Acta Cardiologica Sinica最新文献

Background: Ticagrelor provides faster and more consistent platelet inhibition than clopidogrel; however, its effect on myocardial injury during primary percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI) remains uncertain.

Objectives: The aim of this pilot study was to assess the feasibility and preliminary effects of ticagrelor versus clopidogrel loading on myocardial injury in STEMI patients undergoing PCI, using cardiac magnetic resonance (CMR) imaging.

Methods: Thirty STEMI patients were randomized to receive aspirin with either clopidogrel (300 mg) or ticagrelor (180 mg) before PCI, followed by standard maintenance therapy. Myocardial injury was evaluated 4-10 days post-PCI using CMR parameters (infarct size, myocardial salvage index [MSI], microvascular obstruction [MVO], and infarct transmurality). Enzymatic infarct size and 5-year clinical outcomes were also analyzed.

Results: No significant differences in infarct size, MSI, MVO, or other CMR parameters were detected between the two groups. Left ventricular volume and function were comparable, with no major adverse cardiovascular events, stent thrombosis, or major bleeding over the 5-year follow-up period.

Conclusions: Ticagrelor and clopidogrel showed similar effects on CMR-based myocardial injury and long-term outcomes in STEMI patients undergoing PCI. These pilot findings are hypothesis-generating and support the feasibility and inform sample-size planning for future multicenter trials.

Background: MicroRNAs (miRs) are involved in cardiac remodeling, and tachyarrhythmia can regulate miR expression. While microRNA-1 (miR-1) is essential for genes involved in atrial tachyarrhythmia, the effect of rapid electrical stimulation (RES) on fibroblast-derived exosomal miR-1 is unknown. This study investigated the molecular regulation of exosomal miR-1 and its therapeutic potential in human atrial fibroblasts (HCF-aa) using RES.

Methods: HCF-aa were cultured in a pacer dish and exposed to RES (0.5 V/cm and 10 Hz). We then investigated whether miR-1 expression could be regulated in HCF-aa under RES, and examined the effects on T-box transcription factor 18 (Tbx18) and connexin 43 (Cx43) protein levels.

Results: RES initially upregulated and subsequently downregulated exosomal miR-1 expression. Overexpression of miR-1 reduced Tbx18 levels but increased Cx43 expression in HCF-aa after 64 hours of RES. Conversely, mutant miR-1 and miR-1 antagomir significantly reduced Cx43 expression. Luciferase reporter assays indicated that miR-1 antagomir pretreatment suppressed the transcriptional activity of Tbx18 on the Cx43 promoter, an effect reversed by mutating the Tbx18 binding site. RES for 24 hours increased exosomal miR-1 and led to a reduction in Tbx18 3'-UTR luciferase activity; this effect was mitigated by mutating the hsa-miR-1-3p binding site. Immunohistochemical staining confirmed that miR-1 antagomir downregulated Cx43, while Tbx18 siRNA upregulated Cx43 in RES-exposed HCF-aa.

Conclusions: In HCF-aa under RES, miR-1 and Tbx18 regulated Cx43 expression, with miR-1 modulating Cx43 through Tbx18. These findings provide insights into the molecular mechanisms of cardiac remodeling and offer potential therapeutic targets for treating tachyarrhythmia.

Background: This study aimed to compare access and target lesion patency rates between undersized and apposed/oversized lateral-edge covered stents in patients with hemodialysis access-related central venous occlusive disease (CVOD).

Methods: A retrospective analysis of 76 hemodialysis patients undergoing endovascular treatment for CVOD was conducted. All of the patients received undersized covered stents at the medial edge. Based on lateral-edge sizing, the patients were divided into undersized (n = 14) and apposed/oversized (n = 62) groups. Patency outcomes were compared using the log-rank test, and multivariable analysis was used to identify risk factors associated with the primary outcome.

Results: The 12-month access primary patency rate was significantly higher in the undersized group than in the apposed/oversized group (76.4% vs. 25.9%, p = 0.047). The 12-month target lesion primary patency rate was also higher in the undersized group; however, the difference was not statistically significant (76.4% vs. 52.1%, p = 0.186). Factors associated with the primary outcome included older age (odds ratio [OR] = 1.03, p = 0.011), coronary artery disease (OR = 2.03, p = 0.041), stenting to central veins for access thrombosis (OR = 3.53, p = 0.001), more stents (OR = 3.11, p = 0.002), apposed/oversized lateral stent edge (OR = 2.73, p = 0.044), and higher stent-to-vessel ratio (OR = 1.19, p = 0.022).

Conclusions: The 12-month primary patency rate was better in the undersized group than in the apposed/oversized group. Endovascular treatment with undersized covered stents may be a feasible approach for hemodialysis access-related CVOD. Larger randomized studies are required to confirm these findings.

Background: Transeptal puncture (TSP) is an important technique in catheter ablation and structural interventions. Several novel techniques and equipment have been developed, however they are limited by availability and cost.

Objective: To evaluate the efficacy and safety of a modified TSP technique guided by a 0.014″ angioplasty wire and an electrified Brockenbrough (BRK) stylet.

Methods: One hundred consecutive patients who received the modified TSP technique and another 100 undergoing conventional TSP for pulmonary vein isolation for non-valvular atrial fibrillation from January 2019 to January 2023 were retrospectively analyzed. A historical comparison with three associated studies was performed. Age, gender, left atrial diameter, left ventricular ejection fraction, acute complications, and BRK needle jump distances during TSP were analyzed.

Results: Both groups demonstrated comparable characteristics, including age (conventional TSP vs. modified TSP; 65.8 ± 9.6 vs. 63.63 ± 10.3 years; p = 0.077), sex (conventional TSP vs. modified TSP; males, 75% vs. 67%; p = 0.213), and left atrial diameter (conventional TSP vs. modified TSP; 40.55 ± 7.7 vs. 42.60 ± 8.2 mm; p = 0.069). All received continuous periprocedural nonvitamin K oral anticoagulants and underwent TSP with a BRK needle. There was no acute pericardial effusion or tamponade immediately after TSP or at the end of catheter ablation. Inadvertent jump of the BRK needle was significantly attenuated in the modified TSP group (conventional TSP vs. modified TSP; 0.766 ± 0.19 vs. 1.455 ± 0.48 cm; p < 0.001). No TSP-related complications were observed.

Conclusions: The modified TSP technique using readily available equipment with an electrified stylet and a 0.014″ angioplasty wire is a simple, safe, and cost-effective alternative. This method reduces the built-up tension by mechanical force during tenting and minimizes the risk of inadvertent jumping.

Background: Myocardial ischemia can cause repolarization heterogeneity, manifesting as variations in QT interval; we hypothesized that repolarization heterogeneity could help identify patients with coronary artery disease (CAD). We tested this hypothesis by measuring repolarization heterogeneity with a newly developed multielectrode electrocardiogram (MECG) system, which uses 28 electrodes to increase the spatial resolution of body surface electrical activity.

Methods and results: Male patients admitted for coronary angiography were enrolled. Eighty-five patients were included in the training dataset, and 42 in the validation dataset. QTc heterogeneity indices including QTc dispersion (QTD) and smoothness index of QTc (SI-QTc) were derived from MECG signals. Sixty and 32 patients in the training and validation datasets, respectively, were found to have significant coronary stenosis. The SI-QTc (12.79 ± 4.29 vs. 9.22 ± 2.40 ms, p = 0.0004) and QTD (92.12 ± 34.31 vs. 67.2 ± 19.11 ms, p = 0.0004) of the patients in the training dataset were significantly higher in the CAD patients. The areas under the curve of SI-QTc and QTD in the training dataset were 0.7437 and 0.7433, respectively, for detecting CAD. With cutoff values of SI-QTc ≥ 9.95 ms and QTc dispersion ≥ 69 ms, the sensitivity and specificity for diagnosing CAD were 71.9% and 80.0%, respectively, in the validation dataset.

Conclusions: Resting MECG is a promising noninvasive tool for CAD diagnosis, with sensitivity and specificity comparable to those of the exercise electrocardiography test.

Background: The efficacy, safety, and clinical outcomes in patients switching to generic rosuvastatin compared to those taking other brand-name atorvastatin are unclear.

Methods: Electronic medical records were retrospectively collected from January 1, 2013 to December 31, 2020 of patients who switched medication because of hospital policy from brand-name to generic rosuvastatin after March 14, 2018. Only patients who had taken the medication for at least 1 year prior to and 1 year after that date were enrolled. The records of patients who consistently used brand-name atorvastatin during the same period were also collected. The efficacy of lipid control, potential adverse effects, clinical outcomes of major cardiovascular events (MACE), and medical expenses were compared between the 2 groups. Propensity score matching (PSM) was conducted to balance potential cofounders.

Results: After 1:1 PSM, 592 patients were enrolled in the rosuvastatin and atorvastatin groups, respectively. No significant differences were observed in total cholesterol level (-4.38 ± 23.0 vs. -3.72 ± 26.95 mg/dL, p = 0.702), low-density lipoprotein (-2.38 ± 19.89 vs. -2.42 ± 23.63 mg/dL, p = 0.976), or glycated hemoglobin (-0.05% ± 0.7% vs. -0.08% ± 0.76%, p = 0.543). No significant difference was noted in cumulative MACE rate (2.70% vs. 3.89%, log-rank p = 0.265) after the switch date, and each person in the generic group had a 16% average reduction in medical expenses.

Conclusions: Switching to generic rosuvastatin led to comparable lipid-lowering efficacy, safety, and clinical outcomes and lower medical expenses compared with consistently using brand-name atorvastatin.