RESUMEN
AIMS: Myocardial infarction (MI) is among the main public health problems in the world. This atherosclerotic cardiovascular disease (ASCVD), which seriously endangers human health, progresses to cause heart failure and myocardial fibrosis with a poor prognosis. The gut microbiota plays an important role in health and disease, including obesity and ASCVD. In this study, the protective effect of Lacticaseibacillus rhamnosus GG, known for its anti-inflammatory and antioxidant effects, on isoprenaline (ISO)-induced MI in rats was investigated. METHODS AND RESULTS: Rats were divided into four groups of seven rats in each group as control, ISO, L. rhamnosus, and ISO + L. rhamnosus.The ISO application was made by subcutaneous injection to the rats on the last two days (days 27th and 28th) of the 28-day substance administration. The rats were anesthetized 24 hours after the application of ISO, and blood samples were collected after electrocardiogram (ECG) recordings. To determine myocardial damage and protective effects of L. rhamnosus, serum creatine kinase-MB, cardiac troponin-I, tumor necrosis factor-alpha, interleukin-10, and C-reactive protein (CRP) levels were examined. In addition, ECG recordings were evaluated. While L. rhamnosus had a decreasing effect on cardiac troponin-I, creatine kinase-MB, CRP, and tumor necrosis factor-alpha levels, which increased due to ISO, it had an increasing effect on interleukin-10 levels. Similarly, it decreased the ST-segment elevation caused by ISO while increasing the reduced R wave amplitude.
Asunto(s)
Lacticaseibacillus rhamnosus , Infarto del Miocardio , Humanos , Ratas , Animales , Isoproterenol/efectos adversos , Interleucina-10 , Lacticaseibacillus , Troponina I/efectos adversos , Factor de Necrosis Tumoral alfa/metabolismo , Ratas Wistar , Infarto del Miocardio/inducido químicamente , Infarto del Miocardio/tratamiento farmacológico , Infarto del Miocardio/prevención & control , Creatina Quinasa/efectos adversosRESUMEN
Bergapten (BeG) is explored for its anti-inflammatory and antioxidant properties. Myocardial infarction (MI) is reported to be one of the leading cardiovascular diseases characterized by mitochondrial dysfunction and apoptosis. The main purpose of this study is to assess the cardiopreventive effects of BeG (50 mg/kg) in isoproterenol (ISO)-induced MI in Wistar rats. The increased infarct size after ISO induction was reduced simultaneously on treatment with BeG. Similarly, augmented levels of cardiac biomarkers, namely cardiac troponin T, creatine kinase (CK), cardiac troponin I, and CK-MB were also suppressed by BeG. The increased rate of lipid hydroperoxides and thiobarbituric acid reactive substances owing to the oxidative stress caused by free radical generation in ISO-induced rats were also inhibited by BeG. Antioxidants reduce oxidative stress by scavenging free radicals. ISO induction reduces these antioxidant enzymes glutathione peroxidase, catalase, superoxide dismutase, and glutathione, and levels causing oxidative cardiac damage to the heart tissue. BeG supplementation improved these enzymes synthesis preventing potential damage to the myocardium. Inflammation caused by ISO pretreatment increased the secretion of proinflammatory cytokines in ISO-induced rats. Pretreatment with BeG suppressed these inflammatory cytokines to a normal level in ISO + BeG-treated rats. The histopathological examination of the morphological characteristics showed that the intensity of cardiac damage caused by ISO induction was less in BeG pretreated rats with less inflammatory cells and no necrosis. BeG also showed promising results in the molecular alteration of AMP-activated protein kinase/endothelial nitric oxide synthase/protein kinase B signaling molecules. These observations emphasize the cardioprotective effects of BeG and its potential use as a drug in the near future.
Asunto(s)
Proteínas Quinasas Activadas por AMP , Infarto del Miocardio , 5-Metoxipsoraleno/efectos adversos , Proteínas Quinasas Activadas por AMP/metabolismo , Animales , Antiinflamatorios/farmacología , Antiinflamatorios/uso terapéutico , Antioxidantes/uso terapéutico , Apoptosis , Biomarcadores/metabolismo , Catalasa/metabolismo , Forma MB de la Creatina-Quinasa , Citocinas/metabolismo , Glutatión/metabolismo , Glutatión Peroxidasa/metabolismo , Isoproterenol/toxicidad , Peróxidos Lipídicos/metabolismo , Infarto del Miocardio/inducido químicamente , Infarto del Miocardio/tratamiento farmacológico , Infarto del Miocardio/patología , Miocardio/metabolismo , Óxido Nítrico Sintasa de Tipo III/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Ratas , Ratas Wistar , Transducción de Señal , Superóxido Dismutasa/metabolismo , Sustancias Reactivas al Ácido Tiobarbitúrico/metabolismo , Troponina I/efectos adversos , Troponina I/metabolismo , Troponina T/metabolismo , Troponina T/farmacologíaRESUMEN
BACKGROUND: Although primary graft dysfunction (PGD) is a leading cause of mortality and morbidity early post-heart transplant, relatively little is known regarding mechanisms involved in PGD development. METHODS AND RESULTS: We examined the relationship between cardiac troponin I (cTnI) concentrations in the preservation solution from 43 heart transplant procedures and the development of PGD. Donor hearts were flushed with cold preservation solution (University of Wisconsin [UW] or Custodiol) and stored in the same solution. cTnI concentrations were measured utilizing the i-STAT System and normalized to left ventricular mass. Recipient medical records were reviewed to determine PGD according to the 2014 ISHLT consensus conference. Nineteen patients developed PGD following cardiac transplantation. For both UW and Custodiol, normalized cTnI levels were significantly increased (P = .031 and .034, respectively) for those cases that developed PGD versus no PGD. cTnI levels correlated with duration of ischemic time in the UW group, but not for the Custodiol group. Donor age and donor cTnI (obtained prior to organ procurement) did not correlate with preservation cTnI levels in either UW or Custodiol. CONCLUSIONS: Increased preservation solution cTnI is associated with the development of PGD suggesting preservation injury may be a dominant mechanism for the development of PGD.
Asunto(s)
Trasplante de Corazón , Corazón , Soluciones Preservantes de Órganos/efectos adversos , Disfunción Primaria del Injerto/epidemiología , Troponina I/efectos adversos , Adulto , Biomarcadores/análisis , Femenino , Humanos , Masculino , Persona de Mediana Edad , Soluciones Preservantes de Órganos/química , Donantes de Tejidos , Troponina I/análisisRESUMEN
Objetivo: Avaliar a associação da troponina I e da disfunção miocárdica com mortalidade no choque séptico. Métodos: Coorte de 67 pacientes consecutivos com idade acima de 65 anos, no período de 32 meses, tendo diagnóstico de choque séptico com monitoração da artéria pulmonar. O escore APACHE II foi calculado em todos os pacientes. A mensuração da troponina I foi realizada nas primeira 24 horas de internação e quando havia evolução para disfunção miocárdica. A troponina I foi o teste considerada positiva quando o nível sérico apresentava-se acima de 0,5mg/ml. A disfunção miocárdica foi definida pelos critérios de Le Gall et al. Para análise estatística empregou-se o teste do qui-quadrado, o teste 1 e a análise de sobrevida de kaplan-Meier, considerando-se valor inferior a 5 por cento como nível de significância. Resultados: A média da idade foi 80 anos e do APACHE II foi 19. Houve 39 óbitos (58 por cento) e a disfunção miocárdica ocorreu em 46 por cento dos pacientes. A troponina I foi positiva em 22 dos 31 pacientes que evoluíram com disfunção...
Objective: To evaluate the association between troponin I and myocardial dysfunction with mortality in septicshock. Methods: The cohort followed up for 32 months, monitoring the pulmonary arteries of 67 patientsover 65 years old diagnosed with septic shock. APACHE II scoring was calculated for all patients. Troponin I levels were taken in the first 24 hoursafter admission and when myocardial dysfunction occurred. Troponin I was considered positive for serum levels over 0.5ng/ml. Myocardial dysfunction was defined by Le Galls criteria1. Statistical treatment was provided through chisquare test, t test and analysis of the Kaplan- Meier survival curve, with under 5% consideredstatistically significant. Results: The average age was eighty years old and the average APACHE II score was 19. There were 39 deaths (58%), with myocardial dysfunction present in 46% of the patients. Troponin I was positive in 22 out of 31 patients with myocardial dysfunction. Although myocardialdysfunction demonstrated a borderline p-value (p=0.049) when analyzed by the chi-square test, it presented nocorrelation with mortality through the survival curve analysis (p=0.25). Troponin I was associated not onlywith mortality showed by the chi-square test (p=0.006), but also with the survival curve analysis (p=0.021). There was an association with mortality when positive troponin I was present in myocardial dysfunction.
Asunto(s)
Humanos , Masculino , Femenino , Anciano , Choque Séptico/complicaciones , Choque Séptico/mortalidad , Anciano/fisiología , Troponina I/administración & dosificación , Troponina I/efectos adversosRESUMEN
Las complicaciones cardiovasculares representan la principal causa de muerte en los pacientes con insuficiencia renal en etapa terminal, ya que pueden presentar isquemia silente o síntomas atípicos durante un síndrome coronario agudo. El objetivo del estudio fue evaluar los resultados de troponina I cardiaca (TnIc) en pacientes con insuficiencia renal crónica (IRC) en nuestro hospital. Se realizó un estudio retrospectivo en pacientes con IRC con filtrado glomerular estimado por MDRD 0,05 ng/ml, mientras que el diagnóstico fue angina en el 9% de los pacientes y en el 81 % se encontraron otros diagnósticos. La sensibilidad para la Tnlc con un valor de corte> 0,5 ng/ml fue del 71% y la especificidad del 93%. El número de falsos positivos fue del 31% (20 pacientes). La Tnlc es el marcador de elección para diagnosticar daño miocárdico en, pacientes con IRC
Cardiovascular complications are the first cause of death in patients with end-stage renal disease because they can have silent ischaemia or atypical symptoms during acure coronary syndrome. The aim ofthe study was evaluate cardiac troponin I (cTnI) in patients with chronic renalfailure (CRF). We peiformed a retrospective study on patients with CRF with MDRD 0.05 ng/ml, while the diagnostic was angina in 9% and in 81 % we finded other diagnostics. The sensitivity for cTnI with cut-offvalue > 0.5 ng/ml was 71% and specificity 93%. The number of false positives was 31% (20 patients). cTnI is the preferred biomarker for myocardial damage in patients with CRF