Periostin as a modulator of chronic cardiac remodeling after myocardial infarction.

OBJECTIVE: After acute myocardial infarction, during the cardiac repair phase, periostin is released into the infarct and activates signaling pathways that are essential for the reparative process. However, the role of periostin in chronic cardiac remodeling after myocardial infarction remains to be elucidated. Therefore, the objective of this study was to investigate the relationship between tissue periostin and cardiac variables in the chronic cardiac remodeling induced by myocardial infarction. METHODS: Male Wistar rats were assigned to 2 groups: a simulated surgery group (SHAM; n = 8) and a myocardial infarction group (myocardial infarction; n = 13). After 3 months, morphological, functional and biochemical analyses were performed. The data are expressed as means±SD or medians (including the lower and upper quartiles). RESULTS: Myocardial infarctions induced increased left ventricular diastolic and systolic areas associated with a decreased fractional area change and a posterior wall shortening velocity. With regard to the extracellular matrix variables, the myocardial infarction group presented with higher values of periostin and types I and III collagen and higher interstitial collagen volume fractions and myocardial hydroxyproline concentrations. In addition, periostin was positively correlated with type III collagen levels (r = 0.673, p = 0.029) and diastolic (r = 0.678, p = 0.036) and systolic (r = 0.795, p = 0.006) left ventricular areas. Considering the relationship between periostin and the cardiac function variables, periostin was inversely correlated with both the fractional area change (r = -0.783, p = 0.008) and the posterior wall shortening velocity (r = -0.767, p = 0.012). CONCLUSIONS: Periostin might be a modulator of deleterious cardiac remodeling in the chronic phase after myocardial infarction in rats.

Periostin as a modulator of chronic cardiac remodeling after myocardial infarction

OBJECTIVE: After acute myocardial infarction, during the cardiac repair phase, periostin is released into the infarct and activates signaling pathways that are essential for the reparative process. However, the role of periostin in chronic cardiac remodeling after myocardial infarction remains to be elucidated. Therefore, the objective of this study was to investigate the relationship between tissue periostin and cardiac variables in the chronic cardiac remodeling induced by myocardial infarction. METHODS: Male Wistar rats were assigned to 2 groups: a simulated surgery group (SHAM; n = 8) and a myocardial infarction group (myocardial infarction; n = 13). After 3 months, morphological, functional and biochemical analyses were performed. The data are expressed as means±SD or medians (including the lower and upper quartiles). RESULTS: Myocardial infarctions induced increased left ventricular diastolic and systolic areas associated with a decreased fractional area change and a posterior wall shortening velocity. With regard to the extracellular matrix variables, the myocardial infarction group presented with higher values of periostin and types I and III collagen and higher interstitial collagen volume fractions and myocardial hydroxyproline concentrations. In addition, periostin was positively correlated with type III collagen levels (r = 0.673, p = 0.029) and diastolic (r = 0.678, p = 0.036) and systolic (r = 0.795, p = 0.006) left ventricular areas. Considering the relationship between periostin and the cardiac function variables, periostin was inversely correlated with both the fractional area change (r = -0.783, p = 0.008) and the posterior wall shortening velocity (r = -0.767, p = 0.012). CONCLUSIONS: Periostin might be a modulator of deleterious cardiac remodeling in the chronic phase after myocardial infarction in rats. .

Influence of AIN-93 diet on mortality and cardiac remodeling after myocardial infarction in rats.

BACKGROUND: The AIN-93 diet was proposed by the American Institute of Nutrition with the objective of standardising studies in experimental nutrition. Our objective was to analyze the effects of AIN-93 diet after myocardial infarction in rats. METHODS: Post weaning, the animals were divided into two groups: control (C, n=62), fed the standard diet of our laboratory (Labina); AIN-93 Group (n=70), fed the AIN-93 diet. Achieving 250 g, the animals were subjected to myocardial infarction. RESULTS: Early mortality was increased in AIN-93 animals, associated with lower serum levels of calcium, magnesium, potassium, sodium, and phosphorus. On the other hand, after 90 days, AIN-93 showed smaller normalized left ventricular dimensions. The caloric and carbohydrate intake was smaller, but the fat intake was higher in AIN-93 rats. AIN-93 group also showed increased levels of ß-hydroxyacylcoenzyme A dehydrogenase and citrate synthase. In addition, serum levels of insulin and cardiac levels of malondialdehyde, metalloproteinases-2 and -9, and TNF-α and IFN-γ were decreased in the AIN-93 group. CONCLUSION: AIN-93 diet increased early mortality, while attenuated the chronic remodeling process after experimental coronary occlusion. Therefore, this diet has biological effects and should be use with attention in this model.

Influence of taurine on cardiac remodeling induced by tobacco smoke exposure.

BACKGROUND/AIMS: To investigate the effect of taurine on cardiac remodeling induced by smoking. METHODS: In the first step, rats were allocated into two groups: Group C (n = 14): control; Group T (n = 14): treated with taurine (3% in drinking water), for three months. In the second step, rats were allocated into two groups: Group ETS (n = 9): rats exposed to tobacco smoke; Group ETS-T (n = 9): rats exposed to tobacco smoke and treated with taurine for two months. RESULTS: After three months, taurine presented no effects on morphological or functional variables of normal rats assessed by echocardiogram. On the other hand, after two months, ETS-T group presented higher LV wall thickness (ETS = 1.30 (1.20-1.42); ETS-T = 1.50 (1.40-1.50); p = 0.029), E/A ratio (ETS = 1.13 ± 0.13; ETS-T = 1.37 ± 0.26; p = 0.028), and isovolumetric relaxation time normalized for heart rate (ETS = 53.9 ± 4.33; ETS-T = 72.5 ± 12.0; p < 0.001). The cardiac activity of the lactate dehydrogenase was higher in the ETS-T group (ETS = 204 ± 14 nmol/mg protein; ETS-T = 232 ± 12 nmol/mg protein; p < 0.001). ETS-T group presented lower levels of phospholamban (ETS = 1.00 ± 0.13; ETS-T = 0.82 ± 0.06; p = 0.026), phosphorylated phospholamban at Ser16 (ETS = 1.00 ± 0.14;ETS-T = 0.63 ± 0.10;p = 0.003), and phosphorylated phosfolamban/phospholamban ratio (ETS = 1.01 ± 0.17; ETS-T = 0.77 ± 0.11; p = 0.050). CONCLUSION: In normal rats, taurine produces no effects on cardiac morphological or functional variables. On the other hand, in rats exposed to cigarette smoke, taurine supplementation increases wall thickness and worsens diastolic function, associated with alterations in calcium handling protein and cardiac energy metabolism.

Relevância do padrão de remodelamento ventricular no modelo de infarto do miocárdio em ratos / Relevance of the ventricular remodeling pattern in the model of myocardial infarction in rats

FUNDAMENTO: A relevância do padrão de remodelamento no modelo de ratos infartados não é conhecida. OBJETIVO: Analisar a presença de diferentes padrões de remodelamento nesse modelo e suas implicações funcionais. MÉTODOS: Ratos infartados (n=46) foram divididos de acordo com o padrão de geometria, analisado pelo ecocardiograma: normal (índice de massa normal e espessura relativa normal), remodelamento concêntrico (índice de massa normal e espessura relativa aumentada), hipertrofia concêntrica (índice de massa aumentado e espessura relativa aumentada) e hipertrofia excêntrica (índice de massa aumentado e espessura relativa normal). Os dados estão em mediana e intervalo interquartil. RESULTADOS: Ratos infartados apresentaram apenas dois dos quatro padrões de geometria: padrão normal (15 por cento) e hipertrofia excêntrica - HE (85 por cento). Os grupos de padrão normal e HE não apresentaram diferenças nos valores de fração de variação de área (Normal = 32,1 - 28,8 a 50,7; HE = 31,3 - 26,5 a 36,7; p=0,343). Dos animais infartados, 34 (74 por cento) apresentaram disfunção sistólica, detectada pela fração de variação de área. Considerando os dois padrões de geometria, 77 por cento dos animais com hipertrofia excêntrica e 57 por cento com geometria normal apresentaram disfunção sistólica (p=0,355). A espessura relativa da parede, os padrões de geometria e o índice de massa não foram fator de predição de disfunção ventricular (p>0,05). Por outro lado, o tamanho do infarto foi fator de predição de disfunção ventricular na análise univariada (p<0,001) e na análise multivariada (p=0,004). CONCLUSÃO: Ratos submetidos à oclusão coronariana apresentam dois diferentes padrões de remodelamento, os quais não se constituem em fator de predição de disfunção ventricular.

BACKGROND: The relevance of the remodeling pattern in the model of infarcted rats is not known. OBJECTIVE: To analyze the presence of different patterns of remodeling in this model and its functional implications. METHODS: Infarcted rats (n=47) have been divided according to the geometry pattern, analyzed by echocardiogram: normal (normal mass index and normal relative thickness), concentric remodeling (normal mass index and increased relative thickness), concentric hypertrophy (increased mass index and increased relative thickness) and eccentric hypertrophy (increased mass index and normal relative thickness). Data are median and interquartile range. RESULTS: Infarcted rats showed only two of the four geometric patterns: normal pattern (15 percent) and eccentric hypertrophy - EH (85 percent). Groups of normal pattern and EH showed no differences in the values of fractional area change (Normal = 32.1 - 28.8 to 50.7; EH = 31.3 - 26.5 to 36.7; p = 0.343). Out of the infarcted animals, 34 (74 percent) had systolic dysfunction, detected by fractional area change. Considering these two geometry patterns, 77 percent of animals with eccentric hypertrophy and 57 percent with normal geometry presented systolic dysfunction (p=0.355). The relative wall thickness, the geometric patterns and the body mass index were not predictors of ventricular dysfunction (p> 0.05). On the other hand, infarct size was a predictive factor for ventricular dysfunction in univariate analysis (p<0.001) and multivariate analysis (p = 0.004). CONCLUSION: Rats that underwent coronary occlusion showed two different patterns of remodeling, which do not constitute a predictor of ventricular dysfunction.

Relevance of the ventricular remodeling pattern in the model of myocardial infarction in rats.

BACKGROUND: The relevance of the remodeling pattern in the model of infarcted rats is not known. OBJECTIVE: To analyze the presence of different patterns of remodeling in this model and its functional implications. METHODS: Infarcted rats (n=47) have been divided according to the geometry pattern, analyzed by echocardiogram: normal (normal mass index and normal relative thickness), concentric remodeling (normal mass index and increased relative thickness), concentric hypertrophy (increased mass index and increased relative thickness) and eccentric hypertrophy (increased mass index and normal relative thickness). Data are median and interquartile range. RESULTS: Infarcted rats showed only two of the four geometric patterns: normal pattern (15%) and eccentric hypertrophy - EH (85%). Groups of normal pattern and EH showed no differences in the values of fractional area change (Normal = 32.1 - 28.8 to 50.7; EH = 31.3 - 26.5 to 36.7; p = 0.343). Out of the infarcted animals, 34 (74%) had systolic dysfunction, detected by fractional area change. Considering these two geometry patterns, 77% of animals with eccentric hypertrophy and 57% with normal geometry presented systolic dysfunction (p=0.355). The relative wall thickness, the geometric patterns and the body mass index were not predictors of ventricular dysfunction (p> 0.05). On the other hand, infarct size was a predictive factor for ventricular dysfunction in univariate analysis (p<0.001) and multivariate analysis (p = 0.004). CONCLUSION: Rats that underwent coronary occlusion showed two different patterns of remodeling, which do not constitute a predictor of ventricular dysfunction.