Initial experience with del Nido cardioplegia solution at a Pediatric and Congenital Cardiac Surgery Program in Brazil.

OBJECTIVE: The aim of this study was to evaluate outcome measures between our standard multidose cardioplegia protocol and a del Nido cardioplegia protocol in congenital heart surgery patients. METHODS: Retrospective single-center study including 250 consecutive patients that received del Nido cardioplegia (DN group) with a mandatory reperfusion period of 30% of cross clamp time and 250 patients that received a modified St. Thomas' solution (ST group). Groups were matched by age, weight, gender, and Risk Adjustment for Congenital Heart Surgery (RACHS-1) scores. Preoperative hematocrit and oxygen saturation were also recorded. Outcomes analyzed were the vasoactive inotropic score (VIS), lactate, ventilation time, ventricular dysfunction with low cardiac output syndrome (LCOS), intensive care unit (ICU) length of stay (LOS), hospital LOS, bypass and aortic cross-clamp times, and in-hospital mortality. RESULTS: Both groups were comparable demographically. Statistically significant differences (p ⩽ 0.05) were noted for cardiac dysfunction with LCOS, hematocrit at end of surgery (p = 0.0038), VIS on ICU admission and at end of surgery (p = 0.0111), and ICU LOS (p = 0.00118) with patients in the DN group having more desirable values for those parameters. Other outcome measures did not reach statistical significance. CONCLUSION: In our congenital cardiac surgery population, del Nido cardioplegia strategy was associated with less ventricular dysfunction with LCOS, a lower VIS and decreased ICU LOS compared with patients that received our standard myocardial protection using a modified St. Thomas' solution. Despite the limitation of this study, including its retrospective nature and cohort size, these data supported our transition to incorporate del Nido cardioplegia solution with a mandatory reperfusion period as the preferred myocardial protection method in our program.

The ACE 2 activator diminazene aceturate (DIZE) improves left ventricular diastolic dysfunction following myocardial infarction in rats.

Diminazene aceturate (DIZE) has been reported to enhance the catalytic efficiency of ACE-2 and presumably increases angiotensin 1-7 generation, interfering with cardiac remodeling after myocardial infarction (MI). Our aim was to investigate the chronic effects of DIZE on cardiac dysfunction post-MI. Male Wistar rats underwent myocardial infarction (MI) or SHAM surgery (SO) and were divided into groups treated with DIZE 15 mg/kg/day, s.c. or vehicle (Control). After 4 weeks, the hemodynamic variables were recorded by cardiac catheterism. Hearts were then arrested to obtain the left ventricular (LV) pressure-volume curves in situ. Cardiomyocyte hypertrophy and collagen content were determined by histology. DIZE prevented LV end-diastolic pressure increases in MI rats (MI: 26 ± 3.3 vs. MI-DIZE: 15 ± 1.6 mmHg, P < 0.001) without a significant effect on LV systolic pressure (LVSP). Moreover, DIZE improved LV contractility (+dP/dt, MI: 3014 ± 161 vs. MI-DIZE: 3884 ± 104 mmHg/s, P < 0.001) and relaxation (-dP/dt, MI: -2333 ± 91 vs. MI-DIZE: -2798 ± 120 mmHg/s, P < 0.05). Right ventricular SP was increased in the MI compared to that in the SO group (40 ± 0.6 vs. 30 ± 1.2 mmHg; P < 0.01), and DIZE partially prevented this augmentation. LV stiffness was reduced in MI-DIZE compared with that in MI (0.64 ± 0.01 vs. 0.78 ± 0.02 mmHg/mL; P < 0.01). DIZE treatment reduced the interstitial collagen content by 18% in the surviving LV myocardium. Cardiomyocyte hypertrophy remained unaffected by DIZE treatment. Our findings show that chronic DIZE treatment post-MI attenuates the morphofunctional changes induced by MI in rats. The effects on LV -dP/dt, chamber stiffness and collagen content suggest this drug can be used as a therapeutic agent to reduce interstitial fibrosis and diastolic dysfunction after MI.

High-Fat-Diet-Induced Obesity Produces Spontaneous Ventricular Arrhythmias and Increases the Activity of Ryanodine Receptors in Mice.

Ventricular arrhythmias are a common cause of sudden cardiac death, and their occurrence is higher in obese subjects. Abnormal gating of ryanodine receptors (RyR2), the calcium release channels of the sarcoplasmic reticulum, can produce ventricular arrhythmias. Since obesity promotes oxidative stress and RyR2 are redox-sensitive channels, we investigated whether the RyR2 activity was altered in obese mice. Mice fed a high fat diet (HFD) became obese after eight weeks and exhibited a significant increase in the occurrence of ventricular arrhythmias. Single RyR2 channels isolated from the hearts of obese mice were more active in planar bilayers than those isolated from the hearts of the control mice. At the molecular level, RyR2 channels from HFD-fed mice had substantially fewer free thiol residues, suggesting that redox modifications were responsible for the higher activity. Apocynin, provided in the drinking water, completely prevented the appearance of ventricular arrhythmias in HFD-fed mice, and normalized the activity and content of the free thiol residues of the protein. HFD increased the expression of NOX4, an isoform of NADPH oxidase, in the heart. Our results suggest that HFD increases the activity of RyR2 channels via a redox-dependent mechanism, favoring the appearance of ventricular arrhythmias.

Treatment with Fenofibrate plus a low dose of Benznidazole attenuates cardiac dysfunction in experimental Chagas disease.

Trypanosoma cruzi induces serious cardiac alterations during the chronic infection. Intense inflammatory response observed from the beginning of infection, is critical for the control of parasite proliferation and evolution of Chagas disease. Peroxisome proliferator-activated receptors (PPAR)-α, are known to modulate inflammation. In this study we investigated whether a PPAR-α agonist, Fenofibrate, improves cardiac function and inflammatory parameters in a murine model of T. cruzi infection. BALB/c mice were sequentially infected with two T. cruzi strains of different genetic background. Benznidazole, commonly used as trypanocidal drug, cleared parasites but did not preclude cardiac pathology, resembling what is found in human chronic chagasic cardiomyopathy. Fenofibrate treatment restored to normal values the ejection and shortening fractions, left ventricular end-diastolic, left ventricular end-systolic diameter, and isovolumic relaxation time. Moreover, it reduced cardiac inflammation and fibrosis, decreased the expression of pro-inflammatory (IL-6, TNF-α and NOS2) and heart remodeling mediators (MMP-9 and CTGF), and reduced serum creatine kinase activity. The fact that Fenofibrate partially inhibited NOS2 expression and NO release in the presence of a PPAR-α non-competitive inhibitor, suggested it also acted through PPAR-α-independent pathways. Since IκBα cytosolic degradation was inhibited by Fenofibrate, it can be concluded that the NFκB pathway has a role in its effects. Thus, we demonstrate that Fenofibrate acts through PPAR-α-dependent and -independent pathways. Our study shows that combined treatment with Fenofibrate plus Benznidazole is able both to reverse the cardiac dysfunction associated with the ongoing inflammatory response and fibrosis and to attain parasite clearance in an experimental model of Chagas disease.

N-Acetylcysteine Prevents Low T3 Syndrome and Attenuates Cardiac Dysfunction in a Male Rat Model of Myocardial Infarction.

Nonthyroidal illness syndrome (NTIS) affects patients with myocardial infarction (MI). Oxidative stress has been implicated as a causative factor of NTIS, and reversed via N-acetylcysteine (NAC). Male Wistar rats submitted to left anterior coronary artery occlusion received NAC or placebo. Decreases in triiodothyronine (T3) levels were noted in MI-placebo at 10 and 28 days post-MI, but not in MI-NAC. Groups exhibited similar infarct areas whereas MI-NAC exhibited higher ejection fraction than did MI-placebo. Left ventricular systolic and diastolic diameters were also preserved in MI-NAC, but not in MI-placebo. Ejection fraction was positively correlated with T3 levels. Oxidative balance was deranged only in MI-placebo animals. Increased type 3 iodothyronine deiodinase expression was detected in the cardiomyocytes of MI-placebo compared with normal heart tissue. NAC was shown to diminish type 3 iodothyronine deiodinase expression and activity in MI-NAC. These results show that restoring redox balance by NAC treatment prevents NTIS- related thyroid hormone derangement and preserves heart function in rats subjected to MI.

Cardiac Remodeling: Concepts, Clinical Impact, Pathophysiological Mechanisms and Pharmacologic Treatment / Remodelação Cardíaca: Conceitos, Impacto Clínico, Mecanismos Fisiopatológicos e Tratamento Farmacológico

Abstract 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.

Resumo A remodelação cardíaca é definida como um conjunto de mudanças moleculares, celulares e intersticiais cardíacas, que se manifestam clinicamente por alterações no tamanho, massa, geometria e função do coração, em resposta à determinada agressão. Esse processo resulta em mal prognóstico, pois está associado com a progressão da disfunção ventricular e arritmias malignas. Nessa revisão, são discutidos os conceitos e as implicações clínicas da remodelação, além do papel fisiopatológico de diferentes fatores, incluindo morte celular, metabolismo energético, estresse oxidativo, inflamação, colágeno, proteínas contráteis, transporte de cálcio, geometria e ativação neurohormonal. Finalmente, o artigo apresenta o tratamento farmacológico, que pode ser dividido em três estágios: estratégias consolidadas, promissoras e potenciais.

Cardiac Remodeling: Concepts, Clinical Impact, Pathophysiological Mechanisms and Pharmacologic Treatment.

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.

O etanercepte induz QRS de baixa tensão e disfunção autonômica em camundongos com doença de Chagas experimental / Etanercept induces low QRS voltage and autonomic dysfunction in mice with experimental Chagas disease

FUNDAMENTO: A doença de Chagas é uma doença parasitária tropical causada pelo protozoário flagelado Trypanosoma cruzi. A cardiomiopatia chagásica é caracterizada por distúrbios na regulação autonômica e na condução do potencial de ação nas fases aguda e crônica da infecção. Embora o fator de necrose tumoral alfa (TNF-α) tenha sido associadoà cardiomiopatia em modelos experimentais e em pacientes com doença de Chagas, outros relatos sugerem que o TNF-α pode exercer ações antiparasitárias durante a fase aguda da infecção. OBJETIVOS: Este estudo teve como objetivo determinar os efeitos de um blocker TNF-α solúvel, o etanercepte, em parâmetros eletrocardiográficos na fase aguda da infecção experimental com Trypanosoma cruzi. MÉTODOS: Foram feitos eletrocardiogramas em camundongos infectados não tratados e camundongos infectados que foram tratados com etanercepte 7 dias após a infecção. Os parâmetros de variabilidade onda do eletrocardiograma e frequência cardíaca foram determinados utilizando o Chart para Windows. RESULTADOS: O tratamento com etanercepte resultou em uma baixa tensão do complexo QRS e uma redução da variabilidade da frequência cardíaca em comparação com a ausência de tratamento. No entanto, os camundongos tratados apresentaram um atraso na queda da curva de sobrevivência durante a fase aguda. CONCLUSÃO: Os resultados deste estudo sugerem que, embora o tratamento com etanercepte promova a sobrevivência em camundongos infectados com uma linhagem virulenta de T. cruzi, o bloqueio do TNF-α gera um complexo de baixa tensão e disfunção autonômica durante a fase aguda da infecção. Esses resultados indicam que a mortalidade durante a fase aguda pode ser atribuída a uma resposta inflamatória sistêmica, em vez da disfunção cardíaca.

BACKGROUND: Chagas disease is a tropical parasitic disease caused by the flagellate protozoan Trypanosoma cruzi. Chagasic cardiomyopathy is characterized by disorders of autonomic regulation and action potential conduction in the acute and chronic phases of infection. Although tumor necrosis factor alpha (TNF-α) has been linked to cardiomyopathy in experimental models and in patients with Chagas disease, other reports suggest that TNF-α may exert anti-parasitic actions during the acute phase of infection. OBJECTIVES: This study aimed to determine the effects of a soluble TNF-α agonist, etanercept, on electrocardiographic parameters in the acute phase of experimental infection with Trypanosoma cruzi. METHODS: Electrocardiograms were obtained from untreated infected mice and infected mice who were treated with etanercept 7 days after infection. ECG wave and heart rate variability parameters were determined using Chart for Windows. RESULTS: Etanercept treatment resulted in a low QRS voltage and decreased heart rate variability compared with no treatment. However, the treated mice exhibited a delay in the fall of the survival curve during the acute phase. CONCLUSION: The results of this study suggest that although etanercept treatment promotes survival in mice infected with a virulent T. cruzi strain, TNF-α blockade generates a low voltage complex and autonomic dysfunction during the acute phase of infection. These findings indicate that mortality during the acute phase can be attributed to a systemic inflammatory response rather than cardiac dysfunction.).

Etanercept induces low QRS voltage and autonomic dysfunction in mice with experimental Chagas disease.

BACKGROUND: Chagas disease is a tropical parasitic disease caused by the flagellate protozoan Trypanosoma cruzi. Chagasic cardiomyopathy is characterized by disorders of autonomic regulation and action potential conduction in the acute and chronic phases of infection. Although tumor necrosis factor alpha (TNF-α) has been linked to cardiomyopathy in experimental models and in patients with Chagas disease, other reports suggest that TNF-α may exert anti-parasitic actions during the acute phase of infection. OBJECTIVES: This study aimed to determine the effects of a soluble TNF-α agonist, etanercept, on electrocardiographic parameters in the acute phase of experimental infection with Trypanosoma cruzi. METHODS: Electrocardiograms were obtained from untreated infected mice and infected mice who were treated with etanercept 7 days after infection. ECG wave and heart rate variability parameters were determined using Chart for Windows. RESULTS: Etanercept treatment resulted in a low QRS voltage and decreased heart rate variability compared with no treatment. However, the treated mice exhibited a delay in the fall of the survival curve during the acute phase. CONCLUSION: The results of this study suggest that although etanercept treatment promotes survival in mice infected with a virulent T. cruzi strain, TNF-α blockade generates a low voltage complex and autonomic dysfunction during the acute phase of infection. These findings indicate that mortality during the acute phase can be attributed to a systemic inflammatory response rather than cardiac dysfunction.

Oral administration of an angiotensin-converting enzyme 2 activator ameliorates diabetes-induced cardiac dysfunction.

We evaluated the hypothesis that activation of endogenous angiotensin-converting enzyme (ACE) 2 would improve cardiac dysfunction induced by diabetes. Ten days after diabetes induction (streptozotocin, 50 mg/kg, i.v.), male Wistar rats were treated with the ACE2 activator 1-[[2-(dimethylamino)ethyl]amino]-4-(hydroxymethyl)-7-[[(4-methylphenyl)sulfonyl]oxy]-9H-xanthen-9-one (XNT, 1 mg/kg/day, gavage) or saline (control) for 30 days. Echocardiography was performed to analyze the cardiac function and kinetic fluorogenic assays were used to determine cardiac ACE and ACE2 activities. Cardiac ACE2, ACE, Mas receptor, AT(1) receptor, AT(2) receptor and collagen types I and III mRNA and ACE2, ACE, Mas, AT(1) receptor, AT(2) receptor, ERK1/2, Akt, AMPK-α and AMPK-ß(1) protein were measured by qRT-PCR and western blotting techniques, respectively. Histological sections of hearts were analyzed to evaluate the presence of hypertrophy and fibrosis. Diabetic animals presented hyperglycemia and diastolic dysfunction along with cardiac hypertrophy and fibrosis. XNT treatment prevented further increase in glycemia and improved the cardiac function, as well as the hypertrophy and fibrosis. These effects were associated with increases in cardiac ACE2/ACE ratios (activity: ~26%; mRNA: ~113%; and protein: ~188%) and with a decrease in AT(1) receptor expression. Additionally, XNT inhibited ERK1/2 phosphorylation and prevented changes in AMPK-α and AMPK-ß(1) expressions. XNT treatment did not induce any significant change in AT(2) receptor and Akt expression. These results indicate that activation of intrinsic cardiac ACE2 by oral XNT treatment protects the heart against diabetes-induced dysfunction through mechanisms involving ACE, ACE2, ERK1/2, AMPK-α and AMPK-ß(1) modulations.

Pressure response in Chagasic cardiomyopathy patients after using Sildenafil.

OBJECTIVE: To accurately verify the effect of Sildenafil on blood pressure (BP) and heart rate (HR) in individuals with Chagasic myocardiopathy (CMC) and severe systolic ventricular dysfunction (EF<40%) submitted to physical activity. METHODS: Twelve men with ejection fractions <40% and CMC confirmed by a serological test were assessed. The six-minute walk test (6MWT) was performed before and after administration of 50 mg of Sildenafil, with a 30 minute interval. Heart rate (HR), systolic blood pressure (SBP) and diastolic blood pressure were taken and compared before and after each 6MWT. For statistical analysis purposes, the study was divided into four stages: before the 6MWT and administration of Sildenafil (S1); after the 6MWT but before the administration of Sildenafil (S2); after the administration of Sildenafil but before the 6MWT (S3); and after the administration of Sildenafil and the 6MWT (S4). RESULTS: Participant ages ranged from 47 to 68 years (57.6 +/- 6.4). SBP and DBP after the 6MWT and the administration of Sildenafil (S4) were lower than before taking the drug (S2): 134.2 +/- 15.1 versus 125.5 +/- 14.0 and 88.4 +/- 12.4 versus 83.0 +/- 10.8, respectively. None of the patients reported any symptoms during the 6MWT. There were no differences in the distances walked during the 6MWT before or after taking Sildenafil (487.5+/-15.22 versus 505.3+/-18.45 meters, respectively)-p=0.056, or in HR (before Sildenafil 75.5 +/- 8.79 and 96.8 +/- 10.36 bpm and after 77.1 +/- 9.81 and 96.1 +/- 12.97 bpm). CONCLUSION: A significant reduction in BP after physical activity while using Sildenafil was observed. However, during the six-minute walk test, the patients did not report any symptoms, indicating that this effect is not sufficient to cause clinical manifestations in CMC and heart failure patients.

Resposta pressórica de pacientes com miocardiopatia chagásica ante o uso do sildenafil / Pressure response in chagasic cardiomyopathy patients after using sildenafil

OBJETIVO: Verificar o efeito do sildenafil na pressão arterial (PA) e freqüência cardíaca (FC) de indivíduos portadores de miocardiopata chagásica (MCC) e de disfunção ventricular sistólica grave (FE<40 por cento) submetidos à atividade física. MÉTODOS: Foram avaliados 12 homens com fração de ejeção<40 por cento e MCC confirmada por sorologia. Foi realizado o Teste de 6 minutos (T6M) antes e após a ingestão de sildenafil 50 mg, com intervalo de 30 minutos. Antes e depois de cada T6M aferiram-se a freqüência cardíaca (FC) e a pressão arterial sistólica (PAS) e diastólica (PAD). Para análise estatística, o estudo foi dividido em 4 etapas: Antes do T6M realizado antes do Sildenafil (T1); após o T6M, antes do Sildenafil (T2); após o sildenafil, antes do T6M (T3); após o Sildenafil, após o T6M (T4). RESULTADOS: A idade dos participantes variou entre 47 e 68 anos (57,6±6,4). PAS e PAD após o T6M e uso do sildenafil (T4) mostraram-se menores do que antes do fármaco (T2): 134,2±15,1 versus 125,5±14,0 e 88,4±12,4 versus 83,0±10,8, respectivamente. Nenhum indivíduo referiu sintomas durante a realização do T6M. Não houve diferença na distância total percorrida no T6M antes e depois do uso do sildenafil (487,5±15,22 versus 505,3±18,45 metros, respectivamente) - p=0,056, e na FC (antes sildenafil 75,5±8,79 e 96,8±10,36 bpm e após 77,1±9,81 e 96,1 ± 12,97 bpm). CONCLUSÃO: Observou-se significante diminuição da PA após atividade física sob uso do sildenafil. Entretanto, durante o Teste de 6 minutos, não foram relatados sintomas pelos pacientes, sugerindo, então, que esse efeito parece não ser suficiente para causar manifestações clínicas entre os portadores de MCC e insuficiência cardíaca.

OBJECTIVE: To accurately verify the effect of Sildenafil on blood pressure (BP) and heart rate (HR) in individuals with Chagasic myocardiopathy (CMC) and severe systolic ventricular dysfunction (EF<40 percent) submitted to physical activity. METHODS: Twelve men with ejection fractions <40 percent and CMC confirmed by a serological test were assessed. The six-minute walk test (6MWT) was performed before and after administration of 50 mg of Sildenafil, with a 30 minute interval. Heart rate (HR), systolic blood pressure (SBP) and diastolic blood pressure were taken and compared before and after each 6MWT. For statistical analysis purposes, the study was divided into four stages: before the 6MWT and administration of Sildenafil (S1); after the 6MWT but before the administration of Sildenafil (S2); after the administration of Sildenafil but before the 6MWT (S3); and after the administration of Sildenafil and the 6MWT (S4). RESULTS: Participant ages ranged from 47 to 68 years (57.6 ± 6.4). SBP and DBP after the 6MWT and the administration of Sildenafil (S4) were lower than before taking the drug (S2): 134.2 ± 15.1 versus 125.5 ± 14.0 and 88.4 ± 12.4 versus 83.0 ± 10.8, respectively. None of the patients reported any symptoms during the 6MWT. There were no differences in the distances walked during the 6MWT before or after taking Sildenafil (487.5±15.22 versus 505.3±18.45 meters, respectively)-p=0.056, or in HR (before Sildenafil 75.5 ± 8.79 and 96.8 ± 10.36 bpm and after 77.1 ± 9.81 and 96.1 ± 12.97 bpm). CONCLUSION: Based on these results, it can be concluded that both prediction equations significantly overestimated HRmax measured during maximal GXT in Brazilian elderly women, a finding that may have important implications when prescribing exercise intensity for this population. In addition, HRmax was inversely related to the volunteers' age, suggesting that the chronotropic reserve continues to decline after age 60.

Efectos del Carvedilol sobre la sincronía ventricular en pacientes con insuficiencia cardíaca congestiva / Effects of Carvedilol on ventricular synchrony in patients with congestive heart failure

Introducción: Carvedilol es un bloqueador adrenérgico que mejora el remodelamiento ventricular izquierdo y reduce la morbi-mortalidad de los pacientes con insuficiencia cardíaca congestiva (ICC). Esto podría estar relacionado con una corrección de la sincronía ventricular. Objetivo: Evaluar el efecto de Carvedilol sobre la sincronía en la contracción ventricular en pacientes con ICC. Métodos: Se estudiaron 30 pacientes con ICC estable, capacidad funcional NYHA (CF) II-III, fracción de eyección (FE) < 40 por ciento, los cuales estaban tratados en forma habitual. Se excluyeron pacientes usuarios de betabloqueadores o de marcapaso. Se realizó ventriculografía radioisotópica de equilibrio, al inicio y posterior a la terapia con Carvedilol por 6 meses, para evaluar la función sistólica y la sincronía ventricular. La sincronía interventricular fue calculada mediante la diferencia de promedio de fase de ambos ventrículos y la intraventricular usando la desviación estándar del análisis de fase. Resultados: La edad fue 55 ± 13 años, 71 por ciento hombres, 35 por ciento de etiología isquémica y 29 por ciento con bloqueo completo de rama izquierda (BCRI). Posterior a la terapia con Carvedilol (dosis promedio de 22 mg, rango de 6.25 – 50 mg/día) hubo una mejoría en la CF y en la distancia recorrida en 6 min (499 ± 18 m a 534 ± 17 m ). La FE mejoró de 24 ± 8.3 por ciento a 31 ± 11. 3 por ciento (p<0.001). En los pacientes con peor sincronía, bajo el percentil 50, mejoró la sincronía intraventricular (113 ± ms vs. 94 ± 38 ms, p=0.02) e interventricular (62.8 ± 7 ms vs. 39.4 ± 9 ms, p=0.02). Los pacientes con etiología no isquémica tuvieron una mejoría en la sincronía intraventricular (103.8 ± 7 ms vs 78.3 ± 12 ms, p=0.04) e interventricular (68.1 ± 9 ms vs. 35.3 ± 12 ms, p=0.02). En aquellos sin BCRI mejoró la sincronía intraventricular (112.1 ± 8 ms vs. 88.5 ± 11.2 ms, p=0.01). No hubo cambios significativos en pacientes con causa isquémica o con BCRI. Conclusiones: En pacientes con IC y disfunción ventricular izquierda, Carvedilol mejora la sincronía intra e interventricular. Estos efectos podrían estar relacionados a una acción favorable sobre el remodelamiento cardíaco.

Cocaine-induced myocardial infarction associated with severe reversible systolic dysfunction and pulmonary edema

Myocardial infarction (MI) associated to cocaine use was originally reported in 1982 and cases are being encountered more frequently in our milieu. The literature regarding this diagnosis has included mostly cases of cocaine associated chest pain and MI without serious sequelae. A lesser number of reports however focus on the clinical presentation of severe myocardial dysfunction and severe pulmonary edema, with the mechanism for pulmonary edema still being debated. Although previously described individually, these manifestations are thought to be an uncommon complication of cocaine ingestion. In this article the subject is reviewed and we report our experience with two patients that presented to our care with severe pulmonary edema and concomitant severe left ventricular systolic dysfunction that resolved spontaneously with supportive therapy. It is felt that this clinical picture after cocaine use may be more common than expected. In this article we discuss the possible mechanisms associated to this presentation as well as review the literature regarding this subject.

Pheochromocytoma-induced segmental myocardial dysfunction mimicking an acute myocardial infarction in a patient with normal coronary arteries.

We report a case of pheochromocytoma-induced segmental myocardial dysfunction and electrocardiographic abnormalities mimicking an acute anterior myocardial infarction, probably due to coronary spasm. Coronary angiography showed normal coronaries, and the electrocardiographic and echocardiographic changes resolved completely after therapy with an alpha-adrenergic blocker and tumor removal. Our case illustrates the importance of maintaining a high index of suspicion in patients presenting with an unexpected myocardial event and a hypertensive crisis.

Crise de feocromocitoma simulando um infarto agudo do miocárdio em paciente com artérias coronárias normais / Pheochromocytoma-induced segmental myocardial dysfunction mimicking an acute myocardial infarction in a patient with normal coronary arteries

Relatamos o caso de um paciente com alterações eletrocardiográficas e disfunção miocárdica segmentar induzidas por feocromocitoma, simulando infarto agudo do miocárdio. A angiografia coronariana foi normal e houve normalização completa do eletrocardiograma e ecocardiograma, após terapia com um bloqueador alfa-adrenérgico e ressecção do tumor. Espasmo coronariano foi o provável mecanismo envolvido na produção dessas alterações, ilustrando a importância de manter um alto grau de suspeição clínica em pacientes com evento miocárdico inesperado em meio a uma crise hipertensiva.

Cocaine-induced myocardial infarction associated with severe reversible systolic dysfunction and pulmonary edema.

Myocardial infarction (MI) associated to cocaine use was originally reported in 1982 and cases are being encountered more frequently in our milieu. The literature regarding this diagnosis has included mostly cases of cocaine associated chest pain and MI without serious sequelae. A lesser number of reports however focus on the clinical presentation of severe myocardial dysfunction and severe pulmonary edema, with the mechanism for pulmonary edema still being debated. Although previously described individually, these manifestations are thought to be an uncommon complication of cocaine ingestion. In this article the subject is reviewed and we report our experience with two patients that presented to our care with severe pulmonary edema and concomitant severe left ventricular systolic dysfunction that resolved spontaneously with supportive therapy. It is felt that this clinical picture after cocaine use may be more common than expected. In this article we discuss the possible mechanisms associated to this presentation as well as review the literature regarding this subject.

Do cardiologists at a university hospital adopt the guidelines for the treatment of heart failure?

OBJECTIVE: To verify whether the guidelines for the treatment of heart failure have been adopted at a university hospital. The guidelines recommend the following: use of angiotensin-converting enzyme inhibitors for all patients with systolic ventricular dysfunction, use of digitalis and diuretics for symptomatic patients, use of beta-blockers for patients in functional classes II or III, use of spironolactone for patients in functional classes III or IV. METHODS: We analyzed the prescriptions of 199 patients. All these patients had ejection fraction (EF)

Cardiologistas de um hospital escola adotam as diretrizes para o tratamento da insuficiência cardíaca? / Do cardiologists at a university hospital adopt the guidelines for the treatment of heart failure?

OBJECTIVE: To verify whether the guidelines for the treatment of heart failure have been adopted at a university hospital. The guidelines recommend the following: use of angiotensin-converting enzyme inhibitors for all patients with systolic ventricular dysfunction, use of digitalis and diuretics for symptomatic patients, use of beta-blockers for patients in functional classes II or III, use of spironolactone for patients in functional classes III or IV. METHODS: We analyzed the prescriptions of 199 patients. All these patients had ejection fraction (EF) <=0.50, their ages ranged from 25 to 86 years, and 142 were males. Cardiomyopathy was the most frequent diagnosis: 67 (33.6 percent) patients had dilated cardiomyopathy, 65 (32.6 percent) had ischemic cardiomyopathy. RESULTS: Angiotensin-converting enzyme inhibitors were prescribed for 93 percent of the patients. 71.8 percent also had a prescription for digitalis, 86.9 percent for diuretics, 27.6 percent for spironolactone, 12 percent for beta-blockers, 37.2 percent for acetylsalicylic acid, 6.5 percent for calcium channel antagonists, and 12.5 percent for anticoagulants. In regard to vasodilators, 71 percent of the patients were using captopril (85.2mg/day), 20 percent enalapril (21.4mg/day), 3 percent hydralazine and nitrates. In 71.8 percent of the cases, the dosages prescribed were in accordance with those recommended in the large studies. CONCLUSION: Most patients were prescribed the same doses as those recommended in the large studies. Brazilian patients tolerate well the doses recommended in the studies, and that not using these doses may be a consequence of the physician's fear of prescribing them and not of the patient's intolerance