Search

Background: Current guidelines recommend maintaining a resting heart rate below 100-110 beats per minute (bpm) for patients with atrial fibrillation (AF). However, there is a lack of research on various treatment approaches for patients with both atrial fibrillation and coronary heart disease (AF&CHD). We have discussed the primary therapeutic options for controlling resting heart rate in patients with AF&CHD., Methods: We conducted a post hoc analysis of the AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) trial. Our study included 3986(98.2%) participants with AF, of which 1522 had AF&CHD. The primary outcome was all-cause mortality. We utilized the chi-squared test to identify significant differences in categorical variables. Multivariate Cox regression analysis was performed to compare the risk of death by standard deviation of heart rate visit to visit variability quartile., Results: Compared to the AF group, a higher proportion of patients in the AF&CHD group had histories of smoking, hypertension, diabetes, heart failure, cardiomyopathy, valvular heart disease, peripheral vascular disease, bradycardia, hepatic or renal disease, pulmonary disease, and stroke (all P < 0.001). Additionally, patients with AF&CHD were more likely to undergo coronary artery bypass grafting (CABG) and pacemaker surgeries than those with AF alone. After adjusting for multiple clinical variables, patients with AF&CHD had a significantly higher risk of all-cause mortality compared to the AF group (RR = 1.79, 95% CI: 1.49-2.60; P < 0.01). Nonlinear multivariate curve-fitting analysis identified an optimal resting heart rate of 70 bpm for patients with AF&CHD (P < 0.001). Subgroup analysis revealed that patients with a resting heart rate below 70 bpm had lower all-cause mortality than those with a resting heart rate above 70 bpm (P < 0.001)., Conclusions: For resting heart rates below 70 bpm, our results suggest an inverse causal relationship between genetically determined resting heart rate and all-cause mortality in patients with AF&CHD., Clinical Trial Number: Not applicable., Competing Interests: Declarations. Ethical approval and consent to participate: Not applicable. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests., (© 2024. The Author(s).)

Background: Double kissing (DK) crush approach for patients with coronary bifurcation lesions, particularly localized at distal left main or lesions with increased complexity, is associated with significant reduction in clinical events when compared with provisional stenting. Recently, randomized clinical trial has demonstrated the net clinical benefits by intravascular ultrasound (IVUS)-guided implantation of drug-eluting stent in all-comers. However, the improvement in clinical outcome after DK crush treatment guided by IVUS over angiography guidance for patients with complex bifurcation lesions have never been studied in a randomized fashion., Trial Design: DKCRUSH VIII study is a prospective, multicenter, randomized controlled trial designed to assess superiority of IVUS-guided vs angiography-guided DK crush stenting in patients with complex bifurcation lesions according to DEFINITION criteria. A total of 556 patients with complex bifurcation lesions will be randomly (1:1 of ratio) assigned to IVUS-guided or angiography-guided DK crush stenting group. The primary end point is the rate of 12-month target vessel failure, including cardiac death, target vessel myocardial infarction, or clinically driven target vessel revascularization. The secondary end points consist of the individual component of primary end point, all-cause death, myocardial infarction, and in-stent restenosis. The safety end point is the incidence of definite or probable stent thrombosis. An angiographic follow-up will be performed for all patients at 13 months and clinical follow-up will be continued annually until 3 years after the index procedure., Conclusions: DKCRUSH VIII trial is the first study designed to evaluate the differences in efficacy and safety between IVUS-guided and angiography-guided DK crush stenting in patients with complex true bifurcation lesions. This study will also provide IVUS-derived criteria to define optimal DK crush stenting for bifurcation lesions at higher complexity., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Aim: To establish a novel arrhythmia model in rats., Methods: Coronary artery occlusion was produced in hyperlipidemic rats after the animals were fed a high fat and cholesterol chow for 15 days. The incidence, duration and score of arrhythmias were determined 1 hour after coronary occlusion., Results: The incidence, duration and score of arrhythmia induced by coronary artery occlusion increased significantly in hyperlipidemic rats compared with those in normal rats (P < 0.05). In normal rats, pretreatment with amiodarone 60 mg x kg(-1) or verapamil 25 mg x kg(-1) 3 days before coronary artery occlusion did not influence the incidence, duration and score of arrhythmia (P > 0.05). In hyperlipidemic rats, amiodarone 60 mg x kg(-1) decreased the incidence, duration and score of arrhythmia (P < 0.05), but not verapamil 25 mg x kg(-1) (P > 0.05)., Conclusion: The novel arrhythmia model induced by coronary artery occlusion in hyperlipidemic rats is reliable and similar to the pathophysiological state in human being.

Brain-derived neurotrophic factor (BDNF) is one of the most abundantneurotrophins in the central nervous system. Numerous studies suggestthat BDNF has extensive roles by binding to its specific receptor, tropomyosin-related kinase receptor B (TrkB), and thereby triggering downstream signaling pathways. Recently, growing evidence highlightsthat the BDNF/TrkB pathway is expressed in the cardiovascular system andclosely associated with the development and outcome of cardiovascular diseases (CVD), including coronary artery disease, heart failure, cardiomyopathy, hypertension, and metabolic diseases. Furthermore, circulating BDNF has also been revealed as a new potential biomarker for both diagnosis and prognosis of CVD. In this review, we discuss the current evidence of the emerging role of BDNF/TrkBsignalingand address the challenges that remain in translating these discoveries to novel therapeutic strategies for CVD. [ABSTRACT FROM AUTHOR]

Enhanced external counterpulsation (EECP) significantly augments diastolic blood flow and has been postulated to improve endothelial function by increased shear stress. We examined the effects of EECP on plasma nitric oxide and endothelin-1 (ET-1) levels. Plasma nitrate and nitrite (NOx) and ET-1 levels were measured serially in 13 patients with coronary artery disease who received 1-hour daily treatments of EECP over 6 weeks. During the course of EECP therapy, plasma NOx progressively increased and plasma ET-1 progressively decreased. After 36 hours of EECP, there was a 62 ± 17% increase in plasma NOx compared with baseline (43.6 ± 4.3 vs 27.1 ± 2.6 μmol/L, p <0.0001) and a 36 ± 8% decrease in plasma ET-1 (76.7 ± 9.5 vs 119.5 ± 8.5 pg/L, p <0.0001). At 3 months after completion of EECP, NOx remained 12 ± 11% above baseline (p = 0.002), and ET-1 remained 11 ± 10% below baseline (p = 0.0068). Our data provides neurohormonal evidence to support the hypothesis that EECP improves endothelial function. [Copyright &y& Elsevier]

Brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase B (TrkB) pathway is associated with ischemic heart diseases (IHD). 7,8-dihydroxyflavone (7,8-DHF), BDNF mimetic, is a potent agonist of TrkB. We aimed to investigate the effects and the underlying mechanisms of 7,8-DHF on cardiac ischemia. Myocardial ischemic mouse model was induced by ligation of left anterior descending coronary artery. 7,8-DHF (5 mg/kg) was administered intraperitoneally two days after ischemia for four weeks. Echocardiography, HE staining and transmission electron microscope were used to examine the function, histology and ultrastructure of the heart. H9c2 cells were treated with hydrogen peroxide (H 2 O 2), 7,8-DHF or TrkB inhibitor ANA-12. The effects of 7,8-DHF on cell viability, mitochondrial membrane potential (MMP) and mitochondrial superoxide generation were examined. Furthermore, mitochondrial fission and protein expression of mitochondrial dynamics (Mfn2 [mitofusin 2], OPA1 [optic atrophy 1], Drp1 [dynamin-related protein 1] and Fis-1 [fission 1]) was detected by mitotracker green staining and western blot, respectively. 7,8-DHF attenuated cardiac dysfunction and cardiomyocyte abnormality of myocardial ischemic mice. Moreover, 7,8-DHF increased cell viability and reduced cell death accompanied by improving MMP, inhibiting mitochondrial superoxide and preventing excessive mitochondrial fission of H 2 O 2 -treated H9c2 cells. The cytoprotective effects of 7,8-DHF were antagonized by ANA-12. Mechanistically, 7,8-DHF repressed OMA1-dependent conversion of L-OPA1 into S-OPA1, which was abolished by Akt inhibitor. In conclusion, 7,8-DHF protects against cardiac ischemic injury by inhibiting the proteolytic cleavage of OPA1. These findings provide a novel pharmacological effect of 7,8-DHF on mitochondrial dynamics and a new potential target for IHD. Image 1 • 7,8-DHF attenuates ischemia/H 2 O 2 -induced cardiomyocyte injury. • 7,8-DHF inhibits excessive mitochondrial fission in ischemic heart. • 7,8-DHF inhibits OMA1-dependent conversion of L-OPA1 into S-OPA1. • Akt inhibitor abolished the effects of 7,8-DHF on mitochondrial dynamics. [ABSTRACT FROM AUTHOR]