Health economic analysis and medical cost analysis of children with severe hepatitis B in China: A retrospective study from 2016 to 2022.

BACKGROUND: Hepatitis B poses a heavy burden for children in China, however, the national studies on the distributional characteristics and health care costs of children with severe hepatitis B is still lacking. This study aimed to analyze the disease characteristics, health economic effects, and medical cost for children with severe hepatitis B in China. METHODS: Based on patient information in the Hospital Quality Monitoring System, cases with severe hepatitis B were divided into four groups according to age, and the etiology and symptoms of each group were quantified. The cost of hospitalization was calculated for cases with different disease processes, and severity of disease. The spatial aggregation of cases and the relationship with health economic factors were analyzed by Moran's I  analysis. RESULTS: The total number of children discharged with hepatitis B from January 2016 to April 2022 was 1603, with an average age of 10.5 years. Liver failure cases accounted for 43.48% (697/1603,) of total cases and cirrhosis cases accounted for 11.23% (180/1603,). According to the grouping of disease progression, there were 1292 cases without associated complications, and the median hospitalization cost was $818.12. According to the spatial analysis, the aggregation of cases was statistically significant at the prefectural and provincial levels in 2019, 2020, and 2021 (all P <0.05). The number of severe cases was negatively correlated with gross domestic product (GDP, Moran's I <0) and percentage of urban population (Moran's I <0), and positively correlated with the number of pediatric beds per million population (Moran's I >0). CONCLUSION: The number of severe hepatitis B cases is low in areas with high GDP levels and high urban population ratios, and health care costs have been declining over the years.

Whole-exome sequencing and electrophysiological study reveal a novel loss-of-function mutation of KCNA10 in epinephrine provoked long QT syndrome with familial history of sudden cardiac death.

Congenital long QT syndrome (LQTS) is one type of inherited fatal cardiac arrhythmia that may lead to sudden cardiac death (SCD). Mutations in more than 16 genes have been reported to be associated with LQTS, whereas the genetic causes of about 20% of cases remain unknown. In the present study, we investigated a four-generation pedigree with familial history of syncope and SCD. The proband was a 33-year-old young woman who experienced 3 episodes of syncope when walking at night. The electrocardiogram revealed a markedly epinephrine-provoked prolonged QT interval (QT = 468 ms, QTc = 651 ms) but no obvious arrhythmia in the resting state. Three family members have died of suspected SCD. Whole-exome sequencing and bioinformatic analysis based on pedigree revealed that a novel missense mutation KCNA10 (c.1397G＞A/Arg466Gln) was the potential genetic lesion. Sanger sequencing was performed to confirm the whole-exome sequencing results. This mutation resulted in the KV1.8 channel amino acid residue 466 changing from arginine to glutamine, and the electrophysiological experiments verified it as a loss-of-function mutation of KV1.8, which reduced the K+ currents of KV1.8 and might result in the prolonged QT interval. These findings suggested that KCNA10 (c.1397G＞A) mutation was possibly pathogenic in this enrolled LQTS family, and may provide a new potential genetic target for diagnosis and counseling of stress-related LQTS families as well as the postmortem diagnosis of SCD.

Left Bundle Branch Pacing for Bradycardia in Non-obstructive Hypertrophic Cardiomyopathy Patients: Feasibility, Safety, and Effect.

PURPOSE: Left bundle branch pacing (LBBP) is as an innovative physiological pacing approach. The research on LBBP in non-obstructive hypertrophic cardiomyopathy (NOHCM) patients is scarce. This study aimed to assess the feasibility, safety, and effect of LBBP in bradycardia NOHCM patients with permanent pacemaker (PPM) implantation indication. METHODS: Thirteen consecutive patients with NOHCM who received LBBP were retrospectively enrolled as a hypertrophic cardiomyopathy (HCM) group. Following 1:3 matching, 39 patients without HCM were randomly matched as a control group. Echocardiographic index and pacing parameters were collected. RESULTS: The successful LBBP was achieved in 96.2% of all cases (50/52), and the success rate of the HCM group was 92.3% (12/13). In the HCM group, the paced QRS duration (from the pacing stimulus to QRS end) was 145.6±20.8 ms. The stimulus to left ventricular activation time (s-LVAT) was 87.4±15.2 ms. In the control group, the paced QRS duration was 139.4±17.2 ms, and the s-LVAT was 79.9±14.1 ms. During the implantation, R-wave sensing and the pacing threshold of the HCM group were significantly higher than the control group (20.2±10.5 vs 12.5±5.9 mV, P < 0.05; 0.8±0.3 vs 0.6±0.2V/0.4 ms, P < 0.05). In addition, the fluoroscopic duration and procedural duration were longer in the HCM group (14.8±8.3 vs 10.3±6.6min, P = 0.07; 131.8±50.5 vs 101.4±41.6 min, P < 0.05). The lead insertion depth was 15±2 mm in the HCM group, and no procedure-related complications occurred. During the 12-month follow-up, pacing parameters remained stable and were of no significance in the two groups. The cardiac function did not deteriorate, and the left ventricular outflow tract gradient (LVOTG) did not increase in the follow-up. CONCLUSION: LBBP might be feasible and safe for NOHCM patients with conventional bradycardia pacing indication, and there is no deterioration in cardiac function and LVOTG of patients with NOHCM.

Empagliflozin ameliorates cardiac dysfunction in heart failure mice via regulating mitochondrial dynamics.

Empagliflozin has cardioprotective effects in patients with heart failure (HF). However, the mechanism by which empagliflozin protects against HF remains controversial. Study aimed to evaluate the effect of empagliflozin on myocardial fibrosis and cardiac function in HF mice and its possible mechanism. C57BL/6 mice were induced with HF by ligation of the left anterior descending coronary artery. At 4 weeks postoperation, mice were randomly given normal saline or empagliflozin for 8 weeks. Echocardiography was used to assess cardiac function. Masson's staining, immunohistochemistry and Western blot analysis were used to detect the degree of myocardial fibrosis. Changes in mitochondria were detected by observing mitochondrial morphology, measuring mitochondrial dynamics-related proteins and analysing the levels of adenosine triphosphate (ATP), adenosine monophosphate (AMP) and adenosine diphosphate (ADP). The mitochondrial fission inhibitor, mdivi1, was used to detect the relationship between mitochondrial dysfunction and cardiac dysfunction in HF mice. HF led to myocardial fibrosis and cardiac dysfunction. However, treatment with empagliflozin reduced these effects. Empagliflozin inhibited mitochondrial fission and improved energy metabolic efficiency in HF mice by regulating the expression of mitochondrial dynamics-related proteins. Similarly, mdivi1 attenuated mitochondrial dysfunction and cardiac dysfunction by inhibiting mitochondrial fission in HF mice. Regulation of mitochondrial dynamics, especially inhibition of mitochondrial fission, may be a potential target for reducing cardiac damage in patients with HF. Empagliflozin improved myocardial fibrosis and cardiac dysfunction by modulating mitochondrial dynamics in HF mice. Thus, the cardiac protective effect of empagliflozin may be related to the normalization of mitochondria and the increase in ATP production.

Trimethylamine N-oxide facilitates the progression of atrial fibrillation in rats with type 2 diabetes by aggravating cardiac inflammation and connexin remodeling

Diabetes is an independent risk factor for atrial fibrillation (AF). This study aimed to elucidate the pathophysiology of diabetes-related AF from the perspective of the gut microbial metabolite trimethylamine N-oxide (TMAO). In the present study, male rats received either a normal diet to serve as the control group or a high-fat diet/streptozotocin to induce type 2 diabetes mellitus. Then, diabetic rats were divided into two groups based on the presence or absence of 3,3-dimethyl-1-butanol (DMB, a specific TMAO inhibitor) in drinking water: the diabetic cardiomyopathy (DCM) group and the DCM + DMB group. Eight weeks later, compared with control rats, rats in the DCM group exhibited gut microbiota dysbiosis and systemic TMAO elevation. The inflammatory cytokines IL-1β, IL-6, and TNF-α were markedly increased in the atria of rats in the DCM group. Downregulated expression of connexin 40 and lateralized distribution of connexin 43 were also observed in the atria of DCM rats. AF inducibility was significantly higher in DCM rats than in control rats. Furthermore, DMB treatment effectively ameliorated atrial inflammation and connexin remodeling while markedly reducing plasma TMAO levels. DMB treatment also decreased the vulnerability of diabetic rats to AF. In conclusion, TMAO might promote atrial inflammation and connexin remodeling in the development of diabetes, which may play a key role in mediating diabetes-related AF. (AU)

Trimethylamine N-oxide facilitates the progression of atrial fibrillation in rats with type 2 diabetes by aggravating cardiac inflammation and connexin remodeling.

Diabetes is an independent risk factor for atrial fibrillation (AF). This study aimed to elucidate the pathophysiology of diabetes-related AF from the perspective of the gut microbial metabolite trimethylamine N-oxide (TMAO). In the present study, male rats received either a normal diet to serve as the control group or a high-fat diet/streptozotocin to induce type 2 diabetes mellitus. Then, diabetic rats were divided into two groups based on the presence or absence of 3,3-dimethyl-1-butanol (DMB, a specific TMAO inhibitor) in drinking water: the diabetic cardiomyopathy (DCM) group and the DCM + DMB group. Eight weeks later, compared with control rats, rats in the DCM group exhibited gut microbiota dysbiosis and systemic TMAO elevation. The inflammatory cytokines IL-1ß, IL-6, and TNF-α were markedly increased in the atria of rats in the DCM group. Downregulated expression of connexin 40 and lateralized distribution of connexin 43 were also observed in the atria of DCM rats. AF inducibility was significantly higher in DCM rats than in control rats. Furthermore, DMB treatment effectively ameliorated atrial inflammation and connexin remodeling while markedly reducing plasma TMAO levels. DMB treatment also decreased the vulnerability of diabetic rats to AF. In conclusion, TMAO might promote atrial inflammation and connexin remodeling in the development of diabetes, which may play a key role in mediating diabetes-related AF.

Reversible T-wave inversions during left bundle branch area pacing.

BACKGROUND: Our clinical observation found that T-wave inversions (TWIs) appeared during left bundle branch area pacing (LBBAP); however, the incidence and influencing factors were unclear. The study aimed to investigate the effects of LBBAP on T-wave and explore possible factors associated with TWIs. METHODS: This was a retrospective cohort study. An electrocardiogram (ECG) was acquired at baseline and after LBBAP. Baseline characteristics, ECG parameters, LBBAP parameters, and troponin T (TnT) levels were compared between the non-TWIs and TWIs groups. Multivariable logistic analyses were performed to adjust for potential confounders to identify the predictive factors of TWIs during LBBAP. RESULTS: A total of 398 consecutive patients who underwent successful LBBAP were assessed for inclusion between May 2017 and Jan 2021, and 264 (66.3%) patients had TWIs. The mean (standard deviation [SD]) baseline QRS duration (QRSd) was longer in the TWIs group compared to the non-TWIs group (125.9 [34.5] ms vs. 98.2 [18.1] ms; P <0.001). Multivariable logistic regression analysis suggested that QRSd >120 ms was an independent predictor for TWIs. TWIs were partially or com-pletely recovered in 151/172 (87.8%) patients during follow-up, the median (interquartile range [IQR]) follow-up duration was 10 days (7 days to 5.5 months). TWIs in patients with complete left bundle branch block (CLBBB) occurred more frequently in inferior wall leads (II, III, and aVF) and anterior wall leads (V1-V4) (P <0.05). Patients with complete right bundle branch block (CRBBB) were more prone to TWIs in high lateral wall leads (I and aVL) (P <0.05). There were no significant differences in TnT levels between the TWIs and non-TWIs groups. CONCLUSIONS: TWIs during LBBAP were clinically frequent and recoverable. QRSd >120 ms was independently associated with TWIs.

The Effect of Renal Denervation on Cardiac Diastolic Function in Patients with Hypertension and Paroxysmal Atrial Fibrillation.

Objective: Renal artery denervation (RDN) can treat hypertension and paroxysmal atrial fibrillation (PAF). Hypertension and PAF can affect cardiac diastolic function. The study aimed to evaluate the effect of RDN on cardiac diastolic function in patients with refractory hypertension and PAF. Methods: 190 consecutive patients with hypertension and PAF were recruited. The levels of NT-proBNP and metrics of echocardiography were measured before and after RDN in patients with refractory hypertension and PAF. The 190 patients were divided into the decreasing HR and nondecreasing HR group, the decreasing MAP and nondecreasing MAP group, the HFPEF group, and the normal diastolic function group, respectively. Results: Before RDN, the indices about cardiac diastolic function were out of the normal range. After RDN, the diastolic function improved in the indices of NT-proBNP, E/e', e'. The diastolic function about the indices of NT-proBNP, E/e', e' was improved in the decreasing HR group, the decreasing mean arterial pressure (MAP) group, and the HFPEF group, correspondingly compared to the nondecreasing HR group, the non-decreasing MAP group, and the preoperative normal diastolic function group. In the multivariate analysis, the MAP and HR were the only two indicators significantly associated with the improvement of diastolic function. Conclusion: RDN could improve the diastolic function in patients with refractory hypertension and PAF. Patients with HFPEF could receive benefits through RDN. It was speculated that RDN improved the diastolic function mainly through decreasing HR and MAP.

Clinical Outcomes of Permanent Left Bundle Branch Area Pacing in Patients With Left Bundle Branch Block and Left Ventricular Ejection Fraction >35 vs. ≤35.

Aims: The present study aimed to compare the effects of left bundle branch area pacing (LBBAP) on cardiac function and clinical outcomes in patients with left bundle branch block (LBBB) and left ventricular ejection fraction (LVEF) >35 vs. ≤35%. Methods and Results: Thirty-six consecutive patients with LBBB and LVEF <50% were enrolled. All patients were followed up for a mean of 6 months. The successful LBBAP was defined as a paced QRS complex presented as right bundle branch block (RBBB) morphology and QRSd < 130 ms. Echocardiography parameters, pacing parameters and clinical outcomes were collected. The successful LBBAP was achieved in 77.8% of all cases (28/36). In LVEF > 35% group (70 ± 8 years, 9 male), the success rate was 81.0% (17/21). QRSd significantly decreased from 174 ± 23 ms to 108 ± 13 ms (P < 0.001). The pacing threshold and R-wave amplitude were 0.6 ± 0.2 V @ 0.5 ms and 12 ± 7 mV, respectively. In LVEF ≤ 35% group (69 ± 5 years, 9 male), the success rate was 73.3% (11/15) with QRSd decreasing from 188 ± 25 ms to 107 ± 11 ms (P < 0.001). The hyperresponders to LBBAP (functional recovery and LVEF ≥ 50%) in LVEF > 35% group was 52.9%, which were almost twice of that in LVEF ≤ 35% group (33.3%). Whether patients had LBBAP or left ventricular septal pacing (LVSP), patients in the LVEF > 35% group showed significantly lower incidence of heart failure hospitalizations or death from any cause (hazard ratio in LVEF > 35% group, 0.22; 95%CI, 0.06 to 0.75, P = 0.011). Conclusions: LBBAP can significantly shorten the QRSd and improve cardiac function in LBBB patients with either LVEF > 35 or ≤ 35%. LBBAP should be considered as an effective therapy for preventing the deterioration of cardiac function in early-stage heart failure patients with LBBB and LVEF > 35%.

Discussion of LBBP synchronization effects in HF patients with LBBB and comparison with BiV-CRT.

Left bundle branch block (LBBB) is common in heart failure patients, and could induce dyssynchrony of ventricular contraction, deterioration of cardiac function, and increased mortality. Cardiac resynchronization therapy (CRT) with biventricular pacing reduces ventricular dyssynchrony, heart failure hospitalization, and all-cause mortality in heart failure patients with LBBB. However, there are approximately 30% nonresponders and 10% of patients remain untreated owing to an unsuitable coronary sinus vein. His bundle pacing (HBP) is a more physiological pacing modality which has showed inspiring outcomes in heart failure patients with LBBB, but is limited by implantation challenges, lower success rates, and high pacing capture threshold. Recently, left bundle branch pacing (LBBP), defined as the capture of left bundle branch via transventricular septal approach, has emerged as a newly physiological pacing modality, which is implanted slightly distal to the His bundle. Early clinical studies have demonstrated the procedural feasibility of LBBP with rare complications and high success rate. Recent studies have indicated its potential to be an alternative for CRT. Synchronization effect and the current status of LBBP in the field of CRT are summarized in this paper.

Feasibility and safety of left bundle branch area pacing in very elderly patients (≥80 years).

BACKGROUND: Left bundle branch area pacing (LBBAP) has emerged as a promising physiologic pacing strategy. Though many clinical studies have established the feasibility and safety of LBBAP, the data for very elderly patients are lacking. AIMS: This study aimed to assess the feasibility and safety of LBBAP in very elderly patients (≥80 years). METHODS: Two hundred and forty consecutive patients who received LBBAP implantation were retrospectively enrolled in the present study. Inclusion criteria were patients with atrioventricular block, atrial fibrillation with a slow ventricular response, and heart failure with bundle branch block. The patients were divided into two groups: those aged ≥80 years and those aged <80 years. LBBAP implantation was successfully performed in 48 of 53 (90.6%) very elderly patients and 162 of 187 (86.5%) counterparts. In the very elderly group, the mean (standard deviation [SD]) age was 84 (3) years, mean (SD) paced QRS duration was 112.4 (9.0), and the mean (SD) stimulus to R wave peak time was 82.0 (14.2) ms. Mean (SD) pacing thresholds and mean (SD) R wave sensing were 0.61(0.21) V and 12.1 (4.7) mV at implant. Pacing parameters in very elderly patients were similar to those in their counterparts. During a median follow-up of 6 months, pacing parameters remained stable. Five patients in the very elderly group developed complications (1 with septal perforation during the procedure, 1 with pocket hematoma, 1 with pacing threshold increase, and 2 with micro lead dislodgement during follow-up). CONCLUSION: LBBAP is safe and effective in patients ≥80 years old. LBBAP can be considered as an alternative method for delivering physiological pacing in this special population.

Renal denervation ameliorates cardiac metabolic remodeling in diabetic cardiomyopathy rats by suppressing renal SGLT2 expression.

This study aimed to investigate the effects of renal denervation (RDN) on diabetic cardiomyopathy (DCM) and explore the related mechanisms. Male Sprague-Dawley rats were fed high-fat chow and injected with low-dose streptozotocin to establish a DCM model. Six rats served as controls. The surviving rats were divided into three groups: control group, DCM group and DCM + RDN group. RDN surgery was performed in the fifth week. At the end of the experiment, all rats were subjected to 18F-FDG PET/CT and metabolic cage studies. Cardiac function and structure were evaluated by echocardiography and histology. Myocardial substrate metabolism and mitochondrial function were assessed by multiple methods. In the 13th week, the DCM rats exhibited cardiac hypertrophy and interstitial fibrosis accompanied by diastolic dysfunction. RDN ameliorated DCM-induced cardiac dysfunction (E/A ratio: RDN 1.07 ± 0.18 vs. DCM 0.93 ± 0.12, P < 0.05; E/E' ratio: RDN 10.74 ± 2.48 vs. DCM 13.25 ± 1.99, P < 0.05) and pathological remodeling (collagen volume fraction: RDN 5.05 ± 2.05% vs. DCM 10.62 ± 2.68%, P < 0.05). Abnormal myocardial metabolism in DCM rats was characterized by suppressed glucose metabolism and elevated lipid metabolism. RDN increased myocardial glucose uptake and oxidation while reducing the absorption and utilization of fatty acids. Meanwhile, DCM decreased mitochondrial ATP content, depolarized the membrane potential and inhibited the activity of respiratory chain complexes, but RDN attenuated this mitochondrial damage (ATP: RDN 30.98 ± 7.33 µmol/gprot vs. DCM 22.89 ± 5.90 µmol/gprot, P < 0.05; complexes I, III and IV activity: RDN vs. DCM, P < 0.05). Furthermore, both SGLT2 inhibitor and the combination treatment produced similar effects as RDN alone. Thus, RDN prevented DCM-induced cardiac dysfunction and pathological remodeling, which is related to the improvement of metabolic disorders and mitochondrial dysfunction.

Intestinal Barrier Dysfunction Exacerbates Neuroinflammation via the TLR4 Pathway in Mice With Heart Failure.

AIMS: The present study aimed to investigate alterations in neuroinflammation after heart failure (HF) and explore the potential mechanisms. METHODS: Male wild-type (WT) and Toll-like receptor 4 (TLR4)-knockout (KO) mice were subjected to sham operation or ligation of the left anterior descending coronary artery to induce HF. 8 weeks later, cardiac functions were analyzed by echocardiography, and intestinal barrier functions were examined by measuring tight junction protein expression, intestinal permeability and plasma metabolite levels. Alterations in neuroinflammation in the brain were examined by measuring microglial activation, inflammatory cytokine levels and the proinflammatory signaling pathway. The intestinal barrier protector intestinal alkaline phosphatase (IAP) and intestinal homeostasis inhibitor L-phenylalanine (L-Phe) were used to examine the relationship between intestinal barrier dysfunction and neuroinflammation in mice with HF. RESULTS: Eight weeks later, WT mice with HF displayed obvious increases in intestinal permeability and plasma lipopolysaccharide (LPS) levels, which were accompanied by elevated expression of TLR4 in the brain and enhanced neuroinflammation. Treatment with the intestinal barrier protector IAP significantly attenuated neuroinflammation after HF while effectively increasing plasma LPS levels. TLR4-KO mice showed significant improvements in HF-induced neuroinflammation, which was not markedly affected by intestinal barrier inhibitors or protectors. CONCLUSION: HF could induce intestinal barrier dysfunction and increase gut-to-blood translocation of LPS, which could further promote neuroinflammation through the TLR4 pathway.

Quantification of Acute Myocardial Damage Secondary to Implantation of Electrodes for the Left Bundle Branch Area Pacing

ABSTRACT Background: Different from the traditional right ventricular pacing, the left bundle branch area pacing (LBBAP) is accomplished with deeper lead implantation and more attempts. However, myocardial damage is unclear in LBBAP. Objective: The objective of the study was to observe the change of troponin T and explore possible factors associated with greater myocardial damage in LBBAP. Methods: Patients with an indication for pacemaker implantation underwent attempts for LBBAP by transventricular septal method. Levels of troponin T were determined before operation, 12 h and 1 week after the operation. Parameters of intraoperation and follow-up were recorded and analyzed. Results: In total, successful LBBAP was achieved in 126 patients. The levels of troponin T increased significantly at 12 h after the operation compared with those before operation (96.45 ± 11.07 [69.06] vs. 16.59 ± 1.84 [11.92] ng/L, p < 0.001), while there were no significant differences between pre- and post-operative levels at 1 week. Correlation and regression analysis showed that only the number of attempts was an independent factor related to the change of troponin T. During 1 year of follow-up, LBBAP was safe and feasible with few complications. Conclusions: Myocardial damage of LBBAP was clinically significant. The number of attempts was an independent factor related to the myocardial damage.

Renal Denervation Attenuates Neuroinflammation in the Brain by Regulating Gut-Brain Axis in Rats With Myocardial Infarction.

Aims: The development of neuroinflammation deteriorates the prognosis of myocardial infarction (MI). We aimed to investigate the effect of renal denervation (RDN) on post-MI neuroinflammation in rats and the related mechanisms. Methods and Results: Male adult Sprague-Dawley rats were subjected to sham or ligation of the left anterior descending coronary artery to induce MI. One week later, the MI rats received a sham or RDN procedure. Their cardiac functions were analyzed by echocardiography, and their intestinal structures, permeability, and inflammatory cytokines were tested. The intestinal microbiota were characterized by 16S rDNA sequencing. The degrees of neuroinflammation in the brains of rats were analyzed for microglia activation, inflammatory cytokines, and inflammation-related signal pathways. In comparison with the Control rats, the MI rats exhibited impaired cardiac functions, intestinal injury, increased intestinal barrier permeability, and microbial dysbiosis, accompanied by increased microglia activation and pro-inflammatory cytokine levels in the brain. A RDN procedure dramatically decreased the levels of renal and intestinal sympathetic nerve activity, improved cardiac functions, and mitigated the MI-related intestinal injury and neuroinflammation in the brain of MI rats. Interestingly, the RDN procedure mitigated the MI-increased intestinal barrier permeability and pro-inflammatory cytokines and plasma LPS as well as ameliorated the gut microbial dysbiosis in MI rats. The protective effect of RDN was not significantly affected by treatment with intestinal alkaline phosphatase but significantly reduced by L-phenylalanine treatment in MI rats. Conclusions: RDN attenuated the neuroinflammation in the brain of MI rats, associated with mitigating the MI-related intestinal injury.

Effects of high-intensity interval training in patients with coronary artery disease after percutaneous coronary intervention: A systematic review and meta-analysis.

AIM: To evaluate whether high-intensity interval training (HIIT) was superior to low-intensity training or usual care among patients after percutaneous coronary intervention. The hypothesis was that HIIT would help patients after percutaneous coronary intervention (PCI) improve cardiopulmonary function, lipid profiles and in-stent restenosis. DESIGN: A systematic review and meta-analysis were conducted according to the Preferred Reporting Items for Systematic Review and Meta-analysis (PRISMA)2009 Checklist. METHODS: Randomized controlled trials (RCTs) focusing on HIIT programme in patients after PCI were searched in Cochrane Library, Web of Science Core Collection, EMbase, PubMed, China National Knowledge Infrastructure (CNKI) and SinoMed from the inception to 24 March 2020. Standard Mean difference (SMD) and 95% confidence intervals (CI) were performed to summarize the effect sizes. RESULTS: Six RCTs (247 patients) met the criteria. HIIT programme had a statistically significant effect on raising left ventricular ejection function (LVEF) (SMD = 0.38, 95%CI [0.03, 0.73], I2  = 3%), VO2peak (SMD = 0.94, 95%CI [0.61, 1.28], I2  = 0%), as well as improving the serum level of high-density lipoprotein (SMD = 0.55, 95%CI [0.06, 1.03], I2  = 0%) and late luminal loss (SMD = -0.65, 95%CI [-1.07, -0.23], I2  = 0%). But HIIT had no prominent effect on improving heart rate (SMD = -0.04, 95%CI [-0.29, 0.21], I2  = 0%). Summarily, HIIT programme appears to be favourable for CAD patients after PCI by improving cardiopulmonary function, such as LVEF and VO2peak , as well as reducing late luminal loss in per stented arteries. Nevertheless, HIIT has no advantage for adjusting heart rate. More researches with rigorous methods are warranted to explore the controversy about lipid profiles.

Quantification of Acute Myocardial Damage Secondary to Implantation of Electrodes for the Left Bundle Branch Area Pacing.

BACKGROUND: Different from the traditional right ventricular pacing, the left bundle branch area pacing (LBBAP) is accomplished with deeper lead implantation and more attempts. However, myocardial damage is unclear in LBBAP. OBJECTIVE: The objective of the study was to observe the change of troponin T and explore possible factors associated with greater myocardial damage in LBBAP. METHODS: Patients with an indication for pacemaker implantation underwent attempts for LBBAP by transventricular septal method. Levels of troponin T were determined before operation, 12 h and 1 week after the operation. Parameters of intraoperation and follow-up were recorded and analyzed. RESULTS: In total, successful LBBAP was achieved in 126 patients. The levels of troponin T increased significantly at 12 h after the operation compared with those before operation (96.45 ± 11.07 [69.06] vs. 16.59 ± 1.84 [11.92] ng/L, p < 0.001), while there were no significant differences between pre- and post-operative levels at 1 week. Correlation and regression analysis showed that only the number of attempts was an independent factor related to the change of troponin T. During 1 year of follow-up, LBBAP was safe and feasible with few complications. CONCLUSIONS: Myocardial damage of LBBAP was clinically significant. The number of attempts was an independent factor related to the myocardial damage.

Renal denervation improves chronic intermittent hypoxia induced hypertension and cardiac fibrosis and balances gut microbiota.

AIMS: Investigate the effect of renal denervation (RDN) on chronic intermittent hypoxia (CIH) induced high blood pressure (BP) and cardiac injury, and explore whether the effect is associated with gut microbiota alteration and its product, trimethylamine N-oxide (TMAO). MATERIALS AND METHODS: Thirty six-week-old Sprague Dawley male rats were randomly divided into three groups: Control, CIH (20 cycles h-1, 7-8% at nadir, 8 h.day-1 for 6 weeks) and RDN group. Fecal samples, serum and heart tissue were collected at week 6. 16S rRNA gene sequencing was performed in fecal samples. KEY FINDINGS: Systolic BP in CIH group was significantly elevated compared with Control (164 ± 3 vs. 143 ± 4 mmHg, p = 0.004), while RDN treatment evidently reduced elevated systolic BP (133 ± 5 vs. 164 ± 3 mmHg, p < 0.001). CIH group featured significant cardiac perivascular fibrosis, compared with Control, whereas RDN treatment effectively attenuated perivascular fibrosis. Principal component analysis showed that CIH rats, but not RDN group were noticeably separated from Control. At phyla level, the structure of the biological community of RDN rats converged with that of control rats, which was apparently different in comparison to CIH rats. TMAO levels in the three groups were not significantly different. SIGNIFICANCE: RDN exerts beneficial effect on BP control and perivascular fibrosis in rats exposed to CIH. This effect is associated with its ability to revert the already skewed gut microbiota caused by CIH, but is not via regulation of TMAO.