RESUMEN
Background and aims: It is difficult to document atrial fibrillation (AF) on ECG in patients with non-persistent atrial fibrillation (non-PeAF). There is limited understanding of whether an AI prediction algorithm could predict the occurrence of non-PeAF from the information of normal sinus rhythm (SR) of a 12-lead ECG. This study aimed to derive a precise predictive AI model for screening non-PeAF using SR ECG within 4 weeks. Methods: This retrospective cohort study included patients aged 18 to 99 with SR ECG on 12-lead standard ECG (10 seconds) in Ewha Womans University Medical Center for 3 years. Data were preprocessed into three window periods (which are defined with the duration from SR to non-PeAF detection) - 1 week, 2 weeks, and 4 weeks from the AF detection prospectively. For experiments, we adopted a Residual Neural Network model based on 1D-CNN proposed in a previous study. We used 7,595 SR ECGs (extracted from 215,875 ECGs) with window periods of 1 week, 2 weeks, and 4 weeks for analysis. Results: The prediction algorithm showed an AUC of 0.862 and an F1-score of 0.84 in the 1:4 matched group of a 1-week window period. For the 1:4 matched group of a 2-week window period, it showed an AUC of 0.864 and an F1-score of 0.85. Finally, for the 1:4 matched group of a 4-week window period, it showed an AUC of 0.842 and an F1-score of 0.83. Conclusion: The AI prediction algorithm showed the possibility of risk stratification for early detection of non-PeAF. Moreover, this study showed that a short window period is also sufficient to detect non-PeAF.
RESUMEN
There are limited data about mid-term prognosis according to acute myocardial infarction (AMI) type in female patients with AMI complicated by cardiogenic shock (CS). In this study, we evaluated the impact of AMI type on prognosis in female patients who underwent percutaneous coronary intervention (PCI) for AMI complicated by CS. A total of 184 female patients who underwent PCI for AMI complicated by CS were enrolled from 12 centers in the Republic of Korea. Patients were divided into 2 groups according to AMI type: the ST-segment elevation myocardial infarction (n = 114) and the non-ST-segment elevation myocardial infarction (n = 70) group. Primary outcome was a major adverse cardiac event (MACE) (defined as a composite of cardiac death, myocardial infarction, or repeat revascularization). Propensity-score matching analysis was performed to reduce selection bias and potential confounding factors. During 12-month follow-up, a total of 73 MACEs occurred (ST-segment elevation myocardial infarction group, 47 [41.2%] vs non-ST-segment elevation myocardial infarction group, 26 [37.1%], p = 0.643). Multivariate analysis revealed no significant difference in the incidence of MACE at 12 months between the 2 groups (adjusted hazard ratio 1.16, 95% confidence interval 0.70 to 2.37, p = 0.646). After propensity-score matching, the incidence of MACE at 12 months remained similar between the 2 groups (hazard ratio 1.31, 95% confidence interval 0.69 to 2.52, p = 0.413). The similarity in MACEs between the 2 groups was consistent across a variety of subgroups. In conclusion, after adjusting for baseline differences, AMI clinical type did not appear to increase the risk of MACEs at 12 months in female patients who underwent emergency PCI for AMI complicated by CS.
Asunto(s)
Infarto del Miocardio , Infarto del Miocardio sin Elevación del ST , Intervención Coronaria Percutánea , Infarto del Miocardio con Elevación del ST , Humanos , Femenino , Choque Cardiogénico/etiología , Choque Cardiogénico/complicaciones , Intervención Coronaria Percutánea/efectos adversos , Infarto del Miocardio/complicaciones , Infarto del Miocardio/epidemiología , Pronóstico , Infarto del Miocardio con Elevación del ST/complicaciones , Infarto del Miocardio con Elevación del ST/cirugía , Infarto del Miocardio con Elevación del ST/epidemiología , Infarto del Miocardio sin Elevación del ST/complicaciones , Resultado del TratamientoRESUMEN
Background and aims: This study aimed to examine the association between dynamic smoking habit change and cardiovascular risk in a population newly diagnosed with hypertension, diabetes, and dyslipidemia. Methods: This study included 49,320 individuals who had received health examinations provided by the Korea National Health Insurance Service. To determine the hazard ratios (HRs) and 95% confidence intervals (CIs) for incident major adverse cardiac events (MACE) and all-cause mortality based on dynamic smoking habit changes for 2 years, multivariable Cox proportional hazard models were utilized. Results: During the follow-up, there were 1,004 (2.2%), 3,483 (7.6%), and 334 (0.7%) cases of myocardial infarction, stroke events, and cardiovascular death, respectively. The group with worsening smoking habits had an increased risk of cardiovascular events and death (HR: 1.33, 95% CI: 1.26-1.40) compared to improved smoking habits. The robustness of the results determined by a series of sensitivity analyses further strengthened the main findings. Conclusions: Our findings suggest that worsening of smoking habits, even for a short period of time, may increase the risk of myocardial infarction, stroke, and cardiovascular death in patients diagnosed with hypertension, diabetes, and dyslipidemia. For the primary prevention of cardiovascular events in patients with underlying diseases, dynamic modification of smoking habits should be actively considered.
RESUMEN
SGLT-2 inhibitor, traditionally used for glycemic control, has several beneficial effects that can help manage heart failure (HF). SGLT-2 inhibitors reduce the risk of cardiovascular mortality in patients with HF. As atrial fibrillation (AF) is closely associated with HF and diabetes mellitus (DM) is a risk factor for AF, we assume that SGLT-2 inhibitors will also show therapeutic benefits regarding AF, especially for rhythm control. This trial has a multicenter, prospective, open, blinded endpoint design. It is a 1:1 randomized and controlled study. A total of 716 patients who are newly diagnosed of AF and DM within 1 year will be enrolled from 7 tertiary medical centers. The trial is designed to compare the effects of SGLT-2 inhibitors and other oral hypoglycemic agents on atrial rhythm control in patients with AF and DM. The primary outcome is the recurrence of AF within a year (including post-antiarrhythmic drugs (AAD) or ablation). The secondary outcomes are the ablation rate within a year, change in AF burden, size of the left atrium, NT-proBNP, the AF symptom score, and the quality of life. This trial will prospectively evaluate the effect and safety of SGLT-2 inhibitors on AF rhythm control in patients with DM. It will provide an invaluable dataset on rhythm control in AF with DM for future studies and offer novel information to assist in clinical decisions. (BEYOND trial, ClinicalTrials.gov number: NCT05029115. https://clinicaltrials.gov/ct2/show/NCT05029115).
Asunto(s)
Fibrilación Atrial , Ablación por Catéter , Diabetes Mellitus , Insuficiencia Cardíaca , Inhibidores del Cotransportador de Sodio-Glucosa 2 , Humanos , Fibrilación Atrial/complicaciones , Fibrilación Atrial/tratamiento farmacológico , Inhibidores del Cotransportador de Sodio-Glucosa 2/uso terapéutico , Estudios Prospectivos , Calidad de Vida , Diabetes Mellitus/etiología , Glucosa/uso terapéutico , Sodio , Resultado del Tratamiento , Ablación por Catéter/métodos , Ensayos Clínicos Controlados Aleatorios como Asunto , Estudios Multicéntricos como AsuntoRESUMEN
Oral biofilms coat all surfaces in the oral cavity including the exposed dentin surface. This study aimed to investigate biofilm removal by acid etching procedures and the effects of the residual biofilm on dentin surfaces on composite-dentin adhesion. Dentin discs were assigned to five groups: no biofilm formation (C); biofilm formation and no surface treatment (BF); biofilm formation and acid etching (BF-E); biofilm formation and acid etching followed by chlorhexidine soaking (BF-EC); and biofilm formation and rubbing with pumice, followed by acid etching (BF-RE). Biofilms were formed on saliva-precoated dentin discs by soaking the discs in Streptococcus mutans (S. mutans) suspension. Biofilm removal from the dentin surface was evaluated quantitatively and qualitatively by confocal laser scanning microscopy and scanning electron microscopy, respectively. To compare the bond strength of the biofilm-coated dentin discs with the surface treatments, specimens were assigned to four groups: no biofilm formation and acid etching (C-E); BF-E; BF-EC; and BF-RE. Assessments of the micro-shear bond strength and subsequent failure modes were performed. BF-E and BF-EC did not remove the biofilm, whereas BF-RE partially removed the biofilm attached to the dentin (p < 0.05). The bond strength of BF-RE was significantly higher than those of BF-E and BF-EC, but lower than that of C-E (p < 0.05). In conclusion, mechanical biofilm removal is recommended before etching procedures to enhance adhesion to the biofilm-coated dentin.
RESUMEN
Mitogen-activated protein kinases (MAPKs) are key signal transducers involved in various cellular events such as growth, proliferation, and differentiation. Previous studies have reported that H2O2 leads to phosphorylation of extracellular signal-regulated kinase (ERK), one of the MAPKs in endothelial cells. The current study shows that H2O2 suppressed ERK1/2 activation and phosphorylation at specific concentrations and times in human umbilical vein endothelial cells but not in immortalized mouse aortic endothelial cells or human astrocytoma cell line CRT-MG. Phosphorylation of other MAPK family members (i.e., p38 and JNK) was not suppressed by H2O2. The decrease in ERK1/2 phosphorylation induced by H2O2 was inversely correlated with the level of phosphorylation of Src tyrosine 530. Using siRNA, it was found that H2O2-induced suppression of ERK1/2 was dependent on Csk. Physiological laminar flow abrogated, but oscillatory flow did not affect, the H2O2-induced suppression of ERK1/2 phosphorylation. In conclusion, H2O2-induced Csk translocation to the plasma membrane leads to phosphorylation of Src at the tyrosine 530 residue resulting in a reduction of ERK1/2 phosphorylation. Physiological laminar flow abrogates this effect of H2O2 by inducing phosphorylation of Src tyrosine 419. These findings broaden our understanding of signal transduction mechanisms in the endothelial cells against oxidative stress.
Asunto(s)
Quinasas MAP Reguladas por Señal Extracelular/metabolismo , Células Endoteliales de la Vena Umbilical Humana/metabolismo , Familia-src Quinasas/metabolismo , Animales , Apoptosis , Proteína Tirosina Quinasa CSK , Línea Celular , Endotelio Vascular/citología , Células Endoteliales de la Vena Umbilical Humana/efectos de los fármacos , Humanos , Peróxido de Hidrógeno/farmacología , MAP Quinasa Quinasa 4/metabolismo , Ratones , Proteína Quinasa 1 Activada por Mitógenos/metabolismo , Fosforilación/efectos de los fármacos , ARN Interferente Pequeño , Tirosina/metabolismo , Familia-src Quinasas/genéticaRESUMEN
PURPOSE: This study aimed to investigate the effect of pirfenidone on the IL-1ß-induced hyaluronic acid (HA) increase in orbital fibroblasts from patients with thyroid-associated ophthalmopathy (TAO). METHODS: Primary cultured orbital fibroblasts were obtained from patients with TAO, and the excreted levels of HA from IL-1ß-treated cells with or without pirfenidone were measured. The effect of pirfenidone on IL-1ß-induced hyaluronic acid synthase (HAS) expression was evaluated. The relevance of the mitogen-activated protein kinase (MAPK)-mediated signaling pathway in IL-1ß-induced HAS expression was assessed using specific inhibitors to p38, extracellular signal-regulated kinase (ERK), or c-Jun N-terminal kinase (JNK). The phosphorylation level of each MAPK in IL-1ß-treated cells with or without pirfenidone and the level of AP-1 DNA binding were measured. The inhibitory potency of pirfenidone on HA production was evaluated using dexamethasone as a reference agent. RESULTS: Pirfenidone strongly attenuated the IL-1ß-induced HA release in a dose-dependent manner. The IL-1ß-induced HAS expression was decreased significantly following cotreatment with pirfenidone at the mRNA and protein levels. The production of mRNAs was halted by cotreatment with inhibitors of ERK and p38, but not by inhibitors of JNK. The IL-1ß-induced ERK and p38 phosphorylation, and AP-1 DNA binding were attenuated in the presence of pirfenidone. Pirfenidone showed greater potency than dexamethasone in inhibiting increases in IL-1ß-induced HA. CONCLUSIONS: Pirfenidone attenuates the IL-1ß-induced HA production in orbital fibroblasts from patients with TAO, at least in part, through suppression of the MAPK-mediated HAS expression. These results support the potential use of pirfenidone for treatment of patients with TAO.