An animal model of chronic rheumatic valvulitis induced by formalin-killed streptococci

Rheumatic heart disease is the most severe complication of rheumatic fever. Till date, very few successful animal models of rheumatic valvular disease have been reported. This study aimed at developing a suitable animal model of chronic rheumatic valvulitis for further investigation and prevention of rheumatic heart disease. Lewis rats were immunized with one administration of formalin-killed and sonicated group A streptococci together with Complete Freund’s Adjuvant every 7 days for three cycles followed by group A streptococci alone till killing. Control rats were administered adjuvants and saline. Rats in group 1 were killed 12 weeks after the initial injection. Rats in group 2 and control group were killed 24 weeks after the initial injection. Results 62.5% (5/8) of rats in group 1 developed myocarditis and 50% (4/8) developed valvulitis. Histological examination of cardiac sections showed only cellular infiltrates. In contrast, 75% (6/8) of rats in group 2 developed rheumatic-like myocarditis and 62.5% (5/8) developed chronic valvulitis. Histological manifestations of the hearts in group 2 animals involved not only acute damage such as cellular infiltrates, Aschoff-like cells, verrucous vegetation, but also chronic lesions such as fibrosis, vascular neogenesis. None of the rats (0/8) in control group presented myocarditis or valvulitis. Lewis rat repeatedly immunized with formalin-killed GAS may be a suitable animal model of chronic rheumatic valvulitis. It may be useful for future investigation of the pathogenesis and possible preventive strategies of human rheumatic heart disease.     

The relationship of carditis to the initial attack of Sydenham's chorea

BACKGROUND: The natural history of valvular regurgitation detected by echocardiography in Sydenham's chorea has been lacking. METHODS: Clinical assessment and transthoracic color Doppler echocardiography were independently performed for each patient with an initial attack of Sydenham's chorea and also for each normal control (Khon Kaen University, Thailand; 1991-2001) at the time of their presentations. Serial clinical examinations and echocardiography were done for each patient at 1- and at 5-year follow-up. RESULTS: Of 44 patients, 17 (39%) had carditis (valvulitis) evident by auscultation at the time of the initial attack. Three (11%) of the 27 patients with no clinical evidence of carditis had echocardiographic evidence of acute mitral regurgitation (subclinical valvulitis). All 17 patients with carditis had echocardiographic evidence of acute mitral regurgitation. None of the 88 control children had evidence of pathologically significant valvular regurgitation. Of the 15 patients with carditis regularly followed, the persistence of a mitral regurgitation murmur and of pathologically significant valvular regurgitation by echocardiography were 33% (5/15) and 60% (9/15), respectively, at 1-year follow-up, but the persistence of both was 25% (1/4) at 5-year follow-up. CONCLUSIONS: Color Doppler echocardiography is a useful tool in the early diagnosis of rheumatic carditis (valvulitis) and at 1-year follow-up of rheumatic valvular heart disease in the patients with initial Sydenham's chorea but the incremental benefit beyond 5 years after the initial attack might be minimal.     

Inhibition of adjuvant-induced arthritis by DNA vaccination with the 70-kd or the 90-kd human heat-shock protein: immune cross-regulation with the 60-kd heat-shock protein

OBJECTIVE: Adjuvant arthritis can be induced in Lewis rats by immunization with Mycobacterium tuberculosis (Mt). The mycobacterial 65-kd heat-shock protein (Hsp65) is targeted by arthritogenic T cells. However, Hsp65 and the mycobacterial 71-kd heat-shock protein are also recognized by T cells that can down-regulate adjuvant-induced arthritis (AIA). We have recently demonstrated that vaccination with human Hsp60 DNA inhibits AIA. The present study was undertaken to analyze the role of the T cell responses to self HSP molecules other than Hsp60 in the control of AIA. METHODS: Lewis rats were immunized with DNA vaccines coding for human Hsp70 or Hsp90 (Hsp70 plasmid [pHsp70] or pHsp90), and AIA was induced. The T cell response to Mt, Hsp60, Hsp70, and Hsp90 (proliferation and cytokine release) was studied, and the T cell response to Hsp60 was mapped with overlapping peptides. RESULTS: The Hsp70 or Hsp90 DNA vaccines shifted the arthritogenic T cell response from a Th1 to a Th2/3 phenotype and inhibited AIA. We detected immune crosstalk between Hsp70/90 and Hsp60: both the Hsp70 and Hsp90 DNA vaccines induced Hsp60-specific T cell responses. Similarly, DNA vaccination with Hsp60 induced Hsp70-specific T cell immunity. Epitope mapping studies revealed that Hsp60-specific T cells induced by pHsp70 vaccination reacted with known regulatory Hsp60 epitopes. CONCLUSION: T cell immunity to Hsp70 and to Hsp90, like Hsp60-specific immunity, can modulate the arthritogenic response in AIA. In addition, our results suggest that the regulatory mechanisms induced by Hsp60, Hsp70, and Hsp90 are reinforced by an immune network that connects their reactivities.     

Identification of immunodominant CD4+ T cell epitopes in patients with Yersinia-induced reactive arthritis by cytometric cytokine secretion assay

OBJECTIVE: In reactive arthritis (ReA), a bacteria-specific T cell response to the triggering microbe is detected in synovial fluid. So far, direct characterization of bacteria-specific T cells and identification of the immunodominant fine specificities remain difficult due to the lack of appropriate techniques. The aim of the present study was to directly determine the fine specificity of CD4+ T cells specific to ReA-associated bacteria-derived protein. METHODS: In 2 patients with Yersinia-induced ReA, live Yersinia Hsp60-specific CD4+ T cells were directly isolated from synovial fluid after stimulation with Yersinia-derived protein Hsp60 using a cytometric cytokine secretion assay. Generated short-term T cell lines were then tested in vitro for their peptide epitope specificity. Also, direct cross-reactivity of one line with Chlamydia- and human-derived Hsp60 was assessed. RESULTS: Generated short-term CD4+ T cell lines were highly antigen-specific and revealed single immunodominant peptide epitopes that were confirmed by direct testing with single peptides in both peripheral blood and synovial fluid cells. Yersinia Hsp60-specific T cells of one patient cross-reacted directly with human Hsp60. CONCLUSION: Our results demonstrate the feasibility of direct assessment of live, potentially pathogenic, antigen-specific interferon-gamma+ CD4+ T cells taken from inflammatory lesions of patients with rheumatic diseases such as ReA. This might have implications not only regarding pathogenesis, but also in the design of new immunotherapies.     

Production and characterization of immortalized rat hepatocytes secreting hepatocyte growth factor/scatter factor

BACKGROUND/AIMS: Hepatocyte transplantation is a recently attractive field in the treatment of liver failure and enzyme-deficient diseases. However, procurement of sufficient quantities of hepatocytes is almost impossible. We attempted to create a hepatocyte cell line that could be used for hepatocyte transplantation. METHODOLOGY: L2A2 is a conditionally immortalized rat hepatocyte cell line produced by transfection of temperature-sensitive simian virus T antigen to the hepatocytes in the Lewis rat. Hepatocyte Growth Factor/Scatter Factor (HGF/SF)-secreting L2A2 cells, designated as SF-21, was produced by transfecting human HGF/SF cDNA into L2A2 cells. RESULTS: This cell line was able to produce HGF/SF at the rate of 5-10 ng/10(6) cells/24 hrs, and the recombinant HGF/SF was of the expected size and was functionally active in that it could scatter Madin-Darby canine kidney cells. The SF-21 cells grew faster than its parental cell clone, and survived and proliferated at 37 degrees C in vitro. Also, the SF-21 cells were able to survive and proliferate when transplanted into the spleen of syngeneic rat, and expressed glucose-6-phosphatase. CONCLUSIONS: These HGF/SF-secreting hepatocytes can be used as a model system to test a feasibility of using genetically engineered hepatocyte cell line for hepatocyte transplantation in the rat.     

心肌细胞促凝血活性与风湿热发病关系的探讨

目的 探讨风湿热的发病机制，了解心肌细胞促凝血活性与风湿热发病的关系。方法 用风湿性心脏炎患者的外周血淋巴细胞、血清及Ａ组乙型溶血链球菌膜抗原作为刺激物，测定体外培养的人胚心肌细胞促凝血活性（ＨＰＣＡ）。结果 患者的外周血淋巴细胞能使ＨＰＣＡ明显升高；静止期风心病，风湿性关节炎、其他疾病对照组及健康对照组患者的外周血淋巴细胞均无此特性，迁延活动型风湿性心脏炎患者的血清及Ａ组乙型溶血链球菌膜抗原对Ｈ     

Identification of HLA-A2-restricted T-cell epitopes derived from the MUC1 tumor antigen for broadly applicable vaccine therapies.

The tumor-associated antigen MUC1 is overexpressed on various hematological and epithelial malignancies and is therefore a suitable candidate for broadly applicable vaccine therapies. It was demonstrated that major histocompatibility complex (MHC)-unrestricted cytotoxic T cells can recognize epitopes of the MUC1 protein core localized in the tandem repeat domain. There is increasing evidence now that MHC-restricted T cells can also be induced after immunization with the MUC1 protein or segments of the core tandem repeat. Using a computer analysis of the MUC1 amino acid sequence, we identified two novel peptides with a high binding probability to the HLA-A2 molecule. One of the peptides is derived from the tandem repeat region and the other is derived from the leader sequence of the MUC1 protein, suggesting that, in contrast to previous reports, the MUC1-directed immune responses are not limited to the extracellular tandem repeat domain. Cytotoxic T cells (CTL) were generated from several healthy donors by primary in vitro immunization using peptide-pulsed dendritic cells. The addition of a Pan-HLA-DR binding peptide PADRE as a T-helper epitope during the in vitro priming resulted in an increased cytotoxic activity of the MUC1-specific CTL and a higher production of cytokines such as interleukin-12 and interferon-gamma in the cell cultures, demonstrating the importance of CD4 cells for an efficient CTL priming. The peptide induced CTL lysed tumors endogenously expressing MUC1 in an antigen-specific and HLA-A2-restricted fashion, including breast and pancreatic tumor cells as well as renal cell carcinoma cells, showing that these peptides are shared among many tumors. The use of MUC1-derived peptides could provide a broadly applicable approach for the development of dendritic cell-based vaccination therapies.     

淋巴细胞贴壁试验诊断风湿性心脏意义的探讨

为寻找新的特异性和敏感性的指标，以探讨风湿热的活动性，从而提高风湿热和风心病的诊疗水平。方法用Ａ组乙型溶血链球菌特异性菌膜抗原和１％植物血凝素（ＰＨＡ）作为刺激物，分别测定３８例健康对照组，３０例风湿性心脏病风湿活动组，２４例风湿性心脏病静止组的外周血淋巴细胞贴壁抑制百分率（Ｌｙｍｐｈｏｃｙｔｅ ａｄｈｅｒｅｎｃｅ ｉｎｈｉｂｉｔｉｏｎ ｐｅｒｃｅｎｔ，ＬＡＩＰ）和促凝血活性（Ｐｒｏｃｏａｇｕｌａ     

抗心瓣膜蛋白抗体在风湿性心瓣膜炎中的意义

目的　针对风湿性心瓣膜炎的早期诊断 ,建立一项检测抗心瓣膜蛋白抗体的方法 ,并探讨其临床意义。方法　采用ELISA法检测抗心瓣膜蛋白抗体 (AVP) ,比较 30例风湿性心瓣膜炎、31例风湿性心脏病、2 4例风湿性关节炎和 40名正常人血清中AVP水平 ,并与抗链球菌多糖抗体(ASP)、红细胞沉降率 (ESR)及C反应蛋白 (CRP)作一对比。结果　风湿性心瓣膜炎组AVP水平高于其他三个组 (P <0 0 5 ) ,风湿性心脏病静止组高于后两个组 (P <0 0 5 ) ,而后两组间差异无显著性(P >0 0 5 )。风湿性心瓣膜炎组AVP阳性率高于ESR及CRP。风湿性关节炎组AVP阳性率低于ASP阳性率。结论　AVP具有判断风湿性心瓣膜炎的临床价值 ,且具有较ESR、CRP敏感性高的优点。     

Anticardiolipin antibodies in acute rheumatic fever.

Recent reports describe the association of antiphospholipid antibodies (aPL) with chorea or severe heart valve lesions in systemic lupus erythematosus, lupus-like disease, or the primary antiphospholipid antibody syndrome. We conducted a case series and a case-control investigation of patients with rheumatic fever with Sydenham chorea or other manifestations of rheumatic fever for anticardiolipin antibodies (aCL) during the acute attack and disease remission. Eighty percent of patients were positive for aCL during the rheumatic fever attack vs 40% when inactive (p = 0.035); IgG and IgM aCL increased significantly with disease activity. Individuals with or without Sydenham chorea were equally positive for aCL (76 and 83%, respectively). A significant association was found between IgM aCL and carditis: All patients with valvulitis had IgM aCL (100%) vs 37% of patients without valvular involvement (p = 0.02). aPL may play a role in the pathogenesis of some clinical manifestations of acute rheumatic fever.     

Hemagglutinin protein is a primary target of the measles virus-specific HLA-A2-restricted CD8+ T cell response during measles and after vaccination

To characterize the measles virus (MV)-specific T cell responses important for evaluation of measles vaccines, human leukocyte antigen (HLA)-A2-positive and -negative adults immunized with measles-mumps-rubella vaccine were studied. Both groups developed increases in antibody and in interferon (IFN)- gamma -producing cells in response to pooled hemagglutinin (H) and fusion peptides. HLA-A2-binding peptides were predicted for all MV-encoded proteins and confirmed by T2 cell stabilization. Twenty-nine peptides were tested, and 19 (6 from H) stimulated increased IFN- gamma secretion in a majority of vaccinees. Peptide-loaded HLA-A2 tetramers or immunoglobulin dimers documented MV-specific CD8+ T cell responses after vaccination and during measles and confirmed new A2 epitopes in H (250-259 and 516-525 aa) and matrix (M; 50-58 aa) protein and previously described epitopes in H (30-38 aa), M (211-219 aa), and nonstructural protein C (84-92 aa). No single peptide dominated the response. We conclude that H is an important stimulus for CD8+ T cell as well as for antibody responses in HLA-A2-positive individuals.     

Prospective comparison of clinical and echocardiographic diagnosis of rheumatic carditis: long term follow up of patients with subclinical disease

OBJECTIVE—To determine the frequency of occurrence and long term evolution of subclinical carditis in patients with acute rheumatic fever.
DESIGN—Valvar incompetence was detected by clinical examination and Doppler echocardiographic imaging during the acute and quiescent phases of rheumatic fever. Patients were followed prospectively and submitted to repeat examinations at one and five years after the acute attack. Persistence of acute mitral and aortic lesions detected solely by echocardiography (subclinical disease) was compared with that of disease detected by clinical examination as well (thereby fulfilling the latest 1992 Jones criteria for rheumatic carditis).
SETTING—Three general hospitals with a university affiliation in Chile.
PATIENTS—35 consecutive patients fulfilling the revised Jones criteria for rheumatic fever. Clinical and echocardiographic examination was repeated in 32 patients after one year and in 17 after five years. Ten patients had subclinical carditis on admission, six of whom were followed for five years.
MAIN OUTCOME MEASURES—Auscultatory and echocardiographic evidence of mitral or aortic regurgitation during the acute attack or at follow up.
RESULTS—Mitral or aortic regurgitation was detected by Doppler echocardiographic imaging in 25/35 rheumatic fever patients as opposed to 5/35 by clinical examination (p = 0.03). Doppler echocardiography revealed acute valvar lesions in 10 of 20 rheumatic fever patients who had no auscultatory evidence of rheumatic carditis (subclinical carditis). Three of these subclinical lesions and three of the clinical or auscultatory lesions detected on admission were still present after five years of follow up, emphasising that subclinical lesions are not necessarily transient.
CONCLUSIONS—Doppler echocardiographic imaging improves the detection of rheumatic carditis. Subclinical valve lesions, detected only by Doppler imaging, can persist. Echocardiographic findings should be accepted as a major criterion for the diagnosis of rheumatic fever.


Keywords: rheumatic heart disease; rheumatic fever; echocardiography; carditis     

T cells against the pathogenic and protective epitopes of heat-shock protein 65 are crossreactive and display functional similarity: novel aspect of regulation of autoimmune arthritis

OBJECTIVE: In autoimmune situations, the outcome of immune response against a disease-related antigen is typically viewed in terms of the balance between the pathogenic versus the protective subsets of antigen-reactive T cells. Using the rat adjuvant arthritis (AA) model of human rheumatoid arthritis (RA), we examined the antigen specificity and the functional attributes of the T cell repertoire directed against defined pathogenic versus protective epitopes of heat-shock protein 65 (hsp65), and determined the immunologic basis of the AA-protective effect of subsets of T cells primed by the pathogenic determinant. METHODS: Lewis (RT.1l) rats were pretreated subcutaneously with the pathogenic epitope 177-191 of mycobacterial hsp65 (B177) in adjuvant (incomplete Freund's adjuvant/complete Freund's adjuvant/CpG) and then immunized with heat-killed M. tuberculosis H37Ra for disease induction. The antigen specificity/crossreactivity of the T cells primed by B177 or the AA-protective determinant 465-479 of the homologous rat hsp65 (R465) was tested by using proliferation assay, cytokine ELISA, tolerance induction, and adoptive transfer. RESULTS: Pretreatment of Lewis rats with the arthritogenic determinant B177 using an immunogenic rather than a tolerogenic regimen affords protection against AA instead of initiation or aggravation of AA. This protective effect of B177 is mediated in part by activation of T cells that are crossreactive with R465. CONCLUSION: Downmodulation of AA by a pathogenic foreign epitope involving T cells crossreactive with a distant, protective self-determinant represents a novel aspect of immune regulation, and suggests further exploration of the use of pathogenic epitopes for the treatment of autoimmune arthritis.     

Characterization of neurotensin production by a line of rat medullary thyroid carcinoma cells.

The rMTC 6-23 cell line was derived from a calcitonin-producing rat medullary thyroid carcinoma. During characterization of these cells we discovered that they also synthesize and secrete neurotensin (NT), a tridecapeptide originally isolated from the hypothalamus and not previously associated with C cells. Immunoreactive NT (iNT) was measured with two antisera: HC-8, which recognizes the COOH-terminal eight amino acids, and TG-1, which binds the NH2-terminal region of NT. By use of these antisera, 2 M acetic acid extracts of rMTC 6-23 cells were found to contain 0.7--5.0 pmol of iNT per mg of cell protein. Successive fractionation of iNT from cell extracts by gel filtration, ion-exchange chromatograpy, and reverse-phase high-pressure liquid chromatography showed at each step a peak of iNT that was indistinguishable from synthetic NT in its chromatographic behavior. Biologic activity of the iNT was confirmed by demonstrating the characteristic fall in arterial blood pressure in the rat after intravenous injection of material purified from rMTC 6-23 cells. Calcium (0.5--4.0 mM) stimulated release of iNT in a dose-dependent manner; the effect was maximal at 3--4 mM calcium. K+ (50 mM) stimulated release of iNT that was maximal in the presence of 1.0--1.5 mM calcium. Synthesis and secretion of iNT by these cells were shown during a 16-day growth experiment. These results demonstrate that rMTC 6-23 cells contain NT and suggest the possibility of an association between neurotensin and calcitonin.     

Rheumatic fever

Rheumatic fever is a multisystem inflammatory disease that occurs as a delayed sequel to group A streptococcal pharyngitis. It is less common than it was 50 years ago but is still a major cause of heart disease in developing areas of the world. The relationship between the site of infection, the type of causative organism, and susceptibility of the host is essential in the development of the disease. Its major clinical manifestations include carditis, migratory polyarthritis, chorea, erythema marginatum, and subcutaneous nodules. It can manifest as an acute febrile illness consisting of migratory polyarthritis involving the large joints, as carditis and valvulitis, or as Sydenham's chorea with involvement of the central nervous system. The disorder in its milder form resolves itself without sequelae. Carditis is the condition most associated with increased mortality and morbidity and may be fatal in its severe forms. Penicillin is the most appropriate primary and secondary prophylaxis. Anti- inflammatory agents provide symptomatic relief but do not prevent rheumatic heart disease.     

Human dendritic cells presenting adenovirally expressed antigen elicit Mycobacterium tuberculosis--specific CD8+ T cells

Previous studies in murine and human models have suggested an important role for CD8+ T cells in host defense to Mycobacterium tuberculosis (Mtb). Consequently, a successful tuberculosis vaccine may require the elicitation of sustained CD4+ and CD8+ T cell responses. We tested the hypothesis that the potent CD4+ T cell antigen Mtb39 is also a CD8+ T cell antigen. A recombinant adenovirus-expressing Mtb39 (adenoMtb39) was used to infect monocyte-derived dendritic cells. Using interferon-gamma enzyme-linked immunospot, Mtb39-specific CD8+ T lymphocytes were detected in three healthy individuals with latent tuberculosis infection who also had strong anti-Mtb39-specific CD4+ T cell responses. An Mtb39-specific CD8+ T cell line was generated using Mtb39-expressing dendritic cells. Mtb39-specific T cell clones were obtained by limiting dilution cloning. All seven T cell clones obtained were HLA-B44 restricted. Using a panel of synthetic overlapping peptides representative of Mtb39, the peptide epitope was identified for two clones. Furthermore, all T cell clones recognized Mtb-infected dendritic cells and were cytolytic. We conclude that infection of dendritic cells with adenoviral vectors expressing Mtb proteins allows for measurement of antigen-specific CD8+ T cell responses from peripheral blood mononuclear cells. The technique will be useful in defining CD8+ T cell antigens and in measuring immunogenicity of tuberculosis vaccines.     

Heart-Reactive Antibody,Serum Enzymes and Isoenzymes in the Diagnosis of Acute Rheumatic Fever

Three groups of laboratory tests were assessed for possible clinical application in the diagnosis of rheumatic carditis. Serum antibody cross-reactive with human myocardium and group A streptococcal cell membrane (heart-reactive antibody—H.R.A.) was found in titres above the normal range in most patients with post-streptococcal carditis, arthritis or glomerulonephritis and less often in patients with surgical myocardial damage. Patients with acute rheumatic carditis had lower titres on admission than those with acute rheumatic arthritis alone; after treatment titres rose in the carditis group but fell in children with arthritis. These findings suggested a possible pathogenic role for this antibody in rheumatic carditis, and suggest its determination to be useful in diagnosis. Serum levels of glutamic oxaloacetic transaminase, lactic dehydrogenase and creatine phosphokinase were significantly higher in children with cardiac damage and in those with high titres of H.R.A., but the differences were not sufficiently great to be of clinical value. Relative increases in the fast-migrating isoenzyme of serum lactic dehydrogenase were found in patients with carditis, and its determination is considered to be of potential clinical value.     

Growth of aortic smooth muscle cells from hypertensive obese and lean rats in homologous and heterologous sera

Arterial smooth muscle cells (SMC) were derived from the medial thoracic aortas of three groups of rats: (a) obese, hyperlipidemic, hypertensive koletsky rats (OHT); (b) lean, normolipidemic, hypertensive koletsky rats (LHT) and (c) lean, normotensive Wistar rats (NT). The growth patterns of these cells were subsequently compared in tissue culture media (DMEM) supplemented with pooled 10% homologous or 10% heterologous sera. Morphologically the SMC from all three rat sources grew in culture in typical SMC hill and valley patterns. When the SMC from the three rat sources were cultured in DMEM supplemented with 10% newborn calf serum (NCS) there were no differences in final cell densities and morphologies between the cell types. However, SMC derived from OHT rat aortas grown in DMEM supplemented with pooled 10% homologous serum achieved lower cell densities than SMC derived from LHT and NT rat aortas in their respective homologous sera. There were no differences in final cell densities when LHT SMC and NT SMC were separately cultured inpooled heterologous sera derived from LHT, OHT or NT rats or when OHT cells were cultured in heterologous sera derived from either LHT or NT rats. The OHT serum preferentially affected only the growth and morphology of SMC derived from the obese, hyperlipidemic, hypertensive koletsky rats.     

Prognostic significance of bicycle ergometry test in patients with myocarditis]

A total of 42 patients with rheumatic carditis were examined in the acute-subacute period and following 3-5 years. Seventeen patients were diagnosed as having primary rheumatic carditis, 9 presented with tonsillogenic rheumatic carditis, and 16 had viral rheumatic carditis. The diagnosis of myocarditis was established on the basis of clinical, immunological, and virological findings. The study involved ECG, PhCG, PCG, and bicycle ergometer testing recordings. Groups of patients with good and poor prognosis were identified. Low threshold exercise, exercise-inadequate tachycardia, complex cardiac arrhythmias, phasic myocardial hypodynamic syndrome and volume exercise syndrome that are formed during performance are prognostically poor indicators. More profound electric and mechanic dysfunctions were observed in patients with tonsillogenic or viral myocarditis.     

Daily changing picture in a case of acute rheumatic carditis

A case of acute rheumatic carditis is reported to show the daily electrocardiographic changes during the acute phase of the disease. These changes occurred in the RS-T segments, T waves, and QRS complexes primarily, and were from day to day reversible and recurring. This changing picture indicates the interest and importance attached to the taking of serial tracings in cases of acute rheumatic carditis, for one tracing may be confusing diagnostically.