Acta Cardiologica Sinica最新文献

Background: The resting ankle-brachial index (ABI) is widely used to diagnose lower extremity artery disease (LEAD). However, some LEAD patients have a normal ABI yet require percutaneous transluminal angioplasty (PTA).

Methods: This was a retrospective study of consecutive LEAD patients who underwent PTA. The patients were classified into two groups based on the ABI of the limb that underwent PTA: the ABI-normal group (ABI 0.91-1.40), and ABI-abnormal group (ABI ≤ 0.90 or > 1.40). The primary endpoints were major adverse cardiovascular and cerebral events (MACCEs) and major adverse limb events (MALEs).

Results: Of the 334 patients (mean age: 70 ± 12 years, 60% male), 69 (21%) had a normal ABI, and 265 (79%) had an abnormal ABI. After a median follow-up of 1.5 (0.6-3.1) years, 84 (25%) patients reached the primary or secondary endpoints. The ABI-normal group had a higher proportion of males (73% vs. 57%, p = 0.02) and a higher prevalence of chronic kidney disease (78% vs. 56%, p < 0.01). Angiography revealed less severe lesions in the femoropopliteal artery (p < 0.01) and a lower rate of stent deployment (15% vs. 31%, p < 0.01) in the ABI-normal group than in the ABI-abnormal group. However, the incidence rates of MACCEs (29% vs. 24%, p = 0.56) and MALEs (23% vs. 28%, p = 0.63) were comparable in the two groups.

Conclusions: LEAD patients with a normal ABI often have less severe above-the-knee artery lesions but similar poor outcomes, highlighting the need for additional hemodynamic assessments and increased clinical attention.

Background: The aim of this study was to determine changes in endothelial PAS domain protein-1 (EPAS-1) levels, a biomarker proven to increase with hypoxia, at the time of diagnosis and after treatment in addition to laboratory parameters and scoring systems examined at the time of admission in patients with pulmonary thromboembolism.

Methods: The study included 60 pulmonary embolism (PE) patients followed at the Cardiology clinic and 60 control participants with similar demographic characteristics. Laboratory parameters determined at the time of admission were examined. PE risk and severity scores were calculated, and EPAS-1 levels were also measured. To determine the response, EPAS-1 levels were checked 3 days later and compared with the control group.

Results: There were no differences between the two groups in terms of demographic characteristics and comorbidities. EPAS-1 levels were higher at the time of diagnosis compared to the control group [(3.6 ± 1.42/1.57 ± 0.45), p < 0.001]. EPAS-1 levels were significantly positively correlated with pulmonary embolism severity index (PESI) severity score and risk score in the patient group. EPAS-1 levels decreased after treatment in the patients, and the tendency to decrease was different according to the types of treatment. In the patients who died, EPAS-1 levels continued to increase despite treatment (p = 0.014).

Conclusions: Our study is important in that EPAS-1 levels were correlated with scoring systems and other laboratory parameters used in PE patients, and that it can be used as a predictor in the diagnosis of the disease and play a complementary role in the evaluation of treatment response.

Background: Atherosclerosis progresses after starting renal replacement therapy, and it contributes to high cardiovascular mortality. Carotid intima-media thickness (CIMT) and plaque offer a convenient method to explore the status of systemic atherosclerosis. The aim of this cohort study was to determine the significance of carotid plaque and other factors that may impact the clinical outcomes of end-stage renal disease (ESRD) patients.

Methods: Two hundred and sixty-five patients who received maintenance hemodialysis for more than 3 months were enrolled in the study and closely followed for 2 years with clinical events recorded. The primary endpoint was cardiovascular death.

Results: During the 2-year follow-up period, 11.7% of the patients died from cardiovascular causes; however none were caused by stroke. The patients with carotid plaques were older and had thicker left CIMT and right CIMT, lower serum albumin, higher alanine aminotransferase, higher serum glucose, lower serum creatinine, and higher rates of cardiovascular death and overall mortality. Logistic regression analysis showed that the existence of carotid plaque (odds ratio 3.39, 95% confidence interval: 1.577-7.292, p = 0.002) was significantly correlated with the primary outcome. Plaque also significantly impacted overall survival (log-rank p = 0.024).

Conclusions: The presence of carotid plaque was a risk factor for cardiovascular death in patients with ESRD.

Background: Atherosclerosis accelerates the progression of diabetes and metabolic syndrome. Endothelial to mesenchymal transition (EndMT) has been reported to promote the development of atherosclerosis and the generation of extracellular matrix. However, the mechanism of EndMT in diabetic atherosclerosis has not been fully clarified.

Methods: Human umbilical vein endothelial cells (HUVECs) were treated with high glucose (HG) and transforming growth factor beta 1 (TGF-β1) to induce EndMT. The levels of insulin-like growth factor 2 mRNA-binding protein (IGF2BP), Krüppel-like factor 4 (KLF4), Adhesion-regulating molecule 1 (ADRM1), CD31, vWF, α-SMA and vimentin were detected by qRT-PCR and Western blot. Correlations among IGF2BP1, KLF4 and ADRM1 were analyzed by RIP and ChIP assays. MeRIP-qPCR was used to detect the m⁶A level. The effect of IGF2BP1 on the stability of KLF4 was detected by RNA stability assay. Wound healing and Transwell assays were used to detect HUVEC migration ability.

Results: IGF2BP1, KLF4 and ADRM1 were upregulated in the diabetic atherosclerosis cell model, and IGF2BP1 knockdown inhibited HG combined with TGF-β1-induced EndMT in HUVECs. Mechanically, IGF2BP1 regulated the m⁶A level of KLF4. Functionally, IGF2BP1 upregulated KLF4 to promote HG combined with TGF-β1-induced EndMT in HUVECs. The results proved that IGF2BP1 regulated the KLF4/ADRM1 axis promoting EndMT in diabetic atherosclerosis.

Conclusions: This study demonstrated that IGF2BP1-mediated m⁶A modification of KLF4 and upregulated ADRM1 affect EndMT in diabetic atherosclerosis.

Background: This study aimed to investigate the relationship between cardiorespiratory fitness (CRF) levels and changes in arterial elasticity parameters immediately following maximal exercise in young elite athletes compared to healthy controls. Understanding how CRF influences arterial elasticity could provide insights into optimizing cardiovascular health through exercise interventions.

Methods: The study population comprised 34 elite athletes and 17 healthy controls with similar demographic characteristics. All participants underwent a baseline echocardiographic assessment, followed by a cardiopulmonary exercise test. Echocardiographic measurements, including aortic elasticity parameters derived from M-mode imaging of the ascending aorta, were repeated at 5, 15, and 60 minutes post-exercise. Aortic stiffness index (ASI) was used as the primary measure of arterial elasticity.

Results: The athletes had significantly higher mean VO₂max compared to the controls (50 vs. 38 ml/kg/min, p < 0.01). At rest, the athletes had lower aortic stiffness (ASI: 4.18 vs. 5.92, p < 0.01), indicating better arterial elasticity. A moderate negative correlation was observed between VO₂max and resting ASI (r = -0.51; p < 0.01), suggesting that higher CRF was associated with greater arterial elasticity. Post-exercise, ASI in the athletes returned to baseline levels by 60 minutes, whereas the controls showed a significant reduction in ASI compared to baseline (-0.02 vs. -0.33; p < 0.01).

Conclusions: These findings underscore the importance of CRF in maintaining arterial elasticity and highlight differences in vascular adaptation to exercise between athletes and healthy individuals. The results suggest that exercise interventions should be tailored to individual fitness levels to optimize cardiovascular benefits and improve arterial health.