Use of three-dimensional electroanatomic mapping for epicardial access: needle tracking, electrographic characteristics, and clinical application.

AIMS: Pericardiocentesis is usually completed under fluoroscopy. The electroanatomic mapping (EAM) system allows visualizing puncture needle tip (NT) while displaying the electrogram recorded from NT, making it possible to obtain epicardial access (EA) independent of fluoroscopy. This study was designed to establish and validate a technique by which EA is obtained under guidance of three-dimensional (3D) EAM combined with NT electrogram. METHODS AND RESULTS: 3D shell of the heart was generated, and the NT was made trackable in the EAM system. Unipolar NT electrogram was continuously monitored. Penetration into pericardial sac was determined by an increase in NT potential amplitude and an injury current. A long guidewire of which the tip was also visible in the EAM system was advanced to confirm EA. Epicardial access was successfully obtained without complication in 13 pigs and 22 patients. In the animals, NT potential amplitude was 3.2 ± 1.0 mV when it was located in mediastinum, 5.2 ± 1.6 mV when in contact with fibrous pericardium, and 9.8 ± 2.8 mV after penetrating into pericardial sac (all P ≤ 0.001). In human subjects, it measured 1.54 ± 0.40 mV, 3.61 ± 1.08 mV, and 7.15 ± 2.88 mV, respectively (all P < 0.001). Fluoroscopy time decreased in every 4-5 cases (64 ± 15, 23 ± 17, and 0 s for animals 1-4, 5-8, 9-13, respectively, P = 0.01; 44 ± 23, 31 ± 18, 4±7 s for patients 1-7, 8-14, 15-22, respectively, P < 0.001). In five pigs and seven patients, EA was obtained without X-ray exposure. CONCLUSION: By tracking NT in the 3D EAM system and continuously monitoring the NT electrogram, it is feasible and safe to obtain EA with minimum or no fluoroscopic guidance.

Triglyceride to high-density lipoprotein cholesterol ratio associated with long-term adverse clinical outcomes in patients deferred revascularization following fractional flow reserve.

BACKGROUND: Guidelines on coronary intermediate lesions strongly recommend deferred revascularization after detecting a normal fractional flow reserve (FFR). Researches about triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) on cardiovascular diseases has also been well conducted. However, the association of TG/HDL-C and long-term adverse clinical outcomes remains unknown for patients deferred revascularization following FFR. METHODS: This study retrospectively included 374 coronary artery disease (CAD) patients with non-significant coronary lesions diagnosed by coronary angiography (CAG) and FFR. The main outcome measure was the combination of major adverse cardiovascular and cerebrovascular events (MACCEs). All patients were categorized into three subgroups in terms of TG/HDL-C tertiles (T1 < 0.96, 0.96 ≤ T2 < 1.58, T3 ≥ 1.58). Three different Cox regression models were utilized to reveal the association between TG/HDL-C and prevalence of MACCEs. RESULTS: 47 MACCEs were recorded throughout a median monitoring period of 6.6 years. The Kaplan-Meier survival curves showed a higher MACCEs rate occurred in the higher TG/HDL-C group (5.6% vs. 12.9% vs. 19.4%, log-rank P < 0.01). After adjustment, patients in T3 suffered a 2.6-fold risk compared to the T1 group (T3 vs. T1: HR 2.55, 95% CI 1.05-6.21, P = 0.038; T2 vs. T1: HR 1.71, 95% CI 0.65-4.49, P = 0.075; P for trend = 0.001). The restricted cubic spline (RCS) analysis demonstrated that the HR for MACCEs rose as TG/HDL-C increased. Both the receiver operating characteristic (ROC) and time-dependent ROC proved the excellent predictive ability of TG/HDL-C. CONCLUSION: The study illustrates that TG/HDL-C correlates with the risk of MACCEs in CAD patients deferred revascularization following FFR. TG/HDL-C could serve as a dependable predictor of cardiovascular events over the long term in this population.

Sestrin2 Is Increased in Calcific Aortic Disease and Inhibits Osteoblastic Differentiation in Valvular Interstitial Cells via the Nuclear Factor E2-related Factor 2 Pathway.

ABSTRACT: Sestrin2 (Sesn2) is involved in the progression of cardiovascular diseases, such as hypertension and myocardial infarction. This study aimed to examine Sesn2 expression in human calcific aortic valve disease (CAVD) and explore its possible mechanisms by which Sesn2 participates in this process. CAVD and normal aortic valves were collected. Sesn2 expression and sources were examined, and the results showed that Sesn2 expression was increased in aortic valves from patients with CAVD and was mainly secreted by macrophages. Additionally, U937 macrophages were pretreated with si-Sesn2 or cDNA-Sesn2 and further treated with oxidized low-density lipoprotein (ox-LDL); M1 macrophages and their markers were measured, and we found that pretreatment with si-Sesn2 increased ox-LDL-induced M1 macrophage polarization and marker mRNA levels, whereas pretreatment with cDNA-Sesn2 had the opposite effects. In ox-LDL-treated U937 macrophages, oxidative stress levels were increased in the si-Sesn2 pretreatment group and further increased by si-Nrf2 treatment, whereas oxidative stress levels were decreased in the cDNA-Sesn2 pretreatment group and significantly reversed by ML385, a specific Nrf2 inhibitor. The effects of Sesn2 on ox-LDL-induced oxidative stress and the osteogenic differentiation of ox-LDL-induced valvular interstitial cells (VICs) was examined by down-regulating Nrf2 pathway. When U937 macrophages were co-cultured with VICs, downregulation of Sesn2 increased ox-LDL-induced osteogenic differentiation in VICs, whereas overexpression of Sesn2 exerted the opposite effects. Our study suggests that Sesn2 is increased in CAVD aortic valves and may participate in the development of CAVD by regulating oxidative stress via the Nrf2 pathway.

Radiofrequency ablation for the pre-excitation syndrome of functionally corrected transposition of great arteries.

We reported a 57-year-old female patient who had functionally corrected transposition of the great arteries, severe tricuspid insufficiency, enlarged left atrium and functional right ventricle, which were successfully performed radiofrequency ablation.

Ablation Versus Medical Therapy for Atrial Fibrillation in the Elderly: A Propensity Score-Matched Comparison.

BACKGROUND Whether ablation therapy reduces the risk of death and embolic events in elderly patients with atrial fibrillation (AF) remains unclear. MATERIAL AND METHODS AF patients ≥65 years old receiving either catheter ablation or non-ablation therapy at 2 tertiary and 2 non-tertiary hospitals in Beijing from November 2009 to December 2012 were enrolled. Patients were followed up every 6 months for information on treatment and clinical event occurrence. A propensity score matching algorithm produced comparable 2 groups of patients treated with ablation or non-ablation. Rates of a composite of all-cause death, non-fatal stroke, and peripheral embolism were the primary outcomes. Each composite component and major bleeding were the secondary outcomes. RESULTS There were 596 ablated patients and 1144 patients with non-ablation therapy enrolled. Propensity score algorithm matched 347 comparable pairs of patients. Patient characteristics variables were well balanced. During 523.5 and 497.5 patient-years follow-up, respectively, ablation therapy was associated with a significant lower risk of experiencing the primary composite outcome (hazard ratio [HR]=0.40; 95% confidence interval [CI]: 0.19-0.85), all-cause death (HR=0.13 95% CI: 0.04-0.43), and major bleeding (HR=0.23; 95% CI: 0.12-0.67), without apparent heterogeneity by age, sex, and AF type, and for risk score subgroups. CONCLUSIONS In this propensity-matched elderly sample, ablation therapy was associated with lower risk of composite outcome consisting of all-cause death, non-fatal stroke, and peripheral embolism, and therefore might be an alternative to conservative therapy.

Case Report: Enhancing lead extraction techniques: a novel approach using a loop formed by an ablation catheter and a gooseneck snare.

The difficulty and complexity of lead extraction procedures increase with the age of the lead to be extracted. The extraction of old (>20 years) leads is more time-consuming and requires advanced tools and a complex technique. In this case, we retrieved a very old (>30 years) lead using a loop formed by a catheter and a gooseneck snare. The catheter was rotated to remove the lead-bound sites. The lead was successfully retrieved using a Needle's Eye Snare.

MicroRNA-322-5p targeting Smurf2 regulates the TGF-ß/Smad pathway to protect cardiac function and inhibit myocardial infarction.

Acute coronary artery blockage leads to acute myocardial infarction (AMI). Cardiomyocytes are terminally differentiated cells that rarely divide. Treatments preventing cardiomyocyte loss during AMI have a high therapeutic benefit. Accumulating evidence shows that microRNAs (miRNAs) may play an essential role in cardiovascular diseases. This study aims to explore the biological function and underlying regulatory molecular mechanism of miR-322-5p on myocardial infarction (MI). This study's miR-322-5p is downregulated in MI-injured hearts according to integrative bioinformatics and experimental analyses. In the MI rat model, miR-322-5p overexpression partially eliminated MI-induced changes in myocardial enzymes and oxidative stress markers, improved MI-caused impairment on cardiac functions, inhibited myocardial apoptosis, attenuated MI-caused alterations in TGF-ß, p-Smad2, p-Smad4, and Smad7 protein levels. In oxygen-glucose deprivation (OGD)-injured H9c2 cells, miR-322-5p overexpression partially rescued OGD-inhibited cell viability and attenuated OGD-caused alterations in the TGF-ß/Smad signaling. miR-322-5p directly targeted Smurf2 and inhibited Smurf2 expression. In OGD-injured H9c2 cells, Smurf2 knockdown exerted similar effects to miR-322-5p overexpression upon cell viability and TGF-ß/Smad signaling; moreover, Smurf2 knockdown partially attenuated miR-322-5p inhibition effects on OGD-injured H9c2 cells. In conclusion, miR-322-5p is downregulated in MI rat heart and OGD-stimulated rat cardiomyocytes; the miR-322-5p/Smurf2 axis improves OGD-inhibited cardiomyocyte cell viability and MI-induced cardiac injuries and dysfunction through the TGF-ß/Smad signaling.

Bedside zero-fluoroscopy temporary permanent pacemaker implantation in the electrical storm treatment under the guidance of EnSite 3D system: a case report.

BACKGROUND: Electrical storm (ES) is a clinical emergency characterized by multiple malignant ventricular arrhythmias or ICD discharges within 24 h, requiring early rational management. CASE PRESENTATION: We report a 55-year-old man who underwent aortic valve replacement experienced recurrent ventricular tachycardia/ventricular fibrillation. A temporary permanent pacemaker with the EnSite system was implanted, and significant inhibition of the electrical storm, attributed to the atrial overdrive pacing, ensued. CONCLUSIONS: In emergency regarding an electrical storm, the bedside temporary permanent pacemaker implantation with the EnSite system is concluded to be feasible and safe.

Nerve growth factor (Ngf) gene-driven semaphorin 3a (Sema3a) expression exacerbates thoracic aortic aneurysm dissection in mice.

Thoracic aortic aneurysm and dissection (TAAD) is a life-threatening disease and currently there is no pharmacological therapy. Sympathetic nerve overactivity plays an important role in the development of TAAD. Sympathetic innervation is mainly controlled by nerve growth factor (NGF, a key neural chemoattractant) and semaphoring 3A (Sema3A, a key neural chemorepellent), while the roles of these two factors in aortic sympathetic innervation and especially TAAD are unknown. We hypothesized that genetically manipulating the NGF/Sema3A ratio by the Ngf -driven Sema3a expression approach may reduce aortic sympathetic nerve innervation and mitigate TAAD progression. A mouse strain of Ngf gene-driven Sema3a expression (namely NgfSema3a/Sema3a mouse) was established by inserting the 2A-Sema3A expression frame to the Ngf terminating codon using CRISPR/Cas9 technology. TAAD was induced by ß-aminopropionitrile monofumarate (BAPN) both in NgfSema3a/Sema3a mice and wild type (WT) littermates. Contrary to our expectation, the BAPN-induced TAAD was severer in NgfSema3a/Sema3a mice than in wild-type (WT) mice. In addition, NgfSema3a/Sema3a mice showed higher aortic sympathetic innervation, inflammation and extracellular matrix degradation than the WT mice after BAPN treatment. The aortic vascular smooth muscle cells isolated from NgfSema3a/Sema3a mice and pretreated with BAPN in vivo for two weeks showed stronger capabilities of proliferation and migration than that from the WT mice. We conclude that the strategy of Ngf -driven Sema3a expression cannot suppress but worsens the BAPN-induced TAAD. By investigating the aortic phenotype of NgfSema3a/Sema3a mouse strain, we unexpectedly find a path to exacerbate BAPN-induced TAAD which might be useful in future TAAD studies.

Successful leadless pacemaker implantation in a patient with dextroversion of the heart: A case report.

BACKGROUND: Dextroversion is defined as the presence of dextrocardia with situs solitus, dextro-loop ventricles, and normally related great arteries. Dextrocardia can pose technical challenges when interventional treatments are required. However, the challenges posed by dextroversion can be amplified due to the disruption of typical anatomical relationships, the unpredictable positioning and boundaries of cardiac structures resulting from the shift, and the pathological processes influencing rotation. CASE SUMMARY: A 73-year-old woman with cardiac dextroversion suffered from a recurrence of atrial fibrillation after her radiofrequency catheter ablation and Despite the cessation of antiarrhythmic medications, there were episodes of sinus pauses and symptomatic bradycardia, with heart rates dropping as low as 28 beats per minute. CONCLUSION: Dextroversion makes the implantation of leadless pacemakers more challenging, and appropriate adjustments in fluoroscope angles may be crucial for intracardiac operations. Additionally, when advancing delivery systems, attention should be paid to rotational direction during valve-crossing procedures; changes in the perspective of posture angle between normal cardiac position and dextroversion can serve as references.

Case Report: Fluoroless implantation of left branch bundle pacing in a pregnant patient.

A pregnant patient had symptomatic atrial standstill and indications for pacing therapy with an expected high ventricular pacing ratio. With the consideration of potential pacing-induced cardiomyopathy in the future we conducted zero-fluoro left bundle branch pacing (zLBBP) implantation for heart failure prevention. An ex vivo 3D cardiac model (Medtronic, USA) was used preoperatively to simulate the zLBBP implantation to improve procedure safety and efficiency. Intraoperatively, the simulation steps were followed, and a combination of electroanatomic navigation systems (EANS) and intracardiac echocariography (ICE) were used to ensure that the procedure was performed efficiently and safely.

Removal of a pulmonary artery foreign body during pulse ablation in a patient with atrial fibrillation: A case report.

BACKGROUND: Foreign bodies in the pulmonary circulation have been documented in the literature and are typically caused by interventional procedures. However, reports of pulmonary artery foreign bodies during femoral vein puncture are rare, and there is no description of this complication from the guidewire surface flows into the pulmonary artery during a pulse ablation in a patient with atrial fibrillation. CASE SUMMARY: We described a case in which a linear foreign body suddenly appeared on fluoroscopy image during pulsed ablation of atrial fibrillation. Multiposition angiography showed that the foreign body was currently lodged in the pulmonary artery but was hemodynamically stable. We then chose to use an interventional approach to remove the foreign body from the pulmonary artery. This foreign body was subsequently confirmed to be from the hydrophilic coating of the guidewire surface. This may be related to the difficulties encountered during the puncture of the femoral vein. This is a rare and serious complication of femoral vein puncture. Therefore, we reported this case in order to avoid a similar situation. CONCLUSION: Mismatches between interventional devices from different manufacturers used for femoral venipuncture may result in pulmonary artery foreign bodies.

Preventing effect of astragalus polysaccharide on cardiotoxicity induced by chemotherapy of epirubicin: A pilot study.

To assess the clinical effect of astragalus polysaccharide in preventing cardiotoxicity induced by chemotherapy of epirubicin. Two hundred forty-eight patients with breast cancer or malignant lymphoma were randomly divided into the experimental group (EG) (n = 124) and the control group (CG) (n = 124). The EG received chemotherapy regimen containing anthracycline epirubicin and astragalus injection, while CG received only chemotherapy regimen containing anthracycline epirubicin. We detected myocardial function (cardiac troponin I [cTnI], creatine kinase isoenzyme [CK-MB], left ventricular ejection fraction [LVEF], and the ratio of mitral annular diastolic peak velocity to atrial systolic velocity [E/A]) and incidences of cardiotoxicity to assess cardiac function, they were compared at before the first treatment course (T1), end of the second course (T2) and 6-month follow-up. We also detected proinflammatory cytokines (IL-6 and TNF-α), reactive oxygen species and antioxidant enzymes, glutathione peroxidase (GPx), and superoxide dismutase (SOD) aimed to discover potential mechanism. There were no statistical significances in differences of LVEF and E/A between 2 groups (P > .05) at T1 and T2, while levels of LVEF and E/A of EG were significant higher than those of the CG at 6 month follow-up, with statistically significant differences (P < .05). At T1, there were no statistical significances in differences of cTnI and CK-MB between 2 groups (P > .05); at T2 and 6 months follow-up, the cTnI, and CK-MB levels of EG was significantly lower than those of the CG, with statistically significant differences (P < .05). The incidence of cardiotoxicity of EG was 15% (17/113), which was significant lower than that of the CG (60%, 66/110), with statistically significant difference (P < .05). Moreover, the level of TNF-α, GPx, and SOD did not show significant difference (P > .05). The data in this pilot study suggested that astragalus polysaccharide may be an effective therapy for preventing cardiotoxicity induced by chemotherapy of epirubicin. Furthermore, larger, placebocontrolled, perspective studies are needed to assess the efficacy of astragalus injection treatment for preventing cardiotoxicity induced by chemotherapy of epirubicin.

Percutaneous transhepatic access for catheter ablation of a patient with heterotaxy syndrome complicated with atrial fibrillation: A case report.

BACKGROUND: Atrial fibrillation (AF) is one of the most common arrhythmias, and radiofrequency catheter ablation is the most effective treatment strategy. The inferior vena cava (IVC) is a common approach for radiofrequency ablation of AF. However, this approach may not be applied to some cases such as chronic venous occlusions, surgical ligation of the IVC, and heterotaxy syndrome (HS). CASE SUMMARY: A 68-year-old man with HS suffered from severely symptomatic persistent AF for 9 years, and we successfully ablated by percutaneous transhepatic access. CONCLUSION: In patients without femoral vein access, the use of the hepatic vein for pulmonary vein isolation is a viable alternative for invasive electrophysiology procedures.

Total Bilirubin Level is Associated with the Risk of Left Atrial Appendage Thrombosis in Patients with Non-Valvular Atrial Fibrillation.

Objectives: There are some evidence suggesting that total bilirubin (TBIL) appears to be associated with stroke in patients with nonvalvular atrial fibrillation (NVAF). The left atrial appendage (LAA) is the most common orgin of thrombus in patients with NVAF. The purpose of this study was to assess a possible relationship between plasma TBIL levels and LAA thrombus in NVAF patients. Methods: We retrospectively screened 459 consecutive hospitalized patients with NVAF at three AF centers, who underwent transesophageal echocardiography or cardiac CT. According to the examination results, the patients were divided into either the LAA thrombosis group (41 cases) or the no LAA thrombosis group (418 cases). Independent sample t test, Mann-Whitney U-test and chi-square test were used to compare and analyze the general clinical data of the two groups. Multivariate Logistic regression was used to analyze whether TBIL was a risk factor for LAA thrombosis in patients with NVAF. Pearson correlation analysis was used to explore the correlation between TBIL and other influencing factors. The predictive value of TBIL for LAA thrombosis in patients with NVAF was evaluated by ROC curve. Results: A total of 459 patients were enrolled in this study. Compared with the group without LAA thrombosis, the level of TBIL in LAA thrombosis group was significantly increased (21.34 ± 9.34 umol/L vs. 13.98 ± 4.25 umol/L, P < 0.001). Multivariate logistic regression showed that TBIL level was a risk factor for LAA thrombosis (OR, 1.229; 95% CI, 1.122~1.345; P < 0.001). The AUC of the ROC curve is 0.801 (95% CI, 0.725~0.877; P < 0.001). At 17.4 umol/L of TBIL, the patient may have LAA thrombosis (sensitivity 73.2%; specificity 82.1%). Conclusions: In patients with NVAF, TBIL level is positively associated with LAA thrombosis, and TBIL level may be an index reflecting LAA thrombosis.

FOXO3a-dependent PARKIN negatively regulates cardiac hypertrophy by restoring mitophagy.

BACKGROUND: Sustained cardiac hypertrophy often develops maladaptive myocardial remodeling, and eventually progresses to heart failure and sudden death. Therefore, maladaptive hypertrophy is considered as a critical therapeutic target for many heart diseases. Mitophagy, a crucial mechanism in mitochondria quality control and cellular homeostasis, has been implicated in diverse cardiac disorders such as myocardial infarction, diabetic cardiomyopathy, cardiac hypertrophy and heart failure. However, what role mitophagy plays in heart diseases remains an enigma. PARKIN functions as an E3 ubiquitin protein ligase and mediates mitophagy cascades. It is still unclear whether PARKIN participates in the regulation of cardiac hypertrophy. RESULTS: PARKIN was downregulated in cardiomyocytes and hearts under hypertrophic stress. Enforced expression of PARKIN inhibited Ang II-induced cardiomyocyte hypertrophy. Compared to wide-type mice with Ang II-induced cardiac hypertrophy, Parkin transgenic mice subjected to Ang II administration showed attenuated cardiac hypertrophy and improved cardiac function. In addition, mitophagy machinery was impaired in response to Ang II, which was rescued by overexpression of PARKIN. PARKIN exerted the anti-hypertrophy effect through restoring mitophagy. In further exploring the underlying mechanisms, we found that PARKIN was transcriptionally activated by FOXO3a. FOXO3a promoted mitophagy and suppressed cardiac hypertrophy by targeting Parkin. CONCLUSIONS: The present study reveals a novel cardiac hypertrophy regulating model composed of FOXO3a, PARKIN and mitophagy program. Modulation of their levels may provide a new approach for preventing cardiac hypertrophy and heart failure.

ß-adrenergic activation may promote myosin light chain kinase degradation through calpain in pressure overload-induced cardiac hypertrophy: ß-adrenergic activation results in MLCK degradation.

BACKGROUND: ß-adrenergic activation is able to exacerbate cardiac hypertrophy. Myosin light chain kinase (MLCK) and its phosphorylated substrate, phospho-myosin light chain 2 (p-MLC2), play vital roles in regulating cardiac hypertrophy. However, it is not yet clear whether there is a relationship between ß-adrenergic activation and MLCK in the progression of cardiac hypertrophy. Therefore, we explored this relationship and the underlying mechanisms in this work. METHODS: Cardiac hypertrophy and cardiomyocyte hypertrophy were induced by pressure overload and isoproterenol (ISO) stimulation, respectively. Echocardiography, histological analysis, immunofluorescence and qRT-PCR were used to confirm the successful establishment of the models. A ß-blocker (metoprolol) and a calpain inhibitor (calpeptin) were administered to inhibit ß-adrenergic activity in rats and calpain in cardiomyocytes, respectively. The protein expression levels of MLCK, myosin light chain 2 (MLC2), p-MLC2, myosin phosphatase 2 (MYPT2), calmodulin (CaM) and calpain were measured using western blotting. A cleavage assay was performed to assess the degradation of recombinant human MLCK by recombinant human calpain. RESULTS: The ß-blocker alleviated cardiac hypertrophy and dysfunction, increased MLCK and MLC2 phosphorylation and decreased calpain expression in pressure overload-induced cardiac hypertrophy. Additionally, the calpain inhibitor calpeptin attenuated cardiomyocyte hypertrophy, upregulated MLCK and p-MLC2 and reduced MLCK degradation in ISO-induced cardiomyocyte hypertrophy. Recombinant human calpain degraded recombinant human MLCK in vitro in concentration- and time-dependent manners, and this degradation was inhibited by the calpain inhibitor calpeptin. CONCLUSION: Our study suggested that ß-adrenergic activation may promote the degradation of MLCK through calpain in pressure overload-induced cardiac hypertrophy.

Increased plasma sestrin2 concentrations in patients with chronic heart failure and predicted the occurrence of major adverse cardiac events: A 36-month follow-up cohort study.

BACKGROUND: Previous study had demonstrated that sestrin2 (Sesn2) expression was increased in human failing heart. Although, the circulating Sesn2 concentrations in patients with chronic heart failure (CHF) remains unknown. This study investigated plasma Sesn2 concentrations in patients with CHF and the role between Sesn2 and the occurrence of major adverse cardiac events. METHODS: A total of 80 control subjects and 220 CHF patients were enrolled and the Sesn2 concentrations of each sample were measured. Additionally, the occurrence of major adverse cardiac events in each CHF patient were followed prospectively for 36 months. RESULTS: Increased plasma Sesn2 concentrations were found in CHF patients and gradually increased from New York Heart Association (NYHA) functional class II to IV. The Sesn2 concentrations were positively correlated with N-terminal B-type natriuretic peptide (NT-pro BNP) but negatively correlated with left ventricular ejection fraction (LVEF) in CHF patients. The ROC curve suggested that Sesn2 had a certain value in predicting major adverse cardiac events during CHF patients, although, the predictive role of Sesn2 is not as good as NT-pro BNP. In addition, the multivariate Cox hazard analysis was performed after the CHF patients were divided into 3 groups (low, middle, and high) base on the plasma Sesn2 concentrations category, and the results showed that both high and middle Sesn2 concentrations increased the incidence of major adverse cardiac events when compared with low Sesn2 group. Furthermore, CHF patients with major adverse cardiac events showed higher Sesn2 concentrations when compared with CHF without major adverse cardiac events. The Kaplan-Meier analysis was performed after the CHF patients were divided into 2 groups according to the median Sesn2 concentrations and the results revealed that patients with high Sesn2 concentrations had a higher risk of major adverse cardiac events compared with those with low Sesn2. CONCLUSIONS: Plasma Sesn2 concentrations were increased in CHF patients and positively correlated with the severity of CHF. Increased Sesn2 concentrations significantly increased the occurrence of major adverse cardiac events and suggested poor outcome in CHF patients.