Left ventricular pseudoaneurysm associated with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is associated with several cardiac manifestations but, to our knowledge, there have been no previously published reports on left ventricular (LV) pseudoaneurysm in this disease. We describe a case of a 30-year-old woman with SLE who presented with a disease flare (acute and subacute cutaneous lupus, pericarditis, fever, leukopenia) associated with heart failure syndrome. The patient was diagnosed with a large LV pseudoaneurysm and a bovine pericardium patch closure was performed. Coronary arteries were angiographically normal, and cardiac magnetic resonance imaging did not exhibit detectable myocardial fibrosis or infarction. Trauma, previous cardiac surgery, Chagas disease, and antiphospholipid syndrome were excluded. Histopathology of the pericardium revealed lymphocytic arteriolitis raising the possibility of an autoimmune-mediated mechanism for this complication. The unequivocal concomitant diagnosis of lupus flare, the exclusion of other causes of pseudoaneurysm and the histopathological finding of arteriolitis in this patient reinforces the hypothesis of lupus-mediated lesion.

Mycobacterium chelonae valve endocarditis resulting from contaminated biological prostheses.

OBJECTIVES: A rapid-growing mycobacteria biological prosthetic valve (BPV) endocarditis related to prosthetic manufacturing process is described in Brazil. METHODS: From 1999 to 2008, thirty-nine patients underwent BPV replacement due to culture-negative suspected endocarditis. All these cases had histological sections stained by Ziehl-Neelsen method. Clinical and microbiological data were reviewed in all acid-fast bacilli (AFB) positive cases. The 16S-23S internal transcribed sequence (ITS) was amplified using DNA extracted from paraffin-embedded samples, digested with restrictions enzymes and/or sequenced. RESULTS: Eighteen AFB positive BPV (18/39)(46%) were implanted in 13 patients and were from the same manufacturer. Four of them were implanted in other hospitals. Thirteen BPV were histologically proven endocarditis and five showed a colonization pattern. The examination of six non-implanted "sterile" BPV from this manufacturer resulted in 5 AFB positive. Mycobacterium chelonae was the AFB identified by ITS restriction analysis and sequencing. CONCLUSIONS: Rapid-growing mycobacteria infections must be suspected and Ziehl-Neelsen stain always performed on histology of either early or late BPV endocarditis, particularly when blood cultures are negative.

Coenzyme Q10 exogenous administration attenuates cold stress cardiac injury.

The influence of coenzyme Q10 (CoQ10) in cold stress test (-15 degrees C for 4 hours) cardiac functional impairment was studied in isolated isovolumic heart of control rats (C; n=12) and of placebo (P; n=11) and treated rats (CoQ10; n=10). In addition, electron microscopic evaluation of left ventricular (LV) slices (n=3 in each group) allowed us to analyze the myocardial ultrastructure. Maximal values of developed pressure (DPmax) were similarly decreased in cold stressed animals (C=129+/-3.9 mmHg; P=106+/-6.7 mmHg; CoQ10=91+/-3.9 mmHg); however, volume-induced enhancement of pressure generation (slope of DP volume relations: C=0.248+/-0.0203 mmHg / microl; P=0.2831+/-0.0187 mmHg / microl; CoQ10=0.2387 ( 0.0225 mmHg / microl; p > 0.05), and the duration of systole (C=80+/-1.6 ms; P=78+/-1.3 ms; CoQ10=80+/-2.7 ms) were not altered. Myocardial relaxation, evaluated by the relaxation constant (C=39+/-1.9 ms; P=42+/-3.4 ms; CoQ10=51+/-6.0 ms), as well as resting stress / strain relations were unaffected by cold stress. Myocardial samples showed that pretreatment with CoQ10 attenuates myofibrillar and mitochondrial lesions, and prevents mitochondrial fractional area increase (P: 53.11%>CoQ10: 38.78%=C: 33.87%; p< 0.005) indicating that the exogenous administration of CoQ10 can reduce cold stress myocardial injury.

Detection of Mycoplasma pneumoniae and Chlamydia pneumoniae in ruptured atherosclerotic plaques.

This paper reports what is apparently the first observation of Mycoplasma pneumoniae in association with Chlamydia pneumoniae in thrombosed ruptured atheromas. We performed electron microscopy and in situ hybridization in specimens from three patients who died of acute myocardial infarction. These patients had typical symptoms of acute ischemic syndrome. Mycoplasmas were present mainly in the lipid core of the ruptured thrombosed plaque. Vulnerable atheromas are rich in cholesterol and may favor the growth of mycoplasmas, the only microorganisms that require cholesterol for survival. We suggest that the association of Mycoplasma pneumoniae and Chlamydia pneumoniae may increase the virulence of these microorganisms, favoring proliferation, plaque inflammation and possibly plaque rupture.

Detection of Mycoplasma pneumoniae and Chlamydia pneumoniae in ruptured atherosclerotic plaques

This paper reports what is apparently the first observation of Mycoplasma pneumoniae in association with Chlamydia pneumoniae in thrombosed ruptured atheromas. We performed electron microscopy and in situ hybridization in specimens from three patients who died of acute myocardial infarction. These patients had typical symptoms of acute ischemic syndrome. Mycoplasmas were present mainly in the lipid core of the ruptured thrombosed plaque. Vulnerable atheromas are rich in cholesterol and may favor the growth of mycoplasmas, the only microorganisms that require cholesterol for survival. We suggest that the association of Mycoplasma pneumoniae and Chlamydia pneumoniae may increase the virulence of these microorganisms, favoring proliferation, plaque inflammation and possibly plaque rupture

Prognostic values of stromal proportion and PCNA, Ki-67, and p53 proteins in patients with resected adenocarcinoma of the lung.

Data from 64 patients who underwent surgical resection of lung adenocarcinomas were studied to identify clinicopathologic markers that might provide prognostic information on the clinical behavior of this neoplasia Patient staging was performed in accordance with the tumor-node-metastasis system as follows: Stage I (n = 29), Stage II (n = 11), Stage IIIA (n = 21), and Stage IIIB (n = 3). Overall follow-up time corresponded to the follow-up time for patients who were alive and to the survival time for patients who had died, all of them expressed in months. Data included age, staging, histologic type, morphometric assessment of histologic features related to tumor (stroma and vascularization), and immunohistochemical detection of proliferation cell markers (Ki-67 protein and proliferating cell nuclear antigen) and p53 protein. The morphometric assessment was made by the point-counting procedure. Data analysis included Life Tables for Survival and Cox Regression models. Overall follow-up analysis showed that significant univariate predictors (P < .05) were T stage; N stage; tumor stromal proportion; and immunohistochemical indexes of proliferating cell nuclear antigen, Ki-67, and p53 proteins. Variables that presented independent predictive value for overall follow-up with the multivariate model (P < .05) were sex, T stage, N stage, tumor stromal proportion, and immunohistochemical detection of p53 protein. We conclude that tumor stromal proportion and immunohistochemical detection of p53 protein, controlled for sex, T stage, and N stage, may be of critical value in the evaluation of recurrence of lung adenocarcinoma, serving as indicators for a more accurate prognosis.

Histological evidence of concomitant intramyocardial and epicardial vasculitis in necropsied heart allografts: a possible relationship with graft coronary arteriosclerosis.

BACKGROUND: The significance of medial lymphocytic vasculitis in intramural coronary vessels in heart transplantation is very poorly understood. This study was designed to identify histological evidence of an association between the presence of epicardial coronary lesions and the occurrence of intramyocardial vasculitis and/or myocardial ischemia. METHODS: We analyzed the frequency of medial vasculitis and other myocardial histological alterations in a retrospective study of 24 human cardiac allografts from patients who died of ischemic heart disease and/or myocardial rejection. RESULTS: Medial lymphocytic vasculitis in the myocardium was associated with vasculitis in the vasa vasorum of the epicardial coronary arteries and the presence of microfoci of acute myocardial infarction but was independent of the occurrence of myocardial fiber rejection. Chronic graft epicardial arteriopathy revealed two patterns of lesions. One pattern was similar to that of usual atherosclerosis, compromising mainly the proximal segments of the coronary artery, and was not associated with intramural vasculitis. The other pattern demonstrated diffuse involvement of the epicardial artery associated with vasculitis of its vasa vasorum and lymphocytic vasculitis of the intramural vessels. This second type of epicardial coronary lesion seemed to evolve to fibrotic arteries with thinned walls, frequently demonstrating aneurysmal dilatation with severe fibrosis of the adventitia and poor vasa vasorum. CONCLUSION: Medial vasculitis affecting intramyocardial vessels is associated with adventitial epicardial coronary vasculitis in the transplanted heart. The process of vasculitis may be involved in the development of chronic graft arteriosclerosis and is associated with ischemic myocardial lesions, but seems independent of myocardial fiber rejection.