Patients under Psychiatric Medication Undergoing Cardiac Surgery Have a Higher Risk for Adverse Events.

Objective The percentage of patients undergoing cardiac surgery under some sort of psychiatric medication (PM) is not negligible. Thus, this study aimed to evaluate a possible impact of preoperative PM on the outcome after cardiac surgery. Methods A matched case-control study was conducted by including all patients who underwent myocardial revascularization and/or surgical valve operation in our institution from December 2008 till February 2011 by chart review and institutional quality assurance database (QS) analysis. Results Out of 1,949 patients included, 184 patients (9%) were identified with PM medication (group A). A control group matched for logistic EuroSCORE II, ejection fraction and age was generated (group C). Patients with PM were in mean significantly longer on the intensive care unit (A: 4.94 days; 95% confidence interval (CI), 3.9-5.9 days vs. C: 3.24 days; CI, 2.84-3.64 days; p = 0.003), had longer mechanical ventilation times (A: 36.70 hours; CI, 19.81-53.59 hours vs. C: 20.14 hours; CI, 14.61-25.68 hours; p = 0.258), and significantly more episodes of respiratory insufficiencies (A: 31 episodes [17%] vs. C: 17 episodes [9%]; p = 0.002). Regression analysis revealed preoperative PM as a significant risk factor for respiratory insufficiency (odds ratio: 1.99, CI: 1.0-3.74; p = 0.04). Chest tube drainage (A: 690 mL, CI: 571-808 mL vs. C: 690 mL; CI: 496-884 mL, p = 0.53) and the total amount of red blood cell transfusion units were similar (A: 1.69 units; CI: 1.21-2.18 units vs. C: 1.50 units; CI: 1.04-1.96 units; p = 0.37). Sternal dehiscence requiring sternal refixation was significantly more frequent in A (12 patients [7%] vs. C: 2 patients [1%]; odds ratio: 6.3, CI: 1.4-28.7; p = 0.01). The 30-day mortality was similar in both groups (A: 6 patients [3%] vs. C: 4 patients [2%]; odds ratio: 1.5; CI: 0.4-5.4; p = 0.5); however, the 100-day mortality was near significantly higher in group A (A: 14 patients (8%) vs. C: 6 patients (3%); odds ratio: 2.4, CI: 0.9-6.5, p = 0.057). Conclusion Patients with preoperative PM developed complications more frequently compared with a matched control group. The underlying multifactorial mechanisms remain unclear. Patients under PM need to be identified and particular care including optimal pre- and postoperative psychiatric assistance is recommended.

Cone versus rod disease in a mutant Rpgr mouse caused by different genetic backgrounds.

PURPOSE: To establish mouse models for RPGR-associated diseases by generating and characterizing an Rpgr mutation (in-frame deletion of exon 4) in two different genetic backgrounds (BL/6 and BALB/c). METHODS: Gene targeting in embryonic stem (ES) cells was performed to introduce a in-frame deletion of exon 4 in the Rpgr gene (Rpgr(DeltaEx4)). Subsequently, the mutation was introduced in two different inbred mouse strains by successive breeding. Mutant and wild-type mice of both strains were characterized by electroretinography (ERG) and histology at five time points (1, 3, 6, 9, and 12 months). RPGR transcript amounts were assessed by quantitative RT-PCR. A variety of photoreceptor proteins, including RPGR-ORF15, RPGRIP, PDE6delta/PrBPdelta, rhodopsin, and cone opsin, were localized on retinal sections by immunohistochemistry. RESULTS: Mislocalization of rhodopsin and cone opsin was an early pathologic event in mutant mice of both lines. In contrast, RPGR-ORF15 as well as RPGRIP1 and PDE6delta/PrBPdelta showed similar localizations in mutant and wild-type animals. Functional and histologic studies revealed a mild rod-dominated phenotype in mutant male mice on the BL/6 background, whereas a cone-dominated phenotype was observed for the same mutation in the BALB/c background. CONCLUSIONS: Both Rpgr mutant mouse lines developed retinal disease with a striking effect of the genetic background. Cone-specific modifiers might influence the retinal phenotype in the BALB/c strain. The two lines provide models to study RPGR function in rods and cones, respectively.

Overexpression of RPGR leads to male infertility in mice due to defects in flagellar assembly.

Male infertility is one possible consequence of a group of disorders arising from dysfunction of cilia. Ciliopathies include primary ciliary dyskinesia, polycystic kidney disease, Usher syndrome, nephronophthisis, Bardet-Biedl syndrome, Alstrom syndrome, and Meckel-Gruber syndrome as well as some forms of retinal degenerations. Mutations in the retinitis pigmentosa GTPase regulator gene (RPGR) are best known for leading to retinal degeneration but have also been associated with ciliary dysfunctions affecting other tissues. To further study the involvement of RPGR in ciliopathies, transgenic mouse lines overexpressing RPGR were generated. Animals carrying the transgene in varying copy numbers were investigated. We found that infertility due to aberrant spermatozoa correlated with increased copy numbers. In animals with moderately increased gene copies of Rpgr, structural disorganization in the flagellar midpiece, outer dense fibers, and fibrous sheath was apparent. In contrast, in animals with high copy numbers, condensed sperm heads were present, but the flagellum was absent in the vast majority of spermatozoa, although early steps of flagellar biogenesis were observed. This complexity of defects in flagellar assembly suggests a role of RPGR in intraflagellar transport processes.