Postoperative hypoxemia for patients undergoing Stanford type A aortic dissection.

Clinically, it is widely recognized that surgical treatment is the preferred and reliable option for Stanford type A aortic dissection. Stanford type A aortic dissection is an emergent and serious cardiovascular disease characterized with an acute onset, poor prognosis, and high mortality. However, the incidences of postoperative complications are relatively higher due to the complexity of the disease and its intricate procedure. It has been considered that hypoxemia, one of the most common postoperative complications, plays an important role in having a worse clinical prognosis. Therefore, the effective intervention of postoperative hypoxemia is significant for the improved prognosis of patients with Stanford type A aortic dissection.

Hsa-miR-494-3p attenuates gene HtrA3 transcription to increase inflammatory response in hypoxia/reoxygenation HK2 Cells.

The occurrence of cardiac surgery-associated acute kidney injury (CSA-AKI) increases hospital stay and mortality. MicroRNAs has a crucial role in AKI. This objective of the current study is to explore the function of hsa-miR-494-3p in inflammatory response in human kidney tubular epithelial (HK2) cells with hypoxia/reoxygenation. According to KDIGO standard, patients after cardiac surgery with cardiopulmonary bypass were divided into two groups: AKI (n = 10) and non-AKI patients (n = 8). HK2 were raised in the normal and hypoxia/reoxygenation circumstances and mainly treated by overexpression ofmiR-494-3p and HtrA3. The relationship between miR-494-3p and HtrA3 was determined by dual-luciferase reporter assay. Our result showed that Hsa-miR-494-3p was elevated in the serum of patients with CSA-AKI, and also induced in hypoxic reoxygenated HK2 cells. Hsa-miR-494-3p also increased a hypoxia-reoxygenation induced inflammatory response in HK2 cells. Moreover, as a target gene of miR-494-3p, overexpression of HtrA3 downregulated the hypoxia-reoxygenation induced inflammatory response in HK2 cells. Overexpression of hsa-miR-494-3p-induced inflammatory response was inhibited by overexpression of HtrA3. Collectively, we identified that hsa-miR-494-3p, a miRNA induced in both circulation of AKI patients and hypoxia-reoxygenation-treated HK2 cells, enhanced renal inflammation by targeting HtrA3, which may suggest a possible role as a new therapeutic target for CSA-AKI.

CTBP1­AS2 inhibits proliferation and induces autophagy in ox­LDL­stimulated vascular smooth muscle cells by regulating miR­195­5p/ATG14.

Atherosclerosis (AS) is a chronic progressive disease caused by injury and functional changes in vascular smooth muscle cells (VSMCs). Long non­coding RNAs (lncRNAs) are pivotal regulators in AS development. The present study aimed to explore the roles and molecular mechanisms of lncRNA CTBP1­AS2 in AS progression. A dual­luciferase reporter assay confirmed that miR­195­5p is a downstream target miRNA of lncRNA CTBP1­AS2 and miR­195­5p was increased in AS. The expression levels of miR­195­5p and CTBP1­AS2 in the serums of patients with AS and human aorta vascular smooth muscle cells was increased or decreased, respectively, following treatment with oxidized low­density lipoprotein (ox­LDL). Functional experiments showed that the overexpression of lncRNA CTBP1­AS2 inhibited the proliferation of HA­VSMCs and promoted their autophagy following ox­LDL treatment. This effect could be reversed by treatment with ROC­325, the inhibitor of autophagy, or miR­195­5p mimics. Autophagy related 14 (ATG14) was identified to be a target of miR­195­5p, and lncRNA CTBP1­AS2 promoted ATG14 expression by serving as a competing endogenous RNA of miR­195­5p. The present study revealed that lncRNA CTBP1­AS2 may serve a role in AS by inhibiting the proliferation and promoting the autophagy of VSMCs through ATG14 modulation via miR­195­5p. These data may provide a novel therapeutic target for AS.

A case of abdominal bleeding after mitral valvuloplasty assisted by da Vinci robotic surgery.

A 66-year-old female patient was admitted with abdominal bleeding as an unexpected complication of robotic surgery. Assessments included the patient's medical history, physical examination, laboratory data, and abdominal ultrasound scan results. In our case, laparotomy revealed an injury to the diaphragm and liver of the patient caused by the previous robotic surgery. In conclusion, although abdominal bleeding is a rare condition, it should be taken into consideration as a complication of robotic cardiac surgery.

[Protective role of MMP-9 inhibitor batimastat in acute lung injury after cardiopulmonary bypass].

OBJECTIVE: To investigate the protective effect of exogenous inhibitor of matrix metalloproteinases-9 (MMP-9), batimastat, in the lung injury induced by cardiopulmonary bypass (CPB) in dogs. METHODS: Thirty healthy mongrel puppies were randomly divided into 3 groups: control group, low-dose group [batimastat 10 mg/(kg.d) for 3 days before operation] and high-dose group [batimastat 30 mg/(kg.d) for 3 days before operation]. The off-pump puppies' model of acute lung injury was established, and hemodynamic and respiratory parameters were monitored. The preoperative and postoperative alveolar-arterial oxygen difference (A-aDO(2)) and respiratory index (RI) were calculated. From the beginning of surgery, blood samples were taken at the time 0, 60, 120, and 270 min. Plasma concentrations of MMP-9 were measured by ELISA, and blood MMP-9 mRNA expressions were determined by RT-PCR. The myeloperoxidase (MPO) activity of centrifugal bronchoalveolar lavage fluid were measured by Colorimetry. And MMP-9 activity was determined by Gelatin zymography. Light and electronic microscope were used to observe the morphological changes of lung tissue. A small piece of left lung tissue was taken, weighed and baked to calculate the wet weight (W/D) index. RESULTS: After cardiopulmonary bypass, the concentrations of MMP-9 and mRNA expressions of the control group were increased significantly, and lung injury was apparent. At 270 min, the MMP-9 plasma concentration of high-dose group (17.36 +/- 1.18) microg/L was significant reducing than control group (30.47 +/- 2.22) microg/L (P < 0.05). After operation, A-aDO(2) and RI of high-dose group were significantly improved than control group (P < 0.05). The W/D index of the high-dose group (2.8 +/- 0.48) was significantly lower than that of control group (4.7 +/- 0.6) (P < 0.05). And the pathological changes of lung tissue were significantly improved in the high-dose group. However, there was no significant difference in the MMP-9 mRNA expression in three groups. CONCLUSIONS: Batimastat plays a role in the protection of the lung injury of CBP by reducing the concentration and activity of MMP-9, the degradation of the cell membrane and pulmonary neutrophil infiltration and reduction of pulmonary edema.

[Clinical evaluation of the heart function early after repair of tetralogy of Fallot: follow-up of 43 patients].

OBJECTIVE: To evaluate the heart function of the patients early after the repair of tetralogy of Fallot (TOF). METHODS: Forty-three patients with TOF, 25 males and 18 females, underwent operation at the age of 2.5 - 52 years (16.7 years on average) and were followed up for 1 - 3.5 years. Twenty-one age-matched healthy persons were used as controls. Tissue Doppler imaging (TDI) was used to measure the values of the peak tricuspid ring velocity during early diastole (Ea), late diastole (Aa), systole, and isovolumic contraction, and isovolumetric contraction acceleration (IVA); and isovolumetric contraction time (ICT), isovolumetric relaxation time (IRT), and isovolumetric contraction velocity (IVV) of the right ventricle. Tei index was calculated using the formula: (ICT + IRT)/ET. Treadmill test was used on the patients aged > 17 to measure the maximal heart rate maximal blood pressure, maximal exercise tolerance (MET), and movement time. RESULTS: The peak tricuspid ring velocity during Ea of the repaired TOF group (rTOF group) was 11.5 +/- 2.6 cm/s, significantly lower than that of the control group (17.1 +/- 2.4 cm/s, P < 0.0001), the peak tricuspid ring velocity during Aa of the rTOF group was 9.6 +/- 1.7 cm/s, significantly lower than that of the control group (12.9 +/- 2.9 cm/s, P < 0.001), the E/A of the rTOF group was 1.16 +/- 0.36, significantly lower than that of the control group (1.36 +/- 0.26, P < 0.05). The IVV of the rTOF group was 7.7 +/- 1.8 cm/s, significantly lower than that of the control group (9.9 +/- 1.4 cm/s, P = 0.0030, and the IVA of the rTOF group was 131.7 +/- 37.6 cm/s(2), significantly lower than that of the control group (222.5 +/- 39.2 cm/s(2), P < 0.001). The Tei index of the rTOF group was 0.58 +/- 0.11, significantly higher than that of the control group (0.52 +/- 0.04, P = 0.029). The maximal heart rate maximal blood pressure, MET, and movement time of the rTOF group were all significantly lower than those of the control group (P < 0.05 or P < 0.01). CONCLUSION: The heart function of the patients undergoing repair of TOF fails to recover to the normal level during a short time after the surgery.

Right ventricular dysfunction due to right ventricular outflow tract patch.

Doppler tissue imaging analysis was used to examine the relationship between right ventricular function and right ventricular outflow tract damage in 54 patients with repaired tetralogy of Fallot. The patients were divided into three groups: 16 in whom the right ventricular outflow tract was directly sutured (group DS), 23 who had transventricular patch repair (group TVP), and 15 who had transannular patch repair (group TAP). The control group consisted of 16 age-matched patients who underwent patch closure of a ventricular septal defect (group C). The Tei index was obtained from tricuspid and pulmonary Doppler flow velocities. The right ventricular Tei index was significantly greater in groups TVP and TAP than in group DS. Doppler tissue imaging analysis in groups TVP and TAP showed shorter myocardial systolic velocity, diastolic peak velocity, and atrial diastolic peak velocity, lower peak myocardial velocity and acceleration during isovolumic contraction, and prolonged isovolumic relaxation and contraction times compared to groups DS and C. Right ventricular dysfunction is due to the right ventricular outflow tract patch. Thus, the right ventricular outflow tract may be essential for right ventricular ejection and maintenance of right ventricular function.