阿魏酸钠联合胰激肽原酶治疗早期糖尿病肾病40例临床观察

目的观察阿魏酸钠联合胰激肽原酶治疗早期糖尿病肾病的临床疗效。方法将80例早期糖尿病肾病患者随机分成两组,对照组 40例,给予阿魏酸钠注射液0. 3 g加入0. 9%氯化钠注射液250 mL静脉滴注,每日1次;治疗组40例,在对照组基础上联合胰激肽原酶片240U 口服,每日3次,治疗4周。观察两组治疗前后尿微量白蛋白排泄率（UAER）及血清胱抑素C（Cys C）的变化。结果两组均能降低UAER及CysC水平（p〈0.05）,但治疗组更显著（p〈0.01）。结论阿魏酸钠联合胰激肽原酶治疗早期糖尿病肾病疗效更好。     

利拉鲁肽对糖尿病大鼠肾脏病变的影响

目的探讨利拉鲁肽对糖尿病大鼠肾脏病变的影响。方法高脂高糖饲料喂养1个月后,予小剂量链脲佐菌素（STZ,30mg／kg）腹腔注射诱导建立2型糖尿病大鼠模型。将雄性SD大鼠,随机分为正常对照组（NC组）、糖尿病组（DM组）、利拉鲁肽100μg／kg组（L100组）、利拉鲁肽200μg／kg组（L200组）4组。NC组与DM组均行生理盐水腹腔内注射,利拉鲁肽组分别予利拉鲁肽100μg／kg或200μg／kg腹腔内注射干预每日2次。干预12周后,测体重、肾重、尿白蛋白排泄率、血糖、血肌酐、尿素氮。用光镜、电镜观察各组大鼠肾组织形态、结构的变化。结果利拉鲁肽可抑制糖尿病大鼠肾重／体重指数（KW／BW）、平均肾小球体积（MGV）、系膜面积比（FMA）的增加并降低尿蛋白水平,改善其肾功能（P〈0．05）;可减轻足突融合、基底膜增厚、系膜增生等病理改变。与L100组相比,L200组大鼠肾脏各项指标改善更明显,病理改变减轻更明显。结论利拉鲁肽对糖尿病大鼠肾脏有保护作用,且200μg／kg（每日2次）较100μg／kg（每日2次）的剂量效果更好。     

全方向M型超声心动图对糖尿病心肌病患者左心室收缩功能的研究

目的 探讨全方向M型超声心动图在评价糖尿病心肌病（DCM）左心室心肌局部收缩功能中的效果。方法选择62例DCM患者（研究组）、54例正常人（对照组）作为研究对象,采集各组左心室短轴16个节段的全方向M型超声心动图曲线,分别于收缩期和舒张期测量心内膜运动速度（Ven）、心外膜运动速度（Vep）及相对应的室壁厚度（D）,计算心肌速度梯度（MVG）并进行对照分析。结果 研究组左心室短轴平面多数节段舒张期的MVG低于对照组,差异有统计学意义（P〈0.05）,研究组收缩期只有少部分节段MVG低于对照组,差异有统计学意义（P〈0.05）。结论 DCM患者心脏整体收缩及舒张功能在正常范围时就可出现局部心肌运动功能异常,全方向M型超声心动图可用于定量评价其局部心肌运动功能的变化。     

瞬时外向钾电流在糖尿病心肌病电重构中的作用

目的：探讨糖尿病心肌病（DCM）大鼠心室肌细胞瞬时外向钾电流（Ito）的变化,了解其在电重构中的作用。方法选用20只健康成年SD大鼠,随机分为对照组（n=10）和DCM组（n=10）,并通过病理组织学证实为DCM心肌病理学改变。分别对两组大鼠采用改进的耐钙成年大鼠急性酶分离方法分离心肌细胞,运用膜片钳技术以全细胞模式分别记录两组大鼠心室肌单细胞的Ito和膜电容,并分析比较两组大鼠心室肌Ito的变化。结果与对照组比较,DCM组大鼠左心室心肌细胞的Ito电流密度显著低于对照组[＋70 mV时,（16.80±9.10） pA/pF v s（36.25±5.20）pA/pF]（P〈0.05）,DCM组的Ito的I-V曲线明显较对照组下移。结论 DCM的Ito数量明显减少,在DCM心肌电重构中起着重要作用。 Ito的减少及Ito通道的分布密度不同,可导致动作电位时程与有效不应期发生变化,可能与临床严重心律失常的发生有关。     

前列地尔联合洛汀新治疗早期糖尿病肾病的效果观察

目的：探讨前列地尔联合洛汀新治疗早期糖尿病肾病的效果。方法选取2012年2月~2014年1月本院收治的82例早期糖尿病肾病患者为研究对象,将82例患者遵循随机分配的方式分为对照组（洛汀新组）41例和观察组（前列地尔联合洛汀新组）41例,检测并比较两组患者治疗前后的肾功能及肾血流相关指标。结果观察组患者治疗后1、2周的肾功能及肾血流相关指标均显著优于对照组,差异有统计学意义（P〈0.05）。结论前列地尔联合洛汀新治疗早期糖尿病肾病的效果较好,对患者的肾脏功能及血供改善作用均相对明显。     

格列齐特对2型糖尿病大鼠心肌缺血预适应保护作用的影响

目的 探讨格列齐特对2型糖尿病大鼠离体心脏缺血预适应保护作用的影响。方法 将造模成功的2型糖尿病大鼠随机分为糖尿病缺血预处理组、糖尿病再灌注损伤组、糖尿病缺血预处理+格列齐特组、糖尿病再灌注损伤+格列齐特组。将对照组大鼠随机分为缺血预处理组、再灌注损伤组。分别于平衡灌注后、缺血再灌注开始及再灌注60 min末3个时间点分别收集冠脉流出液,测定乳酸脱氢酶（LDH）、肌酸激酶（CK）、肌酸激酶同工酶（CK-MB）的释放量;在再灌注末,取左心室游离壁心肌组织,进行荧光定量PCR检测心肌ATP敏感性钾离子（KATP）通道组成亚基Kir6.2和SUR2A mRNA的表达;免疫组织化学技术检测其蛋白的表达水平。结果 对于糖尿病非药物治疗大鼠,糖尿病缺血预处理组与糖尿病再灌注损伤组比较,冠脉流出液中LDH、CK、CK-MB无明显差异;Kir6.2和SUR2A mRNA及蛋白表达也均无明显差异。而与糖尿病缺血预处理组、糖尿病再灌注损伤+格列齐特组比较,糖尿病缺血预处理+格列齐特组均降低了糖尿病大鼠心肌缺血预处理后缺血再灌注损伤冠脉流出液中LDH、CK、CK-MB释放量（P<0.05）;也使Kir6.2 mRNA及蛋白表达明显增加（P<0.05）;但SUR2A mRNA表达差异无统计学意义。与糖尿病再灌注损伤+格列齐特组比较,糖尿病缺血预处理+格列齐特组SUR2A蛋白表达水平也增加明显（P<0.05）。结论 格列齐特对心肌缺血预处理的保护作用无不利影响,反而能改善2型糖尿病大鼠心肌缺血预适应的保护作用。     

COVID-19 Severity Potentially Modulated by Cardiovascular-Disease-Associated Immune Dysregulation

Patients with underlying cardiovascular conditions are particularly vulnerable to severe COVID-19. In this project, we aimed to characterize similarities in dysregulated immune pathways between COVID-19 patients and patients with cardiomyopathy, venous thromboembolism (VTE), or coronary artery disease (CAD). We hypothesized that these similarly dysregulated pathways may be critical to how cardiovascular diseases (CVDs) exacerbate COVID-19. To evaluate immune dysregulation in different diseases, we used four separate datasets, including RNA-sequencing data from human left ventricular cardiac muscle samples of patients with dilated or ischemic cardiomyopathy and healthy controls; RNA-sequencing data of whole blood samples from patients with single or recurrent event VTE and healthy controls; RNA-sequencing data of human peripheral blood mononuclear cells (PBMCs) from patients with and without obstructive CAD; and RNA-sequencing data of platelets from COVID-19 subjects and healthy controls. We found similar immune dysregulation profiles between patients with CVDs and COVID-19 patients. Interestingly, cardiomyopathy patients display the most similar immune landscape to COVID-19 patients. Additionally, COVID-19 patients experience greater upregulation of cytokine- and inflammasome-related genes than patients with CVDs. In all, patients with CVDs have a significant overlap of cytokine- and inflammasome-related gene expression profiles with that of COVID-19 patients, possibly explaining their greater vulnerability to severe COVID-19.     

Risk factors for postoperative sepsis-induced cardiomyopathy in patients undergoing general thoracic surgery: a single center experience

BackgroundThe current study aimed to investigate the incidence of sepsis-induced cardiomyopathy (SICM) in patients who received general thoracic surgery, along with the risk factors and management strategies for this complication.MethodsThe clinical records of 163 patients with postoperative sepsis were retrospectively reviewed. After propensity score matching, 144 patients were divided into 2 groups by stroke volume: the SICM group (n=72) and the non-SICM group (n=72).ResultsThe overall incidence of postoperative SICM was 53.99%. Multiple logistic regression analysis showed that stroke volume and C-reactive protein were independent predictors of mortality in patients with postoperative sepsis. Statistical analysis by t-test and χ² test indicated that mortality (P=0.000), B-type natriuretic peptide (P=0.001), left ventricular ejection fraction (P=0.000), the mitral peak velocity of early filling/early diastolic mitral annular velocity (E/e’) (P=0.049), C-reactive protein (P=0.016), procalcitonin (P=0.013), serum creatinine (P=0.016), platelets (P=0.028), and lactic acid (P=0.002) were significantly associated with the occurrence of postoperative SICM. Among these parameters, B-type natriuretic peptide was identified as the best biomarker for predicting SICM by receiver operating characteristic (ROC) curve analysis.ConclusionsIt is vital to improve the diagnosis and standard management of SICM. A combined strategy comprising early detection of suspected infection, adequate use of antibiotics, close monitoring, effective drainage, and supportive care may improve the outcomes of patients with postoperative SICM.     

Surgical septal myectomy outcome for obstructive hypertrophic cardiomyopathy after alcohol septal ablation

BackgroundAlthough surgical treatment of residual obstruction after alcohol septal ablation (ASA) is often challenging in patients with obstructive hypertrophic cardiomyopathy (OHCM) there are very few relevant clinical reports. Thus, outcomes of surgical septal myectomy (SSM) in this subgroup of patients remain to be determined. Therefore, this study aimed to determine the surgical and follow-up outcomes in patients with OHCM exhibiting residual obstruction after ASA.MethodsWe collected case data for 62 patients with OHCM and residual obstruction after ASA who underwent SSM at Fuwai Hospital between January 2002 and June 2019. Propensity score matching with patients having had a myectomy as the only invasive procedure—was conducted in a 1:2 ratio. Echocardiography parameters, surgery results, and follow-up outcomes were compared between the groups.ResultsThe prior ASA group had a higher incidence of complete atrioventricular block (AVB) and subsequently postoperative permanent pacemaker (PPM) implantation than the primary myectomy group (9.7% vs. 1.6%, P=0.01). Two patients died within 30 days after surgery in the prior ASA group, and one patient died in the primary myectomy group, with an operative mortality rate of 3.2% and 0.8%, respectively (P=0.2). The 5-year event-free survival rate was 86.0% in the prior ASA group (median follow-up period: 3.2 years; mean: 3.9±2.6 years; maximum, 10.6 years) and 88.5% in the primary myectomy group (median follow-up period: 2.4 years; mean 2.8±1.7 years; maximum, 9.1 years) (P=0.2). During follow-up, four of 62 (6.5%) patients in the prior ASA group and one of 124 (0.8%) patients in the primary myectomy group progressed to advanced heart failure (P=0.025).ConclusionsPatients with OHCM following ASA are at an increased risk of developing AVB after SSM. Their surgical outcomes, and long-term survival rate were satisfactory and, osimilar to those for patients having had a myectomy as the only invasive procedure. In addition, they had an increased risk of advanced heart failure after SSM in the present study.     

Torsade de pointes induced by intravenous amiodarone therapy accompanied by marked augmentation of the transmural dispersion of repolarization in a patient with tachycardia‐induced‐cardiomyopathy

We report a 77‐year‐old human on renal dialysis for end‐stage renal disease with heart failure and atrial fibrillation (AF) complicated by a high ventricular frequency. The underlying disease was thought as tachycardia‐induced‐cardiomyopathy. Intravenous infusion of amiodarone was initiated, and direct current cardioversion succeeded in converting AF to sinus rhythm. Then, excessive increases in the QT and Tpeak‐Tend (Tp‐e) intervals were seen and hypokalemia induced by hemodialysis led to the development of numerous episodes of torsades de pointes (TdP). Magnesium repletion was effective in preventing TdP, while Tp‐e intervals returned to the previous values 2 days after the discontinuation of amiodarone.