Analysis of prognostic factors for in-hospital mortality in patients with unplanned re-exploration after cardiovascular surgery.

OBJECTIVE: To explore the prognostic factors for in-hospital mortality in patients with unplanned re-exploration after cardiovascular surgery. METHODS: We retrospectively analyzed the data of 100 patients who underwent unplanned re-exploration after cardiovascular surgery in our hospital between May 2010 and May 2020. There were 77 males and 23 females, aged (55.1 ± 15.2) years. Demographic characteristics, surgical information, perioperative complications were collected to establish a database. These patients were divided into surviving and non-surviving groups according to in-hospital mortality. Logistic regression was used for multivariable analysis to explore the prognostic factors of in-hospital mortality. These statistically significant indicators were selected for drawing the receiver operating characteristic curve of the evaluation model, calculating the area under the curve (AUC) and evaluating the effectiveness of the new model with Hosmer-Lemeshow C-statistic. RESULTS: In-hospital mortality in patients with unplanned re-exploration after cardiovascular surgery was 26.0% (26/100). Multivariate logistics regression revealed that the operation time of unplanned re-exploration, the worst blood creatinine value within 48 h before the re-exploration, the worst lactate value within 24 h after the re-exploration, cardiac insufficiency, respiratory insufficiency, and acute kidney injury were independent prognostic factors (P < 0.05). The AUC of the new assessment model constituted by these prognostic factors was 0.910, and the Hosmer-Lemeshow C-statistic was 4.153 (P = 0.762). CONCLUSIONS: Operation time of unplanned re-exploration, worst serum creatinine value within 48 h before re-exploration, worst lactate value within 24 h after re-exploration, cardiac insufficiency, respiratory insufficiency, and acute kidney injury are the main prognostic factors for in-hospital mortality in patients with unplanned re-exploration after cardiovascular surgery. Identifying these prognostic factors can effectively facilitate preventive measures and improve patient outcomes.

Clinical application of pulmonary vascular resistance in patients with pulmonary arterial hypertension.

Pulmonary arterial hypertension is a type of malignant pulmonary vascular disease, which is mainly caused by the increase of pulmonary vascular resistance due to the pathological changes of the pulmonary arteriole itself, which eventually leads to right heart failure and death. As one of the diagnostic indicators of hemodynamics, pulmonary vascular resistance plays an irreplaceable role in the pathophysiology, diagnosis and treatment of pulmonary arterial hypertension. It provides more references for the evaluation of pulmonary arterial hypertension patients. This article summarizes the clinical application of pulmonary vascular resistance in patients with pulmonary arterial hypertension.

A 60-year-old woman with asymptomatic total thoracic-abdominal aortic aneurysm.

INTRODUCTION: Total thoracic-abdominal aortic aneurysm is a rare disease in cardiovascular surgery, with high surgical risk and high mortality. Surgery is considered the most effective treatment for total aortic aneurysms. CASE PRESENTATION: Our group admitted a 60-year-old female patients with asymptomatic complex total thoracic-abdominal aortic aneurysm, and successfully performed two-staged surgery, namely Bentall + Sun's operation in the first-stage and thoracoabdominal aortic replacement in the second-stage. The results of the surgery were satisfactory. CONCLUSIONS: Patients with total thoracic-abdominal aortic aneurysm may not have typical clinical symptoms and require a careful and comprehensive physical examination and related auxiliary examinations by clinicians. Staged repair of total thoracic-abdominal aortic aneurysms is still a safe and effective treatment.

Clinical analysis of redo aortic root replacement after cardiac surgery: a retrospective study.

OBJECTIVES: To explore the etiology, previous cardiac procedure methods and outcomes of redo aortic root replacement after cardiac surgery. METHODS: A retrospective analysis of 41 patients who underwent aortic root replacement surgery in our hospital from February 2010 to February 2020 who underwent at least one cardiac surgery in the past, including 27 males and 14 females, with an average age of 49.5 ± 10.2 years old. Indications for reoperation include: aortic sinus dilation and ascending aortic aneurysm in 20 cases (48.8%), recurrent aortic dissection in 7 cases (17.1%), pseudoaneurysm of aortic root in 4 cases (9.8%), prosthetic valve endocarditis in 5 cases (12.2%) and paravalvular leakage in 5 cases (12.2%). According to whether the previous procedure involved aortic root surgery, they were divided into 2 groups, namely aortic root surgery-involved (ARS) group and non-aortic root surgery-involved (NRS) group. After the patients were discharged from hospitals, follow-ups were carried out through outpatient clinic or telephone for 5 years. Kaplan-Meier was used for survival analysis. RESULTS: All patients underwent Bentall procedure with a median sternum incision. Six patients (14.6%) died during the postoperative hospitalization and 3 patients (8.6%) died during the follow-up. The 1-year, 3-year, and 5-year survival in ARS group were 92.6, 92.6, and 92.6%, respectively; the 1-year, 3-year, and 5-year survival in NRS group were 100, 85.7, and 85.7%, respectively. There was no statistical difference between the two groups in the cause of redo aortic root replacement, procedure time, postoperative complications, postoperative hospital stay, hospital mortality, and 5-year cumulative survival (p > 0.05). CONCLUSIONS: Redo aortic root replacement is difficult and high risk. Bentall procedure is still a reliable surgical option for redo aortic root replacement, with good short- and mid-term results. The prognosis of redo aortic root replacement is not necessarily related to the etiology of patient's surgery and the methods of previous cardiac procedure.

Research progress on the molecular mechanism of coronary microvascular endothelial cell dysfunction.

Coronary microvascular disease is a high-risk factor for many cardiovascular events. However, due to its high concealment and many etiologies, the current understanding of its pathophysiological mechanism is very limited, which greatly limits its clinical diagnosis and treatment. In the process of the occurrence and development of coronary microvascular disease, the damage of coronary microvascular endothelial cell (CMEC) is the core link. CMEC's stress, metabolism, inflammation and other dysfunctions have a causal relationship with coronary microvascular disease, and are also the main features of coronary microvascular disease in the early stage. This article mainly reviews the molecular mechanisms of CMEC damage.

Advanced research on the regulated necrosis mechanism in myocardial ischemia-reperfusion injury.

Myocardial ischemia-reperfusion injury is an important factor that seriously affects the prognosis of patients with myocardial infarction. It can cause myocardial stun, no-reflow phenomenon, reperfusion arrhythmia, and even irreversible cardiomyocyte death. Regulated necrosis is a newly discovered type of regulatory cell death that is different from apoptosis, including necroptosis, pyrolysis, iron death and other forms. Regulated necrosis plays an important role in myocardial infarction, heart failure and other cardiovascular diseases, as well as myocardial ischemia-reperfusion injury and other pathophysiological processes, and is expected to become a new target for intervention in this type of disease.

A 52-year-old man with asymptomatic giant thoracic-abdominal aortic aneurysm.

A 52-year-old man was admitted to our hospital for a "CT-diagnosed thoracic-abdominal aortic aneurysm." One week ago, the patient had repeated dry coughs and went to the local hospital for treatment. A chest radiograph revealed a huge mass in the left thoracic cavity. A further chest computerized tomography examination revealed a thoracic-abdominal aortic aneurysm and was transferred to our hospital for surgical treatment. The patient is almost healthy, with no fever, no severe chest and abdomen pain, no dyspnea, no dysphagia, or other clinical symptoms. Ten years ago, the patient underwent "ascending aorta and total aortic arch replacement surgery" in another cardiovascular hospital due to aortic dissection involving the ascending aorta and aortic arch (Debakey I). The patient's thoracic-abdominal aortic aneurysm is huge and has a high risk of rupture. Recently, the patient has undergone thoracic-abdominal aortic replacement surgery and is recovering well.

Left thorax approach to repair doubly committed juxta-arterial ventricular septal defect with Da Vinci robotic system.

Robotic repair of the ventricular septal defect was performed mainly for perimembranous type via right thorax approach. Minimally invasive strategies for doubly committed juxta-arterial ventricular septal defect were limited. Here, for the first time, we successfully repaired a doubly committed juxta-arterial ventricular septal defect with Da Vinci robotic system via left thorax approach. The technique could provide excellent exposure of surgical field and accurate repair, with the advantage of reducing trauma and shortening the overall length of stay.

Advanced research on the microRNA mechanism in heart failure.

Heart failure is the end stage of most cardiac diseases and also an important cardiovascular disease. Ventricular remodeling, a complicated pathophysiological process involving multiple molecular pathways, is a crucial mechanism for the occurrence and development of heart failure. A microRNA (miRNA) is a highly conservative noncoding molecule containing 18-25 nucleotides. miRNA is different from other RNAs. It mainly serves as an endogenous gene-regulating factor, and is a member of the complex regulatory network. It induces gene repression of target transcripts by affecting mRNA at the post-transcriptional level Vasudevan et al. (2007) . This study aimed at determining the mechanism of miRNA action in heart failure.

[Chromosome 22q11.2 microdeletion and phenotype analysis of patients with non-syndromic tetralogy of Fallot].

OBJECTIVE: To investigate the frequency and clinical phenotypes of 22q11.2 microdeletion in patients with non-syndromic tetralogy of Fallot (TOF). METHODS: Six-eight non-syndromic TOF patients (38 males and 30 females, aged 0-11 years) were selected and evaluated by history, physical examination and review of medical records. After informed consent was obtained, peripheral blood was drawn for genomic DNA extraction. Chromosome 22q11.2 microdeletion was screened by multiplex ligation-dependent probe amplification (MLPA). Suspected cases were confirmed with fluorescence in situ hybridization (FISH). Data was analyzed with SPSS 11.5 software. Phenotype-genotype correlations were assessed using Fisher's exact test. P values less than 0.05 on a 2-sided test were considered to be significant. RESULTS: Six-eight non-syndromic TOF children were screened for a 22q11.2 deletion, among which 59 (86.8%) presented pulmonary stenosis (PS) and 9 (13.2%) presented pulmonary atresia (PA). Seven patients (10.3%) were found to have carried a deletion. Among these, four had TOF-PS, three had TOF-PA. The frequency of 22q11.2 deletion in patients with TOF-PA (3/9, 33.3%) is much higher than that of TOF-PS (4/59, 6.80%) (P< 0.05). CONCLUSION: 22q11.2 microdeletion is present in approximately 10.3% of patients with non-syndromic TOF. The deletion tends to have a higher prevalence in patients with TOF-PA. 22q11.2 deletion should be screened in non-syndromic TOF children and genetic counselling may be provided.

[Evaluation of detection and analysis of chromosome 22q11.2 microdeletion by multiple ligation-dependent probe amplification assay].

OBJECTIVE: To evaluate multiplex ligation-dependent probe amplification (MLPA) assay detection in analysis of chromosome 22q11.2 microdeletion. METHODS: Between March 2008 and September 2009, thirty-two patients including 10 males and 16 females aged between years (3.6±3.1) were selected and evaluated by history, physical examination and medical records. Of these patients, sixteen patients who were previous diagnostic as 22q11.2 microdeletion were in positive control group, the other 16 healthy children were in negative control group. All the patients were detected by MLPA and fluorescence in situ hybridization (FISH) for the presence of a 22q11.2 microdeletion after informed consent. Diagnostic efficacy was assessed by sensitivity, specificity and Kappa analysis. RESULTS: We have applied the two assays of detection of chromosome 22q11.2 microdeletion in 32 patients. Sixteen patients in positive control group were found to have a 22q11.2 deletion and, with the deletion size of 3-Mb. However, as expected, chromosome 22q11.2 deletion was not found in negative control group. The MLPA results were in good agreement with that by FISH. Therefore, MLPA has high sensitivity and specificity. CONCLUSION: MLPA is a rapid, reliable, high-throughput and relatively economical alternative to FISH technology for the diagnosis of 22q11.2 microdeletion. It can provide reliable and helpful information for clinical diagnosis of 22q11.2 microdeletion syndrome.