Clinical risk score for postoperative pneumonia following heart valve surgery / 中华医学杂志(英文版)

BACKGROUND@#Postoperative pneumonia (POP) is one of the most common infections following heart valve surgery (HVS) and is associated with a significant increase in morbidity, mortality, and health care costs. This study aimed to identify the major risk factors associated with the occurrence of POP following HVS and to derive and validate a clinical risk score.@*METHODS@#Adults undergoing open HVS between January 2016 and December 2019 at a single institution were enrolled in this study. Patients were randomly assigned to the derivation and validation sets at 1:1 ratio. A prediction model was developed with multivariable logistic regression analysis in the derivation set. Points were assigned to independent risk factors based on their regression coefficients.@*RESULTS@#POP occurred in 316 of the 3853 patients (8.2%). Multivariable analysis identified ten significant predictors for POP in the derivation set, including older age, smoking history, chronic obstructive pulmonary disease, diabetes mellitus, renal insufficiency, poor cardiac function, heart surgery history, longer cardiopulmonary bypass, blood transfusion, and concomitant coronary and/or aortic surgery. A 22-point risk score based on the multivariable model was then generated, demonstrating good discrimination (C-statistic: 0.81), and calibration (Hosmer-Lemeshow χ2 = 8.234, P = 0.312). The prediction rule also showed adequate discriminative power (C-statistic: 0.83) and calibration (Hosmer-Lemeshow χ2 = 5.606, P = 0.691) in the validation set. Three risk intervals were defined as low-, medium-, and high-risk groups.@*CONCLUSION@#We derived and validated a 22-point risk score for POP following HVS, which may be useful in preventive interventions and risk management.@*TRIAL REGISTRATION@#Chictr.org, ChiCTR1900028127; http://www.chictr.org.cn/showproj.aspx?proj=46932.

Analysis of protective effects of Chaihu Jia Longgu Muli Tang against ischemic stroke by combining traditional Chinese medicine pathogenesis and efficacy with modern pathology and pharmacology / 中国中药杂志

Chaihu Jia Longgu Muli Tang is a classical Chinese formulas treating Shaoyang syndrome complicated with Yangming syndrome according to Treatise on Febrile Diseases. This formula is used in mental disorder, nervous system, gynecologic, andrologic, and cardiovascular disease. However, its therapeutic effect on ischemia stroke and its mechanism is far from clear. In clinical practice, we have found that this formula is effective in treating ischemic stroke, which can shorten the course of the disease and reduce recurrence. The characteristics of this formula include: Shaoyang cardinal disadvantageous syndrome, mental and nervous symptoms, retained fluid punched upward syndrome and accumulation of heat in the stomach and intestines. By combining traditional Chinese medicine (TCM) pathogenesis and efficacy with modern pathology and pharmacology, we proposed that the TCM pathogenesis of stroke, which is characterized by hyperactivity of heat combining with phlegm, stasis and water drink, is consistent with syndromes and corresponding pathology targeted by Chaihu Jia Longgu Muli Tang, including the stress brain edema zone around the ischemic lesion, the increase of intracranial pressure, the excitement of sympathetic nerve, the release of monoamine neurotransmitter, the hypofunction of autonomic nervous system after stroke, and gastrointestinal stress response. Furthermore, the pharmacological mechanism of Chaihu Jia Longgu Muli Tang is concentrated on regulation the neuroendocrinology system centered by hypothalamic-pituitary-adrenal axis (HPA), participating in the process of neuron regeneration and apoptosis, oxidative stress, hyperactivity of sympathetic nerve, and inflammatory reaction. These pathological processes are consistent with the pathological changes after ischemic stroke. Therefore, Chaihu Jia Longgu Muli Tang is a key formula for treating ischemic stroke.

Protein kinase C enhances the swelling-induced chloride current in human atrial myocytes / 华中科技大学学报（医学）（英德文版）

Swelling-activated chloride currents (ICl.swell) are thought to play a role in several physiologic and pathophysiologic processes and thus represent a target for therapeutic approaches. However, the mechanism of ICl.swell regulation remains unclear. In this study, we used the whole-cell patch-clamp technique to examine the role of protein kinase C (PKC) in the regulation of ICl.swell in human atrial myocytes. Atrial myocytes were isolated from the right atrial appendages of patients undergoing coronary artery bypass and enzymatically dissociated. ICl.swell was evoked in hypotonic solution and recorded using the whole-cell patch-clamp technique. The PKC agonist phorbol dibutyrate (PDBu) enhanced ICl.swell in a concentration-dependent manner, which was reversed in isotonic solution and by a chloride current inhibitor, 9-anthracenecarboxylicacid. Furthermore, the PKC inhibitor bis-indolylmaleimide attenuated the effect and 4α-PDBu, an inactive PDBu analog, had no effect on ICl.swell. These results, obtained using the whole-cell patch-clamp technique, demonstrate the ability of PKC to activate ICl,swell in human atrial myocytes. This observation was consistent with a previous study using a single-channel patch-clamp technique, but differed from some findings in other species.

Biventricular repair versus uni-ventricular repair for pulmonary atresia with intact ventrical septum: A systematic review / 华中科技大学学报（医学）（英德文版）

The management of pulmonary atresia with intact ventricular septum (PA/IVS) remains controversial. The goal of separating systematic and pulmonary circulation can be achieved by biventricular or uni-ventricular (Fontan or one and a half ventricle repair) strategies. Although outcomes have been improved, these surgical procedures are still associated with high mortality and morbidity. An optimal strategy for definitive repair has yet to be defined. We searched databases for genetically randomized controlled trials (RCTs) comparing biventricular with uni-ventricular repair for patient with PA/IVS. Data extraction and quality assessment were performed following the guidelines of the Cochrane Collaboration. Primary outcome measures were overall survival, and secondary criteria included exercise function, arrhythmia-free survival and treatment-related mortality. A total number of 669 primary citations were screened for relevant studies. Detailed analysis revealed that no RCTs were found to adequately address the research question and no systematic meta-analysis would have been carried out. Nevertheless, several retrospective analyses and case series addressed the question of finding right balance between biventricular and uni-ventricular repair for patient with PA/IVS. In this review, we will discuss the currently available data.

Combined transgenic inhibition of CaMKII and Ik1 on cardiac remodeling / 生理学报

This study was aimed to establish an experimental mouse model of combined transgenic inhibition of both multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and inward rectifier potassium current (Ik1), and to observe whether the specific inhibition of both CaMKII and Ik1 can bring about any effects on cardiac remodeling. Mice were divided into 4 groups: wild type (WT), CaMKII inhibited (AC3-I), Ik1 inhibited (Kir2.1-AAA) and combined inhibition of both CaMKII and Ik1 (AC3-I+Kir2.1-AAA). Mice in each group received electrocardiogram (ECG) and echocardiography examination. ECG in the condition of isoproterenol (ISO) injection was also checked. The whole cell patch clamp technique was used to measure Ik1 and the transient outward potassium current (Ito) from enzymatically isolated myocytes of left ventricle. In the condition of basal status, no significant changes of heart rate, PR interval and QRS interval were observed. No mouse showed ventricular arrhythmias in all of the 4 groups. After ISO injection, each group presented no significant ventricular arrhythmias either. The indexes measured by M-mode (motion-mode) and two-dimensional echocardiography had no significant differences among the four groups. Ik1 in AC3-I group was significantly higher than those in other three groups (P < 0.01) because of the results brought about by CaMKII inhibition. Among the latter three groups, both Kir2.1-AAA group and AC3-I+Kir2.1-AAA group had a significant reduced Ik1 compared with that of WT group, which was due to the Ik1 inhibition (P < 0.01). Ito in AC3-I group was higher than that of the other three groups (P < 0.01), but there were no significant differences in Ito among WT, Kir2.1-AAA and AC3-I+Kir2.1-AAA groups. Thus, combined transgenic myocardial CaMKII and Ik1 inhibition eliminated the up-regulation of Ik1 in CaMKII inhibited mice, and had no effects on cardiac remodeling including heart structure and function as well as arrhythmias at the basic and ISO conditions. The results of this study may provide a basis for the further investigation of combined inhibition of CaMKII and Ik1 in pathogenic cardiac remodeling.