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3.
BMC Cardiovasc Disord ; 21(1): 258, 2021 05 26.
Artículo en Inglés | MEDLINE | ID: mdl-34039268

RESUMEN

BACKGROUND: Limited data were available on the current trends in optimal medical therapy (OMT) after PCI and its influence on clinical outcomes in China. We aimed to evaluate the utilization and impact of OMT on the main adverse cardiovascular and cerebrovascular events (MACCEs) in post-PCI patients and analyzed the factors predictive of OMT after discharge. METHODS: We collected data from 3812 individuals from 2016.10 to 2017.09 at TEDA International Cardiovascular Hospital. They were classified into an OMT group and a non-OMT group according to their OMT status, which was defined as the combination of dual antiplatelet therapy, statins, ß-blockers, angiotensin-converting enzyme inhibitors or angiotensin receptor blockers after PCI. Multivariable Cox regression models were developed to assess the association between OMT and MACCEs, defined as all-cause mortality, nonfatal myocardial infarction, stroke, and target vessel revascularization. A logistic regression model was established to analyze the factors predictive of OMT. RESULTS: Our results revealed that the proportion of patients receiving OMT and its component drugs decreased over time. A total of 36.0% of patients were still adherent to OMT at the end of follow-up. Binary logistic regression analysis revealed that baseline OMT (P < 0.001, OR = 52.868) was the strongest predictor of OMT after PCI. The Cox hazard model suggested that smoking after PCI was associated with the 1-year risk of MACCE (P = 0.001, HR = 2.060, 95% CI 1.346-3.151), while OMT (P = 0.001, HR = 0.486, 95% CI 0.312-0.756) was an independent protective factor against postoperative MACCEs. CONCLUSIONS: There was still a gap between OMT utilization after PCI and the recommendations in the evidence-based guidelines. Sociodemographic and clinical factors influence the application of OMT. The management of OMT and smoking cessation after PCI should be emphasized.


Asunto(s)
Fármacos Cardiovasculares/uso terapéutico , Enfermedad Coronaria/terapia , Intervención Coronaria Percutánea/tendencias , Pautas de la Práctica en Medicina/tendencias , Anciano , Fármacos Cardiovasculares/efectos adversos , China/epidemiología , Comorbilidad , Enfermedad Coronaria/diagnóstico , Enfermedad Coronaria/mortalidad , Utilización de Medicamentos/tendencias , Femenino , Humanos , Masculino , Cumplimiento de la Medicación , Persona de Mediana Edad , Intervención Coronaria Percutánea/efectos adversos , Intervención Coronaria Percutánea/mortalidad , Estudios Prospectivos , Medición de Riesgo , Factores de Riesgo , Fumar/efectos adversos , Fumar/mortalidad , Cese del Hábito de Fumar , Factores de Tiempo , Resultado del Tratamiento
4.
Oncotarget ; 7(32): 52179-52194, 2016 Aug 09.
Artículo en Inglés | MEDLINE | ID: mdl-27438148

RESUMEN

Type 2 diabetes mellitus is often complicated by osteoporosis, a process which may involve osteoblast autophagy. As melatonin suppresses autophagy under certain conditions, we its investigated the effects on bone autophagy during diabetes. We first assessed different body parameters in a diabetic rat model treated with various concentrations of melatonin. Dynamic biomechanicalmeasurements, bone organization hard slice dyeing and micro-CT were used to observe the rat bone microstructure, and immunohistochemistry was used to determine levels of autophagy biomarkers. We also performed in vitro experiments on human fetal osteoblastic (hFOB1.19) cells cultured with high glucose, different concentrations of melatonin, and ERK pathway inhibitors. And we used Western blotting and immunofluorescence to measure the extent of osteogenesis and autophagy. We found that melatonin improved the bone microstructure in our rat diabetes model and reduced the level of autophagy(50 mg/kg was better than 100 mg/kg). Melatonin also enhanced osteogenesis and suppressed autophagy in osteoblasts cultured at high glucose levels (10 µM was better than 1 mM). This suggests melatonin may reduce the level of autophagy in osteoblasts and delay diabetes-induced osteoporosis by inhibiting the ERK signaling pathway.


Asunto(s)
Autofagia/efectos de los fármacos , Diabetes Mellitus Tipo 2/complicaciones , Melatonina/farmacología , Osteoporosis/prevención & control , Animales , Diabetes Mellitus Experimental/complicaciones , Humanos , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Masculino , Osteoblastos/efectos de los fármacos , Osteogénesis/efectos de los fármacos , Ratas , Ratas Sprague-Dawley , Transducción de Señal/efectos de los fármacos
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