Anti-heart autoantibodies in ischaemic heart disease patients.
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One hundred and ninety-nine ischaemic heart disease (IHD) patients were studied with regard to the prevalence of anti-heart autoantibodies (AHA). The incidence of AHA in IHD patients was 1%: one out of 102 patients who suffered acute myocardial infarction (AMI), one out of seventy-two patients who suffered from acute coronary insufficiency (ACI), and none out of twenty-five patients with other signs and symptoms of IHD, had AHA in their sera. An additional 2% of patients who suffered from AMI developed detectable antibody levels during a follow-up period of 15 days. In comparison,, 53% of patients (eight out of fifteen) who underwent heart surgery and who had no AHA prior to operation, developed these antibodies in their sera during 1-2 weeks following operation. (+info)
Rheumatic chorea in northern Australia: a clinical and epidemiological study.
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To describe the epidemiology and clinical features of Sydenham's chorea in the Aboriginal population of northern Australia a review was conducted of 158 episodes in 108 people: 106 were Aborigines, 79 were female, and the mean age was 10.9 years at first episode. Chorea occurred in 28% of cases of acute rheumatic fever, carditis occurred in 25% of episodes of chorea, and arthritis in 8%. Patients with carditis or arthritis tended to have raised acute phase reactants and streptococcal serology. Two episodes lasted at least 30 months. Mean time to first recurrence of chorea was 2.1 years compared with 1.2 years to second recurrence. Established rheumatic heart disease developed in 58% of cases and was more likely in those presenting with acute carditis, although most people who developed rheumatic heart disease did not have evidence of acute carditis with chorea. Differences in the patterns of chorea and other manifestations of acute rheumatic fever in different populations may hold clues to its pathogenesis. Long term adherence to secondary prophylaxis is crucial following all episodes of acute rheumatic fever, including chorea, to prevent recurrence. (+info)
Superantigen-induced T cell responses in acute rheumatic fever and chronic rheumatic heart disease patients.
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CD4+ and CD8+ T cells from healthy donors, acute rheumatic fever (ARF) and chronic rheumatic heart disease (CRHD) patients responded variably to a superantigen from Streptococcus pyogenes--Streptococcal pyrogenic erythrogenic toxin A (SPE-A). In vitro culture of CD4+ T cells from ARF patients (CD4-ARF) with SPE-A exhibited a Th1 type of response as they produced high levels of IL-2, while CD4+ T cells from CRHD patients (CD4-RHD) secreted IL-4 and IL-10 in large amounts, i.e. Th2 type of cytokine profile. The skewing of human CD4+ T cells (in response to SPE-A stimulation) to Th1 or Th2 type reflects the role of the two subsets in a disorder with differing intensities at the two extremes of the spectrum. Moreover, the anergy induction experiments revealed that CD8-ARF and CD8-RHD undergo anergy (to different extents), whereas CD4+ T cells do not, in response to re-stimulation by SPE-A. These results initially demonstrate that both CD4+ and CD8+ T cells respond differentially to SPE-A, and hence it is an important observation with respect to the pathogenesis of ARF/CRHD. Anergy in CD8+ T cells in the presence of SPE-A in vitro goes a step further to show the clinical relevance of these cells and their possible role in suppression of the disease. (+info)
HLA class II associations with rheumatic heart disease are more evident and consistent among clinically homogeneous patients.
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BACKGROUND: Discrepancies in reported HLA class II associations with rheumatic heart disease (RHD) may have been due to inaccuracies of serological typing reagents and/or lack of defined clinical classification of patients analyzed. The molecular association between HLA and RHD was investigated in patients with defined clinical outcome. METHODS AND RESULTS: Class II allele/haplotype distribution was determined in 2 groups of RHD patients (n=88) and a control group (n=59). Patients were divided into the mitral valve disease (MVD) category (ie, those with mitral regurgitation with or without mitral stenosis) and the multivalvular lesions (MVL) category, with impairment of aortic and/or tricuspid valves in addition to mitral valve damage. The MVD category (n=65) accounted for 74% of patients and included significantly fewer recurrent RF episodes compared with MVL patients (P=0.002). CONCLUSIONS: Significant increases in DRB1*0701 and DQA1*0201 alleles and DRB1*0701-DQA1*0201 haplotypes were found in patients. Removal of the MVL patients from analysis increased the strength of HLA associations among the MVD sample. The frequency of DQA1*0103 allele was decreased and the DQB1*0603 allele was absent from the patient group, suggesting that these alleles may confer protective effects against RHD. DQ alleles in linkage disequilibrium with DR alleles appear to influence risk/protection effect: whereas the DRB1*13-DQA1*0501-3-DQB1*0301 haplotype showed a trend toward risk, the DRB1*13-DQA1*0103-DQB1*0603 haplotype was absent in the RHD sample. Our data indicate that certain class II alleles/haplotypes are associated with risk or protection from RHD and that these associations appear to be stronger and more consistent when analyzed in patients with relatively more homogeneous clinical manifestations. (+info)
The natural history of aortic valve disease after mitral valve surgery.
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OBJECTIVES: The present study evaluates the long-term course of aortic valve disease and the need for aortic valve surgery in patients with rheumatic mitral valve disease who underwent mitral valve surgery. BACKGROUND: Little is known about the natural history of aortic valve disease in patients undergoing mitral valve surgery for rheumatic mitral valve disease. In addition there is no firm policy regarding the appropriate treatment of mild aortic valve disease while replacing the mitral valve. METHODS: One-hundred thirty-one patients (44 male, 87 female; mean age 61+/-13 yr, range 35 to 89) were followed after mitral valve surgery for a mean period of 13+/-7 years. All patients had rheumatic heart disease. Aortic valve function was assessed preoperatively by cardiac catheterization and during follow-up by transthoracic echocardiography. RESULTS: At the time of mitral valve surgery, 59 patients (45%) had mild aortic valve disease: 7 (5%) aortic stenosis (AS), 58 (44%) aortic regurgitation (AR). At the end of follow-up, 96 patients (73%) had aortic valve disease: 33 AS (mild or moderate except in two cases) and 90 AR (mild or moderate except in one case). Among patients without aortic valve disease at the time of the mitral valve surgery, only three patients developed significant aortic valve disease after 25 years of follow-up procedures. Disease progression was noted in three of the seven patients with AS (2 to severe) and in six of the fifty eight with AR (1 to severe). Fifty two (90%) with mild AR remained stable after a mean follow-up period of 16 years. In only three patients (2%) the aortic valve disease progressed significantly after 9, 17 and 22 years. In only six patients of the entire cohort (5%), aortic valve replacement was needed after a mean period of 21 years (range 15 to 33). In four of them the primary indication for the second surgery was dysfunction of the prosthetic mitral valve. CONCLUSIONS: Our findings indicate that, among patients with rheumatic heart disease, a considerable number of patients have mild aortic valve disease at the time of mitral valve surgery. Yet most do not progress to severe disease, and aortic valve replacement is rarely needed after a long follow-up period. Thus, prophylactic valve replacement is not indicated in these cases. (+info)
Predictors of clinical events or restenosis during follow-up after percutaneous mitral balloon valvotomy.
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AIMS: The purpose of this study is to define predictors of events or restenosis during follow-up after percutaneous mitral balloon valvotomy. METHODS AND RESULTS: Percutaneous mitral balloon valvotomy was attempted in 137 patients with severe mitral valve stenosis. In 127 patients follow-up was complete with a mean of 4.2 +/- 2.6 years. Events during follow-up were defined as death, mitral valve surgery or repeat percutaneous mitral balloon valvotomy. Restenosis was defined as a decrease in mitral valve area from > or = 1.5 cm2 following percutaneous mitral balloon valvotomy to < 1.5 cm2. There was 80 +/- 4% event-free survival 4 years after percutaneous mitral balloon valvotomy. Multivariate analysis showed chronic atrial fibrillation at baseline (P = 0.039, relative risk (RR) = 2.5) and a high residual maximal gradient after percutaneous mitral balloon valvotomy (P = 0.004, RR = 2.0 per 5 mmHg) to be independent predictors of an event during follow-up. The restenosis rate was 28.3% after 4 years. Chronic atrial fibrillation at baseline (P = 0.0338, RR = 2.2), a small mitral valve area after percutaneous mitral balloon valvotomy (P = 0.0003, RR = 0.8/0.1 cm2) and a high residual maximal transmitral gradient (P = 0.0252, RR = 1.6/5 mmHg) were all independent predictors of restenosis. CONCLUSION: Patients with chronic atrial fibrillation and a high maximal transmitral gradient after percutaneous mitral balloon valvotomy have a higher risk for events during follow-up. Restenosis is related to the presence of chronic atrial fibrillation at baseline and a suboptimal percutaneous mitral balloon valvotomy result. (+info)
Electron microscopic observations of apoptotic cells in various etiologies of human cardiovascular diseases.
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OBJECTIVE: To observe apoptotic process in various cardiovascular disorders with a particular attention to the ultrastructural morphology of apoptosis in cardiomyocytes, fibroblasts, vascular endothelial cells and smooth muscle cells. METHODS: Transmission electron microscopic observations of the tissue specimens obtained from endomyocardial biopsies or surgical excisions of left ventricular myocardium or calcified aortic valves were carried out in 50 patients with various cardiovascular diseases. RESULTS: The ultrastructural features of apoptosis was consistently observed in cardiomyocytes, fibroblasts, vascular endothelial cells and smooth muscle cells in all diseased tissues. In cardiomyopathies and rheumatic heart diseases apoptosis was commonly observed in the cardiomyocytes. It was often found that fibroblasts underwent apoptosis in calcific aortic valve tissues. Apoptosis of arterial smooth muscle cells was a frequent finding in renal arterial stenosis due to Takayasu's arteritis and fibromuscular dysplasia. Regardless of the cell types, the nuclear hallmarks of apoptosis were identical with minor modifications of the fragmentation of the condensed cells into apoptotic bodies. CONCLUSIONS: Based on electron microscopic findings, it is suggested that the underlying disease processes determine which type of cells predominantly undergoes apoptotic changes in various cardiovascular disorders. In addition, different cells with similar structural morphology may have common ultrastructural features of apoptosis. (+info)
Injuries and noncommunicable diseases: emerging health problems of children in developing countries.
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The present article identifies, for children living in developing countries, the major causes of ill-health that are inadequately covered by established health programmes. Injuries and noncommunicable diseases, notably asthma, epilepsy, dental caries, diabetes mellitus and rheumatic heart disease, are growing in significance. In countries where resources are scarce it is to be expected that increasing importance will be attached to the development and implementation of measures against these problems. Their control may benefit from the application of elements of programmes directed against infectious, nutritional and perinatal disorders, which continue to predominate. (+info)