Biomedical subjects

Cassiano Abreu-Lima

Publications and source records attributed to Cassiano Abreu-Lima.

9 recordsLinked to original sources

PubMed2006

Clinical syndrome suggestive of heart failure is frequently attributable to non-cardiac disorders--population-based study.

AIM: To assess how often the clinical syndrome (CS) of heart failure is attributable to alternative, including non-cardiac, explanations. METHODS AND RESULTS: Cross-sectional evaluation of 739 community participants aged>or=45 years. Subjects with >or=2 symptoms or signs (dyspnoea or fatigue, orthopnoea, nocturnal paroxysmal dyspnoea, third heart sound, jugular venous distension, rales and lower limb oedema) or who were receiving loop diuretics were considered to have the clinical syndrome of heart failure. Attributable fractions were derived based on adjusted odds ratios and the prevalence of underlying disorders among cases. CS was present in 28.0% of women and in 15.2% of men, p<0.001. The multivariate-adjusted fraction of CS attributable to female gender was 40.6%, to age>or=65 years 28.5%, left ventricular systolic dysfunction, left ventricular dilatation or moderate-severe valvular disease 4.9%, diastolic dysfunction or atrial fibrillation 13.0%, obesity 22.6%, coronary heart disease 7.2% and chronic lung disease 6.9%. When additionally adjusting for depressive symptoms, the association with gender and age became much weaker, and 32% of cases were attributable to depressive symptoms. Forty-two percent of subjects with CS had cardiac abnormalities. CONCLUSION: In less than half of subjects with CS was systolic or diastolic heart failure confirmed. Female gender, older age, obesity and depressive symptoms accounted for the largest fraction of CS.

Age Factors↗

PubMed2006

Familial dilated cardiomyopathy with troponin T K210del mutation.

BACKGROUND: It has been estimated that more than 30% of patients with idiopathic dilated cardiomyopathy have a familial form of the disease. The most frequent pattern of inheritance is autosomal dominant and several genes or loci have been implicated, coding for sarcomeric or cytoskeleton proteins. Most of the genotype-phenotype correlations are still under study, but a particular mutation, K210del in the troponin T gene, has been identified in four different families with severe forms of DCM. The pathogenesis of this mutation has been inferred by functional studies but its transmission has not been demonstrated, perhaps due to the high mortality of the affected family members. The aim of this work was to investigate the prevalence of the K210del mutation in Portuguese and Mozambican families with dilated cardiomyopathy. METHODS: We evaluated 27 probands with familial DCM. Forty idiopathic (sporadic) DCM patients and 100 non-related healthy individuals were used as controls. Mutational analysis was performed by amplification of exon 13 of the troponin T gene by the polymerase chain reaction (PCR), determination of molecular weight of PCR products and further sequencing. RESULTS: The K210del mutation in the cardiac troponin T gene was identified in one of the DCM families which presented an aggressive form of the disease, with a high incidence of sudden death, and need for heart transplant at young age. One affected member had sustained left ventricular function recovery after diagnosis. CONCLUSIONS: These results reinforce previous work by others, indicating that this mutation is a bad prognostic factor in familial forms of DCM. The K210del mutation in the troponin T gene, like other mutations in the troponin complex, seems to be especially prevalent in families with rapidly progressive DCM or sudden cardiac death at young age.

Adult↗

PubMed2004

[Autonomic nervous system in heart failure].

The autonomic nervous system (ANS), a complex and self-organized entity, plays a crucial role in cardiovascular regulation. In this review, the authors describe some concepts of anatomo-physiology and cellular/molecular biology of the ANS and of its two major components, the parasympathetic and sympathetic system, both in the normal individual and in the patient with heart failure. Adrenergic and cholinergic neurotransmission, neurotransmitters, adrenergic and cholinergic receptors and intracellular signal transduction are discussed. Some aspects of sympathetic-parasympathetic interaction at the cellular level are described as well as the opposite role of two cyclic nucleotides, cyclic adenosine and guanosine monophosphate. Major emphasis is placed on the beta-adrenergic system, the combination of the beta receptor, G protein complex and adenylyl cyclase. The activation of neurohumoral compensatory mechanisms in heart failure is discussed as well as the increasingly recognized importance of sympathetic overactivation and parasympathetic tonus reducting in this setting. Cellular mechanisms of adrenergic stimulation in heart failure and its consequences are presented, with special focus on down-regulation of beta-1 adrenergic receptors; the authors analyze the steps of phosphorlation and oncoupling, sequestration, internalization and lysosomal degradation, the main result of which is reduced response to catecholamines.

Autonomic Nervous System↗

PubMed2004

[Endothelin system and heart failure: a potential therapeutic target].

Neurohormonal activation is a marker and one of the most important pathophysiologic aspects of heart failure. The hyperactivation and participation of the endothelin system in several manifestations of this syndrome have been widely documented in the last few years. These data support attempts to view the endothelin system as a potential pharmacological target in order to reduce the high morbidity and mortality associated with heart failure. This is a short review of the main aspects of endothelin biology, its mechanisms of action, including those at the molecular level, and its pathophysiological role in heart failure. Finally, the potential benefits of the pharmacological manipulation of the endothelin system as well as some results of clinical trials in this context will be presented.

Endothelins↗

PubMed2004

[Heart failure].

Explore the source record for details and available documents.

Heart Failure↗

PubMed2004

Heart transplantation. A Portuguese hospital center's experience.

Cardiac transplantation is the gold standard therapy for patients below 60 years presenting with severe heart failure (HF) despite maximal medical therapy, who have no other surgical option and no contraindications to this procedure. We evaluated our experience with this important form of heart failure therapy. Between February 1987 and December 2002, 32 patients, aged 37 +/- 16 years, 19 males, with ejection fraction of 18 +/- 7%, underwent heart transplantation in our center. Seven (22%) patients were in NYHA class IV with hemodynamic support. Seventeen (53%) patients had idiopathic dilated cardiomyopathy (DCM), 7 (22%) had ischemic DCM, 3 (9%) had valvular DCM and the remainder had other causes of left ventricular dysfunction. Overall survival rate was 68% at first year post-transplantation, 59% at 5 years and 59% at 10 years. One year after cardiac transplantation, 95% of patients were in NYHA class I and the rest were in NYHA class II. Among the 13 patients who died, in five (18%) death occurred during the first month: the most frequent cause was hemodynamic failure. Causes of late death were: allograft vasculopathy (n = 3), allograft rejection (n = 1), infection (n = 1), sudden death (n = 1), hemodynamic failure (n = 1) and bradyarrhythmia (n = 1). Among the patients followed for more than one year, only three died. Early complications were: infection (8 episodes, 7 of respiratory location), right heart failure (3 patients), pericardial effusion (5 patients) and others (7 patients). Late complications were: a) allograft rejection: 17 (53%) patients, 72 episodes (10 ISHLT grade 3, 6 of whom were treated with intravenous corticotherapy, 8 grade 2 and 54 grade 1); b) infections: 19 (59%) patients; 35 episodes, 25 requiring hospitalization: 10 (28%) involving the respiratory tract, 6 (17%) the oropharynx, 5 (14%) the urinary tract, 4 (11%) the skin and 10 (28%) of undetermined location; c) chronic allograft rejection: 6 (19%) patients; d) arterial hypertension: 14 (45%) patients; d) renal failure: 5 (16%) patients; e) diabetes: 2 (6%) patients; f) cancer: 2 (6%) patients. Patients with severe heart failure and a very poor prognosis who underwent cardiac transplantation in our hospital showed marked improvement in functional capacity and quality of life and had an overall survival similar to the results of international heart transplantation registries. Complications during follow-up were similar to those usually described in the literature.

Adult↗

PubMed2003

B-type natriuretic peptide and left ventricular hypertrophy in hypertensive patients.

AIM: To assess the accuracy of B-type natriuretic peptide (BNP) plasma levels for the diagnosis of left ventricular hypertrophy (LVH) in hypertensive patients. PARTICIPANTS AND METHODS: We studied a sample of 409 adults aged 45 years or older, recruited from residents of Porto by random digit dialing. Data were collected by clinical interview and physical examination, ECG, echocardiogram and venous blood sampling for the measurement of plasma concentrations of BNP. Hypertension (HT) was defined as blood pressure > or = 140/90 mmHg on the day of interview and/or self-reported HT if treated with any antihypertensive medication; LVH was defined as left ventricular mass index (LVMI) > or = 125 g/m2 in men and 110 g/m2 in women. The participants were further classified in four strata according to left ventricular morphology--normal, concentric remodeling, eccentric LVH or concentric LVH. RESULTS: Two hundred and thirty-two (56.7%) individuals were hypertensive, and among these 73 (31.5%) had LVH. BNP levels were significantly higher in these individuals (median [P25-P75] = 55.8 pg/ml [22.6-88.4]) than in hypertensive patients without LVH (29.9 pg/ml [10.0-62.8]), p = 0.003. BNP levels also differed significantly across strata of left ventricular geometry, the main difference depending on the presence or absence of LVH. There was a positive correlation between plasma BNP levels and LVMI (Spearman's P 0.185, p = 0.005). The area under the ROC curve--a parameter for diagnostic accuracy quantification--was 0.62 (95% confidence interval 0.54-0.70), indicating low discriminatory power between normal and abnormal LVMI. CONCLUSION: In the assessed population, BNP levels were higher in hypertensive patients with LVH than in the absence of LVH. However, BNP did not perform well in discriminating between the presence or absence of LVH.

Aged↗

PubMed2002

Chronic left ventricular pseudoaneurism.

We present the case of a 70-year-old white male presenting with an abnormal cardiac silhouette on the chest X-ray and complaining of fatigue in the week before hospital admission. Four months before admission he had a single prolonged ischemic chest pain episode. The ECG revealed an old true posterior myocardial infarction. The transthoracic echocardiogram showed a large left ventricular pseudoaneurysm and surgical resection was performed successfully. The etiology, diagnosis and treatment of left ventricular pseudoaneurysm are reviewed.

Aged↗

PubMed2002

Familial dilated cardiomyopathy.

Dilated cardiomyopathy is a disorder affecting heart muscle, characterized by ventricular dilation and reduced systolic function. It represents the most common cause of heart failure. Until recently, dilated cardiomyopathy was considered an exclusively sporadic and idiopathic disease. Now, as defined by the World Health Organization, cardiomyopathy includes not only the idiopathic form, but secondary ones such as ischemic or hypertensive. It is estimated that familial occurrence accounts for 30% of cases of idiopathic dilated cardiomyopathy. The most common mode of inheritance is the autosomal dominant type. The X-linked, autosomal recessive and mitochondrial forms are less common. Different genes or loci are responsible for the cardiac dilatation, and code for sarcomeric, cytoskeleton and nuclear lamina proteins. The molecular interactions of the mutated proteins with factors such as infectious agents or alcohol could explain the variety of presenting signs and symptoms of this type of cardiomyopathy. Recently the European Society of Cardiology published a definition and a protocol for the study of familial dilated cardiomyopathies. Genetic research in the field of dilated cardiomyopathy can increase our understanding of its pathogenesis and lead to new treatment modalities for the disease.

Cardiomyopathy, Dilated↗