Preoperative decline in skeletal muscle strength of patients with cardiovascular disease affects postoperative pulmonary complication occurrence: a single-center retrospective study.

BACKGROUND: Dynapenia, defined as age-related skeletal muscle strength decline, has been reported as a poor prognostic factor in patients with cardiovascular disease. Decline in skeletal muscle strength (DS), the main symptom of dynapenia, may be an important clinical indicator in patients undergoing cardiac surgery. However, the relationship between DS and postoperative pulmonary complication occurrence is unclear. Herein, we investigated the relationship between preoperative DS and postoperative pulmonary complication occurrence in patients undergoing cardiac surgery. METHODS: We enrolled 125 patients who underwent cardiac surgery. DS was determined by low grip strength and quadriceps isometric strength. The patients were divided into DS and non-DS groups. The relationship between the clinical characteristics and preoperative physical function was compared, and factors associated with postoperative pulmonary complication occurrence were investigated using multivariate logistic regression analysis. RESULTS: There were 42 (33.6%) patients in the DS group and 83 (66.4%) patients in the non-DS group. Compared with the non-DS group, the DS group was significantly older and had a higher body mass index and Japan SCORE (operative mortality rate and major complication rate). The DS group also had a lower estimated glomerular filtration rate and preoperative Barthel index than the non-DS group. Furthermore the DS group had a significantly higher incidence of postoperative pulmonary complications and length of intensive care unit stay, and their postoperative rehabilitation was prolonged compared to the non-DS group. Multivariate logistic regression analysis revealed that DS was a determinant of postoperative pulmonary complications (odds ratio 4.26, 95% confidence interval 1.63‒11.14). CONCLUSIONS: We showed that preoperative DS was an independent risk factor for postoperative pulmonary complications in patients undergoing cardiac surgery. Skeletal muscle strength before cardiac surgery may be an important clinical indicator for predicting the prognosis of patients from post-surgery to discharge and for planning postoperative rehabilitation programs.

Morphometric study of the human mitral annulus: guide for mitral valve surgery.

BACKGROUND: during mitral valve surgery, it is important for surgeons to understand the anatomy of the mitral valve annulus to prevent surgical complications. This study aimed to perform morphometry of the mitral annulus to facilitate secure suturing during ring annuloplasty or replacement of the mitral valve. METHODS: an anatomical study was carried out on 7 human hearts. We divided the mitral valve annulus into sections containing 8 different points. It was noted that the annulus was a complex structure which has fibrous continuity with the mitral leaflets, and with or without the aortic annulus. RESULTS: there was always a segment of the annular fibrous structure which was facing directly toward the left ventricular cavity. The length of the segment ranged from 1.0 to 3.4 mm. In terms of the size of the annulus, there were large variations within the subject and among the subjects. The shortest distance between the mitral annulus and left circumflex coronary artery was at the anterolateral commissure, and the length was 3.3 mm. CONCLUSION: this study has improved understanding of the anatomy of the mitral annulus, which could help surgeons to avoid operative complications. Based on this study, several suggestions are made for placing sutures for mitral valve replacement and mitral ring annuloplasty.

Evidence of a vicious cycle in mitral regurgitation with prolapse: secondary tethering attributed to primary prolapse demonstrated by three-dimensional echocardiography exacerbates regurgitation.

BACKGROUND: In patients with mitral valve prolapse, nonprolapsed leaflets are often apically tented. We hypothesized that secondary left ventricular dilatation attributed to primary mitral regurgitation (MR) causes papillary muscle (PM) displacement, resulting in this leaflet tenting/tethering, and that secondary tethering further exacerbates malcoaptation and contributes to MR severity. METHODS AND RESULTS: Three-dimensional transesophageal echocardiography was performed in 25 patients with posterior mitral leaflet prolapse with an intact anterior mitral leaflet (AML) and 20 controls. From 3D zoom data sets, 11 equidistant antero-posterior cut planes of the mitral valve at midsystole were obtained. In each plane, tenting area of nonprolapsed leaflet and prolapse area of prolapsed leaflet were measured. Prolapse/tenting volume of each region was obtained as the product of interslice distance and the prolapse/tenting area. AML tenting volume and whole leaflet prolapse/tenting volume were then obtained. The PM tethering distance between PM tips and anterior mitral annulus was measured from 3D full-volume data sets. The severity of MR was quantified by vena contracta area extracted from color 3D transesophageal echocardiography data sets. AML tenting volume was significantly larger in patients with posterior mitral leaflet prolapse compared with that in controls (1.2 ± 0.5 versus 0.6 ± 0.2 mL/m(2); P<0.001). Multivariate regression analysis identified independent contribution to AML tenting volume from an increase in PM tethering distance. Multivariate regression analysis identified independent contributions to MR severity (vena contracta area) from both whole leaflet tenting volume (r=0.44; P<0.05) and prolapse volume (r=0.44; P<0.05). AML tenting volume decreased along with left ventricular volume and PM tethering distance postrepair (n=8; P<0.01). CONCLUSIONS: These results suggest that primary mitral valve prolapse with MR causes secondary mitral leaflet tethering with PM displacement by left ventricular dilatation, which further exacerbates valve leakage, constituting a vicious cycle that would suggest a pathophysiologic rationale for early surgical repair.

[Surgical management of acute aortic dissection complicated with cerebral malperfusion].

Although type A acute aortic dissection is considered a surgical emergency, the optimal treatment of patients with preoperative cerebral malperfusion remains controversial. From September 1994 to December 2005, 68 consecutive patients with type A aortic dissection underwent emergent surgical treatment. Eight patients showed preoperative newly-developed neurological deficits. The hospital mortality rate was 25% (2 of the 8 patients). Of the 8 patients, 1 with preoperative coma died due to severe brain injury. Another with acute myocardial infarction and left hemiparesis died due to low output syndrome in the immediate postoperative period. Three of the others had persistent left hemiplegia. One of these patients showed new paraplegia early postoperatively. The preoperative neurological deficit of the remaining 3 patients had improved in some degree. The optimal strategy should be taken individually under the accurate and prompt evaluations of hemodynamic and neurological state in such patients.

Perineuronal nets protect against amyloid beta-protein neurotoxicity in cultured cortical neurons.

Perineuronal nets (PNs) consisting of chondroitin sulfate proteoglycans (CSPGs) and hyaluronic acid are associated with distinct neuronal populations in mammalian brain. Cortical areas abundant in PNs have been known to be less affected by neurotoxicity in human Alzheimer's disease. In the present study, we examined whether PNs protect the neurotoxicity caused by amyloid beta-protein (Abeta), a major constituent of senile plaques in Alzheimer's disease using cortical neurons of dissociated culture. Double labeling experiments using confocal microscopy showed that the neurons associated with PNs were visualized with the anti-CSPG antibody in dissociated cortical culture. The analysis of reverse transcription-polymerase chain reaction revealed that mRNA expression of chondroitin sulfotransferases, CSPG-specific enzymes, was detected in neuronal culture, indicating that cultured cortical neurons are able to synthesize CSPGs and construct PNs structure. The treatment of Abeta1-42 showed significant neurotoxicity on PNs-free cortical neurons, however, it did not reveal neurotoxicity on PNs-associated neurons. Moreover, it was shown that the treatment of Abeta1-42 was able to kill PNs-associated neurons after the removal of chondroitin sulfate (CS) glycosaminoglycans with chondroitinase ABC. The treatment of glutamate killed not only PNs-free cortical neurons but also PNs-associated neurons. These results suggest that CS glycosaminoglycans on PNs are responsible for protecting neurons from Abeta1-42 neurotoxicity.