Acta cardiologica最新文献

Background: Epicardial pacing is a preferred and almost inevitable pacing method, especially in young children, the site of epicardial lead is a major determinant of adverse cardiac remodelling and dysfunction, resulting in a disease termed pacing-induced cardiomyopathy (PICM). This study evaluates the clinical and echocardiographic outcomes of paediatric patients diagnosed with PICM and treated with cardiac resynchronisation therapy.

Methods: A retrospective analysis was conducted on paediatric patients (≤18 years) diagnosed with PICM and resynchronised between 2006 and 2024. Demographic, clinical, electrocardiographic, and echocardiographic data were collected. Echocardiographic assessments included left ventricular ejection fraction (LVEF), fractional shortening (FS), and ventricular diameters.

Results: Eleven patients (mean age: 5.7 ± 4.3 years) were identified. The mean time for the development of LV dysfunction was 28.1 ± 28.8 months. All patients had pacing percentage of 100%, with a mean QRS duration of 164 ± 23 msec and LVEF of 43 ± 15% at diagnosis. The site of pacing was the right ventricular free wall in 6/11 and outflow in 4/11 patients. Following resynchronisation, LVEF improved to 67 ± 6%, FS increased to 37 ± 4%, and QRS duration decreased to 129 ± 24 msec. BNP levels significantly declined, and no procedural complications occurred.

Conclusion: Although lead implantation in the right ventricular anterior wall may be technically feasible through the existing incision in the early postoperative period, it should be avoided due to the risk of potential complications and the likelihood of requiring additional interventions in the future.

Background: mTOR inhibitors released from drug-eluting stents (DESs) play a critical role in the pathogenesis of in-stent neoatherosclerosis (ISNA), contributing to the development of late in-stent restenosis (ISR). Circular RNAs (circRNAs) are emerging as key regulators in various pathophysiological processes, but their involvement in ISNA remains unclear.

Methods: The expression pattern of circRNAs in human umbilical vein endothelial cells (HUVECs) treated with everolimus (EVL) was analysed using RNA sequencing. The expression levels of circRNAs, miR-1-5p, and the downstream targets ACVR2B/StarD13 were measured by quantitative real-time PCR. The effects of circPTK2 on cell proliferation, migration, apoptosis, and permeability in EVL-treated endothelial cells were assessed using cell counting kit-8, scratch, Annexin-V FITC and PI double-staining, and transwell assays. Bioinformatics analysis and dual luciferase assay were used to identify the interaction between circPTK2 and miR-1-5p. The association between circPTK2, miR-1-5p, and ACVR2B/StarD13 was further evaluated by functional rescue experiments.

Results: CircPTK2 was significantly upregulated in EVL-treated HUVECs. Knockdown of circPTK2 reversed the EVL-induced suppression of cell viability and migration, reduced apoptosis, and alleviated endothelial barrier leakage. Conversely, circPTK2 overexpression produced the opposite effects. Mechanistically, circPTK2 acted as a sponge for miR-1-5p, leading to increased expression of its target genes ACVR2B and StarD13. Silencing ACVR2B or StarD13 partially attenuated the exacerbating effects of miR-1-5p inhibition on EVL-induced endothelial dysfunction. Moreover, inflammatory conditions affected the expressions of circPTK2, miR-1-5p, and ACVR2B/StarD13.

Conclusions: CircPTK2 regulates EVL-induced endothelial dysfunction via the miR-1-5p/ACVR2B/StarD13 axis, providing novel insights for the treatment of late ISR after DES implantation.

Objective: To evaluate the subclinical left ventricular (LV) myocardial dysfunction by myocardial layer-specific and dyssynchorony analysis in patients with obstructive sleep apnoea syndrome (OSAS) with normal left ventricular ejection fraction (LVEF) and without any confounding disease that can cause myocardial dysfunction.

Methods: A total of 32 patients with moderate (n = 14) or severe (n = 18) OSAS and 20 controls underwent both standard conventional echocardiography assessment, myocardial layer-specific and dyssynchorony analysis. Changes in the levels of norepinephrine (NE) were analysed.

Results: Patients in the OSAS group had higher BMI (p = .002) and BSA (p = .017), significantly increased DBP (p < .001) and NE (p = .028) level than those in control group. Compared with the controls, OSAS patients had thickened left ventricular posterior wall (LVPWT) (p < .001) and lager LVMI/H^2.7 (p = .04). Three layers (endocardial, myocardial and epicardia) in the apical long-axis view, apical 4 C and 2 C views were decreased in both moderate and severe OSAS groups. PSD was significantly increased in severe OSAS patients (p = .044), TTP in the severe OSAS group was significantly shorter than in control group in the ant-sept wall (p = .04) and inferior wall (p = .03) from basal segment, inferior wall (p = .005) from the middle segment, and all segments from apical segments. PSD and TTP in the moderate OSAS group had no significant differences when compared with control group.

Conclusions: Despite normal LVEF, three layers (endocardial, myocardial and epicardia) of LV wall are decreased in OSOA patients, patients in the severe OSAS group suffer from myocardial systolic dyssynchrony earlier compared with controls.

Background: Contrast-induced acute kidney injury (CI-AKI) occurs as a result of the use of contrast media during coronary interventions and can lead to serious complications.

Aim: To investigate the predictive value of the pre-procedural aggregate index of systemic inflamation (AISI) for the development of CI-AKI in patients with chronic coronary artery disease suspicion who underwent coronary angiography (CAG) or percutaneous coronary intervention (PCI).

Methods: This retrospective cohort study conducted on 166 patients with chronic coronary artery disease suspicion who underwent CAG or PCI. The neutrophil-to-lymphocyte ratio (NLR), systemic immune-inflammation index (SII) and AISI levels were calculated. The relationship between these parameters and the development of CI-AKI within 72 h after intervention was analysed.

Results: CI-AKI occurred in 25 patients (15.1%). Upon conducting a likelihood ratio test to compare full and reduced models, it was found that in the reduced model, variables such as NLR, SII and AISI were independently predictors of CI-AKI, The NLR model (Odds ratio (OR) =1.32, 95% CI [1.16-1.52]), SII model (OR =3.41, 95% CI [1.92-6.08]), and AISI model (OR =4.81, 95% CI [2.42-9.60]). An increase in AISI was linearly associated with CI-AKI and showed the highest prediction for CI-AKI.

Conclusion: These findings demonstrate that AISI is a significant independent predictor for CI-AKI in patients undergoing CAG or PCI.

Background: Reduced cardiovascular event risk is observed with eicosapentaenoic acid (EPA), but EPA mixed with docosahexaenoic acid (EPA/DHA) does not show consistent benefit. Comparative effects of EPA versus EPA/DHA on coronary plaque remain unclear.

Methods: We systematically reviewed trials measuring coronary plaque volume in patients randomised to statin + EPA or statin + EPA/DHA therapy compared to statin monotherapy, and used network meta-analysis to compare percent change in total and lipid coronary plaque volumes on these treatments.

Results: Among 553 articles, ten trials comprising 860 patients met inclusion criteria. Among statin, statin + EPA, and statin + EPA/DHA respectively, random effects analysis yielded changes of +1.9% [-3.4%, +7.2%], -10.0% [-17.5%, -2.5%], and -3.3% [-14.2%, +7.5%] in total plaque volume and +1.3% [-4.7%, +7.4%], -21.5% [-32.1%, -10.8%], and -6.1% [-18.9%, +6.7%] in lipid volume. Compared with statin, statin + EPA achieved greater percent reduction in coronary plaque volumes (total volume: SMD = 0.60, p < 0.0001; lipid volume: SMD = 1.1, p = 0.0017) but statin + EPA/DHA showed no difference (total volume: SMD = 0.19, p = 0.19; lipid volume: SMD = 0.43, p = 0.38).

Conclusions: EPA but not EPA/DHA is associated with reductions in coronary plaque burden when given as adjunct to statins in patients with coronary artery disease.