Cardiac resynchronization therapy in heart failure patients by using left bundle branch pacing.

Background: Left bundle branch pacing (LBBP) is emerging as an effective alternative to achieve cardiac resynchronization therapy (CRT) and improve heart function. The purpose of our study was to investigate the feasibility and efficacy of LBBP in heart failure patients with left ventricular ejection fraction (LVEF) <50% and left bundle branch block (LBBB). Methods: All patients with complete LBBB and LVEF <50% were retrospectively included in the study from April 2018 to April 2021 and underwent CRT via LBBP implantation. ECG, pacing parameters, the New York Heart Association (NYHA) functional class, echocardiographic measurements, and complications were recorded and analyzed at implant and during follow-up of 1, 6, and 12 months. Results: Left bundle branch pacing was successful in all 34 patients (mean age 65.6 ± 11.2 years, 67.6% men). A significant decrease in QRS duration (QRSd) was observed after the LBBP operation for 1 month (153.2 ± 1.7 vs. 111.9 ± 2.6 ms, p < 0.01). LBB capture threshold and R-wave amplitude remained stable at 12-month follow-up when compared with implantation values (0.62 ± 0.13 V @ 0.4 ms vs. 0.73 ± 0.21 V @ 0.4 ms, 12.02 ± 5.68 mV vs. 8.58 ± 4.09 mV, respectively). LVEF increased significantly (35.28 ± 1.70% vs. 51.09 ± 1.71%, p < 0.01) accompanied with reduced left ventricular end-diastolic dimension (LVEDd; 65.3 ± 1.99 vs. 53.58 ± 2.07 mm, p < 0.01) and left atrial dimension (LAD; 49.03 ± 1.32 vs. 40.67 ± 1.58 mm, p < 0.01). Normalized LVEF (LVEF ≥ 50%) was found in 70.5% of patients at 12 months. The NYHA classification, brain natriuretic peptide (BNP), and 6-minute walk test (6MWT) were significantly improved at follow-up of 12 months (all p < 0.01 vs. baseline). No deaths or heart failure hospitalizations were observed during the follow-up period. Conclusion: The current work suggested that LBBP was feasible with a high success implantation rate and effective to correct LBBB and improved left ventricular structure and function with a low and stable pacing threshold.

Microalbuminuria Complicated with Low Estimated Glomerular Filtration Rate: Early Risk Factors for Contrast-Induced Acute Kidney Injury After Coronary Intervention.

BACKGROUND We aimed to investigate the impact of microalbuminuria complicated with low estimate glomerular filtration rate (eGFR) on the incidence and prognosis of contrast-induced acute kidney injury (CI-AKI) in patients with coronary artery disease after coronary intervention. MATERIAL AND METHODS A total of 943 patients were enrolled in the study. Based on microalbumin/creatinine (ACR) measurements, the patients were divided into a microalbuminuria cohort (MA; 222 patients) and a normal albuminuria cohort (NA; 721 patients). According to eGFR levels, the cohorts were further subdivided into normal, mild, moderate, and severe renal dysfunction groups. The basic data and indicators of all enrolled patients were collected. The patients were followed up at 30 days, 6 months, 1 year, and 3 years after surgery. RESULTS The overall incidence of CI-AKI in the MA cohort was higher than that in the NA cohort (17.6% vs 8.2%, P.

Effect of Combining Furosemide With Standard Hydration Therapy on Contrast-Induced Acute Kidney Injury Following Coronary Angiography or Intervention in a High-Risk Population.

This study aimed to investigate whether combining furosemide with standard hydration therapy results in increased preventive effects on contrast-induced acute kidney injury (CI-AKI) following coronary angiography (CA) or percutaneous coronary intervention (PCI). Patients (n = 230) were enrolled in the study and were randomized to the furosemide group or the control group. Patients in the furosemide group received 0.2 to 0.5 mg/kg of furosemide as a continuous intravenous infusion for 24 hours postoperatively and the same standard hydration regimen received by the control group. Blood samples were obtained 24 hours before and 48 hours after the procedure and urine volume was recorded postprocedure. Patients were followed up for an average of 6 months after the procedure. The incidence of CI-AKI in the furosemide group was significantly lower than that in the control group (8.7% vs 18.3%, P = .034). Multivariate logistic regression showed that age-glomerular filtration rate-ejection fraction score and V/estimated glomerular filtration rate ratio were independent risk factors for CI-AKI. During the average 6-month follow-up, incidence of major adverse cardiovascular events (MACEs) in the furosemide group was also significantly lower. Furosemide combined with standard hydration therapy may reduce the incidence of CI-AKI and MACEs following CA or PCI.

Circulating cell-free mitochondrial deoxyribonucleic acid is increased in coronary heart disease patients with diabetes mellitus.

AIMS/INTRODUCTION: Circulating cell-free mitochondrial deoxyribonucleic acid (ccf-mtDNA) is presumably derived from injured tissues or cells in the body and has been suggested to be potential biomarker in several diseases. The present study explored whether mtDNA could be used as a biomarker to evaluate disease in coronary heart disease (CHD) patients with or without diabetes mellitus (DM). MATERIALS AND METHODS: A total of 50 CHD patients with type 2 diabetes, 50 CHD patients without type 2 diabetes, and 50 age- and sex-matched patients without CHD and DM (non-CHD-DM) were recruited. Ccf-mtDNA levels were assessed by measuring the nicotinamide adenine dinucleotide dehydrogenase 1 gene using quantitative real-time polymerase chain reaction. Receiver operating characteristic curve analysis of plasma mtDNA in CHD with or without DM was also determined. Multivariate logistic regression analyses were carried out to determine the correlation between the mtDNA levels and traditional CHD risk factors. RESULTS: The plasma ccf-mtDNA levels were significantly elevated in CHD patients with DM compared with those without and non-CHD-DM. The area under the receiver operating characteristic curves of mtDNA in CHD patients with DM vs non-CHD-DM was 0.907%. Correlation analyses of the mtDNA levels and traditional CHD risk factors showed that the mtDNA levels were significantly correlated with fasting blood glucose in CHD patients with DM. CONCLUSIONS: Ccf-mtDNA levels can be used as a biomarker in CHD patients with DM.

Influence of phenotype conversion of epicardial adipocytes on the coronary atherosclerosis and its potential molecular mechanism.

OBJECTIVE: To investigate the phenotype conversion of epicardial adipocytes and its potential molecular mechanism during the occurrence and development of coronary atherosclerosis. METHODS: A total of 30 health male New Zealand white rabbits were used. In experiment group (n=15), rabbits were fed with high fat food to establish atherosclerosis animal model; rabbits in control group (n=15) were fed with normal food. RESULTS: At week 0, UCP-1 and PPARγ mRNA expressions in EAT and sBAT were significantly higher than in eWAT, and leptin mRNA expression lower than (P<0.05). In experiment group, the mRNA expressions of UCP-1 and PPARγ reduced gradually, but leptin mRNA increased progressively in EAT (P<0.05). UCP-1 expression reduced gradually, the newly generated blood vessels reduced significantly, but leptin and RAM11 increased gradually (P<0.05). The adipocyte volume in EAT increased gradually, but the adipocyte number reduced progressively (P<0.05). The number of mitochondria with multiple crests reduced gradually in EAT; IL-6 reduced the mRNA expressions of UCP-1 and PPARγ in adipocytes of BAT in a dose dependent manner, but it increased the mRNA expressions of leptin and STAT3 (P<0.05). In the presence of IL-6, JSI-124 increased the mRNA expressions of UCP-1 and PPAR-γ in adipocytes of BAT in a dose dependent manner, but it reduced the mRNA expressions of leptin and STAT3 (P<0.05). CONCLUSION: During the progression of atherosclerosis, there is a phenotype conversion of EAT from BAT to WAT, which further promotes the focal occurrence and development of atherosclerosis; IL-6 may activate JAK-STAT3 pathway to induce this conversion.

Associations of C1q/TNF-Related Protein-9 Levels in Serum and Epicardial Adipose Tissue with Coronary Atherosclerosis in Humans.

OBJECTIVE: To investigate the correlation of CTRP9 with coronary atherosclerosis. METHODS: Coronary angiography confirmed CAD in 241 patients (62 received CABG) and non-CAD in 121 (55 received valve replacement). RESULTS: Serum levels of LDL-C, CRP, TNF-α, IL-6, and leptin in CAD patients were significantly higher than those in non-CAD patients (P < 0.05), but APN and CTRP9 were lower (P < 0.05). Serum levels of CTRP9 and APN were negatively related to BMI, HOMA-IR, TNF-α, IL-6, and leptin but positively to HDL-C (P < 0.05) in CAD patients. After adjustment of APN, CTRP9 was still related to the above parameters. Serum CTRP9 was a protective factor of CAD (P < 0.05). When compared with non-CAD patients, leptin mRNA expression increased dramatically, while CTRP9 mRNA expression reduced markedly in epicardial adipose tissue of CAD patients (P < 0.05). The leptin expression and macrophage count in CAD group were significantly higher than in non-CAD group, but CAD patients had a markedly lower CTRP9 expression (P < 0.05). CONCLUSIONS: Circulating and coronary CTRP9 plays an important role in the inflammation and coronary atherosclerosis of CAD patients. Serum CTRP9 is an independent protective factor of CAD.

Plasma nuclear and mitochondrial DNA levels in acute myocardial infarction patients.

OBJECTIVE: Plasma nuclear and mitochondrial DNA (mtDNA) levels are altered in many diseases. However, it is not known whether they are also altered in acute myocardial infarction (AMI). In the present study, we examined plasma nuclear and mtDNA levels in the patients with AMI before and after a percutaneous coronary intervention (PCI) to explore their potential as biomarkers. METHODS AND RESULTS: Plasma nuclear and mtDNA levels were measured by quantitative PCR in 25 AMI patients, 25 non-myocardial infarction (MI) control participants (with MI risk), and 20 healthy individuals during the study period. The concentrations of nuclear and mtDNA were significantly higher in the AMI group on hospital day 1 than that in the non-MI controls (nuclear: 0.4948±0.0830 vs. 0.2047±0.0222 ng/µl, P<0.05; mitochondrial: 3.754±0.384 vs. 1.851±0.3483 ng/µl, P<0.05) and healthy individuals (nuclear: 0.4948±0.0830 vs. 0.1683±0.0254 ng/µl, P=0.001; mitochondrial: 3.754±0.384 vs. 0.1517±0.0924 ng/µl, P<0.05) and decreased shortly after PCI. CONCLUSION: Both plasma nuclear and mtDNA levels are elevated in AMI patients, but return to normal levels immediately after PCI, suggesting that they are potentially novel biomarkers for AMI.

Reversible cardiogenic shock caused by atrioventricular junctional rhythm after percutaneous coronary intervention.

An 82-year-old female patient undergoing cardiogenic shock caused by atrioventricular junctional rhythm immediately after percutaneous coronary intervention (PCI) is described. Pharmacotherapy was invalid, and subsequent application of atrial pacing reversed the cardiogenic shock. PCI-related injury of sinuatrial nodal artery leading to acute atrial contractility loss, accompanied by atrioventricular junctional arrhythmia, was diagnosed. We recommend that preoperative risk evaluation be required for multi-risk patients. Likewise, emergent measures should to be established in advance. This case reminds us that atrial pacing can be an optimal management technique once cardiogenic shock has occurred.

[Impact of anti-OX-LDL antibodies on CD36 mRNA expression in monocytes].

AIM: To investigate the impact of antibodies to oxidized low-density lipoprotein (OX-LDL) on CD36 mRNA expression in monocytes and explore the mechanism underlying the impact on the formation of foam cells. METHODS: U937 cells and the monocytes of New Zealand rabbit were respectively cultured in vitro and divided into 4 groups: the control group (cultured in nutrient medium of RPMI1640), the OX-LDL group (with additional OX-LDL of 50 µg/L in nutrient medium), the OX-LDL+Ab-OX-LDL group (with additional OX-LDL of 50 µg/L and Ab-OX-LDL of 100 µg/L in nutrient medium) and the Ab-OX-LDL group (with additional Ab-OX-LDL of 100 µg/L in nutrient medium). After 24-hour culture, the expression of CD36 mRNA was detected by semi-quantitative RT-PCR. RESULTS: The expression of CD36 mRNA, either in the OX-LDL group or in the OX-LDL+Ab-OX-LDL group, was higher than that in the control group. After intervened by Ab-OX-LDL, the expression was respectively down-regulated by 64.80% in U937 cells and 35.18% in the monocytes of rabbit, which was statistically significant between the two species. CONCLUSION: Antibodies to OX-LDL could negatively regulate the expression of CD36 mRNA in monocytes, and prevent monocyte in taking OX-LDL through the pathway of antigen CD36.

[Membrane testosterone receptors in cultured vascular smooth muscle cells].

OBJECTIVE: To determine the presence of membrane testosterone receptors in cultured vascular smooth muscle cells (VSMC), and investigate their relationship with classical intracellular androgen receptors (iAR). METHODS: VSMCs were cultured from the thoracic aorta of male Sprague-Dawley rats by the explant method. Subconfluent VSMCs were incubated with serum-free medium for 24 h to obtain quiescent non-dividing cells, and then treated with the indicated agents. The aliquots of VSMCs were labeled with testosterone-BSA-FITC (T-BSA-FITC) and analyzed by flow cytometry. Classical iARs in intact- and permeabilized-cells were detected with anti-iAR antibodies and FITC-labeled secondary antibodies by immunofluorescence, followed by flow cytometry analysis. RESULTS: Incubation of VSMCs with T-BSA-FITC obviously increased their relative fluorescence intensity at 10 sec as compared with the untreated controls (P < 0.01), and so did it at 10 min in comparison with the treatment with BSA-FITC alone or together with free testosterone (P < 0.01). Pretreatment with iAR antagonist flutamide exhibited no significant influence on the relative fluorescence intensity of VSMCs (P = 0.318). Traditional iARs were not detectable on the surface of intact VSMCs, although permeabilized cells contained iARs. CONCLUSION: VSMCs contain testosterone receptors in the plasma membrane, and these membrane receptors are not identical to classical iARs.

[Testosterone at physiological level inhibits PGF2alpha-induced increase in intracellular Ca2+ in cultured vascular smooth muscle cells].

OBJECTIVE: To explore the acute effects of testosterone at the physiological level on PGF2alpha-induced increase in intracellular Ca2+ in cultured vascular smooth muscle cells (VSMCs). METHODS: VSMCs from the thoracic aorta of male Sprague-Dawley rats were cultured using the explant method. The subconfluent VSMCs were incubated with serum-free medium for 24 hours to obtain quiescent non-dividing cells and then treated with the indicated agents. For the measurement of [Ca2+]i, the VSMCs were loaded with fura-2. Changes of [Ca2+]i were determined ratiometrically with a Nikon TE-2000E system. RESULTS: The resting level of [Ca2+]i was around 100 nmol/L in the VSMCs. Exposing cells to perfusate containing 10 micromol/L PGF2alpha triggered an immediate and transient peak in [Ca2+]i, which gradually decreased afterwards. Interference at the peak with the physiological concentration (40 nmol/L) of testosterone significantly decreased the peak-to-baseline time of [Ca2+]i, compared with ethanol vehicle (104.9 +/- 27.0 s vs 153.5 +/- 40.4 s, P < 0.01). Pretreatment with testosterone at 40 nmol/L for 2 minutes also reduced the peak-to-baseline time of [Ca2+]i significantly in comparison with the ethanol control (120.6 +/- 32.0 s vs 151.4 +/- 27.4 s, P < 0.01), but it had no significant effect on the peak level of PGF2alpha-induced intracellular Ca2+ (390.0 +/- 126.0 nmol/L vs 403.4 +/- 160.7 nmol/L, P > 0.05). CONCLUSION: Testosterone at physiological concentration inhibits PGF2alpha-induced Ca2+ fluxes, probably via receptor-operated calcium channels by a non-genomic mechanism in VSMCs, which may be involved in the vasodilatory effect of testosterone.