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We review the evidence for the presence of stem/progenitor cells in the heart and the preclinical and clinical data using diverse cell types for the therapy of cardiac diseases. We highlight the failure of adult stem/progenitor cells to ameliorate heart function in most cardiac diseases, with the possible exception of refractory angina. The use of pluripotent stem cell-derived cardiomyocytes is analysed as a viable alternative therapeutic option but still needs further research at preclinical and clinical stages. We also discuss the use of direct reprogramming of cardiac fibroblasts into cardiomyocytes and the use of extracellular vesicles as therapeutic agents in ischemic and non-ischemic cardiac diseases. Finally, gene therapies and genome editing for the treatment of hereditary cardiac diseases, ablation of genes responsible for atherosclerotic disease, or modulation of gene expression in the heart are discussed.

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The precise mechanisms underlying the cardiovascular complications due to acute kidney injury (AKI) and the retention of uremic toxins like p-cresyl sulfate (PCS) remain incompletely understood. The objective of this study was to evaluate the renocardiac effects of PCS administration in animals subjected to AKI induced by ischemia and reperfusion (IR) injury. C57BL6 mice were subjected to distinct protocols: (i) administration with PCS (20, 40, or 60 mg/L/day) for 15 days and (ii) AKI due to unilateral IR injury associated with PCS administration for 15 days. The 20 mg/L dose of PCS led to a decrease in renal mass, an increase in the gene expression of Cystatin C and kidney injury molecule 1 (KIM-1), and a decrease in the α-actin in the heart. During AKI, PCS increased the renal injury biomarkers compared to control; however, it did not exacerbate these markers. Furthermore, PCS did not enhance the cardiac hypertrophy observed after 15 days of IR. An increase, but not potentialized, in the cardiac levels of interleukin (IL)-1ß and IL-6 in the IR group treated with PCS, as well as in the injured kidney, was also noticed. In short, PCS administration did not intensify kidney injury, inflammation, and cardiac outcomes after AKI.

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BACKGROUND AND AIMS: Developing novel therapies to battle the global public health burden of heart failure remains challenging. This study investigates the underlying mechanisms and potential treatment for 4-hydroxynonenal (4-HNE) deleterious effects in heart failure. METHODS: Biochemical, functional, and histochemical measurements were applied to identify 4-HNE adducts in rat and human failing hearts. In vitro studies were performed to validate 4-HNE targets. RESULTS: 4-HNE, a reactive aldehyde by-product of mitochondrial dysfunction in heart failure, covalently inhibits Dicer, an RNase III endonuclease essential for microRNA (miRNA) biogenesis. 4-HNE inhibition of Dicer impairs miRNA processing. Mechanistically, 4-HNE binds to recombinant human Dicer through an intermolecular interaction that disrupts both activity and stability of Dicer in a concentration- and time-dependent manner. Dithiothreitol neutralization of 4-HNE or replacing 4-HNE-targeted residues in Dicer prevents 4-HNE inhibition of Dicer in vitro. Interestingly, end-stage human failing hearts from three different heart failure aetiologies display defective 4-HNE clearance, decreased Dicer activity, and miRNA biogenesis impairment. Notably, boosting 4-HNE clearance through pharmacological re-activation of mitochondrial aldehyde dehydrogenase 2 (ALDH2) using Alda-1 or its improved orally bioavailable derivative AD-9308 restores Dicer activity. ALDH2 is a major enzyme responsible for 4-HNE removal. Importantly, this response is accompanied by improved miRNA maturation and cardiac function/remodelling in a pre-clinical model of heart failure. CONCLUSIONS: 4-HNE inhibition of Dicer directly impairs miRNA biogenesis in heart failure. Strikingly, decreasing cardiac 4-HNE levels through pharmacological ALDH2 activation is sufficient to re-establish Dicer activity and miRNA biogenesis; thereby representing potential treatment for patients with heart failure.

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Background and Aims Developing novel therapies to battle the global public health burden of heart failure remains challenging. This study investigates the underlying mechanisms and potential treatment for 4-hydroxynonenal (4-HNE) deleterious effects in heart failure. Methods Biochemical, functional, and histochemical measurements were applied to identify 4-HNE adducts in rat and human failing hearts. In vitro studies were performed to validate 4-HNE targets. Results 4-HNE, a reactive aldehyde by-product of mitochondrial dysfunction in heart failure, covalently inhibits Dicer, an RNase III endonuclease essential for microRNA (miRNA) biogenesis. 4-HNE inhibition of Dicer impairs miRNA processing. Mechanistically, 4-HNE binds to recombinant human Dicer through an intermolecular interaction that disrupts both activity and stability of Dicer in a concentration- and time-dependent manner. Dithiothreitol neutralization of 4-HNE or replacing 4-HNE-targeted residues in Dicer prevents 4-HNE inhibition of Dicer in vitro. Interestingly, end-stage human failing hearts from three different heart failure aetiologies display defective 4-HNE clearance, decreased Dicer activity, and miRNA biogenesis impairment. Notably, boosting 4-HNE clearance through pharmacological re-activation of mitochondrial aldehyde dehydrogenase 2 (ALDH2) using Alda-1 or its improved orally bioavailable derivative AD-9308 restores Dicer activity. ALDH2 is a major enzyme responsible for 4-HNE removal. Importantly, this response is accompanied by improved miRNA maturation and cardiac function/remodelling in a pre-clinical model of heart failure. Conclusions 4-HNE inhibition of Dicer directly impairs miRNA biogenesis in heart failure. Strikingly, decreasing cardiac 4-HNE levels through pharmacological ALDH2 activation is sufficient to re-establish Dicer activity and miRNA biogenesis; thereby representing potential treatment for patients with heart failure.

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Over the development of eukaryotic cells, intrinsic mechanisms have been developed in order to provide the ability to defend against aggressive agents. In this sense, a group of proteins plays a crucial role in controlling the production of several proteins, guaranteeing cell survival. The heat shock proteins (HSPs), are a family of proteins that have been linked to different cellular functions, being activated under conditions of cellular stress, not only imposed by thermal variation but also toxins, radiation, infectious agents, hypoxia, etc. Regarding pathological situations as seen in cardiorenal syndrome (CRS), HSPs have been shown to be important mediators involved in the control of gene transcription and intracellular signaling, in addition to be an important connector with the immune system. CRS is classified as acute or chronic and according to the first organ to suffer the injury, which can be the heart (CRS type 1 and type 2), kidneys (CRS type 3 and 4) or both (CRS type 5). In all types of CRS, the immune system, redox balance, mitochondrial dysfunction, and tissue remodeling have been the subject of numerous studies in the literature in order to elucidate mechanisms and propose new therapeutic strategies. In this sense, HSPs have been targeted by researchers as important connectors between kidney and heart. Thus, the present review has a focus to present the state of the art regarding the role of HSPs in the pathophysiology of cardiac and renal alterations, as well their role in the kidney-heart axis.

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The prevalence of cardiovascular mortality is higher in men than in age-matched premenopausal women. Gender differences are linked to circulating sex-related steroid hormone levels and their cardio-specific actions, which are critical factors involved in the prevalence and features of age-associated cardiovascular disease. In women, estrogens have been described as cardioprotective agents, while in men, testosterone is the main sex steroid hormone. The effects of testosterone as a metabolic regulator and cardioprotective agent in aging men are poorly understood. With advancing age, testosterone levels gradually decrease in men, an effect associated with increasing fat mass, decrease in lean body mass, dyslipidemia, insulin resistance and adjustment in energy substrate metabolism. Aging is associated with a decline in metabolism, characterized by modifications in cardiac function, excitation-contraction coupling, and lower efficacy to generate energy. Testosterone deficiency -as found in elderly men- rapidly becomes an epidemic condition, associated with prominent cardiometabolic disorders. Therefore, it is highly probable that senior men showing low testosterone levels will display symptoms of androgen deficiency, presenting an unfavorable metabolic profile and increased cardiovascular risk. Moreover, recent reports establish that testosterone replacement improves cardiomyocyte bioenergetics, increases glucose metabolism and reduces insulin resistance in elderly men. Thus, testosterone-related metabolic signaling and gene expression may constitute relevant therapeutic target for preventing, or treating, age- and gender-related cardiometabolic diseases in men. Here, we will discuss the impact of current evidence showing how cardiac metabolism is regulated by androgen levels in aging men.

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Emerging data indicate a substantial decrease in global physical activity levels during the period of social isolation adopted worldwide to contain the spread of the coronavirus disease 2019 (COVID-19). Confinement-induced decreases in physical activity levels and increases in sedentary behavior may provoke a rapid deterioration of cardiovascular health and premature deaths among populations with increased cardiovascular risk. Even short-term (1-4 wk) inactivity has been linked with detrimental effects in cardiovascular function and structure and increased cardiovascular risk factors. In this unprecedented and critical scenario, home-based physical activity programs arise as a clinically relevant intervention to promote health benefits to cardiac patients. Many studies have demonstrated the feasibility, safety, and efficacy of different models of home-based exercise programs in the primary and secondary prevention of cardiovascular diseases and major cardiovascular events among different populations. This body of knowledge can inform evidence-based policies to be urgently implemented to counteract the impact of increased physical inactivity and sedentary behavior during the COVID-19 outbreak, thereby alleviating the global burden of cardiovascular disease.

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BACKGROUND: The present study analyzed the synergistic protective effect of ß-alanine and taurine against myocardial ischemia/reperfusion. Myocardial infarct size, lipid peroxidation, and levels of glutathione peroxidase (Gpx), superoxide dismutase (SOD), reduced glutathione (GSH), catalase, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), reactive oxygen species (ROS), apoptosis, and the mRNA and protein expression of Janus kinase 2 (JAK2) and signal transducer and activator 3 of transcription (STAT3) were determined. The molecular docking was carried out by using AutoDock 4.2.1. RESULTS: Combined treatment with ß-alanine and taurine reduced myocardial infarct size, lipid peroxidation, inflammatory marker, ROS levels, and apoptosis and increased Gpx, SOD activity, GSH, and catalase activity. Furthermore, combined treatment significantly reduced JAK2 and STAT3 mRNA and protein expression compared with the control. The small molecule was docked over the SH2 domain of a STAT3, and binding mode was determined to investigate the inhibitory potential of ß-alanine and taurine. ß-Alanine bound to SH2 domain with ΔG of -7.34 kcal/mol and KI of 1.91 µM. Taurine bound to SH2 domain with ΔG of -7.38 kcal/mol and KI of 1.95 µM. CONCLUSION: Taken together, these results suggest that the combined supplementation of ß-alanine and taurine should be further investigated as an effective therapeutic approach in achieving cardioprotection in myocardial ischemia/reperfusion.

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The advances in biotechnology, biomechanics, and biomaterials can be used to develop organ models that aim to accurately emulate their natural counterparts. Heart disease, one of the leading causes of death in modern society, has attracted particular attention in the field of tissue engineering. To avoid incorrect prognosis of patients suffering from heart disease, or from adverse consequences of classical therapeutic approaches, as well as to address the shortage of heart donors, new solutions are urgently needed. Biotechnological advances in cardiac tissue engineering from a bioreactor perspective, in which recapitulation of functional, biochemical, and physiological characteristics of the cardiac tissue can be used to recreate its natural microenvironment, are reviewed. Detailed examples of functional and preclinical applications of engineered cardiac constructs and the state-of-the-art systems from a bioreactor perspective are provided. Finally, the current trends and future directions of the field for its translation to clinical settings are discussed.

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Acute coronary syndrome (ACS) is the leading cause of death in elderly patients worldwide. Due its participation in apoptosis, fibrosis, and angiogenesis, transforming growth factor-ß (TGF-ß) isoforms had been categorized as risk factors for cardiovascular diseases. However, due their contradictory activities, a cardioprotective role has been suggested. The aim was to measure the plasma levels of TGF-ß1, 2, and 3 proteins in patients with ACS. This was a case-control study including 225 subjects. The three activated isoforms were measured in serum using the Bio-Plex Pro TGF-ß assay by means of magnetic beads; the fluorescence intensity of reporter signal was read in a Bio-Plex Magpix instrument. We observed a significant reduction of the three activated isoforms of TGF-ß in patients with ACS. The three TGF-ß isoforms were positively correlated with each other in moderate-to-strong manner. TGFß-2 was inversely correlated with glucose and low-density lipoprotein (LDL)-cholesterol, whereas TGF-ß3 was inversely correlated with the serum cholesterol concentration. The production of TGF-ß1, TGF-ß2, and TGF-ß3 are decreased in the serum of patients with ACS. Further follow-up controlled studies with a larger sample size are needed, in order to test whether TGF-ß isoforms could be useful as biomarkers that complement the diagnosis of ACS.

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Objetivos: construir um instrumento para aplicação do processo de enfermagem para pacientes hospitalizados em unidades cardiológicas; treinar os enfermeiros destas unidades para o uso do instrumento e; avaliar a qualidade dos registros antes e após o treinamento por meio do Quality of Diagnosis, Interventions and Outcomes (Q-DIO). Métodos: Trata-se de um estudo quase-experimental que avaliou os registros de enfermagem de prontuários de pacientes de unidades cardiológicas, de um hospital universitário na cidade do Rio de Janeiro/RJ. Foi realizado em duas fases: a elaboração do instrumento para aplicação do processo de enfermagem para os pacientes com distúrbios cardiológicos hospitalizados, baseado na linguagem padronizada NANDA-I, NIC E NOC (NNN) baseada em uma revisão integrativa sobre registros de enfermagem para pacientes com doenças cardiovasculares e na sequência foi realizado um treinamento com enfermeiros das unidades cardiológicas sobre registro de enfermagem e uso do instrumento. O Q-DIO foi aplicado para avaliação da qualidade dos registros antes e após o treinamento. Resultados: O instrumento elaborado possibilitou o registro de enfermagem pautado nos domínios da NANDA-I e a seleção dos diagnósticos, intervenções e resultados foi de acordo com a literatura. O treinamento foi realizado com enfermeiros das unidades cardiológicas e proporcionou uma troca de experiências teórico-práticas positivas. Após o treinamento com os enfermeiros sobre o uso de linguagens padronizadas NNN e o uso do instrumento, o escore total do Q-DIO aumentou no momento pós-intervenção (14,8±5,7vs.29,0±10,5; p=0,003). Conclusão: A qualidade dos registros foi considerada satisfatória após treinamento e utilização do instrumento para aplicação do processo de enfermagem, no entanto, são necessárias mais pesquisas experimentais sobre o processo de enfermagem e sobre a qualidade do registro de enfermagem principalmente referente às intervenções de enfermagem

Goals: to build an instrument for the application of the nursing process for hospitalized patients in cardiac units; to train nurse of these units for the use o the instrument and; to assess the quality of the records before and after the treatment through the Quality of Diagnosis, Interventions and Outcomes (Q-DIO). Methods: It is a quasi-experimental study that evaluated the nursing records of patients of cardiac units of an academic hospital in the city of Rio de Janeiro/RJ. It was performed in two phases: the elaboration of the instrument for the application of the nursing process for hospitalized patients with cardiac disorders based on a standardized language NANDA-I, NIC E NOC (NNN) based on a integrative revision about the nursing records for patients with cardiac diseases and in the sequence it was performed a training with nurses from cardiac units about the nursing records and the usage of the instrument. The Q-DIO was applied for the evaluation of the quality of the records before and after the training. Outcomes: The elaborated instrument enabled the nursing records based on NANDA-I domains and the diagnosis selection, interventions and results was according to the literature. The training was performed with nurses from cardiac units and provided a positive theoretical-practical exchange of experiences. After the training with the nurses about the use of the NNN standardized language and the use of the instrument, the total score of the Q-DIO increased in the post-intervention moment (14,8±5,7vs.29,0±10,5; p=0,003). Conclusion: The quality of the records was considered satisfactory, after training and the usage of the instrument for the application of the nursing process, however it is necessary to have more experimental research about the nursing process and about the quality of the nursing process mainly for the nursing interventions

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Objetivo: Evaluar mediante un estudio prospectivo, observacional y transversal, la incidencia de la aorta bivalva y su asociación con patología aórtica en el laboratorio de ecocardiografía. Material y métodos: Se analizaron todos los enfermos consecutivos estudiados mediante ecocardiografía del 1º de septiembre de 2009 al 14 de enero de 2011 en búsqueda de aorta bivalva y su asociación con otra patología aórtica. Resultados: Se realizó un total de 2,750 estudios en este periodo de tiempo. En 72 (2.6%) no fue posible precisar con claridad el número de valvas. Se detectaron 137 enfermos con aorta bivalva (4.9%). El promedio de edad fue 13.3 años ± 9.6, mediana de 11 años, 81 fueron hombres (59.1%) y 56 fueron mujeres (40.9%), 14 (10.2%) tuvieron por lo demás corazón estructuralmente normal. En 99 (72.3%) se encontraron lesiones relacionadas con patología aórtica: 50 (36.5%) fueron coartación aórtica, 22 (16.1%) doble lesión aórtica, 10 (7.3%) estenosis subaórtica, 9 (6.6%) estenosis aórtica, 1 (0.7%) dilatación aneurismática de raíz aórtica con coartación aórtica, 2 (1.5%) con dilatación aórtica no significativa de la raíz aórtica, 3 (2.2%) insuficiencia aórtica, 1 (0.7%) interrupción del arco aórtico, 1 (0.7%) desarrolló endocarditis, y en 24 casos (17.5%) con aorta bivalva se encontraron lesiones no relacionadas con patología aórtica. Conclusiones: La aorta bivalva en un laboratorio de ecocardiografía es relativamente frecuente: 4.9% en este trabajo. En los pacientes con corazón estructuralmente normal se encontró aorta bivalva en el 0.5% de la población. La presencia de aorta bivalva estuvo asociada con lesión significativa en ella misma o con otras lesiones del tracto de salida izquierdo en el 3.6% de los casos. La dilatación aórtica y coartación aórtica estuvieron presentes en un paciente (0.7%). La presencia de endocarditis bacteriana asociada a aorta bivalva la encontramos en el 0.7%. Es importante el seguimiento a largo plazo de aquellos pacientes que presentan aorta bivalva dado que hasta en un 30% de los casos pueden desarrollar complicaciones.

Objective: To evaluate by a prospective, observational and cross study the incidence of bicuspid aorta valve and associated aortic disease in the echocardiography laboratory. Material and methods: We analyzed all the consecutive patients studied by echocardiography from the 1st of September 2009 to January 14, 2011, in search of bicuspid aortic bivalve and its associations. Results: A total of 2,750 studies were made in this period of time. In 72 (2.6%) was not possible to specify clearly the number of valves. There were detected 137 patients with bicuspid aortic (4.9%). The age average was 13.27 years ± 9.64, median 11 years, 81 were men (59.1%), 56 women (40.9%), 14 (10.2%) were otherwise structurally normal heart. It was found that 99 (72.3%) had aortic disease-related injuries: 50 (36.5%) had aortic coarctation, 22 (16.1%) double aortic lesion, 10 (7.3%) subaortic stenosis, 9 (6.6%) aortic stenosis, 1 (0.7%) dilation of aortic root aneurysm with aortic coarctation, 2 (1.5%) no significant expansion of the root aortic, 3 (2.2%) aortic regurgitation, 1 (0.7%) interrupted aortic arch, 1 (0.7%) developed endocarditis a in 24 cases (17.5%) with bicuspid aortic lesions were not related to aortic disease. Conclusions: The bicuspid aorta in an echocardiography lab is relatively frequent: 4.9% in this work. In patients with structurally normal heart bicuspid aorta were found in 0.5% of the population. The presence of bicuspid aorta was associated with significant injury to herself or with other lesions of the left outflow tract in 3.6% of cases. The aortic dilatation and aortic coarctation was present in 0.7% patients. The presence of bacterial endocarditis associated with bicuspid aortic found in 0.7%. It is important to the long-term monitoring of those patients with bicuspid aortic as much as 30% of cases can develop complications.

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Cardiovascular diseases are the most common cause of death worldwide. In Kuwait, death related to cardio vascular diseases may account for about 40%. Thus, it will be the greatest health care burden of the twenty-first century. Hypertension and diabetes are the two major risk factors in the development of cardiac hypertrophy, ischemic heart disease, cardiac failure, cardiac arrhythmias and myocardial infarction. The kallikrein-kinin components (plasma and urinary kininogens, kallikreins, kininases and kinins) are able to regulate BP and blood glucose levels via promoting; vasodilator, natriuretic effects and glucose metabolism. These components are located in the cardiac tissue, kidney and vascular smooth muscle. The kinin system is found to be abnormally depressed in various experimental animal models of hypertension and diabetes which might be responsible for inducing cardiac complications. It has been pointed out that the development of a compound having renal kallikrein-like activity may serve the purpose of excreting excessive sodium from the kidney in the treatment of hypertension. Also it has been demonstrated that transgenic mice over-expressing renal tissue kallikrein were hypotensive and that administration of aprotinin, a tissue kallikrein inhibitor, restored the BP of the transgenic mice. These findings highlight a role of tissue kallikrein in the regulation of BP. It has been proposed that tissue kallikrein gene delivery into various hypertensive models exhibits protection, such as reduction in high BP, attenuation of cardiac hypertrophy, inhibition of renal damage and stenosis. This may indicate the prospect of this kallikrein gene therapy for cardiovascular pathology. Several reports indicate that urinary kallikrein excretion is decreased in essential hypertension in humans and in models of experimental hypertension. Thus, reduced urinary kallikrein may reflect a deficiency in the endogenous kallikrein/kinin vasodilatory system that contributes to the pathogenesis of hypertension. Previous studies conducted in white and black population in the USA demonstrated that urinary kallikrein excretion is diminished in family members at risk for hereditary (essential) hypertension and that urinary kallikrein is one of the major genetic markers associated with family history of hypertension. Also evidence for genetic linkage between the kallikrein locus and blood pressure has been reported in the rat. Previous studies have suggested that diminished urinary kallikrein excretion is associated with salt sensitivity of blood pressure. Kallikrein excretion is also diminished in African-Americans and deficiency of the kallikreinkinin renal vasodilatory system may explain many of the unique features of essential hypertension and heart diseases in some black subjects.

Las enfermedades cardiovasculares son la causa más frecuente de muerte en todo el mundo. En Kuwait, la muerte relacionada a enfermedades cardiovasculares puede llegar al 40%. De este modo, será la mayor carga para el sistema de salud del siglo XXI. La hipertensión y la diabetes son los dos factores de riesgo mayores en la producción de hipertrofia cardíaca, cardiopatía isquémica, insuficiencia cardíaca, arritmias cardíacas e infarto de miocardio. Los componentes del sistema calicreína-quinina (quininógenos plasmáticos y urinarios, calicreínas, quininasas y quininas) regulan la PA y los niveles de glucosa sanguínea mediante estimulación de la vasodilatación, efectos natriuréticos y metabolismo de la glucosa. Esos componentes se localizan en el tejido cardíaco, riñón y células musculares lisas. El sistema quinina se encuentra deprimido anormalmente en varios modelos animales experimentales de hipertensión y diabetes que podrían ser responsables de la aparición de complicaciones cardíacas. Se ha señalado que el hallar un compuesto con actividad renal similar a la calicreína puede ser útil al propósito de excretar el exceso de sodio por el riñón en el tratamiento de la hipertensión. También se demostró que los ratones transgénicos que sobreexpresan calicreína por el tejido renal eran hipotensos y que la administración de aprotinina, un inhibidor de la calicreína tisular, restaura la PA de los ratones transgénicos. Esos hallazgos realzaron el papel de la calicreína tisular en la regulación de la PA. Se ha propuesto que el gen de la calicreína tisular entregado en varios modelos de hipertensión ejerce protección, como reducción de la PA aumentada, atenuación de la hipertrofia cardíaca, inhibición de la estenosis y del daño renal. Esto puede indicar la posibilidad de este tratamiento con gen de calicreína para trastronos cardiovasculares. Varios informes indican que la excreción urinaria de calicreína está disminuida en la hipertensión esencial en humanos y en modelos de hipertensión experimental. De este modo, la reducción de la calicreína urinaria puede reflejar una deficiencia en el sistema vasodilatador endógeno calicreína/quinina que contribuye a la patogénesis de la hipertensión. Algunos estudios previos realizados en la población blanca y negra en los EE.UU. demostraron que la excreción urinaria de calicreína está disminuida en miembros familiares con riesgo de hipertensión hereditaria (esencial) y que la calicreína urinaria es uno de los mayores marcadores genéticos asociado con historia familiar de hipertensión. También se informó la existencia de unión genética entre el locus de la calicreína y la presión sanguínea, en ratas. Algunos estudios sugirieron que la excreción urinaria disminuida de calicreína se asocia con sensibilidad de la presión sanguínea a la sal. La excreción de calicreína también está disminuida en afroamericanos y la deficiencia del sistema renal vasodilatador de calicreína-quinina puede explicar muchas de las características singulares de la hipertensión y de las enfermedades cardíacas en algunos sujetos de raza negra.

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No presente trabalho, são mostrados resultados de um estudo piloto direcionado à detecção de seqüências de enterovirus em tecido cardíaco obtido a partir de biópsias endomiocárdicas de pacientes com doenças cardíacas na região Amazônica. Seis amostras coletadas de três pacientes foram analisadas por RT-PCR obtendo-se três espécimes positivos e três negativos. Esses achados preliminares sugerem a participação dos enterovirus na etiologia de doenças cardíacas, principalmente miocardites, e justificam estudos mais amplos nesse assunto.

In the present report we describe the results from a pilot study aimed at detecting enterovirus sequence in cardiac tissues, obtained through endomyocardial biopsies, from patients suffering from cardiac diseases in the Amazon region. Six samples that were collected from three patients were analysed by RT-PCR showing 3 positive and 3 negative results. These preliminary findings suggest the participation of enteroviruses in the etiology of cardiac diseases, mainly myocarditis, and warrant further and broader local studies on this subject.

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