Effect of variable annular reduction on functional tricuspid regurgitation and right ventricular dynamics in an ovine model of tachycardia-induced cardiomyopathy

ObjectiveTo investigate the effect of variable tricuspid annular reduction (TAR) on functional tricuspid regurgitation (FTR) and right ventricular (RV) dynamics in ovine tachycardia-induced cardiomyopathy.MethodsNine adult sheep underwent implantation of a pacemaker with an epicardial lead and were paced at 200 to 240 bpm until the development of biventricular dysfunction and functional TR was noted. During reoperation on cardiopulmonary bypass, 6 sonomicrometry crystals were placed around the tricuspid annulus (TA) and 14 were placed on the RV epicardium. Annuloplasty suture was placed around the TA and externalized to an epicardial tourniquet. After weaning from cardiopulmonary bypass, echocardiographic, hemodynamic, and sonomicrometry data were acquired at baseline and during 5 progressive TARs achieved with suture cinching. TA area and RV free wall strains and function were calculated from crystal coordinates.ResultsAfter pacing, changes in left ventricular (LV) ejection fraction and RV fractional area decreased significantly. Mean TA diameter increased from 25.1 ± 2.9 mm to 31.5 ± 3.3 mm (P = .005), and median TR (range, 0-3+) increased from 0 (0) to 3 (2) (P = .004). Progressive suture cinching reduced the TA area by 18 ± 6%, 38 ± 11%, 56 ± 10%, 67 ± 9%, and 76 ± 8%. Only aggressive annular reductions (67% and 76%) decreased TR significantly, but these were associated with deterioration of RV function and strain. A moderate annular reduction of 56% led to a substantial reduction of TR with little deleterious effect on regional RV function.ConclusionsA moderate TAR of approximately 50% may be most advantageous for correction of functional TR and simultaneous maintenance of regional RV performance. Additional subvalvular interventions may be needed to achieve complete valvular competence.     

组织运动二尖瓣环位移技术评价糖尿病合并代谢综合征患者左心室收缩功能的临床研究

目的采用超声组织运动二尖瓣环位移技术（TMAD） 评价射血分数正常的2型糖尿病（T2DM） 合并代谢综合征（MS）患者的左心室收缩功能。方法收集左心室射血分数保留的T2DM患者（T2DM组）94 例,根据是否合并MS,将T2DM组分为合并MS组（CMS组）与不合并MS组（NMS组）,同期收集年龄、性别 相匹配的50例志愿者作为对照组。采用超声心动图测量左心室舒张期容积（LVEDV）、左心室射血分数（LVEF） 及二尖瓣血流速度等常规参数。采用二维斑点追踪技术（2D STE）测量TMAD参数：二尖瓣环室间隔位点位移 （TMAD1）、侧壁位点位移（TMAD2）、平均位移（TMADmid）及平均位移率（TMADmid%）,比较各组各参数 的差异。结果T2DM组患者和对照组的常规超声心动图参数结果比较,差异有统计学意义（P <0.05）;与对照 组相比,T2DM患者的LVEDV增加（P <0.05）,Mitral E/A减低（P <0.05）;而LVEDD及LVEF比较,差异无统 计学意义（P >0.05）。对照组、CMS组及NMS组TMAD参数比较,差异有统计学意义（P <0.05）;与对照组比 较,CMS 组及NMS 组患者TMAD1、TMAD2、TMADmid 及TMADmid%均降低（P <0.05）,且CMS 组患者 TMAD参数均低于NMS组（P <0.05）。结论射血分数保留的T2DM患者左心室收缩功能仍降低,且合并MS 的T2DM患者左心室收缩功能降低更显著。TMAD参数可作为临床评价左心室收缩功能的新参数,具有操作简 单,准确、灵敏等优点。     

The Pathophysiological Link between Right Atrial Remodeling and Functional Tricuspid Regurgitation in Patients with Atrial Fibrillation: A Three-Dimensional Echocardiography Study

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Accelerated premature stress-induced senescence of young annulus fibrosus cells of rats by high glucose-induced oxidative stress

Purposes

Diabetes mellitus (DM) is thought to be an important aetiological factor in intervertebral disc degeneration. A glucose-mediated increase of oxidative stress is a major causative factor in development of diseases associated with DM. The aim of this study was to investigate the effect of high glucose on mitochondrial damage, oxidative stress and senescence of young annulus fibrosus (AF) cells.

Methods

AF cells were isolated from four-week-old young rats, cultured, and placed in either 10 % FBS (normal control) or 10 % FBS plus two different high glucose concentrations (0.1 M and 0.2 M) (experimental conditions) for one and three days. We identified and quantified the mitochondrial damage and reactive oxygen species (ROS) (oxidative stress). We also identified and quantified the occurrence of senescence and telomerase activity. Finally, the expressions of proteins were determined related to replicative senescence (p53-p21-pRB) and stress-induced senescence (p16-pRB).

Results

Two high glucoses enhanced the mitochondrial damage in young rat AF cells, which resulted in an excessive generation of ROS in a dose- and time-dependent manner for one and three days compared to normal control. Two high glucose concentrations increased the occurrence of senescence of young AF cells in a dose- and time-dependent manner. Telomerase activity declined in a dose- and time-dependent manner. Both high glucose treatments increased the expressions of p16 and pRB proteins in young rat AF cells for one and three days. However, compared to normal control, the expressions of p53 and p21 proteins were decreased in young rat AF cells treated with both high glucoses for one and three days.

Conclusions

The present study demonstrated that high glucose-induced oxidative stress accelerates premature stress-induced senescence in young rat AF cells in a dose- and time-dependent manner rather than replicative senescence. These results suggest that prevention of excessive generation of oxidative stress by strict blood glucose control could be important to prevent or to delay premature intervertebral disc degeneration in young patients with DM.