Is having a moderate or low history, electrocardiogram, age, risk factors, troponin risk score a handicap for long-term mortality?

OBJECTIVE: History, electrocardiogram, age, risk factors, troponin risk score and troponin level follow-up are used to safely discharge low-risk patients with suspected non-ST elevation acute coronary syndrome from the emergency department for a 1-month period. We aimed to comprehensively investigate the 6-month mortality of patients with the history, electrocardiogram, age, risk factors, troponin risk score. METHODS: A total of 949 non-ST elevation acute coronary syndrome patients admitted to the emergency department from 01.01.2019 to 01.10.2019 were included in this retrospective study. History, electrocardiogram, age, risk factors, troponin scores of all patients were calculated by two emergency clinicians and a cardiologist. We compared the 6-month mortality of the groups. RESULTS: The mean age of the patients was 67.9 (56.4-79) years; 57.3% were male and 42.7% were female. Six-month mortality was significantly lower in the high-risk history, electrocardiogram, age, risk factors, troponin score group than in the low- and moderate-risk groups: 11/80 (12.1%), 58/206 (22%), and 150/444 (25.3%), respectively (p=0.019). CONCLUSION: Patients with high history, electrocardiogram, age, risk factors, troponin risk scores are generally treated with coronary angioplasty as soon as possible. We found that the mortality rate of this group of patients was lower in the long term compared with others. Efforts are also needed to reduce the mortality of moderate and low-risk patients. Further studies are needed on the factors affecting the 6-month mortality of moderate and low-risk acute coronary syndrome patients.

Is having a moderate or low history, electrocardiogram, age, risk factors, troponin risk score a handicap for long-term mortality?

SUMMARY OBJECTIVE: History, electrocardiogram, age, risk factors, troponin risk score and troponin level follow-up are used to safely discharge low-risk patients with suspected non-ST elevation acute coronary syndrome from the emergency department for a 1-month period. We aimed to comprehensively investigate the 6-month mortality of patients with the history, electrocardiogram, age, risk factors, troponin risk score. METHODS: A total of 949 non-ST elevation acute coronary syndrome patients admitted to the emergency department from 01.01.2019 to 01.10.2019 were included in this retrospective study. History, electrocardiogram, age, risk factors, troponin scores of all patients were calculated by two emergency clinicians and a cardiologist. We compared the 6-month mortality of the groups. RESULTS: The mean age of the patients was 67.9 (56.4-79) years; 57.3% were male and 42.7% were female. Six-month mortality was significantly lower in the high-risk history, electrocardiogram, age, risk factors, troponin score group than in the low- and moderate-risk groups: 11/80 (12.1%), 58/206 (22%), and 150/444 (25.3%), respectively (p=0.019). CONCLUSION: Patients with high history, electrocardiogram, age, risk factors, troponin risk scores are generally treated with coronary angioplasty as soon as possible. We found that the mortality rate of this group of patients was lower in the long term compared with others. Efforts are also needed to reduce the mortality of moderate and low-risk patients. Further studies are needed on the factors affecting the 6-month mortality of moderate and low-risk acute coronary syndrome patients.

The neuroprotective effect of Sulindac after ischemia-reperfusion injury in rats.

PURPOSE: To investigate the neuroprotective effects of Sulindac on the hippocampal complex after global cerebral ischemia/reperfusion (I/R) injury in rats. METHODS: Thirty one Sprague-Dawley rats were used, distributed into group I (sham) n:7 were used as control. For group II (n:8), III (n:8) and IV (n:8) rats, cerebral ischemia was performed via the occlusion of bilateral internal carotid artery for 45 minutes and continued with reperfusion process. 0.3 mL/kg/h 0.9 % sodium chloride was infused intraperitoneally to the Group II rats before ischemia, 5µg/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group III rats before ischemia and 5µg/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group IV rats after ischemia and before reperfusion process. The levels of MDA, GSH and MPO activity were measured in the left hippocampus tissue. The hippocampal tissue of all group members were taken for histopathological study. RESULTS: The MDA and MPO levels increased from group I (control) to group II (I/R) (P<0.05) and decreased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05). Beside these, the GSH levels decreased from group I (control) to group II (I/R) (P<0.05) and increased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05).The number of apoptotic neurons increased from group I (control) to group II (I/R) (P<0.05) and decreased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05). CONCLUSION: The Sulindac may have neuroprotective effects on ischemic neural tissue to prevent the reperfusion injury after ischemia.

The neuroprotective effect of Sulindac after ischemia-reperfusion injury in rats

To investigate the neuroprotective effects of Sulindac on the hippocampal complex after global cerebral ischemia/reperfusion (I/R) injury in rats. Thirty one Sprague-Dawley rats were used, distributed into group I (sham) n:7 were used as control. For group II (n:8), III (n:8) and IV (n:8) rats, cerebral ischemia was performed via the occlusion of bilateral internal carotid artery for 45 minutes and continued with reperfusion process. 0.3 mL/kg/h 0.9 % sodium chloride was infused intraperitoneally to the Group II rats before ischemia, 5μg/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group III rats before ischemia and 5μg/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group IV rats after ischemia and before reperfusion process. The levels of MDA, GSH and MPO activity were measured in the left hippocampus tissue. The hippocampal tissue of all group members were taken for histopathological study. The MDA and MPO levels increased from group I (control) to group II (I/R) (P<0.05) and decreased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05). Beside these, the GSH levels decreased from group I (control) to group II (I/R) (P<0.05) and increased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05).The number of apoptotic neurons increased from group I (control) to group II (I/R) (P<0.05) and decreased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05). The Sulindac may have neuroprotective effects on ischemic neural tissue to prevent the reperfusion injury after ischemia.

The neuroprotective effect of Sulindac after ischemia-reperfusion injury in rats

To investigate the neuroprotective effects of Sulindac on the hippocampal complex after global cerebral ischemia/reperfusion (I/R) injury in rats. Thirty one Sprague-Dawley rats were used, distributed into group I (sham) n:7 were used as control. For group II (n:8), III (n:8) and IV (n:8) rats, cerebral ischemia was performed via the occlusion of bilateral internal carotid artery for 45 minutes and continued with reperfusion process. 0.3 mL/kg/h 0.9 % sodium chloride was infused intraperitoneally to the Group II rats before ischemia, 5μg/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group III rats before ischemia and 5μg/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group IV rats after ischemia and before reperfusion process. The levels of MDA, GSH and MPO activity were measured in the left hippocampus tissue. The hippocampal tissue of all group members were taken for histopathological study. The MDA and MPO levels increased from group I (control) to group II (I/R) (P<0.05) and decreased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05). Beside these, the GSH levels decreased from group I (control) to group II (I/R) (P<0.05) and increased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05).The number of apoptotic neurons increased from group I (control) to group II (I/R) (P<0.05) and decreased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P<0.05). The Sulindac may have neuroprotective effects on ischemic neural tissue to prevent the reperfusion injury after ischemia.(AU)

The effects of electromagnetic fields on the ultrastructure of heart / Efectos de los campos electromagnéticos en la ultraestructura del corazón

Increasingly the use and convenience of electrical appliances in our daily lives are the cause of harmful effects caused by electromagnetic fields (EMF). The aim of this study was to research the effect of EMF on the ultrastructure of the heart in EMF exposed rats. In this study 45 male Sprague Dawley rats ranging in weight between 260 and 280 grams were used. The rats were divided into 3 groups, control (n:15), Sham (n:15) and EMF group (n: 15) and exposed for 14 days 3 hours per day; gauss levels at 2.5 were applied to the EMF group, while the sham group in the same environment in Plexiglas cage was kept for 14 days 3 hours per day without magnetic field exposure. Control group at 14/10 hours light dark cycle fed in normal cages for 14 days. After two weeks rats were sacrificed by 50mg/kg of Ketalar anesthesia and heart tissue fixed in 2.5 gluteraldehide. Routine follow up with electron microscopic assessment. Mitochondrial structures and cellular structures observed in all the groups were normal. Myofibrillar loss, dilatation of smooth endoplasmic reticulum, mitochondrial swelling or cristalysis was not observed. Intercalated disc degeneration and apoptosis of nucleus was not observed. Therefore, and as a result of our study we did not observe differences between control and EMF groups.

El uso y la comodidad de los aparatos eléctricos en nuestra vida cotidiana cada vez más son causa de efectos perjudiciales debido a los campos electromagnéticos(CEM).El objetivo de este estudio fue investigar el efecto de los CEM sobre la ultraestructura del corazón en ratas. Fueron utilizadas 45ratas Sprague Daw ley, con peso entre 260 y 280gramos. Las ratas fueron divididas en 3 grupos: control (n: 15); Sham (n:15), y grupo expuesto a CEM (n:15) durante 14 días,3 horas por día. Se aplicó niveles de 2,5gaussal grupo expuesto a CEM, mientras que el grupo de tratamiento simulado en el mismo entorno en jaulas plexiglás se mantuvo durante 14 días 3 horas día, sin exposición a campo electromagnético. Grupo control alimentado en jaulas normales durante 14 días con ciclo luz/oscuridad de 14/10. Al termino de dos semanas las ratas fueron sacrificadas por medio de anestesia Ketalar 50mg/kg y el tejido del corazón fijado engluteraldehido al 2,5. Se realizó seguimiento de rutina con correspondiente evaluación de microscopía electrónica. Las estructuras mitocondriales y celular es observadas en todos los grupos eran normales. No se observó pérdida miofibrilar, tampoco aumento del volumen mitocondrial ni dilatación del retículo endoplásmico lisoocristalysis. No se observó degeneración de los discosintercaladoso apoptosis de núcleo. Por lo tanto,y como resultado de nuestro estudio no encontramos diferencias entre los grupos control y CEM.