Prognostic Value of Pulmonary Vascular Resistance by Magnetic Resonance in Systolic Heart Failure

Abstract Background: Pulmonary hypertension is associated with poor prognosis in heart failure. However, non-invasive diagnosis is still challenging in clinical practice. Objective: We sought to assess the prognostic utility of non-invasive estimation of pulmonary vascular resistances (PVR) by cardiovascular magnetic resonance to predict adverse cardiovascular outcomes in heart failure with reduced ejection fraction (HFrEF). Methods: Prospective registry of patients with left ventricular ejection fraction (LVEF) < 40% and recently admitted for decompensated heart failure during three years. PVRwere calculated based on right ventricular ejection fraction and average velocity of the pulmonary artery estimated during cardiac magnetic resonance. Readmission for heart failure and all-cause mortality were considered as adverse events at follow-up. Results: 105 patients (average LVEF 26.0 ±7.7%, ischemic etiology 43%) were included. Patients with adverse events at long-term follow-up had higher values of PVR (6.93 ± 1.9 vs. 4.6 ± 1.7estimated Wood Units (eWu), p < 0.001). In multivariate Cox regression analysis, PVR ≥ 5 eWu(cutoff value according to ROC curve) was independently associated with increased risk of adverse events at 9 months follow-up (HR2.98; 95% CI 1.12-7.88; p < 0.03). Conclusions: In patients with HFrEF, the presence of PVR ≥ 5.0 Wu is associated with significantly worse clinical outcome at follow-up. Non-invasive estimation of PVR by cardiac magnetic resonance might be useful for risk stratification in HFrEF, irrespective of etiology, presence of late gadolinium enhancement or LVEF.

Functional Class in Children with Idiopathic Dilated Cardiomyopathy. A pilot Study

Abstract Background: Idiopathic dilated cardiomyopathy (IDCM), most common cardiac cause of pediatric deaths, mortality descriptor: a low left ventricular ejection fraction (LVEF) and low functional capacity (FC). FC is never self reported by children. Objective: The aims of this study were (i) To evaluate whether functional classifications according to the children, parents and medical staff were associated. (iv) To evaluate whether there was correlation between VO2 max and Weber's classification. Method: Prepubertal children with IDCM and HF (by previous IDCM and preserved LVEF) were selected, evaluated and compared. All children were assessed by testing, CPET and functional class classification. Results: Chi-square test showed association between a CFm and CFp (1, n = 31) = 20.6; p = 0.002. There was no significant association between CFp and CFc (1, n = 31) = 6.7; p = 0.4. CFm and CFc were not associated as well (1, n = 31) = 1.7; p = 0.8. Weber's classification was associated to CFm (1, n = 19) = 11.8; p = 0.003, to CFp (1, n = 19) = 20.4; p = 0.0001and CFc (1, n = 19) = 6.4; p = 0.04). Conclusion: Drawing were helpful for children's self NYHA classification, which were associated to Weber's stratification.

Fractal Dimension in Quantifying Experimental-Pulmonary-Hypertension-Induced Cardiac Dysfunction in Rats

Abstract Background: Right-sided heart failure has high morbidity and mortality, and may be caused by pulmonary arterial hypertension. Fractal dimension is a differentiated and innovative method used in histological evaluations that allows the characterization of irregular and complex structures and the quantification of structural tissue changes. Objective: To assess the use of fractal dimension in cardiomyocytes of rats with monocrotaline-induced pulmonary arterial hypertension, in addition to providing histological and functional analysis. Methods: Male Wistar rats were divided into 2 groups: control (C; n = 8) and monocrotaline-induced pulmonary arterial hypertension (M; n = 8). Five weeks after pulmonary arterial hypertension induction with monocrotaline, echocardiography was performed and the animals were euthanized. The heart was dissected, the ventricles weighed to assess anatomical parameters, and histological slides were prepared and stained with hematoxylin/eosin for fractal dimension analysis, performed using box-counting method. Data normality was tested (Shapiro-Wilk test), and the groups were compared with non-paired Student t test or Mann Whitney test (p < 0.05). Results: Higher fractal dimension values were observed in group M as compared to group C (1.39 ± 0.05 vs. 1.37 ± 0.04; p < 0.05). Echocardiography showed lower pulmonary artery flow velocity, pulmonary acceleration time and ejection time values in group M, suggesting function worsening in those animals. Conclusion: The changes observed confirm pulmonary-arterial-hypertension-induced cardiac dysfunction, and point to fractal dimension as an effective method to evaluate cardiac morphological changes induced by ventricular dysfunction.

Estudos sobre thrombose cardiaca e endocardite parietal de origem não valvular

1.-Since the parietal endocarditis represents a chapter generally neglected, owing to the relative lack of cases, and somewhat confused because there various terms have been applied to a very same morbid condition, it justifies the work which previously we tried to accomplish, of nosographic classification. Taking into account the functional disturbances and the anatomical changes, all cases of parietal endocarditis referred to in the litterature were distributed by the following groups: A-Group-Valvulo-parietal endocarditis. 1st . type-Valvulo-parietal endocarditis per continuum. 2nd. type-Metastatic valvulo-parietal endocarditis. 3rd. type-Valvulo-parietal endocarditis of the mitral stenosis. B-Group-Genuine parietal endocarditis. a) with primary lesions in the myocardium. b) with primary lesions in the endocardium. 4th type-Fibrous chronic parietal endocarditis (B A Ü M L E R), « endocarditis parietalis simplex». 5th type-Septic acute parietal endocarditis (LESCHKE), «endocarditis parietalis septica». 6th type-Subacute parietal endocarditis (MAGARINOS TORRES), «endocarditis muralis lenta». 2.-Studying a group of 14 cases of fibrous endomyocarditis with formation of thrombi, and carrying together pathological and bacteriological examinations it has been found that some of such cases represent an infectious parietal endocarditis, sometimes post-puerperal, of subacute or slow course, the endocardic vegetations being contamined by pathogenic microörganisms of which the most frequent is the Diplococcus pneumoniae, in most cases of attenuated virulence. Along with the infectious parietal endocarditis, there occur arterial and venous thromboses (abdominal aorta, common illiac and femural arteries and external jugular veins). The case 5,120 is a typical one of this condition which we name subacute parietal endocarditis (endocarditis parietalis s. muralis lenta). 3.-The endocarditis muralis lenta encloses an affection reputed to be of rare occurrence, the «myocardite subaigüe primitive», of which JOSSERAND and GALLAVARDIN published in 1901 the first cases, and ROQUE and LEVY, another, in 1914. The «myocardite subaigüe primitive» was, wrongly, in our opinion, included by WALZER in the syndrome of myocardia of LAUBRY and WALZER, considering that, in the refered cases of JOSSERAND and GALLAVARDIN and in that of ROQUE and LEVY, there are described rather considerable inflammatory changes in the myocardium and endocardium. The designation «myocardia» was however especially created by LAUBRY and WALZER for the cases of heart failure in which the most careful aetiologic inquiries and the most minucious clinical examination were unable to explain, and in which, yet, the post-mortem examination did not reveal any anatomical change at all, it being forcible to admit, then, a primary functional change of the cardiac muscle fibre. This special cardiac condition is thoroughly exemplified in the observation that WALZER reproduces on pages 1 to 7 of his book. 4.-The clinical picture of the subacute parietal endocarditis is that of heart failure with oedemas, effusion in the serous cavities and passive chronic congestion of the lungs, liver, kideys and spleen associated, to that of an infectious disease of subacute course. The fever is rather transient oscillating around 99.5 F., being intersected with apyretic periods of irregular duration; it is not dependent on any evident extracardiac septic infection. In other cases the fever is slight, particularly in the final stage of the disease, when the heart failure is well established. The rule is to observe then, hypothermy. The cardiac-vascular signs consist of enlargement of the cardiac dullness, smoothing of the cardiac sounds, absence of organic murmurs and accentuated and persistent tachycardia up to a certain point independent of fever. The galloprhythm is present, in most cases. The signs of the pulmonary infarct are rather expressed by the aspect of the sputum, which is foamy and blood-streaked than by the classic signs. Cerebral embolism was a terminal accident on various cases. Yet, in some of them, along with the signs of septicemia and of cardiac insufficiency, occurred vascular, arterial (abdominal aorta, common illiac and femurals arteries) and venous (extern jugular veins) thromboses. 5. The autopsy revealed an inflammatory process located on the parietal endocardium, accompanied by abundant formation of ancient and recent thrombi, being the apex of the left ventricle, the junction of the anterior wall of the same ventricle, with the interventricular septum, and the right auricular appendage, the usual seats of the inflammatory changes. The region of the left branch of HIS’ bundle is spared. The other changes found consist of fibrosis of the myocardium (healed infarcts and circumscribed interstitial myocarditis), of recent visceral infarcts chiefly in lungs, spleen and brain, of recent or old infarcts in the kidneys (embolic nephrocirrhosis) and in the spleen, and of vascular thromboses (abdominal aorta, common illiacs and femurals arteries and external jugular veins), aside from hydrothorax, hydroperitoneum, cutaneous oedema, chronic passive congestion of the liver, lungs, spleen and kidneys and slight ictericia. 6. In the subacute parietal endocarditis the primary lesions sometimes locate themselves at the myocardium, depending on the ischemic necrosis associated to the arteriosclerosis of the coronariae arteries, or on an specific myocarditis. Other times, the absence of these conditions is suggestive of a primary attack to the parietal endocardium which is then the primary seat of the lesions. It matters little whatever may be the initial pathogenic mechanism; once injured the parietal endocardium and there being settled the infectious injury, the endocarditis develops with peculiar clinical and anatomical characters of remarkable uniformity, constituting an anatomo-clinical syndrome. 7.-The histologic sections show that recent lesions…

Diagnosing pulmonary embolism in outpatients with clinical assessment, D-dimer measurement, venous ultrasound, and helical computed tomography: a multicenter management study.

PURPOSE: To evaluate a diagnostic strategy for pulmonary embolism that combined clinical assessment, plasma D-dimer measurement, lower limb venous ultrasonography, and helical computed tomography (CT). METHODS: A cohort of 965 consecutive patients presenting to the emergency departments of three general and teaching hospitals with clinically suspected pulmonary embolism underwent sequential noninvasive testing. Clinical probability was assessed by a prediction rule combined with implicit judgment. All patients were followed for 3 months. RESULTS: A normal D-dimer level (&lt;500 microg/L by a rapid enzyme-linked immunosorbent assay) ruled out venous thromboembolism in 280 patients (29%), and finding a deep vein thrombosis by ultrasonography established the diagnosis in 92 patients (9.5%). Helical CT was required in only 593 patients (61%) and showed pulmonary embolism in 124 patients (12.8%). Pulmonary embolism was considered ruled out in the 450 patients (46.6%) with a negative ultrasound and CT scan and a low-to-intermediate clinical probability. The 8 patients with a negative ultrasound and CT scan despite a high clinical probability proceeded to pulmonary angiography (positive: 2; negative: 6). Helical CT was inconclusive in 11 patients (pulmonary embolism: 4; no pulmonary embolism: 7). The overall prevalence of pulmonary embolism was 23%. Patients classified as not having pulmonary embolism were not anticoagulated during follow-up and had a 3-month thromboembolic risk of 1.0% (95% confidence interval: 0.5% to 2.1%). CONCLUSION: A noninvasive diagnostic strategy combining clinical assessment, D-dimer measurement, ultrasonography, and helical CT yielded a diagnosis in 99% of outpatients suspected of pulmonary embolism, and appeared to be safe, provided that CT was combined with ultrasonography to rule out the disease.

Diagnostic d'embolie pulmonaire: problématique résiduelle des D-dimères faussement positifs [The unresolved issue of false-positive D-dimer results in the diagnostic workup of pulmonary embolism].

The unresolved issue of false-positive D-dimer results in the diagnostic workup of pulmonary embolism Pulmonary embolism (PE) remains a difficult diagnosis as it lacks specific symptoms and clinical signs. After the determination of the pretest PE probability by a validated clinical score, D-dimers (DD) is the initial blood test in the majority of patients whose probability is low or intermediate. The low specificity of DD results in a high number of false-positives that then require thoracic angio-CT. A new clinical decision rule, called the Pulmonary Embolism Rule-out criteria (PERC), identifies patients at such low risk that PE can be safely ruled-out without a DD test. Its safety has been confirmed in US emergency departments, but retrospective European studies showed that it would lead to 5-7% of undiagnosed PE. Alternative strategies are needed to reduce the proportion of false-positive DD results.

Patogenesis of pipe-stem fibrosis of the liver (experimental observation on murine Schistosomiasis)

Mice infected with 30 cercariae of Schistosoma mansoni developed portal and septal fibrosis due to the massive and concentrated deposition of eggs in the periportal areas which occurred following the 16th week after infection. The lesion resembled pipe-stem fibrosis seen in human hepatosplenic schistosomiasis in the following characters: portal fibrosis interconnecting portal spaces as well as portal spaces and central canals; portal inflammation; periovular granulomas; vascular obstruction and telangiectasia. The liver parenchyma maintained its normal architecture. Vascular injection techniques with Indian ink and vinylite revealed that the portal system developed numerous dilated collateral venules coming from the large and medium-sized portal branches, about 10 weeks after schistosome infection. The lodging of schistosome eggs into these collaterals resulted in granulomatous inflammation and fibrosis along all the portal tracts, thus forming the pipe-stem lesion. Although not readily demonstrable grossly, the pipe-stem fibrosis of murine schistosomiasis has many similarities with the human lesion and can be considered to have the same basic pathogenesis.

Cell-matrix interactions in Schistosomal portal fibrosis: a dynamic event

In recent years, one of the most significant progress in the understanding of liver diseases was the demonstration that liver fibrosis is a dynamic process resulting from a balance between synthesis and degradation of several matrix components, collagen in particular. Thus, fibrosis has been found to be a very early event during liver diseases, be it of toxic, viral or parasitic origin, and to be spontaneously reversible, either partially or totally. In liver fibrosis cell matrix interactions are dependent on the existence of the many factors (sometimes acting in combination) which produce the same events at the cellular and molecular levels. These events are: (i) the recruitment of fiber-producing cells, (ii) their proliferation, (iii) the secretion of matrix constituents of the extracellular matrix, and (iv) the remodeling and degradation of the newly formed matrix. All these events represent, at least in principle, a target for a therapeutic intervention aimed at influencing the experimentally induced hepatic fibrosis. In this context, hepatosplenic schistosomiasis is of particular interest, being an immune cell-mediated granulomatous disease and a model of liver fibrosis allowing extensive studies in human and animals as well as providing original in vitro models.

Pulmonary involvement in Schistosomiasis mansoni

The post-treatment pulmonary alterations were evaluated in patients (Study 1) and in mice (Study 2) infected with Schistosoma mansoni. Study 1: the patients were examined pre and post-treatment (with ora oxamniquine) and the following exams were performed: sputum for eosinophils and chest x-ray. Study 2: four groups of mice (total = 64) were studied; Group I (infected and treated with oxamniquine); II (infected and not treated); III (not infected and treated) and IV (not infected and not treated). All were x-rayed to check for pulmonary abnormalities pre and post-treatment and lung specimens were studied by optical microscopy and immunofluorescence. We have found abnormalities in the parameters checked in both studies and the results suggest an immunological reaction, probably due to deposition of immune complexes in the lungs, with subsequent activation of the complement system. The experimental study showed that the alterations are not dependent of the presence of eggs and/or worms of S. mansoni in the lungs, thus corroborating the hypothesis of deposition of circulating material.

Transcatheter stent-valve implantation in a stenotic pulmonary conduit via a sub-xyphoidian access

Patients who develop a severe stenosis in biological pulmonary conduits previously implanted for pulmonary outflow trunk reconstructions are treated either by surgical re-replacement, or by transcatheter stent-valve implantation through a femoral vein access. A catheter-based sub-xyphoidian access through the right ventricle for stent-valve positioning in a pulmonary conduit has rarely been proposed. We describe the case of a 20-year-old man who underwent a pulmonary trunk reconstruction for a congenital pulmonary valve dysplasia and a few years later developed a stenosis in the pulmonary conduit. He was successfully treated with a 23 mm Edwards Sapien stent-valve implantation in pulmonary position, through an unusual right ventricular, sub-xyphoidian access and without contrast medium injections and pleura opening.

Microbiota abnormalities in inflammatory airway diseases - Potential for therapy.

Increasingly the development of novel therapeutic strategies is taking into consideration the contribution of the intestinal microbiota to health and disease. Dysbiosis of the microbial communities colonizing the human intestinal tract has been described for a variety of chronic diseases, such as inflammatory bowel disease, obesity and asthma. In particular, reduction of several so-called probiotic species including Lactobacilli and Bifidobacteria that are generally considered to be beneficial, as well as an outgrowth of potentially pathogenic bacteria is often reported. Thus a tempting therapeutic approach is to shape the constituents of the microbiota in an attempt to restore the microbial balance towards the growth of 'health-promoting' bacterial species. A twist to this scenario is the recent discovery that the respiratory tract also harbors a microbiota under steady-state conditions. Investigators have shown that the microbial composition of the airway flora is different between healthy lungs and those with chronic lung diseases, such as asthma, chronic obstructive pulmonary disease as well as cystic fibrosis. This is an emerging field, and thus far there is very limited data showing a direct contribution of the airway microbiota to the onset and progression of disease. However, should future studies provide such evidence, the airway microbiota might soon join the intestinal microbiota as a target for therapeutic intervention. In this review, we highlight the major advances that have been made describing the microbiota in chronic lung disease and discuss current and future approaches concerning manipulation of the microbiota for the treatment and prevention of disease.