[The mid-term outcomes of minimally invasive plasty for severe tricuspid regurgitation after cardiac surgery].

Objectives: To evaluate the efficacy of minimally invasive surgery in patients with late severe tricuspid regurgitation after cardiac surgery, and to evaluate the role of leaflets augmentation technique in tricuspid valvuloplasty. Methods: From January 2015 to June 2019, 85 patients undergoing tricuspid valve repair procedure with minimally invasive approach at Department of Cardiovascular Surgery, Guangdong provincial People's Hospital were enrolled. There were 22 males and 63 females, aging of (53.6±12.4) years (range: 15 to 75 years). The interval between the prior and current operations was (16.0±7.3) years (range: 0.2 to 35.0 years). The diameter of right atrium and right ventricle was (77.3±17.2) mm and (61.0±8.4) mm, respectively. Tricuspid regurgitation was severe or extremely severe, the tricuspid regurgitation area was (19.0±10.3) cm(2). All patients underwent minimally invasive tricuspid valvuloplasty or tricuspid valve replacement on beating-heart with totally endoscopic technique and port-access approach through right chest wall. The operations included tricuspid valve replacement and tricuspid valvuloplasty, the technique of tricuspid valvuloplasty including leaflets augmentation with patch, ring implantation, chordae tendineaes reconstruction, release of papillary muscle, edge to edge method, etc. Postoperative hospitalization days, the time of ICU stay, blood transfusion rate, ventilator time and the results of echocardiography were recorded. Follow-up was completed regularly by WeChat, telephone and outpatient visit. Results: Sixty-five patients underwent tricuspid valve repair, and 20 patients underwent tricuspid valve replacement because of prosthetic failure and plasty failure. Five patients died during hospitalization, with mortality rate 5.9%. One patient was transferred to local hospital for anti-infection treatment, the other 79 patients were discharged from hospital in well condition and followed-up. The postoperative hospitalization time was 7.0 (5.5) days (M(Q(R))) days, the mean ventilator time was 18.0 (16.2) hours, and the mean ICU stay time was 68.0 (75.5) hours. There were 35 patients without blood conduction transfusion, the transfusion rate was only 58.9% (50/85). Four cases of severe, 9 cases of moderate and 67 cases of mild to zero tricuspid regurgitation were examined before being discharged, with tricuspid regurgitation area of (2.8±3.5) cm(2) (range: 0 to 19.1 cm(2)). The follow-up time was 1 to 38 months. Two patients died during follow-up, one patient died from infective endocarditis and mitral perivalvular leakage, the other one died of intractable right heart failure. One patient was implanted with permanent pacemaker due to Ⅲ atrioventricular block. Valvular re-replacement was performed in 2 patients who were re-admitted for the artificial valve infection and mechanical valve obstruction. No re-operation of tricuspid valve. Conclusions: Totally endoscopic minimally invasive technique provided satisfactory surgical outcomes for critically sick patients with severe tricuspid regurgitation following cardiac surgery. The application of leaflets augmentation technique achieved ideal repair effect for previously unrepairable lesions.

In vitro study on cytotoxicity and intracellular formaldehyde concentration changes after exposure to formaldehyde and its derivatives.

HeLa cells were exposed to formaldehyde and its metabolic derivatives, methanol, formic acid, and acetaldehyde, to investigate that the toxicity of formaldehyde is not caused by the chemical group. After 1 h of treatment with formaldehyde, mitochondrial assays showed that low concentrations (e.g. 10 µmol/L) of formaldehyde promoted growth of the HeLa cells, while higher concentrations (e.g. ≥62.5 µmol/L) inhibited cell growth; while all four chemicals at a concentration of 125 µmol/L affected cell growth, formaldehyde affected the largest. Reactive oxygen species concentration increased with the concentration of the exposure chemical. The endogenous formaldehyde content increased the most in the formaldehyde group, but in other three groups, it did not increase as the exposure concentration increased. Expression of dehydrogenase (formaldehyde dehydrogenase (FDH)) in the formaldehyde (10.40) and methanol (10.60) groups increased significantly compared with the control (1), while it was similar to the control in formic acid (0.90) and acetaldehyde (1.10) groups. Our results suggest that formaldehyde could affect cell activity and even enter cells. Exposure to formaldehyde changes the endogenous formaldehyde concentration in cells within 24 h, and this induces expression of FDH for formaldehyde degradation to maintain the formaldehyde balance. The toxicity of formaldehyde is not caused by the carbon atoms in the aldehyde, hydroxyl, or carboxyl groups. Formaldehyde is hypothesized to be an important signaling molecule in the regulation of cell growth and maintenance of the endogenous formaldehyde level.