Abstract Background Acute heart failure (AHF) poses significant diagnostic challenges in the emergency room (ER) because of its varied clinical presentation and limitations of traditional diagnostic methods. This study aimed to develop and evaluate a deep-learning model using electrocardiogram (ECG) data to enhance AHF identification in the ER. Methods In this retrospective cohort study, we analyzed the ECG data of 19,285 patients who visited ERs of three hospitals between 2016 and 2020; 9,119 with available left ventricular ejection fraction and N-terminal prohormone of brain natriuretic peptide level data and who were diagnosed with AHF were included in the study. We extracted morphological and clinical parameters from ECG data to train and validate four machine learning models: baseline linear regression and more advanced models including XGBoost, Light GBM, and CatBoost. Results The CatBoost algorithm outperformed other models, showing superior area under the receiver operating characteristic and area under the precision–recall curve diagnostic accuracy across both internal (0.89 ± 0.01 and 0.89 ± 0.01) and external (0.90 and 0.89) validation datasets, respectively. The model demonstrated high accuracy, precision, recall, and f1 score, indicating robust performance in AHF identification. Conclusion The developed machine learning model significantly enhanced AHF detection in the ER using conventional 12-lead ECGs combined with clinical data. These findings suggest that ECGs, a common tool in the ER, can effectively help screen for AHF.
Angiography remains the gold standard for guiding percutaneous coronary intervention (PCI). However, it is prone to suboptimal stent results due to the visual estimation of coronary measurements. Although the benefit of intravascular ultrasound (IVUS)-guided PCI is becoming increasingly recognised, IVUS is not affordable for many catheterisation laboratories. Thus, a more practical and standardised angiography-based approach is necessary to support stent implantation.
There have been limited data on the impact of hyperuricemia on long-term clinical outcomes after percutaneous coronary intervention (PCI) for in-stent restenosis (ISR). From January 2009 to July 2015, 317 patients who underwent repeat PCI for ISR were divided into two groups: patients with normal serum uric acid (UA) levels (normal UA group) and patients with higher serum UA levels (higher UA group). The higher UA group included patients with serum UA levels > 6.8 mg/dL or patients who were taking anti-hyperuricemic medication. During a median follow-up period of 1088 days, the cumulative incidence rates of major adverse event (MAE), including a composite of all-cause death, non-fatal myocardial infarction, and any revascularization, were similar between the two groups (higher UA 36.4% vs. normal UA 29.9%, p = 0.389, log-rank p = 0.367). Follow-up angiographic data showed similar outcomes of late lumen loss (0.8 ± 0.9 mm vs. 0.8 ± 1.1 mm, p = 0.895) and binary restenosis rate (28.1% vs. 34.7%, p = 0.622). Multivariate Cox regression analysis indicated higher levels of low-density lipoprotein cholesterol (hazard ratio [HR] 1.011, 95% confidence interval [CI] 1.003–1.019, p = 0.006) and lower left ventricular ejection fraction (HR 0.972, 95% CI 0.948–0.996, p = 0.022), but not UA levels, to be the independent risk predictors of MAE. Hyperuricemia is not associated with poor clinical outcomes after repeat PCI for ISR lesions.
To establish normal references of acceleration time-to-ejection time (At/Et) ratio of fetus at 25 to 40 weeks of gestation. A cross-sectional prospective study was conducted on 138 fetuses of normal singleton pregnancies between 24 and 40 weeks. At/Et ratio was measured in the main pulmonary artery of fetus. Measurement was analysed according to gestational age. We present nomogram for At/Et ratio in normal singleton pregnancy. At/Et ratio was increased as gestational age advanced. This study established a normogram for At/Et ratio in normal singleton pregnancy and demonstrated a correlation between this ratio and gestational age. The observed changes throughout gestational age are showing an increase in perfusion as well as a decrease in the vascular resistance and pressure.
We compared the efficacy and safety of low-intensity atorvastatin and ezetimibe combination therapy with moderate-intensity atorvastatin monotherapy in patients requiring cholesterol-lowering therapy.At 19 centers in Korea, 290 patients were randomized to 4 groups: atorvastatin 5 mg and ezetimibe 10 mg (A5E), ezetimibe 10 mg (E), atorvastatin 5 mg (A5), and atorvastatin 10 mg (A10). Clinical and laboratory examinations were performed at baseline, and at 4-week and 8-week follow-ups. The primary endpoint was percentage change from baseline in low-density lipoprotein (LDL) cholesterol levels at the 8-week follow-up. Secondary endpoints included percentage changes from baseline in additional lipid parameters.Baseline characteristics were similar among the study groups. At the 8-week follow-up, percentage changes in LDL cholesterol levels were significantly greater in the A5E group (49.2%) than in the E (18.7%), A5 (27.9%), and A10 (36.4%) groups. Similar findings were observed regarding the percentage changes in total cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B levels. Triglyceride levels were also significantly decreased in the A5E group than in the E group, whereas high-density lipoprotein levels substantially increased in the A5E group than in the E group. In patients with low- and intermediate-cardiovascular risk, 93.3% achieved the target LDL cholesterol levels in the A5E group, 40.0% in the E group, 66.7% in the A5 group, and 92.9% in the A10 group. In addition, 31.4% of patients in the A5E group, 8.1% in E, 9.7% in A5, and 7.3% in the A10 group reached the target levels of both LDL cholesterol < 70 mg/dL and reduction of LDL ≥ 50% from baseline.The addition of ezetimibe to low-intensity atorvastatin had a greater effect on lowering LDL cholesterol than moderate-intensity atorvastatin alone, offering an effective treatment option for cholesterol management, especially in patients with low and intermediate risks.
Background Beta-blockers are often not the preferred treatment for patients with vasospastic angina. However, nebivolol, beta-blocker with nitric oxide-releasing effect, could theoretically improve coronary vasospasm. We compared nebivolol versus diltiazem in improving coronary vasospasm and quality of life in patients with hypertensive vasospastic angina during a 12-week follow-up. Methods Fifty-one hypertensive patients with documented coronary vasospasm were randomly allocated into 3 treatment groups: (1) Nebivolol Group (5mg for 2 weeks/10mg for 10 weeks); (2) Diltiazem Group (90mg for 2 weeks/180mg for 10 weeks); (3) Low-dose Combination Group (2.5mg + 45mg for 2 weeks/5mg + 90mg for 10 weeks). The primary endpoint was to compare the percent changes in coronary vasospasm at 12 weeks from baseline among the 3 groups. The secondary endpoints included changes in quality of life based on the Seattle Angina Questionnaire and changes in blood pressure at 12 weeks from baseline. Results Significant improvements in coronary vasospasm were found in all groups; however, the improvement in percent changes in coronary artery spasm was greatest in the Diltiazem Group (50.4±8.8% vs. 67.8±12.8% vs. 46.8±12.3%, Nebivolol Group vs. Diltiazem Group p = 0.008; Nebivolol Group vs. Low-dose Combination Group p = 0.999; Diltiazem Group vs. Low-dose Combination Group p = 0.017). The overall Seattle Angina Questionnaire scores were significantly elevated at 12 weeks compared to the baseline in entire study population. There were no significant differences between the three groups in the overall Seattle Angina Questionnaire score changes and blood pressure changes. Conclusions Both nebivolol and diltiazem showed significant coronary vasospasm reduction effect, but the effect was greater for diltiazem.
Background: Cell sheet technology has magnified as an important transplantation skill. Mouse adipose derived stem cells (mADSCs) can secrete various growth factors, which promote the repair of damaged cardiomyocyte and protecting cells from death. In addition, autologous cell source to easily obtain from patients are promising candidates for cell therapy in cardiovascular field. Methods: mADSCs were confirmed stem cell properties and secreted cytokines were evaluated in vitro. Eighteen acute myocardial infarction (AMI) rats were divide into 3 group; sham (n=6), suspended mADSCs (n=6), and mADSCs sheet (n=6) groups. In the mADSCs sheet group, 60х106 cells were cultured for 2 days onto temperature-responsive polymers and the sheets were then transplanted over the infarct region. In additional, the sheet was made of carboxyfluorescein diacetate succinimidyl ester (CFDA) -labelled mADSCs to confirmed cell survival. Engraftment and differentiation were blindly assessed after 28 days. Results: The mADSCs expressed Sca-1+ and represented multi-differentiation potential. Interestingly, EGF and IGF levels significantly increased in the mADSCs sheet. Significant improvements in ejection fraction and fraction shortening value were observed in the mADSCs sheet and suspended mADSCs groups compared with the sham group at 14 and 28 days. But, it was not higher significance level in the mADSCs sheet group than in the suspended mADSCs group. Engraftment range and fibrosis area of infarct region were significantly higher in the mADSCs sheet group compared to the other two groups at 4, 14 and 28 days. In significant expressed cytokines (bFGF, IL-1a, IL-1ra, CT-1, EGF, TGFb1, IGF-1, IGF-2 and MCP-1) were observed in the mADSCs sheet group compared with the other 2 groups at 28 days after transplantation. In addition, in the mADSCs sheet was confirmed endothelial differentiation by Von Willebrand factor (vWF) at 4, 14 and 28 days. Conclusions: Transplantation of mADSCs sheet into rat infarcted myocardium increased engraftment and survival of transplanted cells. The mADSCs sheet is very useful for the study of stem cell proliferation and differentiation as well as for cell therapy in cardiovascular field.
Abstract Background Stent thrombosis (ST) is a potentially fatal complication after percutaneous coronary intervention (PCI). The association between P2Y12 reaction unit (PRU) level and stent thrombosis occurrence is not fully elucidated. Methods Based on the multicenter, observational PTRG-DES (Platelet function and genoType-Related long-term proGnosis in DES-treated patients) registry of patients with drug-eluting stents (DES) implantation, a total of 11,714 patients with PRU values were identified. The independent predictors of early stent thrombosis (EST) were assessed. The primary outcome after EST was the composite of cardiac death, myocardial infarction and any revascularisation. Key secondary outcomes were all-cause death, cardiac death, myocardial infarction, and any revascularisation. Results EST, defined as definite ST in less than 1 month after index PCI, was identified in a total of 51 patients. The PRU value was significantly higher in the EST group (263.5 ± 70.8 vs. 217.5 ± 78.7, p<0.001). In multivariable analysis, having a PRU value of ≥252 (OR, 5.10; 95% CI, 1.58-16.46; p=0.006) and an ARU value of ≥414 (OR 4.85; 95% CI, 1.07-21.97; p=0.040) were significant predictors of EST. The use of first-generation DES (OR 3.56; 95% CI, 0.98-12.99; p=0.054) also posed a higher risk for EST occurrence with a borderline significance. Cumulative incidence of the primary composite outcome was significantly higher in patients with EST (HR 18.7; 95% CI 12.8-27.3; p<0.001). Conclusion In patients treated with clopidogrel after successful DES implantation, EST was associated with higher PRU values, and a greater rate of adverse outcomes, including all-cause death and MI.
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