RESUMEN
OBJECTIVE: Sodium-glucose cotransporter 2 (SGLT2) inhibitors, such as empagliflozin are antidiabetic drugs that have recently been reported to have cardio-protective action; however, their effect on cardiac structure and function in heart failure with reduced ejection fraction (HFrEF) has not yet been determined. This study evaluates the efficacy of empagliflozin on left ventricular (LV) volumes in type 2 diabetes or prediabetes patients with HFrEF. METHODS: This randomised, double-blind, trial study was conducted on 104 patients with type 2 diabetes or prediabetes with HFrEF referred to Imam Khomeini and Golestan hospitals in Ahvaz, Iran. The patients were randomised to receive empagliflozin (10 mg once daily) in addition to standard treatments of HFrEF or receive only standard treatments (control group) for six months. During the six months of follow-up, changes in LV volumes, LVEF, hospitalisation for heart failure (HF) were evaluated. RESULTS: Empagliflozin reduced LVEDVI and LVESVI by 10.0 and 8.0 mL/m2 (p < 0.0001). Furthermore, a significant increase in LVEF was observed in the empagliflozin group (p < 0.0001) without any significant change in the control group (p = 0.389). The hospitalisation rate was lower in the empagliflozin group than the control group (3.8% vs. 23.1%; p = 0.008). CONCLUSIONS: Empagliflozin is effective in reducing LV volumes and hospitalisation rate in patients with type 2 diabetes and prediabetes and HFrEF. Therefore, treatment with empagliflozin for six months was associated with a significant reduction in adverse cardiovascular outcomes in these patients.
Asunto(s)
Compuestos de Bencidrilo , Diabetes Mellitus Tipo 2 , Glucósidos , Insuficiencia Cardíaca , Estado Prediabético , Inhibidores del Cotransportador de Sodio-Glucosa 2 , Volumen Sistólico , Humanos , Compuestos de Bencidrilo/uso terapéutico , Diabetes Mellitus Tipo 2/complicaciones , Diabetes Mellitus Tipo 2/tratamiento farmacológico , Diabetes Mellitus Tipo 2/fisiopatología , Glucósidos/uso terapéutico , Masculino , Volumen Sistólico/fisiología , Volumen Sistólico/efectos de los fármacos , Femenino , Insuficiencia Cardíaca/fisiopatología , Insuficiencia Cardíaca/tratamiento farmacológico , Inhibidores del Cotransportador de Sodio-Glucosa 2/uso terapéutico , Método Doble Ciego , Estado Prediabético/tratamiento farmacológico , Estado Prediabético/fisiopatología , Estado Prediabético/complicaciones , Persona de Mediana Edad , Resultado del Tratamiento , Función Ventricular Izquierda/efectos de los fármacos , Función Ventricular Izquierda/fisiología , Anciano , Ventrículos Cardíacos/fisiopatología , Ventrículos Cardíacos/diagnóstico por imagen , Ventrículos Cardíacos/efectos de los fármacos , Irán/epidemiología , Estudios de SeguimientoRESUMEN
Embolic material forms in many parts of the body and can affect anywhere in the body. Pulmonary embolism and embolic stroke are the most common presentations of embolic disorders in the body. Embolic events have different causes, and the heart is one of the most important places where emboli originate. One of the uncommon causes of embolic events is non-bacterial thrombotic endocarditis (NBTE), which can occur in patients with advanced cancer. NBTE can lead to embolism. Embolisation may occur in some organs including the central nervous system, kidneys, spleen, limb extremities, and coronary arteries. The authors aim to describe a rare case with concurrent pulmonary embolism (PE) and embolic stroke caused by non-bacterial thrombotic endocarditis (NBTE) in a woman with breast cancer.
RESUMEN
The present study was conducted to identify the effect of vasopressin (AVP) on electrocardiographic changes produced by ischemia-reperfusion. Male rats were divided into seven groups (n=8-13) subjected to 30min ischemia and 120 min reperfusion. In protocol I (control group), saline was administered before ischemia. In protocol II, different doses of AVP (0.015, 0.03, 0.06 and 0.12µg/rat) were infused 10 min before ischemia. In protocol III SR49059 (1 mg/kg), was injected 20 min prior to ischemia with and without the effective dose of AVP (0.03 g/rat). Ischemia-induced arrhythmia and myocardial infarct size (IS) were measured. Different doses of vasopressin decreased IS. There were no significant differences in PR, QRS duration and &DGR;T/amp;DGR;ST ratio between control and intervention groups in ischemia. ST elevation was significantly increased in control and AVP 0.015, 0.03, 0.06 groups during ischemia. In AVP 0.12 group there was no significant difference in ST deviation between the baseline and ischemia phase. JT interval was significantly increased in control and antagonist group during ischemia. AVP 0.12µ/rat prevented the increase of JT interval in ischemia compared to the baseline. In summary, AVP mediated preconditioning improved ST resolution, prevented prolongation of JT interval and decreased the likelihood of subsequently ventricular arrhythmia.
