Effects of Pera Orange Juice and Moro Orange Juice in Healthy Rats: A Metabolomic Approach.

Cardiovascular disease is a leading cause of death worldwide. Heart failure is a cardiovascular disease with high prevalence, morbidity, and mortality. Several natural compounds have been studied for attenuating pathological cardiac remodeling. Orange juice has been associated with cardiovascular disease prevention by attenuating oxidative stress. However, most studies have evaluated isolated phytochemicals rather than whole orange juice and usually under pathological conditions. In this study, we evaluated plasma metabolomics in healthy rats receiving Pera or Moro orange juice to identify possible metabolic pathways and their effects on the heart. METHODS: Sixty male Wistar rats were allocated into 3 groups: control (C), Pera orange juice (PO), and Moro orange juice (MO). PO and MO groups received Pera orange juice or Moro orange juice, respectively, and C received water with maltodextrin (100 g/L). Echocardiogram and euthanasia were performed after 4 weeks. Plasma metabolomic analysis was performed by high-resolution mass spectrometry. Type I collagen was evaluated in picrosirius red-stained slides and matrix metalloproteinase (MMP)-2 activity by zymography. MMP-9, tissue inhibitor of metalloproteinase (TIMP)-2, TIMP-4, type I collagen, and TNF-α protein expression were evaluated by Western blotting. RESULTS: We differentially identified three metabolites in PO (N-docosahexaenoyl-phenylalanine, diglyceride, and phosphatidylethanolamine) and six in MO (N-formylmaleamic acid, N2-acetyl-L-ornithine, casegravol isovalerate, abscisic alcohol 11-glucoside, cyclic phosphatidic acid, and torvoside C), compared to controls, which are recognized for their possible roles in cardiac remodeling, such as extracellular matrix regulation, inflammation, oxidative stress, and membrane integrity. Cardiac function, collagen level, MMP-2 activity, and MMP-9, TIMP-2, TIMP-4, type I collagen, and TNF-α protein expression did not differ between groups. CONCLUSION: Ingestion of Pera and Moro orange juice induces changes in plasma metabolites related to the regulation of extracellular matrix, inflammation, oxidative stress, and membrane integrity in healthy rats. Moro orange juice induces a larger number of differentially expressed metabolites than Pera orange juice. Alterations in plasma metabolomics induced by both orange juice are not associated with modifications in cardiac extracellular matrix components. Our results allow us to postulate that orange juice may have beneficial effects on pathological cardiac remodeling.

Influence of Consumption of Orange Juice (Citrus Sinensis) on Cardiac Remodeling of Rats Submitted to Myocardial Infarction. / Influência do Consumo de Suco de Laranja (Citrus Sinensis) na Remodelação Cardíaca de Ratos Submetidos a Infarto do Miocárdio.

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.

FUNDAMENTO: O suco de laranja (SL) é rico em polifenóis com propriedades anti-inflamatórias e antioxidantes. Após o infarto do miocárdio (IM), mudanças complexas ocorrem na estrutura e na função cardíacas, processo conhecido como remodelação cardíaca (RC). O estresse oxidativo e a inflamação podem modular esse processo. Nossa hipótese foi a de que o consumo de SL atenua a RC após o IM. OBJETIVOS: Avaliar a influência do SL sobre a RC após IM pela análise de variáveis funcionais, morfológicas, de estresse oxidativo, de inflação, e de metabolismo energético. MÉTODOS: Um total de 242 ratos machos pesando entre 200 e 250g foram submetidos a um procedimento cirúrgico (ligação da artéria coronária ou cirurgia simulada). Sete dia após a cirurgia, os animais sobreviventes foram divididos para um dos quatro grupos: 1) SM, animais sham que receberam água e maltodextrina (n= 20); 2) SSL, animais sham que receberam SL (n= 20); 3) IM, animais infartados que receberam água e maltodextrina (n= 40); e 4) ISL, animais infartados que receberam SL (n = 40). A análise estatística foi realizada pelo teste de ANOVA com dois fatores com o teste de Holm-Sidak. Os resultados foram apresentados em média ± desvio padrão, e o nível de significância adotado foi de 5%. RESULTADOS: Três meses depois, o IM levou à hipertrofia do ventrículo esquerdo (VE), com disfunção sistólica e diastólica, e aumento nos mediadores inflamatórios e de estresse oxidativo. Os animais que consumiram SL apresentaram menor atividade da glutationa peroxidase e maior expressão da heme-oxigenase-1 (HO-1). CONCLUSÃO: O SL atenuou a RC, e a HO-1 pode exercer um importante papel nesse processo.

Influência do Consumo de Suco de Laranja (Citrus Sinensis) na Remodelação Cardíaca de Ratos Submetidos a Infarto do Miocárdio / Influence of Consumption of Orange Juice (Citrus Sinensis) on Cardiac Remodeling of Rats Submitted to Myocardial Infarction

Resumo Fundamento O suco de laranja (SL) é rico em polifenóis com propriedades anti-inflamatórias e antioxidantes. Após o infarto do miocárdio (IM), mudanças complexas ocorrem na estrutura e na função cardíacas, processo conhecido como remodelação cardíaca (RC). O estresse oxidativo e a inflamação podem modular esse processo. Nossa hipótese foi a de que o consumo de SL atenua a RC após o IM. Objetivos Avaliar a influência do SL sobre a RC após IM pela análise de variáveis funcionais, morfológicas, de estresse oxidativo, de inflação, e de metabolismo energético. Métodos Um total de 242 ratos machos pesando entre 200 e 250g foram submetidos a um procedimento cirúrgico (ligação da artéria coronária ou cirurgia simulada). Sete dia após a cirurgia, os animais sobreviventes foram divididos para um dos quatro grupos: 1) SM, animais sham que receberam água e maltodextrina (n= 20); 2) SSL, animais sham que receberam SL (n= 20); 3) IM, animais infartados que receberam água e maltodextrina (n= 40); e 4) ISL, animais infartados que receberam SL (n = 40). A análise estatística foi realizada pelo teste de ANOVA com dois fatores com o teste de Holm-Sidak. Os resultados foram apresentados em média ± desvio padrão, e o nível de significância adotado foi de 5%. Resultados Três meses depois, o IM levou à hipertrofia do ventrículo esquerdo (VE), com disfunção sistólica e diastólica, e aumento nos mediadores inflamatórios e de estresse oxidativo. Os animais que consumiram SL apresentaram menor atividade da glutationa peroxidase e maior expressão da heme-oxigenase-1 (HO-1). Conclusão O SL atenuou a RC, e a HO-1 pode exercer um importante papel nesse processo.

Abstract 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.

Exercise during transition from compensated left ventricular hypertrophy to heart failure in aortic stenosis rats.

We evaluated the influence of aerobic exercise on cardiac remodelling during the transition from compensated left ventricular (LV) hypertrophy to clinical heart failure in aortic stenosis (AS) rats. Eighteen weeks after AS induction, rats were assigned into sedentary (AS) and exercised (AS-Ex) groups. Results were compared to Sham rats. Exercise was performed on treadmill for 8 weeks. Exercise improved functional capacity. Echocardiogram showed no differences between AS-Ex and AS groups. After exercise, fractional shortening and ejection fraction were lower in AS-Ex than Sham. Myocyte diameter and interstitial collagen fraction were higher in AS and AS-Ex than Sham; however, myocyte diameter was higher in AS-Ex than AS. Myocardial oxidative stress, evaluated by lipid hydroperoxide concentration, was higher in AS than Sham and was normalized by exercise. Gene expression of the NADPH oxidase subunits NOX2 and NOX4, which participate in ROS generation, did not differ between groups. Activity of the antioxidant enzyme superoxide dismutase was lower in AS and AS-Ex than Sham and glutathione peroxidase was lower in AS-Ex than Sham. Total and reduced myocardial glutathione, which is involved in cellular defence against oxidative stress, was lower in AS than Sham and total glutathione was higher in AS-Ex than AS. The MAPK JNK was higher in AS-Ex than Sham and AS groups. Phosphorylated P38 was lower in AS-Ex than AS. Despite improving functional capacity, aerobic exercise does not change LV function in AS rats. Exercise restores myocardial glutathione, reduces oxidative stress, impairs JNK signalling and further induces myocyte hypertrophy.

Cardiac Remodeling Induced by All-Trans Retinoic Acid is Detrimental in Normal Rats.

BACKGROUND/AIMS: This study aimed to discern whether the cardiac alterations caused by retinoic acid (RA) in normal adult rats are physiologic or pathologic. METHODS AND RESULTS: Wistar rats were assigned into four groups: control animals (C, n = 20) received a standard rat chow; animals fed a diet supplemented with 0.3 mg/kg/day all-trans-RA (AR1, n = 20); animals fed a diet supplemented with 5 mg/kg/day all-trans-RA (AR2, n = 20); and animals fed a diet supplemented with 10 mg/kg/day all-trans-RA (AR3, n = 20). After 2 months, the animals were submitted to echocardiogram, isolated heart study, histology, energy metabolism status, oxidative stress condition, and the signaling pathway involved in the cardiac remodeling induced by RA. RA increased myocyte cross-sectional area in a dose-dependent manner. The treatment did not change the morphological and functional variables, assessed by echocardiogram and isolated heart study. In contrast, RA changed catalases, superoxide dismutase, and glutathione peroxidases and was associated with increased values of lipid hydroperoxide, suggesting oxidative stress. RA also reduced citrate synthase, enzymatic mitochondrial complex II, ATP synthase, and enzymes of fatty acid metabolism and was associated with increased enzymes involved in glucose use. In addition, RA increased JNK 1/2 expression, without changes in TGF-ß, PI3K, AKT, NFκB, S6K, and ERK. CONCLUSION: In normal rats, RA induces cardiac hypertrophy in a dose-dependent manner. The non-participation of the PI3K/Akt pathway, associated with the participation of the JNK pathway, oxidative stress, and changes in energy metabolism, suggests that cardiac remodeling induced by RA supplementation is deleterious.

Strain Pattern on Electrocardiogram Is Associated with Increased Carotid Intima-Media Thickness in Patients with Aortic Valve Stenosis.

BACKGROUND: Coronary artery disease is present in at least 30% of patients with degenerative aortic stenosis (AS). Atherosclerosis also performs an important role in the progression of AS, because of the similarities of pathological mechanisms in both conditions. The electrocardiogram (EKG) strain pattern is associated with structural myocardial change and subendocardial ischemia and has been worldwide used as a marker of AS severity. We hypothesized that EKG strain pattern would be a marker of atherosclerosis as well in AS patients. The aim of this study was to associate the presence of EKG strain pattern in AS patients with the carotid intima-media thickness (CIMT). METHODS: Fifty-two consecutive patients referred from the cardiology clinic with moderate or severe AS were included in the study and underwent clinical evaluation, EKG, transthoracic echocardiography, and carotid ultrasonography, following statistical analysis of the results. RESULTS: There was a significant association between left ventricular EKG strain and increased CIMT (P = 0.001). The presence of strain increased the odds of abnormal CIMT (P = 0.004, odds ratio 9.7, 95% confidence interval 2.4-45.0), in a model adjusted for age and clinical diagnosis of systemic arterial hypertension. Additionally, EKG strain was associated with the presence of atherosclerotic plaque in at least one carotid artery (P = 0.011). CONCLUSION: Our results suggest that AS patients with EKG strain pattern should be further investigated for the diagnosis of subclinical atherosclerotic disease.

The role of lipotoxicity in smoke cardiomyopathy.

BACKGROUND/AIMS: Experimental and clinical studies have shown the direct toxic effects of cigarette smoke (CS) on the myocardium, independent of vascular effects. However, the underlying mechanisms are not well known. METHODS: Wistar rats were allocated to control (C) and cigarette smoke (CS) groups. CS rats were exposed to cigarette smoke for 2 months. RESULTS: After that morphometric, functional and biochemical parameters were measured. The echocardiographic study showed enlargement of the left atria, increase in the left ventricular systolic volume and reduced systolic function. Within the cardiac metabolism, exposure to CS decreased beta hydroxy acyl coenzyme A dehydrogenases and citrate synthases and increased lactate dehydrogenases. Peroxisome proliferator-activated receptor alpha (PPARα) and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) were expressed similarly in both groups. CS increased serum lipids and myocardial triacylglycerols (TGs). These data suggest that impairment in fatty acid oxidation and the accumulation of cardiac lipids characterize lipotoxicity. CS group exhibited increased oxidative stress and decreased antioxidant defense. Finally, the myocyte cross-sectional area and active Caspase 3 were increased in the CS group. CONCLUSION: The cardiac remodeling that was observed in the CS exposure model may be explained by abnormalities in energy metabolism, including lipotoxicity and oxidative stress.

Infarct size as predictor of systolic functional recovery after myocardial infarction.

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.

Infarct Size as Predictor of Systolic Functional Recovery after Myocardial Infarction / Tamanho do Infarto como Preditor de Recuperação da Função Sistólica após Infarto do Miocárdio

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. .

Fundamento: Os efeitos da terapêutica moderna na recuperação funcional após o infarto agudo do miocárdio não são conhecidos. Objetivos: Avaliar os fatores preditores da recuperação funcional sistólica após infarto agudo do miocárdio de parede anterior em pacientes submetidos à terapia moderna (reperfusão, antiagregação plaquetária agressiva, inibidores da enzima conversora da angiotensina e betabloqueadores). Métodos: Foram incluídos 94 pacientes consecutivos com infarto agudo do miocárdio com supradesnivelamento do segmento ST. Ecocardiogramas foram realizados na fase intra-hospitalar e após 6 meses. Disfunção sistólica foi definida pela presença de fração de ejeção de valor < 50%. Resultados: No ecocardiograma inicial, 64% dos pacientes apresentaram disfunção sistólica. Os pacientes com disfunção ventricular apresentaram tamanhos maiores de infarto, avaliados pelas enzimas creatinofosfoquinase total e isoenzima MB, que os pacientes sem disfunção. Adicionalmente, 24,5% dos pacientes inicialmente com disfunção sistólica apresentaram recuperação no período de 6 meses após o infarto agudo do miocárdio. Os pacientes que recuperaram a função ventricular apresentaram menores tamanhos de infarto, mas maiores valores da fração de ejeção e tempo de desaceleração da onda E que pacientes sem recuperação. Na análise multivariada, observa-se que o tamanho de infarto foi o único fator preditor independente de recuperação funcional após 6 meses de infarto, quando ajustado pela idade, sexo, fração de ejeção e tempo de desaceleração da onda E. Conclusão: Apesar do tratamento agressivo, a disfunção ventricular ...

Waist circumference, but not body mass index, is a predictor of ventricular remodeling after anterior myocardial infarction.

OBJECTIVE: The impact of obesity on ventricular remodeling after myocardial infarction (MI) is still poorly understood. Therefore, the aim of this study was to evaluate the role of waist circumference (WC) and body mass index as predictors of cardiac remodeling in patients after an anterior MI. METHODS: Eighty-three consecutive patients with anterior MI were prospectively evaluated. Clinical characteristics and echocardiographic data were analyzed at admission and at a 6-mo follow-up. Ventricular remodeling was defined as a 10% increase in left ventricular end-systolic or end-diastolic diameter at the 6-mo follow-up. RESULTS: In our study, 83 consecutive patients were evaluated (72% men). Ventricular remodeling was present in 31% of the patients (77% men). Patients with remodeling had higher creatine phosphokinase and creatine phosphokinase-MB peak values, a higher resting heart rate, a larger left atrial diameter, and a larger interventricular septum diastolic thickness. In addition, patients with remodeling had lower peak velocity of early ventricular filling deceleration time and ejection fraction. Patients with remodeling presented higher WC values (with remodeling, 99.2 ± 10.4 cm; without remodeling, 93.9 ± 10.8 cm, P = 0.04), but there were no differences in the body mass index values. In the logistic regression analysis, WC, adjusted by age, gender, ejection fraction, and creatine phosphokinase levels, was an independent predictor of left ventricular remodeling (odds ratio 1.067, 95% confidence interval 1.001-1.129, P = 0.02). CONCLUSION: Waist circumference, but not body mass index, is a predictor of ventricular remodeling after an anterior MI. Therefore, the WC of these patients should be measured in clinical practice.

Prevalence and predictors of ventricular remodeling after anterior myocardial infarction in the era of modern medical therapy.

BACKGROUND: The consequences of aggressive therapy following a myocardial infarction (MI) on ventricular remodeling are not well established. Thus, the objective of this study was to analyze the prevalence, clinical characteristics, and predictors of left ventricular remodeling in the era of modern medical therapy. MATERIAL/METHODS: Clinical characteristics and echocardiographic data were analyzed in 66 consecutive patients with anterior infarction at admission and at 6-month follow-up. Ventricular remodeling was defined as an increase of 10% in ventricular end-systolic or end-diastolic diameter. RESULTS: In our study, 58% of patients presented with ventricular remodeling. Patients with remodeling possessed higher total plasma creatine kinase (CPK), MB-fraction (CPK-MB), heart rate, heart failure, shortness of breath, and reperfusion therapy than patients without remodeling. In contrast, patients with remodeling had a smaller ejection fraction, E-Wave deceleration time (EDT), and early (E' Wave) and late (A' Wave) diastolic mitral annulus velocity (average of septal and lateral walls), but a higher E/E' than patients without remodeling. Patients with remodeling used more diuretics, digoxin, oral anticoagulants and aldosterone antagonists than patients without remodeling. In the multivariate analyses, only E' Wave was an independent predictor of ventricular remodeling. Each 1 unit increase in the E' Wave was associated with a 59% increased odds of ventricular remodeling. CONCLUSIONS: In patients with anterior MI, despite contemporary treatment, ventricular remodeling is still a common event. In addition, diastolic function can have an important role as a predictor of remodeling in this scenario.

Predictors of right ventricle dysfunction after anterior myocardial infarction.

BACKGROUND: Regardless significant therapeutic advances, mortality and morbidity after myocardial infarction (MI) are still high. For a long time, the importance of right ventricle (RV) function has been neglected. Recently, RV dysfunction has also been associated with poor outcomes in the setting of heart failure. The shape, location, and contraction conditions make the RV chamber assessment technically challenging. METHODS: Our study identified clinical characteristics and left ventricle (LV) echocardiographic data performed 3-5 days after MI that could be associated with RV dysfunction (RV fractional area change [FAC] < 35%) 6 months after MI. RESULTS: The RV dysfunction group consisted of 11 patients (RV FAC 29.4% ± 5.2) and the no RV dysfunction group of 71 patients (RV FAC 43.7% ± 5.1); (P < 0.001). Both groups presented the same baseline clinical characteristics. Left atrium (LA), interventricular septum (IVS), and left ventricular posterior wall (LVPW) were larger in RV dysfunction than in no RV dysfunction. Conversely, E wave deceleration time (EDT) was lower in RV dysfunction when compared with no RV dysfunction. Left atrium(adj) (adjusted by gender, age, infarct size, and body mass index) (odds ratio [OR], 1.22; confidence interval [CI], 1.016-1.47; P = 0.032), interventricular septum(adj) (OR, 1.49; CI, 1.01-2.23; P = 0.044), and E wave deceleration time(adj) (OR, 0.98; CI, 0.97-0.98; P = 0.029) assessed soon after MI predicted RV failure after 6-months. CONCLUSIONS: LV diastolic dysfunction, resulting from anterior MI and assessed 3-5 days after the event, may play an important role in predicting RV dysfunction 6 months later.

A intervenção coronária percutânea melhora a função diastólica do ventrículo esquerdo em pacientes com angina pectoris? / Percutaneous coronary intervention improves left ventricular diastolic function in patients with stable angina?

Objetivo: Avaliar pelo ecocardiograma, o efeito da intervenção coronária percutânea (ICP) nos índices de função diastólica do ventrículo esquerdo (VE), obtidos por meio do Doppler tissular e da medida do volume atrial esquerdo (VAE), três meses após a realizaçãodo procedimento. Métodos: Estudo longitudinal e prospectivo, incluindo 66 (40 homens) pacientes consecutivos, com estenose crítica em uma artéria coronária. Ecocardiograma transtorácico foi realizado 24 horas antes da ICP e três meses após o procedimento. Com o Doppler tissular foi determinado o pico de velocidade das ondas E’ e A’, da região septal e lateral do anel mitral e a relação E’/A’, considerando-se a média de tais medidas. Com o Doppler de fluxo foi determinada a velocidade de pico da onda E do fluxograma mitral e, a partir desta, a relação E/E’. O VAE foi determinado pelo método de Simpson. As medidas ecodopplercardiográficas seguiram as recomendações da American Society of Echocardiography. Resultados: A idade média dos pacientes estudados foi de 61 + 14 anos e a ICP foi realizada em apenas um vaso. Determinando-se a média dos valores da onda E’, da relação E’/A’, E/E’ e VAEde todos os pacientes, observamos que não houve variação, estatisticamente significante desses índices, após a ICP. Conclusão: O presente estudo mostrou que a ICP de um vaso, com lesão grave, não é suficiente para causar melhora da função diastólica do VE em pacientes com angina estável, quando avaliada pelo Doppler tissular e VAE.

Objective: The aim of this study was to evaluate by echocardiogram, the effect of percutaneous coronary intervention (PCI) in left ventricular (LV) diastolic function indices, obtained by tissue Doppler imaging and measurement of left atrial volume (LAV), three months after the procedure. Methods: This was a longitudinal and prospective study including 66 (40 men) consecutive patients with critical stenosis in one coronary vessel. Transthoracic echocardiography was performed 24 hours before and three months after PCI.Medial and lateral mitral annulus peak velocity of the waves E’ and A’, and the averaged ratio E’/A’ were obtained. Early transmitral flow velocity was measured, E wave and the ratio E/E’ was calculated. The LAV was determined by the Simpson’s method. Dopplerechocardiography measurements followed the recommendations of the American Society of Echocardiography. Results: Mean age was 61 + years. PCI was performed in a single vessel. By determining the average value of the wave E ‘of E’/A’, E/E’ and LAV of allpatients, we found no statistically significant variations in these indices after PCI. Conclusion: This study showed that PCI of a single vessel with a severe lesion, is not sufficient to improve of LV diastolic function in patients with stable angina, evaluated by tissue Doppler and LAV.

Digitalis-like induced arrhythmia in a patient with rheumatic mitral regurgitation complicated by preeclampsia.

OBJECTIVE: To report a case of cardiac arrhythmia related to a low dose of endovenous lanatoside C. CASE REPORT: A 23-year-old pregnant woman with mitral regurgitation complicated with preeclampsia and pulmonary edema presented 2 episodes of atrial tachycardia induced by a intravenous digitalis (2 mg, IV and 1 mg, IV, respectively). CONCLUSION: This case calls attention to the need for further studies analysing the security of digoxin use in preeclampsia.

Association between atherosclerotic aortic plaques and left ventricular hypertrophy in patients with cerebrovascular events.

BACKGROUND AND PURPOSE: The purpose of this research was to evaluate whether an association exists between the presence of atherosclerotic plaque in the thoracic aorta and left ventricular hypertrophy (LVH) in patients with a cerebrovascular event. METHODS: We included 116 consecutive patients (79 men; mean age, 62+/-12.4 years) with previous history of stroke or transient ischemic attack in a cross-sectional study. Transthoracic echocardiogram was performed to diagnose LVH and transesophageal echocardiogram for the detection of atheromas of the thoracic aorta. Continuous variables were analyzed by Student t or Mann-Whitney tests and categorized variables by Goodman test. From the significant association of LVH and age with atheromatous disease of the aorta, an adjustment to the multivariate logistic model was made using high blood pressure history or age as covariates. All of the statistical tests were carried out at a level of 5% significance. RESULTS: Almost half of the patients (43.1%) presented atherosclerotic lesions in the aorta. LVH was present in 90.0% of patients with plaque and in only 30.3% of patients without plaque. Using high blood pressure as a covariate, the risk of patients with LVH presenting atherosclerotic plaque in the aorta was 18.23-fold greater than the risk for patients without LVH (95% CI, 5.68 to 58.54; P<0.0001). Adding age into the model, the risk increased to 26.36 (95% CI, 7.14 to 97.30; P<0.0001). CONCLUSIONS: LVH detected by conventional echocardiogram is associated with high risk of atherosclerotic plaque in the aorta and would be used as a criterion for indication of transesophageal echocardiography in patients with previous stroke or transient ischemic attack LVH.