Impact of 1-week preoperative auto-CPAP treatment on postoperative outcomes in patients undergoing heart valve replacement surgery: a prospective randomized controlled trial.

Background: Whether preoperative continuous positive airway pressure (CPAP) treatment improves postoperative outcomes in patients undergoing cardiac valve replacement (CVR) remains unknown. Hypothesis: This study was to evaluate the effects of 1-week perioperative auto-continuous positive airway pressure (CPAP) treatment on postoperative heart and pulmonary outcomes in patients with obstructive sleep apnea (OSA) and valvular heart disease. Methods: Thirty-two patients with OSA and valvular heart disease were randomly assigned to 1-week CPAP (n = 15) group and non-CPAP treatments (n = 17) group. After the treatment, all patients underwent CVR surgery. The length of ICU and hospital stays, postoperative cardiac and respiratory complications were assessed and compared between the 2 groups. Results: The results showed there was no significant difference in the baseline characteristics between the CPAP and non-CPAP treatment groups. The length of postoperative ICU and hospital stays, as well as the duration of mechanical ventilation were significantly reduced in the CPAP treatment group compared to the non-CPAP treatment group; however, there were no significant differences in cardiac complications (postoperative arrhythmias, pacemaker use, first dose of dopamine in the ICU, and first dose of dobutamine in the ICU), and respiratory complications (reintubation and pneumonia). Conclusion: We concluded that in patients underwent CVR, preoperative use of auto-CPAP for OSA significantly decreased the duration of mechanical ventilation, and postoperative stays in the ICU and hospital.Clinical Trial Registration: https://ClinicalTrials.gov, identifier NCT03398733.

Mathematical models for intraoperative prediction of metastasis to regional lymph nodes in patients with clinical stage I non-small cell lung cancer.

It remains challenging to determine the regions of metastasis to lymph nodes during operation for clinical stage I non-small cell lung cancer (NSCLC). This study aimed to establish intraoperative mathematical models with nomograms for predicting the hilar-intrapulmonary node metastasis (HNM) and the mediastinal node metastasis (MNM) in patients with clinical stage I NSCLC. The clinicopathological variables of 585 patients in a derivation cohort who underwent thoracoscopic lobectomy with complete lymph node dissection were retrospectively analyzed for their association with the HNM or the MNM. After analyzing the variables, we developed multivariable logistic models with nomograms to estimate the risk of lymph node metastasis in different regions. The predictive efficacy was then validated in a validation cohort of 418 patients. It was confirmed that carcinoembryonic antigen (>5.75 ng/mL), CYFRA211 (>2.85 ng/mL), the maximum diameter of tumor (>2.75 cm), tumor differentiation (grade III), bronchial mucosa and cartilage invasion, and vascular invasion were predictors of HNM, and carcinoembryonic antigen (>8.25 ng/mL), CYFRA211 (>2.95 ng/mL), the maximum diameter of tumor (>2.75 cm), tumor differentiation (grade III), bronchial mucosa and cartilage invasion, vascular invasion, and visceral pleural invasion were predictors of MNM. The validation of the prediction models based on the above results demonstrated good discriminatory power. Our predictive models are helpful in the decision-making process of specific therapeutic strategies for the regional lymph node metastasis in patients with clinical stage I NSCLC.

A method to improve multi-node power transmission efficiency of inductively coupled mooring cable.

The inductively coupled mooring cable is an important tool for monitoring the ocean hydrological data. The mooring cable is an open-loop structure that uses a section of seawater as the transmission medium. The power transmission efficiency of this structure is very low due to the large power loss of the seawater medium, and it is rarely studied. In this paper, a contactless power transmission circuit with seawater loss is analyzed, and the theoretical model of multi-node power transmission of the inductively coupled mooring system is established. In this model, the improvement of the output power and transmission efficiency is only related to the frequency selection and the properties of the magnetic core itself, such as the magnetic core material. Moreover, the optimal scheme is selected according to the output power requirements. The experimental results show that when the input current (Irms) is 2 A, the output power of a single node is 12 W, the total output power is 120 W, and the total transmission efficiency reaches 50%.

Perirenal adipose afferent nerves sustain pathological high blood pressure in rats.

Hypertension is a pathological condition of persistent high blood pressure (BP) of which the underlying neural mechanisms remain obscure. Here, we show that the afferent nerves in perirenal adipose tissue (PRAT) contribute to maintain pathological high BP, without affecting physiological BP. Bilateral PRAT ablation or denervation leads to a long-term reduction of high BP in spontaneous hypertensive rats (SHR), but has no effect on normal BP in control rats. Further, gain- and loss-of-function and neuron transcriptomics studies show that augmented activities and remodeling of L1-L2 dorsal root ganglia neurons are responsible for hypertension in SHR. Moreover, we went on to show that calcitonin gene-related peptide (CGRP) is a key endogenous suppressor of hypertension that is sequestered by pro-hypertensive PRAT in SHRs. Taken together, we identify PRAT afferent nerves as a pro-hypertensive node that sustains high BP via suppressing CGRP, thereby providing a therapeutic target to tackle primary hypertension.

Long noncoding RNA ArfGAP with RhoGAP domain, ankyrin repeat and PH domain 1 antisense RNA 1 recruits enhancer of zeste 2 polycomb repressive complex 2 subunit to promote the proliferation, migration and invasion of lung adenocarcinoma cells.

The detailed function of ARAP1-AS1, the antisense RNA of Arf-GAP with Rho-GAP domain, ANK repeat and PH domain-containing protein 1 (ARAP1), in lung adenocarcinoma (LUAD) has not been clearly elucidated and required further investigation. Our study is committed to exploring the role of ARAP1-AS1 in LUAD. Gene expression in LUAD was measured by real-time quantitative polymerase-chain reaction (RT-qPCR). The influence of ARAP1-AS1 on LUAD cell malignant behaviors was evaluated by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony formation assay, Transwell invasion assay and wound healing assay. Subcellular fractionation assay detected the cellular localization of ARAP1-AS1 in LUAD. The protein levels were subjected to western blotting. RNA immunoprecipitation (RIP) and luciferase reporter assay were employed to verify the interaction between ARAP1-AS1, ARAP1 and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2). Our investigation identified that ARAP1-AS1 was upregulated in LUAD cells and tissues. ARAP1-AS1 silencing repressed LUAD cell growth and migration. Furthermore, ARAP1-AS1 knockdown altered the expression of its sense mRNA, ARAP1. ARAP1-AS1 could recruit EZH2 to inhibit ARAP1 expression. Additionally, the downregulation of ARAP1 reversed ARAP1-AS1 downregulation-induced repression of cell growth and migration in LUAD. In conclusion, ARAP1-AS1 recruited EZH2 to silence ARAP1, facilitating cell proliferation, migration and invasion in LUAD. Our study demonstrated the possibility of ARAP1-AS1 to be a novel therapeutic target for LUAD. [Figure: see text].

FAK-targeting PROTAC demonstrates enhanced antitumor activity against KRAS mutant non-small cell lung cancer.

Focal adhesion kinase (FAK) has been established as a promising therapeutic target for KRAS mutant non-small cell lung cancer (NSCLC). However, phase II clinical trials of a FAK inhibitor (Defactinib) have only shown modest antitumor activity. To address this challenge, here we report the use of a FAK-targeting proteolysis targeting chimera (D-PROTAC) to treat KRAS mutant NSCLC. We validated that D-PROTAC could efficiently eliminate FAK protein via the ubiquitin-proteasome pathway in KRAS mutant NSCLC A427 cells, causing over 90% degradation at 800 nM. After comparing both in vitro and in vivo therapeutic efficacies, we demonstrated that D-PRTOAC outperformed Defactinib in inhibiting tumor growth. Specifically, D-PROTAC at 800 nM reduced cell viability, migration, and invasion by ∼80%. Furthermore, a ∼85% suppression of tumor growth was elicited by D-PROTAC when intratumorally administrated at 10 mg/kg in subcutaneous A427-bearing mice. These results thus demonstrate for the first time that PROTACs may serve as promising therapeutic agents for the intractable NSCLC harboring KRAS mutations.

Prognosis of early stage pulmonary mucinous adenocarcinoma with different treatments.

BACKGROUND: The effects of surgical approach and adjuvant chemotherapy (AC) of early stage pulmonary mucinous adenocarcinoma (MAD) have not been thoroughly studied yet. This study intends to clarify whether AC provides clinical benefit to the early stage MAD patients and the survival difference between surgical approaches. METHODS: All cases of stage I MAD were identified from the SEER database during the period of 2009-2014. The primary cohort was divided into AC and surgery (S) groups. Meanwhile, the patients with tumor ≤1 cm were divided into lobectomy and sublobar resection group. Clinical characteristics, treatments and survival data including overall survival (OS) and cancer-specific survival (CSS) were analyzed. RESULTS: A total of 1,816 patients were included in the final cohort. Referring to surgical procedure, 140 patients received lobectomy and 75 patients received sublobar resection. AC showed worse survival outcomes than surgery alone (OS: 71.2 vs. 93.4 months; CSS: 74.9 vs. 101.1 months). No significant difference was observed between lobectomy group and sublobar resection group (OS: 97.3 vs. 93.1 months; CSS: 103.7 vs. 101.3 months). Consistent results were also shown after the propensity score matching analysis (PSM) was applied. CONCLUSIONS: Early stage of MAD has an ideal prognosis. AC may bring adverse effects which would lower OS and CSS of stage I MAD patients. No significant difference is observed in the comparison of prognosis between lobectomy and sublobar resection in tumor size ≤1 cm MAD patients.

Prediction of lymph node metastatic status in superficial esophageal squamous cell carcinoma using an assessment model combining clinical characteristics and pathologic results: A retrospective cohort study.

BACKGROUND: It is important to identify the risk of lymph node metastasis (LNM) in patients with superficial esophageal squamous carcinoma (SESC) who have received endoscopic resection (ER). We aimed to develop a risk-predicting model for metastasis of SESC to lymph nodes using clinicopathological features and pathological results. METHODS: Clinical data on 539 consecutive patients who underwent esophagectomy for SESC in our hospital were collected. Their post-surgical pathological results were assessed and analyzed. Multivariate logistic regression was used to identify all independent risk factors associated with LNM that then were incorporated into the prediction model. RESULTS: LNM was identified in 53 of 366 patients and 30 of 173 patients by positive histopathological results in the training and validation cohorts. The risk factors associated with LNM were large tumor size, poor tumor grade, deep invasion, and presence of angiolymphatic invasion. The model achieved good discriminatory ability of 0.80 (95%CI, 0.74-0.86) and 0.81 (95%CI, 0.75-0.86) in predicting LNM in the training and validation cohorts respectively. A LNM-predicting nomogram was formed with an area under curve of 0.80 (95% CI, 0.74-0.86), which had well-fitted calibration curves. CONCLUSIONS: A prediction model was constructed to generates 3 categories for estimated LNM risk in SESC patients. It provides a practical way of estimation of LNM risk in SESC patients who had received ER.

Cardiac Sympathetic Denervation Suppresses Atrial Fibrillation and Blood Pressure in a Chronic Intermittent Hypoxia Rat Model of Obstructive Sleep Apnea.

Background Chronic intermittent hypoxia ( CIH ) is a distinct pathological mechanism of obstructive sleep apnea ( OSA ), which is recognized as an independent risk factor for cardiovascular diseases. The aims of this study were to ascertain whether CIH induces atrial fibrillation ( AF ), to determine whether cardiac sympathetic denervation ( CSD ) can prevent it and suppress blood pressure, and to explore the potential molecular mechanisms involved. Methods and Results Sixty Sprague-Dawley male rats were randomly divided into 4 groups: sham, CSD , CIH , CIH + CSD . The rats were exposed either to CIH 8 hours daily or normoxia for 6 weeks. Cardiac pathology and structure were analyzed by hematoxylin and eosin staining and echocardiogram. ECG, blood pressure, body weight, and blood gas were recorded. Connexin 43 and tyrosine hydroxylase were detected by western blot, immunohistochemistry, and immunofluorescence. CIH induced atrial remodeling, and increased AF inducibility. CSD treatment reduced postapneic blood pressure rises and AF susceptibility, which could attenuate CIH -associated structural atrial arrhythmogenic remodeling. In addition, CIH -induced sympathetic nerve hyperinnervation and CSD treatment reduced sympathetic innervation, which may affect CIH -induced AF -associated sympathovagal imbalance. Connexin 43 was specifically downregulated in CIH , whereas CSD treatment increased its expression. Conclusions These results suggested CIH induces atrial remodeling, increases AF inducibility, results in sympathetic nerve hyperinnervation, and decreases connexin 43 expression, but CSD treatment reduces AF susceptibility, postapneic blood pressure increase, sympathetic innervation, and the alteration of Cx43, which may be a key point in the genesis of CIH -induced AF .

Overexpression of filamin c in chronic intermittent hypoxia-induced cardiomyocyte apoptosis is a potential cardioprotective target for obstructive sleep apnea.

PURPOSE: Chronic intermittent hypoxia (CIH) is key pathological mechanism of obstructive sleep apnea (OSA), which induced cardiac dysfunction. Filamin c (FLNC) is a muscle-restricted isoform and predominantly expressed in muscle tissue. In this study, we utilized a recently developed CIH rat model to mimic OSA, investigated the expression of FLNC in cardiomyocytes, and examined the correlations of FLNC with active caspase-3 to ascertain whether FLNC regulates the survival of cardiomyocytes. METHODS: Forty Sprague-Dawley rats were randomly divided into normoxia and CIH groups. All rats were exposed either to normoxia or CIH 8 h daily for 6 weeks. Echocardiogram and HE staining were used to examine cardiac pathology, structure, and function. Body weight, heart weight, and blood gas values were recorded, respectively. The FLNC, Bax, Bcl-2, BNIP 3, and active caspase-3 proteins were detected by western blot; FLNC was examined by immunohistochemistry and immunofluorescence. Association of FLNC with cardiomyocyte apoptosis was detected by immunofluorescence. RESULTS: CIH induced cardiac injuries and caused arterial blood gas disorder. FLNC significantly increased in CIH-induced cardiomyocytes than that in normoxia tissues. Pro-apoptotic BNIP 3 and Bax proteins were significantly increased in CIH, whereas anti-apoptotic member Bcl-2 was decreased. Active caspase-3, a universal marker of apoptosis, was significantly increased in CIH group. Co-localizations of FLNC and active caspase-3 were observed in CIH group. CONCLUSIONS: These results suggested FLNC is implicated in the pathogenesis of CIH-induced cardiomyocyte apoptosis, and FLNC may serve as a novel cardioprotective target for OSA patients.

Simultaneously surgical management of adult complex coarctation of aorta concomitant with intracardiac abnormality.

BACKGROUND: To explore surgical management of complex coarctation of aorta (COA) concomitant with intracardiac abnormality, in order to provide recommendations for safe and reliable treatment. METHODS: Totally, six adult cases demonstrating complex COA concomitant with intracardiac abnormality were reviewed from our department between May 2012 and June 2017. Four patients were male and two patients were female, the age range being 43.8±10.6 years old. The associated intracardiac abnormality included 3 aortic root aneurysms, 3 aortic insufficiency, 1 aortic stenosis, 3 mitral regurgitation (MR), 1 coronary artery disease (CAD), 1 patent ductus arteriosus (PDA) and 1 ventricular septal defect (VSD). All patients received extra-anatomic aortic bypass approach to tackle complex COA. The extra-anatomic aortic bypasses comprised 4 ascending-descending aortic bypass grafting and 2 ascending-abdominal aortic bypass grafting. Simultaneous intracardiac abnormality repair procedures comprised 3 Bentall procedures, 1 aortic valve replacement, 3 mitral valve repairs, 1 coronary artery bypass grafting, 1 PDA repair and 1 VSD repair. RESULTS: There was no early or late mortality. None of the patients suffered from stroke or paraplegia. Only 1 patient received reexploration for hemostasis because of post-pericardial anastomosis bleeding. The same patient suffered from acute renal failure, but completely recovered after 7-day hemodialysis. All other patients had uneventful post-operative recoveries. The follow-up (mean 37±22.9 months) showed that all patients survived and all patients' blood pressures significantly decreased (pre-operative 165.8±16.3mmHg versus post-operative 121.5±10.8 mmHg, P<0.05). All patients have significantly reduced ankle-brachial pressure gradients (pre-operative 63.3±17.2 mmHg versus post-operative 29.1±4.3 mmHg, P<0.05). All aortic grafts maintained patent flow. CONCLUSIONS: Simultaneous management of complex COA concomitant with intracardiac abnormality is a safe and reliable surgical method.

A hybrid approach for patent ductus arteriosus closure using the Amplatzer Duct Occluder.

OBJECTIVE: We performed closure of the patent ductus arteriosus (PDA) using a hybrid approach with an Amplatzer Duct Occluder. METHODS: Six patients (two males and four females) underwent PDA closure at a mean age of 7.8 months (range 2-24 months) and a mean weight of 6.6 kg (range 4.5-13 kg). The main pulmonary artery (MPA) was exposed via a minimally invasive left parasternal second intercostal space incision. Under transesophageal echocardiography guidance, the PDA occluder was implanted via direct puncture of the MPA. RESULTS: The procedure was successful in all patients with no residual shunt. There were no hospital deaths, and the postoperative course was uneventful. All patients were discharged on the 3rd to 4th day. There was no residual shunt in any patient on midterm follow-up. CONCLUSIONS: The novel hybrid approach is a safe, minimal invasive procedure. Further experience and longer follow-up of these patients is necessary to conclude whether this technique is applicable to all the patients with a PDA.

Iodine stimulates estrogen receptor singling and its systemic level is increased in surgical patients due to topical absorption.

Iodine is crucial for thyroid hormone production. However, recent epidemiologic studies have shown that breast cancer patients have an elevated risk of developing thyroid cancer and vice versa. A notable finding in this study is that iodine stimulated the transcriptional activity of estrogen receptor-α (ER-α) in breast cancer cells. Iodine stimulated expression of several ER-α regulated gene including PS2, Cathepsin D, CyclinD1, and PR both in vitro and in nude mice, which is consistent with its stimulation of both anchorage-dependent and -independent growth of ER-α positive breast cancer cells and the effect to dampen tumor shrinkage of MCF-7 xenograft in ovariectomized nude mice. Analyses of clinical urine samples from breast cancer patients undergoing surgery demonstrated that urinary iodine levels were significantly higher than that in controls; and this increased level is due to the antiseptic use of iodine during breast surgery. The present study indicates that excess iodine intake may be an unfavorable factor in breast cancer by stimulation of ER-α transcriptional activity.

Idiopathic isolated fibrotic atrial cardiomyopathy underlies unexplained scar-related atrial tachycardia in younger patients.

Aims: Unexplained scar-related atrial tachycardia (AT) has been frequently encountered in clinical practice. We hypothesized that idiopathic, isolated fibrotic atrial cardiomyopathy (ACM) underlies this rhythm disorder. This study was aimed to characterize the underlying substrate and to explore the aetiology of this unexplained scar-related AT. Methods and results: Twenty-six (11 men, aged 46 ± 13 years) of 52 non-surgical scar-related AT patients identified by three-dimensional voltage mapping were enrolled in this prospective observational study. Multimodality image examinations (echocardiography, cardiac magnetic resonance, 99Tc single-photon emission computed tomography), ventricular voltage mapping, and intracardiac pressure curve recording ruled out ventricular involvement. Catheter ablation was acutely successful for all the patients, and pacemaker implantation was performed in seven patients who presented sinus node dysfunction or atrial standstill after termination of the AT. In three patients with multiple AT recurrences, the diseased areas of the right atrium were resected and dechannelled via mini-invasive surgical interventions. Histological examinations revealed profound fibrosis without amyloidosis or adipose deposition. Viral and familial investigations yielded negative results. Fibrosis progression over a median of 45 (5-109) months of follow-up manifested as atrial arrhythmia recurrence in seven patients and atrial lead non-capture due to newly developed atrial standstill in two patients. Two patients suffered four ischaemic stroke events before receiving anticoagulation treatment. Conclusion: Isolated, fibrotic ACM may underlie the idiopathic scar-related ATs. This novel cardiomyopathy has unique clinical characteristics with high morbidity including stroke and warrants specific therapeutic strategies. Further investigations are required to determine the aetiology and mechanism.

Inusual endocarditis grave por Kodamaea ohmeriasociada a linfohistiocitosis hemofagocítica / A rare life-threatening kodamaea ohmeriendocarditis associated with hemophagocytic lymphohistiocytosis

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Biomechanical characterization of a novel ring connector for sutureless aortic anastomosis.

The surgical treatment for aortic diseases remains a challenge for any cardiac surgeon. The use of sutureless ring connector in aortic anastomosis can simplify the procedure and shorten anastomosis time. Therefore, we developed a novel device for sutureless aortic anastomosis. A series of experiments were carried out for tensile and leakproof-capacity assessments to verify the feasibility of the ring connector by using fresh swine aorta samples. In in vivo test, the ring connector was implanted in 6 swine with follow-up of 6 months. Radiographic and pathological studies of the aorta were performed. In the tensile tests, the strength was 32.7±5.9 Newton (N) in the sutureless anastomosis group, compared with 73.3±12.5 N in the control group by traditional manual suture. In the leakproof-capacity assessment, no sign of either leakage or bursting was evident at 280 mmHg of internal pressure in the aorta samples. In in vivo tests, it took 9.47±0.3 minutes for the sutureless anastomosis, compared with 15.58±1.39 minutes for hand-sewn suturing. Insertion was easy and rapid. Radiographic and pathological studies were performed at first month, third month and sixth month after surgery, each time obtained from the two swine, showed patency of the anastomosis and no signs of stenosis, blood leakage, migration or pseudoaneurysm formation, except one paralyzed swine developed of thrombo-occlusion at the site of the sutureless anastomosis. The result indicates that this novel ring connector offers considerable promise for sutureless aortic anastomosis.

Bilateral superior cervical ganglionectomy attenuates the progression of ß-aminopropionitrile-induced aortic dissection in rats.

AIMS: Aortic dissection (AD) represents one of the most common aortic emergencies with high incidence of morbidity and mortality. Clinical studies have shown that the increased excitability of the sympathetic nerve may be associated with the formation of AD. In this study, we examined the effects of bilateral superior cervical sympathectomy (SCGx) on the progression of ß-aminopropionitrile (BAPN)-induced AD in rats. MAIN METHODS: Sprague-Dawley rats were randomly divided into three groups, including BAPN, BAPN+SCGx and control groups. For terminal measurements, the mean arterial pressure (MAP) and heart rate (HR) were monitored and the basal sympathetic nerve activity (SNA) was assessed through recording the variation in arterial pressure in response to hexamethonium application. Pathological changes in the aortic wall were observed by histological staining. Matrix metalloproteinase-2 (MMP-2) and MMP-9 concentrations within the aortic wall were analyzed by western blot. KEY FINDINGS: The results show that BAPN administration could elevate SNA and cause the formation of AD in rats with a high incidence (67.7%), while SCGx treatment inhibited the elevation of SNA and significantly reduced the incidence (20%). SCGx may suppress the formation of BAPN-induced AD via restraining the rise of HR and reducing the MMP-9 concentration in aortic wall. SIGNIFICANCE: These results indicate that surgical techniques such as sympathetic nerve block may be a potentially useful therapy for the prevention of AD.

Sex-dependent aortic valve pathology in patients with rheumatic heart disease.

BACKGROUND: Rheumatic heart disease is an autoimmune disease caused by group A streptococci infection and frequently affects the aortic valve. Sex differences are common in the disease progression, treatment, and outcome. However, little is known about the sex differences in the pathology of aortic valves in rheumatic heart disease. DESIGN: We studied the end-stage calcific aortic valves from male versus female patients to reveal the sex-dependent pathology differences and molecular changes associated with requiring valve replacement. METHODS: Aortic valves from 39 patients with rheumatic heart disease (19 males and 20 females) were collected at the time of aortic valve replacement for comparative pathology, immunohistochemistry, and gene expression analyses. Clinical characteristics were also analyzed and compared between the two groups. RESULTS: Aortic valves from female patients exhibited increased expression of collagens, infiltration of monocytes/macrophages and neovascularization. Aortic valves from female patients also had increased expression of inflammatory genes involved in the NFKB pathway (phosphorylated NFKB p65 subunit, IL8, and NOS3) and Th1 cytokine genes (IFNA and IL12B). The severe valve pathology in female patients was correlated with a higher serum level of anti-streptolysin O antibodies. CONCLUSION: Inflammation is more prominent in aortic valves of female patients with rheumatic heart disease. This sex difference may contribute to the severe valve pathology and worse outcome of female patients.

Cardiac autotransplantation for repair of left ventricular rupture after mitral valve replacement.

Left ventricular rupture is an infrequent but potentially fatal complication of mitral valve replacement. Here, we report a case of large posterior mid-ventricular rupture following mitral valve replacement, which was successfully treated by a sandwich style repair and autotransplantation.