05 for DPC group. However, there was no significant difference between the IPC and DPC groups (P > 0.05). Flameng score: IPC group (0.44 +/- 0.13), DPC group (0.47 +/- 0.10), I/R group (1.78 +/- 0.14), blank control group (1.70 +/- 0.03) and DMSO group (1.68 +/- 0.06). The Flameng score of the IPC and DPC groups was statistically significantly different as compared to the I/R group, blank control group and DMSO group (P < 0.01), but no significant difference was detected between the IPC and DPC groups (P > 0.05). CONCLUSION: IPC and DPC have a protective effect on myocardial mitochondria, and their mechanism of action may be related to activation and over-expression of PGC-1alpha.

[Diabetes counteracts the protective effect of the diazoxide preconditioning on ischemic reperfused rat heart].

OBJECTIVE: To explore the impact of diabetic condition on the protective effect of diazoxide preconditioning (DPC) on ischemic-reperfused (I/R) myocardium in rats. METHODS: Thirty normal male Sprague-Dawley rats were divided into 3 groups, including non-diabetic control group, non-diabetic I/R group, and non-diabetic I/R DPC group. Thirty diabetic male rats were also divided into the same 3 groups. The Langendorff isolated heart perfusion models were established. The control groups had a 90 min perfusion without any intervention. The I/R groups had a 30 min equilibration period, a 30 min ischemia, and a 30 min reperfusion. The I/R DPC groups had a 10 min equilibration, two cycles of 100 micromol/L diazoxide perfusion, 5 min each, followed by a 5 min diazoxide-free period before the 30 min ischemia and a 30 min reperfusion. The recovery rate of the left ventricular function, including cardiac output, left ventricular developed pressure (LVDP), and the maximum change rate of left ventricular pressure rise and fall (+/- dp/dt(max)) were recorded. The activity of creatine kinase in coronary outflow and activities of malonyldialdehyde, and superoxide dismutase in myocardium were detected. Myocardial water content was also assessed. RESULTS: In non-diabetic rats, the content of creatine kinase, malonyldialdehyde and water content were significantly decreased in I/R DPC group compared with those in I/R group. Furthermore, in I/R DPC group, the activity of superoxide dismutase and the recovery rate of the left ventricular function, including cardiac output, LVDP and +/- dp/dt(max), were significantly increased compared with those in I/R group (P < 0.05). By contrast, there were no significant changes between I/R DPC group and I/R group in diabetic rats (P > 0.05). CONCLUSION: Diabetes counteracts the protective effect of the diazoxide preconditioning on ischemic reperfused rat heart, which may be related with acute insulin resistance in cardiomyocytes.

Role of nitric oxide during early phase myocardial ischemic preconditioning in rats.

BACKGROUND: To date, there have been no reports on altered nitric oxide (NO) content in ischemia/reperfusion with regard to in vivo preconditioning procedures. These studies are important for understanding the mechanisms of NO during early myocardial ischemic preconditioning. The aim of the present study was to investigate the mechanisms of NO during early myocardial ischemic preconditioning by measuring levels of NO and cyclic guanosine monophosphate (cGMP), as well as activity of nitric oxide synthase (NOS) in ischemia/reperfusion with respect to preconditioning in rats. METHODS: Sixty-six female Sprague-Dawley rats were randomly divided into four groups: ischemic preconditioning group (IP), ischemia/reperfusion group (I/R), control group (CON), and preconditioning procedure group (PC). In the PC group, rats were further divided into PC1-, PC1 +, PC2-, PC2 +, PC3-, and PC3 + subgroups. Rats underwent left coronary artery occlusion and reperfusion, and subsequently, NOS activity and levels were assessed with spectrophotometric analysis. cGMP contents were measured with radioimmunoassay. RESULTS: The level of NO and cGMP, as well as the activity of NOS, were significantly higher in the IP group compared to the I/R and CON groups (P < 0.05). During preconditioning prior to prolonged ischemia, NO and cGMP levels varied markedly with ischemia and reperfusion. The levels of NO repeatedly increased when the heart was exposed to three episodes of 5-minute ischemia, and were almost completely reversed during each reperfusion period. NO and cGMP levels were significantly different between the 5-minute period of ischemia and the same period of reperfusion during preconditioning. CONCLUSIONS: NO plays an important role during early phase myocardial ischemic preconditioning in rats. NO and cGMP could be triggers and mediators of early phase myocardial ischemic preconditioning. Altered NOS activity following ischemic stress could be the primary inducer of higher NO levels detected. NO and cGMP fluctuations might be the trigger for protection during early phase myocardial ischemic preconditioning.

[Protective effect of ischemia and diazoxide preconditioning on postischemic reperfused myocardium and possible mechanism thereof].

OBJECTIVE: To study the protective mechanism of ischemic preconditioning (IPC) and diazoxide preconditioning (DPC) against myocardium ischemia-reperfusion (I/R) injury. METHODS: The hearts were taken out from 30 male Wistar rats and were divided randomly into 3 equal groups: I/R group undergoing 30-min equilibration perfusion and 30-min ischemia and then 60-min reperfusion, IPC group undergoing 10-min equilibration perfusion and then two cycles of 5 min ischemia interspersed with 5 min reperfusion prior to 30 min ischemia and a 60-min reperfusion, and DPC group undergoing 10-min equilibration perfusion and 2 cycles of 5 min of 100 microM diazoxide perfusion followed by 5-min drug-free period before the 30 min ischemia and 60-min reperfusion. Frozen sections of myocardium at the cardiac apex were made and immunohistochemical staining was used to detect the expression of peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC-1alpha). Ultrathin sections 70 nm thick were made and transmission electron microscopy was used to detect the structure of the mitochondria with the Flameng scoring system. RESULTS: The PGC-1alpha expression of the IPC and DPC groups were significantly higher than that of the I/R group (P<0.01 and P<0.05), however, there was no significant difference in PGC-1alpha is expression between the IPC and DPC groups (P >0.05). The Flameng scores of the IPC and DPC groups were 0.44 +/- 0.13 and 0.47 +/- 0.10 respectively, both significantly higher than that of the I/R group (1.78 +/- 0.14, both P <0.01), however, there was no significant difference between IPC and DPC groups (P>0.05). CONCLUSION: IPC and DPC can protect myocyte mitochondria from the injury of ischemia/ reperfusion. The cardioprotective effects of IPC and DPC may be concerned with the activation and high expression of PGC-1alpha.

[Clinical analysis of surgical procedures and outcomes for corrected transposition of great arteries with heart anomaly].

OBJECTIVE: To determine the outcome of anatomically corrective repair and traditional repair of corrected transposition of great arteries (c-TGA) with heart anomaly. METHODS: From April 2002 to December 2006, nineteen patients including fourteen male and five female with c-TGA, underwent operations, age ranged from 2 to 22 years old and weight ranged from 10 to 48 kg. Fifteen of them received anatomically corrective repair and the other four received traditional repair. Eighteen patients were referred to SLL (segmental anatomy) in situs solitus while fifteen of them with levocardia and three with dextrocardia. One patient was referred to IDD (segmental anatomy) in situs inversus with levocardia. Associated cardiac lesions included ventricular defect in eighteen patients, double outlet of right ventricle in one patient, pulmonary stenosis in seventeen patients and pulmonary hypertension in two patients. The operative procedures to anatomically correct atrioventricular discordance included an atrial switch plus a ventricle-arterial switch. The atrial switch was performed using the modified Senning procedure (n=13), Senning procedure (n=1) and Mustard procedure (n=1). The ventricle-arterial switch was performed using a Rastelli procedure (n=13) or an arterial switch (n=2). The patients underwent Mustard and Rastelli procedure had received bi-direct Gleen shunt due to postoperative high pressure of superior vena cava. Three patients underwent traditional cardiac repair because of small ventricular septal defect and one patient was reoperated to undergo traditional cardiac repair because of left ventricular failure after received anatomically corrective repair. RESULTS: In the patients received anatomically corrective repair, there was one early operative death received a modified Senning atrial switch and an arterial switch. The cause of death was acute myocardial failure due to imperfect coronary transfer. The postoperative complications included severe low cardiac output syndrome (n=1), temporary atrioventricular block (n=1) and thorax cavity fluidify (n=1). The survivors were followed up for 6 months to 4 years. All were sinus cardiac rhythm and in NYHA class I or II. There was no death in the patients received traditional repair. Four patients were followed up for 1 year. Three patients were in NYHA I or II class and one patient in class II. CONCLUSIONS: Anatomically corrective repair of c-TGA can be performed with good operative survival and intermediate-term outcome. The patients with good right ventricular function and well developed tricuspid valve who were difficult to undergo anatomically corrective repair might be fit to receive traditional repair.

[Study of cardiopulmonary adaptation during exercise in patients after extracardiac conduit total cavopulmonary connection].

OBJECTIVE: To study cardiopulmonary physiology during exercise in patients after extracardiac total cavopulmonary connection (ECTCPC). METHODS: Twenty-six patients were studied after ECTCPC by exercise testing with bicycle treadmill protocol. Heart rate (HR), blood pressure (BP), respiratory frequency (RF) and pulse oxygen saturation (SpO(2)) were measured continuously; twenty-six patients suffered from Fallot 4 underwent biventricular repair were also studied as control group. RESULTS: In ECTCPC group, HR, BP, SpO(2) and RF all increased with exercise below 3 grade; when exceed 4 grade, BP, SpO(2) decreased and RF kept increasing. Compared with control group, HR, RF were higher (t = 2.13, P < 0.05; t = 2.31, P < 0.05), SpO(2) was lower (t = 2.46, P < 0.05) under the quiescent condition; When exceed 3 grade, HR, BP, SpO(2) decreased more significantly, but RF increased continuously. In fenestration group after ECTCPC, HR reached the top at 5 grades, but in group without fenestration it reached the top at 3 grades; In the whole process of exercising, RF kept higher and SpO(2) kept lower in fenestration group. CONCLUSIONS: The ECTCPC patients showed obviously exercise limitation. Totally bypass of sinoatrial node in this operation may have some adverse effects on the integer regulation of HR.

Coexisting ventricular septal defect affects the features of ruptured sinus of Valsalva aneurysms.

OBJECTIVES: To determine the correlation exists between ventricular septal defect (VSD) and ruptured sinus of Valsalva aneurysm (RSVA). Methods: Between September 2003 and April 2014, 80 RSVA patients underwent surgical repair. These patients were retrospectively divided into two groups: the VSD group (38 cases) and the non-VSD group (42 cases).  Results: Rupture points of SVA originated more frequently in the right coronary sinus (RCS) of patients in the VSD group than those in the non-VSD group (p=0.002). In the VSD group, more than 92.1% tended to rupture into the right ventricular outflow tract. The rupture points are diverse in the non-VSD group. A significant difference was found in rupture points of RSVA between the two groups (p less than 0.001). Patients in the VSD group presented with aortic valve disease more often than those in the non-VSD group (p less than 0.001). A total of 67 patients were repaired with a patch at the opening of RSVA; of those, all patients in VSD group and 29 patients in non-VSD group were repaired with a patch. Nine patients in non-VSD group received transcatheter closure of RSVA. Conclusion: The presence or absence of VSD affects the rupture points of SVA, aortic valve disease involved, and therapeutic schedule. Ruptured sinus of Valsalva aneurysm type should be clinically modified on the basis of presence or absence of VSD.

[Clinical analysis on surgical treatment of single atrium].

OBJECTIVE: To summarize the experience of surgical treatment of single atrium. METHODS: From August 1984 to August 2004, there were 33 patients with single atrium in our study. Plastic surgery for mitral valves were performed for 30 cases with mitral insufficiency. Plastic surgery for tricuspid valves were performed for 18 cases with tricuspid valve insufficiency. There were 3 cases only with complete absence of atrial septum. There were 14 cases with left superior vena cava. All new atrial septums were made with patches including 24 autologous pericardial patches and 9 terylene patches. Complicate abnormalities were corrected in the same time. Tow suture techniques were used in operations to prevent conductive system block, and plastic surgery for mitral valves were performed until the mitral valves were sufficiency. RESULTS: There weren't death and conductive system block after operation in the group. One case was low-grade mitral insufficiency and the others weren't mitral insufficiency. Twenty-five cases were followed up from 3 months to 11 years, and they could work and study normally. CONCLUSIONS: Single atrium should be operated as early as possible. The key of surgery is to prevent conductive system block, to properly correct mitral insufficiency and to drastically correct complicated abnormality. The new atrial septum should be made by patch and an autologous pericardial patch is the first selection.

[Surgical treatments and results of pulmonary atresia with ventricular septal defect].

OBJECTIVE: To evaluate the indication and operative program of ventricular septal defect with pulmonary atresia (VSD-PA). METHODS: From June 1984 to March 2005, there were 32 patients with VSD-PA, which underwent 33 operations. Among them, 15 were males and 17 were females. The ages ranged from 6 months to 9 years. There were 9 patients with aortopulmonary collateral arteries. The operations included central aorta-pulmonary shunts 3 cases, one stage complete repair 27 cases and one stage unifocalization with VSD open 2 cases. RESULTS: There were early 5 death including one death after aorta-pulmonary shunt and 4 deaths after one stage complete repair. The causes of death were severe low cardiac output (2 patients), respiratory function failure (1 patient), multiorgan function failure (1 patient) and severe infect (1 patient). Twenty-one patients were followed up from 3 months to 15.5 years. Heart function (NYHA) was class I or II in 19 cases and class III or IV in 2 cases. CONCLUSIONS: The operative indication and methods mainly depend on the developing of pulmonary arteries and aortopulmonary collateral arteries. Completely surgical repair of patients with VSD-PA can be achieved with acceptable mortality.

[The treatments and results of tetralogy of Fallot with major aortopulmonary collateral arteries].

OBJECTIVE: To evaluate the indication and operative program of complete repair of tetralogy of Fallot with major aortopulmonary collateral arteries (TOF-MAPCA). METHODS: From January 2000 to May 2004, 9 patients with TOF-MAPCA including 5 patients with pulmonary atresia underwent complete surgical repair, 6 of them were male and 3 were female. The ages ranged from 3 to 9 years. All patients underwent corrected operations with moderate hypothermia and cardiopulmonary bypass. Transcatheter occlusion of MAPCA was performed in 5 patients just before corrected operation. Ligation of MAPCA was performed in 1 patient in the same time of cardiac corrected operation. Midline one-stage complete unifocalization and repair were performed in 3 patients with pulmonary atresia. RESULTS: There was one early death. The cause of death was spinal cord hemorrhage. There was no death then. Eight patients were followed up from 3 month to 4 years. Heart function (NYHA) was class I or II in 7 patients and III in 1 patient. CONCLUSIONS: Completely surgical repair of patients with TOF-MAPCA should be performed as early as possible, which can achieve with satisfactory results by transcatheter occlusion of MAPCA or one-stage unifocalization.

[The effects of inhaled nitric oxide on pulmonary vascular resistance in patients after total cavopulmonary connection].

OBJECTIVE: To study the effects of inhaled nitric oxide (NO) on pulmonary vascular resistance in patients after total cavopulmonary connection (TCPC). METHODS: Fifty-two patients after TCPC were evaluated, of them 24 patients were administered with inhaled nitric oxide in the early postoperative period. The cardiac index (CI) and pulmonary vascular resistance (PVR) were compared before and after inhaled NO. RESULTS: In experimental group, after inhaled NO, partial pressure of oxygen in artery/fraction of inspired oxygen increased from 161 +/- 17 to 193 +/- 23 (t = 2.75, P < 0.01); CI from (2.86 +/- 0.24) L.min(-1).m(-2) to (3.13 +/- 0.22) L.min(-1).m(-2) (t = 2.25, P < 0.05); PVR decreased from (4.2 +/- 0.5) U/m(2) to (3.8 +/- 1.4) U/m(2) (t = 2.29, P < 0.05); central venous pressure (CVP) from (17.0 +/- 1.8) mm Hg to (15.0 +/- 1.1) mm Hg, decreased 11.7%. Compared with the control group, respirator time decreased from (86 +/- 27) h to (54 +/- 18) h (t = 2.29, P < 0.05); ICU time from (6 +/- 2) d to (4 +/- 2) d (t = 2.32, P < 0.05); But hydrothorax drainage and length of stay had no significant difference. CONCLUSIONS: Though inhaled NO, there is no significant long-term effects in patients after TCPC, but it may play an important role in the management of low cardiac output syndrome and high cava pressure caused by reactive elevated pulmonary vascular resistance in the early postoperative period of TCPC.

[Surgical treatment on residual shunt after repair of ventricular septal defect].

OBJECTIVE: To summarize the experience in surgical treatment of residual shunt after repair of ventricular septal defect and investigate the position of the residual shunts. METHODS: Between January 1979 and May 2003, re-operations on residual shunt after repair of ventricular septal defect were performed in 37 patients with congenital heart disease including ventricular septal defect, tetralogy of Fallot, double outlet right ventricle in 19, 17 and 1 patients, respectively. It accounted for 0.21% (37/18000) of open heart operations performed during these years. The patients included 26 males and 11 females with age from 3 months to 53 years (mean 16 +/- 12 years). The residual shunt was diagnosed by postoperative murmur and echocardiography. Twenty-six cases were repaired with patch and 11 cases were closed directly with mattresses sutures. RESULTS: Two patients (2/37, 5%) died within 48 hrs postoperatively. The results in other 35 patients followed up after surgery from 3 months to 15 years were satisfactory. CONCLUSIONS: Most of the residual shunts occurred in base of septal leaflet of tricuspid valve, the second and the first transfer suture respectively. Effects of reoperations on residual shunts were satisfactory.

[Surgical treatment of secundum atrial septal defects in adults over 30 years old].

OBJECTIVE: To summarize the experience of surgical treatment of secundum atrial septal defects in adults over 30 years old. METHODS: There were 469 patients with secundum atrial septal defects in our study (male 144, female 325; ages 30-68, mean 38.6 years old). There were 105 cases with pulmonary hypertension and 458 cases with arrhythmia in the group. Surgical closure of defects were performed in all patients. Surgical closure of 358 cases were done by patches including 305 autologous pericardial patches. The low dose (6 x 10(-6)) nitric oxide inhalation was used in 25 postoperative patients with pulmonary hypertension. Right sided maze procedures were done in 5 cases with atrial fibrillation. RESULTS: Surgical mortality was 0.6% (3 cases), the others were healed. In the group, there were 180 cases with arrhythmia, 27 cases with left ventricular function amyoplasia, 28 cases with low cardiac output syndrome, 12 cases in secondary operation for bleeding and 1 case with air-embolism. The level of mean pulmonary artery pressure of 25 postoperative patients with pulmonary hypertension inhaled nitric oxide was down 28.5%. After right sided maze procedures were done in 5 cases with atrial fibrillation, atrial fibrillation disappeared. 352 cases were followed up from 3 months to 20 years (mean 5.6 years). Twenty-nine cases were in class I-II of cardiac function, and the others were better than class I of cardiac function. CONCLUSIONS: Atrial septal defects in adult should be operated as early as possible. When patch is needed, an autologous pericardial patch is the first selection. Inhaled nitric oxide is an effective method to postoperative pulmonary hypertension. The maze operation should be performed for atrial septal defect with atrial fibrillation while the surgical closure of defect was done. During and after operation, much attention should be paid to preventing and curing arrhythmia and protecting and supporting left heart function.

Carvedilol for prevention of atrial fibrillation after cardiac surgery: a meta-analysis.

BACKGROUND: Postoperative atrial fibrillation (POAF) remains the most common complication after cardiac surgery. Current guidelines recommend ß-blockers to prevent POAF. Carvedilol is a non-selective ß-adrenergic blocker with anti-inflammatory, antioxidant, and multiple cationic channel blocking properties. These unique properties of carvedilol have generated interest in its use as a prophylaxis for POAF. OBJECTIVE: To investigate the efficacy of carvedilol in preventing POAF. METHODS: PubMed from the inception to September 2013 was searched for studies assessing the effect of carvedilol on POAF occurrence. Pooled relative risk (RR) with 95% confidence interval (CI) was calculated using random- or fixed-effect models when appropriate. Six comparative trials (three randomized controlled trials and three nonrandomized controlled trials) including 765 participants met the inclusion criteria. RESULTS: Carvedilol was associated with a significant reduction in POAF (relative risk [RR] 0.49, 95% confidence interval [CI] 0.37 to 0.64, p<0.001). Subgroup analyses yielded similar results. In a subgroup analysis, carvedilol appeared to be superior to metoprolol for the prevention of POAF (RR 0.51, 95% CI 0.37 to 0.70, p<0.001). No evidence of heterogeneity was observed. CONCLUSIONS: In conclusion, carvedilol may effectively reduce the incidence of POAF in patients undergoing cardiac surgery. It appeared to be superior to metoprolol. A large-scale, well-designed randomized controlled trial is needed to conclusively answer the question regarding the utility of carvedilol in the prevention of POAF.

Overexpression of ornithine decarboxylase suppresses thapsigargin-induced apoptosis.

Ornithine decarboxylase (ODC), the key enzyme of polyamine biosynthesis, has paradoxical roles in apoptosis. Our published papers show overexpression of ODC prevents the apoptosis induced by many cytotoxic drugs. Thapsigargin (TG) is an inhibitor of the sarcoplasmic/endoplasmic reticulum (ER) Ca(2+) ATPase (SERCA) pumps and causes ER stress-induced apoptosis. We used ODC overexpressing cell lines to examine whether overexpression of ODC inhibits TG-induced apoptosis. Our results indicated overexpression of ODC attenuated TG-induced apoptosis. Overexpression of ODC blocked procaspase-4 cleavage and phosphorylation of protein kinase-like ER-resident kinase (PERK), triggered by TG. It also attenuated the increase in CAAT/enhancer binding protein homologous protein (CHOP). Cells with overexpressed ODC had greater Bcl-2 expression. Overexpression of ODC preserved the expression of Bcl-2, inhibited the increase in Bak and stabilized mitochondrial membrane potential without the influences of TG. Cytochrome c release and down-stream caspase activation were blocked. That is, overexpression of ODC inhibits the mitochondria-mediated apoptotic pathway, induced by TG. Finally, overexpression of ODC maintains the protein and mRNA expression of SERCA. In conclusion, overexpression of ODC suppresses TG-induced apoptosis by blocking caspase-4 activation and PERK phosphorylation, attenuating CHOP expression and inhibiting the mitochondria-mediated apoptotic pathway.