Atrial septal defect repair through limited lateral thoracotomy in children

Objective We have developed a surgical method for atrial septal defect repair through a limited right lateral thoracotomy in which the incision line begins 2 cm caudal from the lower angle of the scapula and ends at the midaxial line, thereby improving patient satisfaction with the cosmetic results of treatment. Methods We performed a retrospective review of 28 patients who underwent isolated atrial septal defect repair through a limited right lateral thoracotomy between January 2002 and August 2004. The mean age and mean body weight at the time of the operation were 85.8 months (range 9–236 months) and 23.0 kg (range 8.0–56.0 kg), respectively. All repaired defects were the ostium secundum type. Results There was no operative or late mortality and no late morbidity after a mean follow-up of 26 months (range 12–41 months). Echocardiography showed no residual shunt in any of the patients. The mean length of the skin incision was 7.8 cm (range 5.0–11.0 cm), and almost all the patients had satisfactory cosmetic results. Conclusion The atrial septal defect repair through a limited right lateral thoracotomy in pediatric patients showed satisfactory surgical results and excellent cosmetic results.     

In normal development pulmonary veins are connected to the sinus venosus segment in the left atrium

Background: Classic theories descibe that the common pulmonary vein develops as an outgrowth from either the sinus venosus or atrial segment. Recent studies show that the pulmonary veins are connected to the sinu-atrial region before its differentiation into a sinus venosus and atrial segment. Methods: The development of the sinu-atrial region with regard to the developing common pulmonary vein and the growth of the atrial septum was investigated in avian embryos, using both scanning electron microscopy and immunohistochemistry. Embryos ranging between stage HH12 and HH28 were incubated with QH-1 that recognizes quail endothelial cells and precursors, HNK-1, that appears in this study to detect the myocardium of the sinus venosus, or with HHF-35, being specific for muscle actins. Also vascular casts of the heart were produced by injecting prepolymerized Mercox into the vascular system. Results: In preseptation stages the common pulmonary vein drains into the left part of the sinus venosus, that is clearly demarcated by the sinuatrial fold and HNK-1 expression. During atrial septation the left part of the sinus venosus, in contrast to the right part, loses its HNK-1 antigen from stage HH23 onwards, while at the same time the sinu-atrial fold in the left atrial dorsal wall flattens and disappears. From stage HH25 onwards HNK-1 expression is restricted to the right part of the sinus venosus, which contributes to the right atrium. The myocardial atrial septum never expresses the HNK-1 antigen, suggesting that the septum is of atrial origin. Discussion: It appeared that the sinus venosus does not only contribute to the sinus venarum of the right atrium, but also to the left atrium. © 1995 Wiley-Liss, Inc.     

Interaction of class III antiarrhythmic drugs with muscarinic M2 and M3 receptors: radioligand binding and functional studies

We have recently reported that class III antiarrhythmic drugs inhibit the muscarinic acetylcholine (ACh) receptor-operated K⁺ current (I _K, ACh) in guinea-pig atrial cells by different molecular mechanisms. The data obtained from the patch-clamp study suggest that d,l-sotalol inhibits I _{K, ACh} by blocking the muscarinic receptors, whereas MS-551 inhibits the K⁺ current by blocking the muscarinic receptors and depressing the function of the K⁺ channel itself and/or the guanine nucleotide-binding protein (G protein). This study was undertaken to determine whether the class III antiarrhythmic drugs d,l-sotalol and MS-551 interact with the muscarinic receptors of cardiac and peripheral tissues. Both drugs inhibited concentration dependently the specific [³H]N-methylscopolamine ([³H]-NMS) binding to membrane preparations obtained from guinea-pig atria and submandibular glands. The competition curves of these drugs for [³H]-NMS binding to glandular membranes were monophasic, suggesting competition with [³H]-NMS at a single site. Although the competition curve of d,l-sotalol for [³H]-NMS binding to atrial membranes was monophasic, that of MS-551 was biphasic and showed high- and low-affinity states of binding. d,l-Sotalol showed slightly, but significantly, higher affinity for cardiac-type muscarinic receptors (M₂) than for glandular-type muscarinic receptors (M₃). The inhibition constant (K _i) for MS-551 in glandular membranes was also slightly greater than the high-affinity K _i value for the drug in atrial membranes. In guinea-pig left atria and ilea, d,l-sotalol shifted the concentration-response curves for the negative inotropic effect and the contracting effect of carbachol in a parallel manner. The slopes of Schild plot were not significantly different from unity, suggesting competitive antagonism, and the pA₂ for d,l-sotalol in left atria was slightly greater than that in ilea. MS-551 also shifted the concentration response curve for the negative inotropic effect of carbachol in atrial preparations to a greater extent than that for the contracting effect in ileal preparations, although MS-551 failed to show a pure competitive antagonism. These results suggest that both d,l-sotalol and MS-551 interact with cardiac M₂ and peripheral M₃ receptors, and that at high concentrations they exert anticholinergic activity in cardiac and peripheral tissues.     

Differential coupling of m-cholinoceptors to Gi/Go-proteins in failing human myocardium

Muscarinic acetylcholine receptors (mAChRs) mediate their main cardiac effects via pertussis toxin-sensitive G-proteins. Physiological effects differ considerably between atrium and ventricle, and it is unknown to which extent these differences derive from selective receptor-G-protein coupling or further downstream events. We have characterized specific coupling between mAChRs and Gi/Go-protein isoforms in atrial and ventricular myocardium by agonist-dependent photoaffinity labeling with [(32)P]azidoanilido GTP (aaGTP) and immunoprecipitation in sarcolemmal membranes from terminally failing human hearts. The total amount of mAChRs, as determined by specific binding of [(3)H]QNB, was significantly higher in right-atrial (RA +/- SEM, 959 +/- 68 fmol/mg, n = 4) than in left-ventricular membranes (LV, 582 +/- 53 fmol/mg, n = 6). Standardized immunoblots revealed that Gialpha-2 was the predominant subtype in both regions. A 40-kDa splice variant of Goalpha (Goalpha-1 and/or Goalpha-3) was almost exclusively detectable in RA. Levels of Gialpha-3 and a 39-kDa splice variant of Goalpha (Goalpha-2) were also higher in RA. Basal aaGTP binding was higher in RA than in LV for all Gialpha/Goalpha subtypes. The carbachol (10 micromol/l)-induced increase in aaGTP binding was significantly higher in RA than in LV for Goalpha-1/3 (336 +/- 95% of LV, n = 4) and for Gialpha-3 (211 +/- 83%), lower for Gialpha-2 (42 +/- 5%), and was similar in both regions for Goalpha-2 (130 +/- 62%). The differential coupling of mAChRs in human RA and LV suggests that the initiation of different physiological responses to mAChR stimulation starts with signal sorting at the receptor-G-protein level.     

Changes in DNA content,number of nuclei and cellular dimensions of young rat atrial myocytes in response to left coronary artery ligation

Studies of enzymatically isolated myocytes from atria of young male Sprague-Dawley rats at 11 days after left coronary artery ligation show that a major response of atrial myocytes to ventricular infarction is binucleation. In sham-operated animals, 23.2% of left and 15.5% of right atrial myocytes were binucleated, compared to 77.8% of left and 40.5% of right atrial myocytes of infarcted animals. Examination of 150 g and 250 g unoperated control animals indicate that this response is occurring at a time when a small but significant amount of binucleation is also occurring as a normal part of growth. Using a Feulgen-acriflavine-SO₂ method for cytofluorometry, a significant increase in ploidy was seen in left atrial myocytes of infarcted animals over those of sham or control animals. The number of left atrial myocytes in infarcted animals having a ploidy level above 3C was 10.8% above sham values. The mean length of binucleated myocytes of left atrium was significantly greater in infarcted animals (119.8 μm) than in sham-operated animals (97 μm) and the mean length of mononucleated myocytes was greater in infarcted animals (104.1 μm) than in sham-operated animals (77 μm). Thus, cardiac myocytes are capable of a substantial response to a stressful situation by increases in cell length, number of nuclei and ploidy. Study of a model system such as the rat atrium may yield an understanding of the mechanisms involved in the induction of these nuclear changes.     

综合抗凝溶栓治疗对左心房、机械瓣血栓的疗效

目的：探讨华法令、低分子肝素钙、硫酸氯毗格雷和尿激酶联合治疗人工瓣膜置换术后血栓形成的疗效及安全性。方法：32例人工瓣膜置换术后血栓形成患者应用华法令、低分子肝素钙、硫酸氯毗格雷（机械瓣加用尿激酶）联合治疗，观察血压，心功能，凝血指标，血、尿常规及副作用。结果：经治疗8～20d后血栓消失21例（65．6％），明显缩小10例（31．3％），出现少量出血7例（21．9％），经及时处理后缓解，无严重出血。结论：华法令、低分子肝素钙、硫酸氯吡格雷和尿激酶联合治疗人工瓣膜置换术后血栓安全有效。     

应变率成像定量评价孤立性房颤患者局部左房功能的研究

目的:探讨应变率成像技术定量评估孤立性房颤患者左房局部功能的临床应用价值。材料与方法:随机选取来我院就诊的孤立性房颤患者50例,行常规超声心动图检查,在超声组织速度成像状态下获取心尖四腔、两腔、左室长轴切面动态图像,将左房间隔壁、侧壁、前壁、下壁、前间隔和后壁分别按照基底段、中间段和心尖段划分为18个节段。观察左房各壁的基底段和中间段,测量收缩期峰值应变率(SR-LAs)和舒张期应变率(SR-LAe和SR-LAa),并与40例健康人相应节段心肌比较。结果:正常对照组40例480个被研究心肌节段,470个节段的应变率-时间曲线的形态整体有一定的规律性,SR-LAs、SR-LAe和SR-LAa值随个体变化不大。孤立性房颤患者组被研究600个心肌节段,应变率-时间曲线显示523个节段失去正常形态,轮廓杂乱,波峰低小、消失甚至倒置,峰值较正常心肌节段明显降低(P0.05)。结论:用应变率成像技术能够无创的定量评价孤立性房颤所致的左房功能异常。