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Background: Orange juice (OJ) is rich in polyphenols with anti-inflammatory and antioxidant properties. After myocardial infarction (MI), complex changes occur in cardiac structure and function, which is known as cardiac remodeling (CR). Oxidative stress and inflammation can modulate this process. We hypothesized that the consumption of OJ attenuates the CR after MI., Objectives: To evaluate the influence of OJ on CR after MI by analysis of functional, morphological, oxidative stress, inflammation, and energy metabolism variables., Methods: A total of 242 male rats weighing 200-250 g were submitted to a surgical procedure (coronary artery ligation or simulated surgery). Seven days after surgery, survivors were assigned to one of the four groups 1) SM, sham animals with water and maltodextrin (n= 20); 2) SOJ, sham animals with OJ (n= 20); 3) IM, infarcted animals with water and maltodextrin (n= 40); and 4) IOJ, infarcted animals with OJ (n = 40). Statistical analysis was performed by the two-way ANOVA supplemented by Holm-Sidak. Results are presented as mean ± standard deviation, the level of significance adopted was 5%., Results: After 3 months, MI led to left ventricular (LV) hypertrophy, with systolic and diastolic dysfunction, and increased oxidative stress and inflammatory mediators. OJ intake reduced LV cavity and improved systolic and diastolic function. The OJ animals presented lower activity of glutathione peroxidase and higher expression of heme-oxygenase-1 (HO-1)., Conclusion: OJ attenuated CR in infarcted rats and HO-1 may be play an important role in this process.

Background: Vitamin D (VD) has been shown to play an important role in cardiac function. However, this vitamin exerts a biphasic "dose response" curve in cardiovascular pathophysiology and may cause deleterious effects, even in non-toxic doses. VD exerts its cellular functions by binding to VD receptor. Additionally, it was identified that the thioredoxin-interacting protein (TXNIP) expression is positively regulated by VD. TXNIP modulate different cell signaling pathways that may be important for cardiac remodeling., Objective: To evaluate whether VD supplementation lead to cardiac remodeling and if TXNIP and thioredoxin (Trx) proteins are associated with the process., Methods: A total of 250 Male Wistar rats were allocated into three groups: control (C, n=21), with no VD supplementation; VD3 (n = 22) and VD10 (n=21), supplemented with 3,000 and 10,000 IU of VD/ kg of chow respectively, for two months. The groups were compared by one-way analysis of variance (ANOVA) and Holm-Sidak post hoc analysis, (variables with normal distribution), or by Kruskal-Wallis test and Dunn's test post hoc analysis. The significance level for all tests was 5%., Results: TXNIP protein expression was higher and Trx activity was lower in VD10. The animals supplemented with VD showed increased lipid hydroperoxide and decreased superoxide dismutase and glutathione peroxidase. The protein Bcl-2 was lower in VD10. There was a decrease in fatty acid β-oxidation, tricarboxylic acid cycle and electron transport chain with shift to increase in glycolytic pathway., Conclusion: VD supplementation led to cardiac remodeling and this process may be modulated by TXNIP and Trx proteins and consequently oxidative stress.

Background: Physical exercise has been considered an important non-pharmacological therapy for the prevention and treatment of cardiovascular diseases. However, its effects on minor cardiac remodeling are not clear., Objective: To evaluate the influence of aerobic exercise on the functional capacity, cardiac structure, left ventricular (LV) function, and gene expression of NADPH oxidase subunits in rats with small-sized myocardial infarction (MI)., Methods: Three months after MI induction, Wistar rats were divided into three groups: Sham; sedentary MI (MI-SED); and aerobic exercised MI (MI-AE). The rats exercised on a treadmill three times a week for 12 weeks. An echocardiogram was performed before and after training. The infarction size was evaluated by histology, and gene expression was assessed by RT-PCR. The significance level for statistical analysis was set at 5%., Results: Rats with MI lower than 30% of the LV total area were included in the study. Functional capacity was higher in MI-AE than in Sham and MI-SED rats. The infarction size did not differ between groups. Infarcted rats had increased LV diastolic and systolic diameter, left atrial diameter, and LV mass, with systolic dysfunction. Relative wall thickness was lower in MI-SED than in the MI-AE and Sham groups. Gene expression of the NADPH oxidase subunits NOX2, NOX4, p22phox, and p47phox did not differ between groups., Conclusion: Small-sized MI changes cardiac structure and LV systolic function. Late aerobic exercise is able to improve functional capacity and cardiac remodeling by preserving the left ventricular geometry. NADPH oxidase subunits gene expression is not involved in cardiac remodeling or modulated by aerobic exercise in rats with small-sized MI.

Background: Euterpe oleracea Mart. (açaí) is a fruit with high antioxidant capacity and could be an adjuvant strategy to attenuate ischemia-reperfusion injury., Objective: To evaluate the influence of açaí in global ischemia-reperfusion model in rats., Methods: Wistar rats were assigned to 2 groups: Control (C: receiving standard chow; n = 9) and Açaí (A: receiving standard chow supplemented with 5% açaí; n = 10). After six weeks, the animals were subjected to the global ischemia-reperfusion protocol and an isolated heart study to evaluate left ventricular function. Level of significance adopted: 5%., Results: There was no difference between the groups in initial body weight, final body weight and daily feed intake. Group A presented lower lipid hydroperoxide myocardial concentration and higher catalase activity, superoxide dismutase and glutathione peroxidase than group C. We also observed increased myocardial activity of b-hydroxyacyl coenzyme-A dehydrogenase, pyruvate dehydrogenase, citrate synthase, complex I, complex II and ATP synthase in the A group as well as lower activity of the lactate dehydrogenase and phosphofructokinase enzymes. The systolic function was similar between the groups, and the A group presented poorer diastolic function than the C group. We did not observe any difference between the groups in relation to myocardial infarction area, total and phosphorylated NF-kB, total and acetylated FOXO1, SIRT1 and Nrf-2 protein expression., Conclusion: despite improving energy metabolism and attenuating oxidative stress, açai supplementation did not decrease the infarcted area or improve left ventricular function in the global ischemia-reperfusion model.

Background: Tobacco smoke exposure is an important risk factor for cardiac remodeling. Under this condition, inflammation, oxidative stress, energy metabolism abnormalities, apoptosis, and hypertrophy are present. Pentoxifylline has anti‑inflammatory, anti-apoptotic, anti-thrombotic and anti-proliferative properties., Objective: The present study tested the hypothesis that pentoxifylline would attenuate cardiac remodeling induced by smoking., Methods: Wistar rats were distributed in four groups: Control (C), Pentoxifylline (PX), Tobacco Smoke (TS), and PX-TS. After two months, echocardiography, invasive blood pressure measurement, biochemical, and histological studies were performed. The groups were compared by two-way ANOVA with a significance level of 5%., Results: TS increased left atrium diameter and area, which was attenuated by PX. In the isolated heart study, TS lowered the positive derivate (+dp/dt), and this was attenuated by PX. The antioxidants enzyme superoxide dismutase and glutathione peroxidase were decreased in the TS group; PX recovered these activities. TS increased lactate dehydrogenase (LDH) and decreased 3-hydroxyacyl Coenzyme A dehydrogenases (OH-DHA) and citrate synthase (CS). PX attenuated LDH, 3-OH-DHA and CS alterations in TS-PX group. TS increased IL-10, ICAM-1, and caspase-3. PX did not influence these variables., Conclusion: TS induced cardiac remodeling, associated with increased inflammation, oxidative stress, apoptosis, and changed energy metabolism. PX attenuated cardiac remodeling by reducing oxidative stress and improving cardiac bioenergetics, but did not act upon cardiac cytokines and apoptosis.

Background: Heart failure prediction after acute myocardial infarction may have important clinical implications., Objective: To analyze the functional echocardiographic variables associated with heart failure in an infarction model in rats., Methods: The animals were divided into two groups: control and infarction. Subsequently, the infarcted animals were divided into groups: with and without heart failure. The predictive values were assessed by logistic regression. The cutoff values predictive of heart failure were determined using ROC curves., Results: Six months after surgery, 88 infarcted animals and 43 control animals were included in the study. Myocardial infarction increased left cavity diameters and the mass and wall thickness of the left ventricle. Additionally, myocardial infarction resulted in systolic and diastolic dysfunction, characterized by lower area variation fraction values, posterior wall shortening velocity, E-wave deceleration time, associated with higher values of E / A ratio and isovolumic relaxation time adjusted by heart rate. Among the infarcted animals, 54 (61%) developed heart failure. Rats with heart failure have higher left cavity mass index and diameter, associated with worsening of functional variables. The area variation fraction, the E/A ratio, E-wave deceleration time and isovolumic relaxation time adjusted by heart rate were functional variables predictors of heart failure. The cutoff values of functional variables associated with heart failure were: area variation fraction < 31.18%; E / A > 3.077; E-wave deceleration time < 42.11 and isovolumic relaxation time adjusted by heart rate < 69.08., Conclusion: In rats followed for 6 months after myocardial infarction, the area variation fraction, E/A ratio, E-wave deceleration time and isovolumic relaxation time adjusted by heart rate are predictors of heart failure onset.

Cardiac remodeling is defined as a group of molecular, cellular and interstitial changes that manifest clinically as changes in size, mass, geometry and function of the heart after injury. The process results in poor prognosis because of its association with ventricular dysfunction and malignant arrhythmias. Here, we discuss the concepts and clinical implications of cardiac remodeling, and the pathophysiological role of different factors, including cell death, energy metabolism, oxidative stress, inflammation, collagen, contractile proteins, calcium transport, geometry and neurohormonal activation. Finally, the article describes the pharmacological treatment of cardiac remodeling, which can be divided into three different stages of strategies: consolidated, promising and potential strategies.

Background: Abdominal obesity is an important cardiovascular risk factor. Therefore, identifying the best method for measuring waist circumference (WC) is a priority., Objective: To evaluate the eight methods of measuring WC in patients with acute coronary syndrome (ACS) as a predictor of cardiovascular complications during hospitalization., Methods: Prospective study of patients with ACS. The measurement of WC was performed by eight known methods: midpoint between the last rib and the iliac crest (1), point of minimum circumference (2); immediately above the iliac crest (3), umbilicus (4), one inch above the umbilicus (5), one centimeter above the umbilicus (6), smallest rib and (7) the point of greatest circumference around the waist (8). Complications included: angina, arrhythmia, heart failure, cardiogenic shock, hypotension, pericarditis and death. Logistic regression tests were used for predictive factors., Results: A total of 55 patients were evaluated. During the hospitalization period, which corresponded on average to seven days, 37 (67%) patients had complications, with the exception of death, which was not observed in any of the cases. Of these complications, the only one that was associated with WC was angina, and with every cm of WC increase, the risk for angina increased from 7.5 to 9.9%, depending on the measurement site. It is noteworthy the fact that there was no difference between the different methods of measuring WC as a predictor of angina., Conclusion: The eight methods of measuring WC are also predictors of recurrent angina after acute coronary syndromes.

Background: The effects of modern therapy on functional recovery after acute myocardial infarction (AMI) are unknown., Objectives: To evaluate the predictors of systolic functional recovery after anterior wall AMI in patients undergoing modern therapy (reperfusion, aggressive platelet antiaggregant therapy, angiotensin-converting enzyme inhibitors and beta-blockers)., Methods: A total of 94 consecutive patients with AMI with ST-segment elevation were enrolled. Echocardiograms were performed during the in-hospital phase and after 6 months. Systolic dysfunction was defined as ejection fraction value < 50%., Results: In the initial echocardiogram, 64% of patients had systolic dysfunction. Patients with ventricular dysfunction had greater infarct size, assessed by the measurement of total and isoenzyme MB creatine kinase enzymes, than patients without dysfunction. Additionally, 24.5% of patients that initially had systolic dysfunction showed recovery within 6 months after AMI. Patients who recovered ventricular function had smaller infarct sizes, but larger values of ejection fraction and E-wave deceleration time than patients without recovery. At the multivariate analysis, it can be observed that infarct size was the only independent predictor of functional recovery after 6 months of AMI when adjusted for age, gender, ejection fraction and E-wave deceleration time., Conclusion: In spite of aggressive treatment, systolic ventricular dysfunction remains a frequent event after the anterior wall myocardial infarction. Additionally, 25% of patients show functional recovery. Finally, infarct size was the only significant predictor of functional recovery after six months of acute myocardial infarction.

Background: Intervention studies have shown an increased mortality in patients who received beta-carotene. However, the mechanisms involved in this phenomenon are still unknown., Objective: Evaluate the influence of beta-carotene on oxidative stress and the expression of connexin 43 in rat hearts., Methods: Wistar rats, weighing approximately 100 g, were allocated in two groups: CONTROL GROUP (n=30), that received the diet routinely used in our laboratory, and Beta-Carotene Group (n = 28), which received beta-carotene (in crystal form, added and mixed to the diet) at a dose of 500 mg of beta-carotene/kg of diet. The animals received the treatment until they reached 200-250 g, when they were sacrificed. Samples of blood, liver and heart were collected to perform Western blotting and immunohistochemistry for connexin 43; morphometric studies, dosages of beta-carotene by high-performance liquid chromatography as well as reduced glutathione, oxidized glutathione and lipids hydroperoxides were performed by biochemical analysis., Results: Beta-carotene was detected only in the liver of Beta-Carotene Group animals (288 ± 94.7 µg/kg). Levels of reduced/oxidized glutathione were higher in the liver and heart of Beta-Carotene Group animals (liver -, Control Group: 42.60 ± 1.62; liver - Beta-Carotene Group: 57.40 ± 5.90; p = 0.04; heart: -, Control Group: 117.40 ± 1.01; heart - Beta-Carotene Group: 121.81 ± 1.32 nmol/mg protein; p = 0.03). The content of total connexin 43 was larger in Beta-Carotene Group., Conclusion: Beta-carotene demonstrated a positive effect, characterized by the increase of intercellular communication and improvement of anti-oxidizing defense system. In this model, mechanism does not explain the increased mortality rate observed with the beta-carotene supplementation in clinical studies.

Background: The relevance of left ventricular (LV) geometric pattern after myocardial infarction is not known., Objectives: To analyze the presence of different LV geometric patterns and their impact as a predictor of remodeling in patients with myocardial infarction., Methods: Patients with anterior acute myocardial infarction (n = 80) were divided according to the geometric pattern: normal (normal left ventricular mass index [LVMI] and normal relative wall thickness [RWT]), concentric remodeling (normal LVMI and increased RWT), concentric hypertrophy (increased LVMI and RWT) and eccentric hypertrophy (increased LVMI and normal RWT). After six months, echocardiographic assessment was repeated., Results: Four patients died. Of the survivors, 41 showed remodeling (R +), whereas 39 did not (R-). Considering the geometric pattern, the cases were distributed as follows: 24 patients with normal pattern, 13 with concentric remodeling, 29 with concentric hypertrophy and 14 with eccentric hypertrophy. Patients who showed remodeling had larger infarction sizes analyzed by peak CPK (R + = 4,610 (1,688-7,970), R- = 1,442 (775-4247), p <0.001) and CK-MB (R + = 441 (246 - 666), R- = 183 (101-465), p <0.001), trend towards higher prevalence of concentric remodeling (R+ = 10, R- = 3, p = 0.08) and lower prevalence of eccentric hypertrophy (R + = 2 R- = 12, p = 0.006). In the multivariate regression analysis, infarction size was a predictor (OR = 1.01, p = 0.020) and eccentric hypertrophy was a protective factor (OR = 0.189, p = 0.046) of ventricular remodeling after coronary occlusion., Conclusion: The LV geometric pattern of can have an impact on the remodeling process in patients with myocardial infarction.

Background: The role of serum metalloproteinases (MMP) after myocardial infarction (MI) is unknown., Objective: The aim of this study was to evaluate the role of serum MMP-2 and -9 as predictors of ventricular remodeling six months after anterior MI., Methods: We prospectively enrolled patients after their first anterior MI. MMP activity was assayed 12 to 72 hours after the MI. An echocardiogram was performed during the hospitalization and six months later., Results: We included 29 patients; 62% exhibited ventricular remodeling. The patients who exhibited remodeling had higher infarct size based on creatine phosphokinase (CPK) peak values (p = 0.037), higher prevalence of in-hospital congestive heart failure (p = 0.004), and decreased ejection fraction (EF) (p = 0.007). The patients with ventricular remodeling had significantly lower serum levels of inactive MMP-9 (p = 0.007) and significantly higher levels of the active form of MMP-2 (p = 0.011). In a multivariate logistic regression model, adjusted by age, CPK peak, EF and prevalence of heart failure, MMP-2 and -9 serum levels remained associated with remodeling (p = 0.033 and 0.044, respectively)., Conclusions: Higher serum levels of inactive MMP-9 were associated with the preservation of left ventricular volumes, and higher serum levels of the active form of MMP-2 were a predictor of remodeling 6 months after MI.

Background: In a previous study utilizing the rat model, exposure to tobacco smoke for 5 weeks increased survival after AMI, despite similar age and infarct size between the smokers and nonsmokers, and absence of reperfusion., Objective: Thus, this study aimed to analyze the effects of exposure to tobacco smoke on intensity, distribution or phosphorylation of connexin 43 in the rat heart., Methods: Wistar rats weighing 100 g were randomly allocated into 2 groups: 1) CONTROL (n = 25); 2) Exposed to tobacco smoke (ETS), n = 23. After 5 weeks, left ventricular morphometric analysis, immunohistochemistry and western blotting for connexin 43 (Cx43) were performed., Results: Collagen volume fraction, cross-sectional areas, and ventricular weight were not statistically different between control and ETS. ETS showed lower stain intensity of Cx43 at intercalated disks (, Control: 2.32 ± 0.19; ETS: 1.73 ± 0.18; p = 0.04). The distribution of CX43 at intercalated disks did not differ between the groups (, Control: 3.73 ± 0.12; ETS: 3.20 ± 0.17; p = 0.18). ETS rats showed higher levels of dephosphorylated form of Cx43 (CONTROL: 0.45 ± 0.11; ETS: 0.90 ± 0.11; p = 0.03). On the other hand, total Cx43 did not differ between control and ETS groups (, Control: 0.75 ± 0.19; ETS: 0.93 ± 0.27; p = 0.58)., Conclusion: Exposure to tobacco smoke resulted in cardiac gap junction remodeling, characterized by alterations in the quantity and phosphorylation of the Cx43, in rats hearts. This finding could explain the smoker's paradox observed in some studies.

Over the last decade, several studies were conducted on the gastrointestinal changes associated to chronic heart failure. This article presents a literature review on the physiopathology and clinical consequences of pathological digestive changes of heart failure patients. Structural and functional abnormalities of the gastrointestinal tract, such as edema of absorptive mucosa and intestinal bacterial overgrowth, have been leading to serious clinical consequences. Some of these consequences are cardiac cachexia, systemic inflammatory activation and anemia. These conditions, alone or in combination, may lead to worsening of the pre-existing ventricular dysfunction. Although currently there is no therapy specifically earmarked for gastrointestinal changes associated to heart failure, the understanding of digestive abnormalities is germane for the prevention and management of systemic consequences.

Background: The prediction of the ventricular remodeling process after acute myocardial infarction (AMI) may have important clinical implications., Objective: To analyze echocardiographic variables predictors of remodeling in the infarction model in rats. MEHTODS: The animals underwent echocardiography in two moments, five days and three months after infarction (AMI group) or sham surgery (control group). Linear regression was used to identify the echocardiographic variables on the fifth day after the infarction, which were predictive of remodeling after three months of coronary occlusion. We considered as a criterion of remodeling in this study, the values of left ventricular diastolic diameter (LVDD) after three months of infarction., Results: The infarction induced increase in the left chambers, associated with changes in systolic and diastolic functions. The variables body weight, left ventricular wall stress index (LVWSI), systolic area (SA), diastolic area (DA), LVDD, left ventricular systolic diameter (LVSD), area variation fraction (AVF), ejection fraction (EF), percent of endocardial shortening (%Short), posterior wall shortening velocity (PWSV) and infarct size assessed five days after infarction were predictors of LVDD after three months. At the multivariate regression analysis, we included the size of infarction, the LVWSI and PWSV. The LVWSI (coefficient: 4.402, standard error: 2.221, p = 0.05), but not the size of infarction and PWSV, was a predictor of remodeling after three months of infarction., Conclusion: LVPSI was an independent predictor of remodeling three months after the myocardial infarction and could be included in the clinical stratification after the coronary occlusion.

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.

Background: The left ventricular (LV) sphericity is a factor associated with ventricular dysfunction, but it is not well-characterized in the experimental infarction model in rats., Objective: To analyze the association between the sphericity index (SI), the ventricular function and the infarcted area in an experimental rat model., Methods: Six months after the infarction (AMI, n=33) or simulated surgery (SHAM, n=18), the animals were submitted to an echocardiogram. The SI was obtained through the ratio between the diastolic areas at the LV long axis and the short axis., Results: The AMI group presented the lowest index of sphericity (1.32 x 0.23 vs 1.57 x 0.33; p=0.002), systolic function and relative thickness (0.13 x 0.003 vs 0.18 x 0.04; p<0.001) and the highest index of parietal stress (1.27 x 0.33 vs 0.88 x 0.25; p<0.001). There was a significant correlation between the infarct size and sphericity (p=0.046). At the linear regression analysis, the infarct size (p=0.014), but not the sphericity (p=0.683) and the parietal stress (p=0.176), was the predictive factor of the systolic function. Eccentric remodeling (p=0.011), but not sphericity (p=0.183) or the infarct size (p=0.101), was a predictive factor of parietal stress. Additionally, the infarct size (p=0.046), but not the eccentric remodeling (0.705), was a predictive factor of sphericity. The infarct size (p=0.015) and the parietal stress (p=0.011), but not the sphericity (p=0.705), were the predictors of eccentric remodeling., Conclusion: The sphericity is associated, but it is not a determinant factor of parietal stress, of eccentric remodeling and ventricular systolic function in an experimental infarction model in rats.

Background: The relevance of the remodeling pattern in the model of rats exposed to cigarette smoke is not known., Objective: Analyzing the presence of different remodeling patterns in this model and its relation with the ventricular function., Methods: Smoking rats (n=47) have been divided according to the geometry pattern, analyzed by echocardiogram: normal (normal mass index and normal relative wall thickness), concentric remodeling (normal mass index and increased relative wall thickness), concentric hypertrophy (increased mass index and increased relative wall thickness) and eccentric hypertrophy (increased mass index and normal relative wall thickness)., Results: Smoking rats presented one of the following geometry patterns: normal pattern, 51%; eccentric hypertrophy; 32%; concentric hypertrophy, 13% and concentric remodeling, 4%. The normal and eccentric hypertrophy groups presented smaller ejection fraction values and fractional shortening than the concentric hypertrophy group. Thirteen animals (28%) presented systolic dysfunction detected by the ejection fraction and by fractional shortening. In the single regression analysis, geometry patterns and mass index could not predict ventricular dysfunction (p<). On the other hand, the increased relative thickness of the wall could predict ventricular dysfunction in the single regression analysis (p<0.001) and in the multiple regression analysis after adjustment to the mass index (p=0.003)., Conclusion: Rats exposed to cigarette smoke presented one of the four different remodeling patterns. Among the geometric variables analyzed, only the increased relative thickness of the left ventricle wall could predict ventricular dysfunction in this model.

One of the most often used strategies to study the physiopathological alterations caused by coronary occlusion is the use of the experimental infarction model in rats. Among other factors, this is due to the similarities in the physiopathological alterations that occur after the infarction in humans. One must consider, however, that this model has characteristics that can hinder the use as well as the interpretation of eventual outcomes. Thus, this review aims at analyzing the main characteristics of the experimental infarction model in rats, discussing the coronary occlusion technique, the consequences and the methods of morphological and functional assessment of the infarction and its clinical implications.

Background: The mechanisms involved in the biggest remodeling caused by the post-infarct beta-carotene are unknown., Objective: To analyze the role of lipoperoxidation in the ventricular remodeling after infarct of the myocardium in rats supplemented with beta-carotene., Methods: Rats were infarcted and divided into two groups: C (control) and BC (500mg/kg/regimen). After six months, echocardiogram and biochemical evaluation were performed. The t test was used, with 5% significance., Results: The animals from BC group presented highest means of the diastolic (C = 1.57 +/- 0.4 mm(2)/g, BC = 2.09 +/- 0.3 mm(2)/g; p < 0.001) and systolic (C = 1.05 +/- 0.3 mm(2)/g, BC = 1.61 +/- 0.3 mm(2)/g; p < 0.001) areas of LV, which were adapted according to the rat's body weight. The systolic function of LV, evaluated by the area variation fraction, was lower in the animals supplemented with beta-carotene (C = 31.9 +/- 9.3%, BC = 23.6 +/- 5.1%; p = 0.006). The animals supplemented with beta-carotene presented higher values of the E/A relation (C = 2.7 +/- 2.5, BC = 5.1 +/- 2.8; p = 0.036). No differences were found between the groups concerning the cardiac levels of the GSH (C = 21 +/- 8 nmol/mg of protein, BC = 37 +/- 15 nmol/mg of protein; p = 0.086), GSSG (C = 0.4 (0.3-0.5) nmol/g of protein, BC = 0.8 (0.4-1.0; p = 0.19) of protein; p = 0.246) and lipoperoxides (C = 0.4 +/- 0.2 nmol/mg of tissue, BC = 0.2 +/- 0.1 nmol/mg of tissue; p = 0.086)., Conclusion: The highest remodeling in infarcted rats supplemented with beta-carotene does not depend on the lipoperoxidation.

Background: The role of the adrenergic system on ventricular remodeling induced by cigarette smoking is unknown., Objectives: To investigate the influence of propranolol on ventricular remodeling induced by exposure to tobacco smoke., Methods: Rats were divided into three groups: 1) C, n=10--control group; 2) F, n=10--animals exposed to tobacco smoke; 3) BB, n=10--animals receiving propranolol and exposed to tobacco smoke (40 mg/kg/day). After 2 months, the animals underwent echocardiographic and morphometric analyses. One-way ANOVA (mean +/- standard deviation) or the Kruskal-Wallis test (median and interquartile interval) was used., Results: Group BB showed a lower heart rate than group F (C = 358 +/- 74 bpm, F = 374 +/- 53 bpm, BB = 297 +/- 30; P = 0.02). Group F showed greater end-diastolic diameters (C = 18.6 +/- 3.4 mm/kg, F = 22.8 +/- 1.8 mm/kg, BB = 21.7 +/- 1.8 mm/kg; P = 0.003) and left ventricular (LV) end-systolic diameters (C = 8.6 +/- 2.1 mm/kg, F = 11.3 +/- 1.3 mm/kg, BB = 9.9 +/- 1.2 mm/kg; P = 0.004), adjusted for body weight (BW) and a tendency towards a lower ejection fraction (C = 0.90 +/- 0.03, F = 0.87 +/- 0.03, BB =0.90 +/- 0.02; P = 0.07) than group C. Group BB showed a tendency towards a lower LV/BW ratio than group F (C = 1.94 (1.87 - 1.97), F = 2.03 (1.9-2.1) mg/g, BB = 1.89 (1.86-1.94); P = 0.09)., Conclusion: Administration of propranolol attenuated some of the variables of ventricular remodeling induced by the exposure to tobacco smoke in rats.

Thiamine deficiency may present four classic clinical forms: peripheral polyneuropathy, anorexia and muscular weakness (dry beriberi); high output heart failure with signs of congestion (wet beriberi); beriberi associated with shock (Shoshin beriberi) and Wernicke's encephalopathy. In this report we describe a picture that is suggestive of severe pulmonary hypertension and cor pulmonale, with jugular stasis, congestive hepatitis and generalized edema that reversed completely after the administration of thiamine.

Objective: To analyze the effects of beta-carotene on the ventricular remodeling process following myocardial infarction (MI) in rats exposed to cigarette smoke., Methods: After acute myocardial infarction (AMI), the animals were divided into four groups: 1) Group C, 24 animals that were given standard diet; 2) Group BC, 26 animals that were given beta-carotene; 3) Group ECS, 26 animals that were given standard diet and were exposed to cigarette smoke; and 4) Group BC+ECS, 20 animals that were given beta-carotene and were exposed to cigarette smoke. After six months, a morphofunctional study was performed. We used a 5% significance level., Results: As regards diastolic areas (DA) and systolic areas (SA), the values for the BC group were higher than those for the C group. If DA/body weight (BW) and SA/BW are considered, the values for group BC+ECS were higher than the values for group C. As regards the fractional area change, we observed significant differences between ECS (lower values) and C (higher values) and between BC (lower values) and C (higher values). Differences between groups regarding infarction size were not observed. The ECS group presented higher values for myocyte cross-section area (MCA) than control animals. Additionally, the BC+ECS group presented higher MCA values than the BC, ECS and C groups., Conclusion: After myocardial infarction, smoking and beta-carotene intensified the heart remodeling process; harmful effects of the remodeling process were heightened when the two treatments were used in conjunction.

Objective: To evaluate the differences between three methods for the measurement of experimental infarction in rats in comparison to the traditional method., Methods: Histological analysis of the infarction area (AREA), histological analysis of the internal cavity perimeter (PER) and echocardiogram analysis of the internal perimeter (ECHO) were compared to the traditional method (histological analysis of the epicardial and endocardial circumferences of the infarction region - CIR). Repeated ANOVA measurements were used in conjunction with the Dunn multiple comparison test, the Bland and Altman concordance method and the Spearman correlation test. Significance was established as p < 0.05., Results: The data of 122 animals were analyzed, 3 to 6 months after the infarction. Infarction size assessments revealed differences between CIR and the other three methods (p < 0.001): CIR = 42.4% (35.9-48.8), PER = 50.3% (39.1-57.0), AREA = 27.3% (20.2-34.3), ECHO = 46.1% (39.9-52.6). Therefore, measurement by area underestimated the infarct size by 15%, whereas the echocardiogram and histological internal perimeter measurements overestimated the infarct size by 4% and 5%, respectively. In relation to ECHO and PER, even though the difference between the methods was only 1.27%, the concordance interval ranged from 24.1% to -26.7%, suggesting a low level of concordance between the methods. In relation to associations, statistically significant correlations were found between: CIR and PER (r = 0.88 and p < 0.0001); CIR and AREA (r = 0.87 and p < 0.0001) and CIR and ECHO (r = 0.42 and p < 0.0001)., Conclusion: Despite the high level of correlation, there was a low level of concordance between the methods to define infarct size.

Objective: To evaluate the role of cigarette smoke exposure (CSE) on ventricular remodeling following acute myocardial infarction (AMI)., Methods: Rats were submitted to myocardial infarction and divided into two groups: C (control, n = 31) and F (CSE: 40 cigarettes/day, n = 22). After 6 months, the survivors were submitted to echocardiogram, functional study with isolated heart, and morphometric analysis. For comparison purposes, we used the t test (mean +/- standard deviation) or the Mann-Whitney test (with median and 25th and 75th percentiles)., Results: The CSE animals tended to have larger diastolic (C = 1.5 +/- 0.4 mm2, F = 1.9 +/- 0.4 mm2; p = 0.08) and systolic (C = 1.05 +/- 0.3 mm2, F = 1.32 +/- 0.4 mm2; p = 0.08) left ventricular(LV) areas. The systolic function of the LV, assessed according to the fractional area change, tended to be impaired in CSE animals (C = 31.9 +/- 9.3%, F = 25.5 +/- 7.6%; p = 0.08). The dp/dt values for CSE animals were statistically lower (C = 1474 +/- 397 mmHg, F = 916 +/- 261 mmHg; p = 0.02) than for control animals. The CSE animals presented higher right ventricle (RV) weight adjusted for body weight (C = 0.8 +/- 0.3 mg/g, F = 1.3 +/- 0.4 mg/g; p = 0.01), higher content of water in lungs (C = 4.8 (4.3-4.8)%, F = 5.4 (5.1-5.5); p = 0.03), and larger LV myocyte cross-sectional areas (C = 239.8 +/- 5.8 microm2, F = 253.9 +/- 7.9 microm2; p = 0.01)., Conclusion: Cigarette smoke exposure intensifies ventricular remodeling following acute myocardial infarction.

Objective: To compare cardiac structural changes in experimental pressure and volume overload models., Methods: The study analysis included renovascular hypertensive rats (RVH, n = 8), normotensive rats with volume overload caused by an aortocaval fistula (ACF, n = 10) and control rats (CONT, n = 8). After four weeks, tail cuff blood pressure (SBP) was recorded. Rats were killed, the hearts were excised and the right and left ventricles (RV&LV) were weighed (RVW&LVW). Using histological sections, myocyte cross sectional areas (MA). LV wall thickness (LVWT) LV cavity diameter (LVD), normalized LVWT (LVWT/LVD) and collagen volume fraction (CVF) were measured. The comparisons were made using the ANOVA and Tukey test for a significance level of 5%., Results: Tail cuff blood pressure (mmHg) was higher in the RVH group (RVH = 187 +/- 22; CONT = 125 +/- 10; ACF = 122 +/- 6, p < 0.05). LV hypertrophy was observed in the RVH and ACF groups. The ACF group presented a significant increase in size of LVD, compared to CONT and RVH. The absolute and normalized ventricular wall thickness were similar among the groups. The RVH group presented a significant increase in CVF compared to CONT group and ACF group., Conclusion: Cardiac remodeling patterns following volume or pressure overload are distinct, suggesting that their implications on ventricular dysfunction are not interchangeable.

Objective: To assess the role of the AT1 receptor blocker and the angiotensin-converting enzyme inhibitor in cardiac remodeling induced by aortic stenosis in rats., Methods: Wistar rats were divided into the following 4 groups: 1) C--control (n=13); 2) AoS--aortic stenosis (n=11); 3) LIS--AoS treated with lisinopril, 20 mg/kg/day (n=11); and 4) LOS--AoS treated with losartan, 40 mg/kg/day (n=9). The treatments were initiated 3 days before surgery. After 6 weeks, the animals underwent echocardiographic study, and quantification of the hydroxyproline (HOP) concentration and the left ventricular (LV) myocyte cross-sectional area (CSA)., Results: Aortic stenosis induced an increase in left ventricular wall thickness. The LIS and LOS groups showed no difference as compared with the control group. The AoS and LIS rats had greater left atrial diameters than the control rats did, while no difference was observed in the LOS animals. The AoS animals had greater values of shortening percentage than control animals did. This fact was modified with neither LIS nor LOS. The cross-sectional area of the animals in the AoS group was greater than that in the control group. However, treatment with LOS and LIS attenuated the AoS-induced increase in area. Aortic stenosis caused an increase in HOP concentration, while the LOS group showed no difference as compared with the control group., Conclusion: Blockade of the renin-angiotensin system with AT1 blocker and ACEI may attenuate the development of heart hypertrophy, but only the blockade of AT1 receptors attenuates left ventricular interstitial fibrosis.

Objective: To determine the cardiac structural and functional alterations caused by cigarette smoke exposure in rats., Methods: The animals were randomly distributed into the following 2 groups: 1) smokers (S), comprising 10 animals exposed to cigarette smoke at a rate of 40 cigarettes/day; and 2) control (C), comprising 10 animals not exposed to cigarette smoke. After 4 months, the animals underwent morphological and functional study with echocardiography. The variables studied were analyzed by use of the t test or the Mann-Whitney test., Results: The smoking rats had a greater left atrium (S=4.2+/-0.7 mm; C=3.5+/-0.6 mm; P<0.05), and greater left ventricular diastolic (S=7.9+/-0.7 mm; C=7.2+/-0.5 mm; P<0.05) and systolic (S=4.1+/-0.5; C=3.4+/-0.5; P<0.05) diameters. The left ventricular mass index was greater in the smoking animals (S=1.5 mg/kg+/-0.2; C=1.3 mg/kg+/-0.2; P<0.05), and the ejection fraction (S=0.85+/-0.03; C=0.89+/-0.03; P<0.05) and the shortening fraction (S=47.8%+/-3.7; C=52.7%+/-4.6; P<0.05) were greater in the control group. No differences were observed in the diastolic transmitral flow variables (E wave, A wave, and E/A ratio)., Conclusion: Chronic cigarette smoke exposure results in cardiac remodeling with a decrease in ventricular functional capacity.

Objective: To assess the effect of growth hormone (GH) on myocardial remodeling in infarcted rats., Methods: This study comprised 24 Wistar rats divided into 3 groups as follows: 1) AMI-GH group--comprising 8 rats that underwent infarction and were treated with GH; 2) AMI group--comprising 8 rats that underwent infarction and received only the diluent of the GH solution; and 3) control group (C group)--comprising 8 rats that underwent simulated infarction. After 30 days, the animals underwent functional study through echocardiography, and the changes in myocardial contractility of the isolated left ventricular (LV) papillary muscle were studied., Results: The echocardiography identified an increase in the diastolic (C=7.32+/-0.49; AMI=8.50+/-0.73; AMI-GH=9.34+/-0.73; P<0.05) and systolic (C=3.38+/-0.47, AMI=5.16+/-1.24; AMI-GH=5.96+/-1.54; P<0.05) diameters (mm) in the LV of the infarcted animals. The AMI-GH group animals had a lower ejection fraction (%) (C=0.9+/-0.03; AMI=0.76+/-0.12; AMI-GH= 0.72+/- 0.14; P<0.05 for C vs AMI-GH) compared with those in controls. The study of the isolated left ventricular papillary muscle showed that the AMI-GH group had changes (C=1.50+/-0.59; AMI=1.28+/-0.38; AMI-GH=1.98+/-0.41; P<0.05 for C vs AMI-GH) only in the tension at rest (TR - g/mm2) and in the time delta for a 50% decrease in the tension developed (TR50, ms) after stimulation with calcium (C=23.75+/-9.16; AMI=-16.56+/-14.82; AMI-GH=-4.69+/-8.39; P<0.05 for C vs AMI-GH) and in the delta of tension developed (TD, g/mm2) after stimulation with isoproterenol (C=0.99+/-0.17; AMI=0.54+/-0.62; AMI-GH=0.08+/-0.75; P<0.05 for C vs AMI-GH) compared with those in control animals., Conclusion: The early administration of GH in the experimental infarction model in rats may result in adverse effects on the process of ventricular remodeling.

Objective: To compare 30-day mortality in patients receiving different types of medication from 1992 to 1997, when no consensual treatment for acute myocardial infarction was available, versus 30-day mortality in patients being treated between 2000 and 2002 after standardization of that treatment was obtained in our service., Methods: In the first and second study periods, 172 and 143 patients, respectively, admitted with the diagnosis of acute myocardial infarction were retrospectively assessed. Their diagnoses were confirmed, and the following statistical tests were performed: the chi-square test for comparing proportions and the Student t test and the Mann-Whitney test for comparing the means or medians., Results: The analysis showed no difference in regard to white men with a mean age of 61 years in the 2 study periods. In regard to the traditional risk factors, a difference was observed only in the incidence of dyslipidemia (17 and 29%). In regard to the therapeutic strategy adopted, the following was observed: 1) a significant increase in the use of thrombolytic agents (39 and 61.5%), acetylsalicylic acid (70.9 and 96.5%), beta-blockers (34.8 and 67.8%), angiotensin-converting enzyme inhibitors (45.9 and 74.8%), and nitrates (61 and 85.3%); and 2) a significant reduction in the use of calcium channel blockers (16.8 and 5.3%), antiarrhythmics (29.1 and 9.7%), and diuretics (50.6 and 26.6%). The use of inotropic agents did not differ between the study periods (29.6 and 32.1%). The 30-day mortality showed a statistically significant reduction from 22.7 to 10.5%., Conclusion: The implementation of standard protocols for the treatment of acute myocardial infarction was accompanied by a significant reduction in the 30-day mortality rate.

Objective: To assess the behavior of cardiac variables in animals exposed to cigarette smoke., Methods: Two groups of Wistar rats were studied as follows: control group (C), comprising 28 animals; and smoking group (S), comprising 23 animals exposed to cigarette smoke for 30 days. Left ventricular cardiac function was assessed in vivo with transthoracic echocardiography, and myocardial performance was analyzed in vitro in preparations of isolated left ventricular papillary muscle. The cardiac muscle was assessed in isometric contractions with an extracellular calcium concentration of 2.5 mmol/L., Results: No statistical difference was observed in the values of the body variables of the rats and in the mechanical data obtained from the papillary muscle between the control and smoking groups. The values of left ventricular systolic diameter were significantly greater in the smoking animals than in the control animals (C=3.39 +/- 0.4 mm and S=3.71 +/- 0.51 mm, P=0.02). A significant reduction was observed in systolic shortening fraction (C=56.7 +/- 4.2% and S=53.5 +/- 5.3%, P=0.02) and in ejection fraction (C=0.92 +/- 0.02 and S=0.89 +/- 0.04, P=0.01)., Conclusion: The rats exposed to cigarette smoke had a reduction in left ventricular systolic function, although their myocardial function was preserved.

Objective: To evaluate clinical profiles, predictors of 30-day mortality, and the adherence to international recommendations for the treatment of myocardial infarction in an academic medical center hospital., Methods: We retrospectively studied 172 patients with acute myocardial infarction, admitted in the intensive care unit from January 1992 to December 1997., Results: Most patients were male (68%), white (97%), and over 60 years old (59%). The main risk factor for coronary atherosclerotic disease was systemic blood hypertension (63%). Among all the variables studied, reperfusion therapy, smoking, hypertension, cardiogenic shock, and age were the predictors of 30-day mortality. Most commonly used medications were: acetylsalicylic acid (71%), nitrates (61%), diuretics (51%), angiotensin-converting enzyme inhibitors (46%), thrombolytic therapy (39%), and beta-blockers (35%)., Conclusion: The absence of reperfusion therapy, smoking status, hypertension, cardiogenic shock, and advanced age are predictors of 30-day mortality in patients with acute myocardial infarction. In addition, some medications that are undoubtedly beneficial have been under-used after acute myocardial infarction.