Acute Perimyocarditis Research Articles

Troponin elevation in coronary vs. non-coronary disease

Acute myocardial infarction is defined as myocardial cell death due to prolonged myocardial ischaemia. Cardiac troponins (cTn) are the most sensitive and specific biochemical markers of myocardial injury and with the new high-sensitivity troponin methods very minor damages on the heart muscle can be detected. However, elevated cTn levels indicate cardiac injury, but do not define the cause of the injury. Thus, cTn elevations are common in many disease states and do not necessarily indicate the presence of a thrombotic acute coronary syndrome (ACS). In the clinical work it may be difficult to interpret dynamic changes of troponin in conditions such as stroke, pulmonary embolism, sepsis, acute perimyocarditis, Tako-tsubo, acute heart failure, and tachycardia. There are no guidelines to treat patients with elevated cTn levels and no coronary disease. The current strategy of treatment of patients with elevated troponin and non-acute coronary syndrome involves treating the underlying causes. The aim of this paper is to review data from studies of non-ACS patients with acutely elevated troponin who in clinical practice may be difficult to discriminate from ACS patients.

Popis případu akutní perimyokarditidy

Popis případu akutní perimyokarditidy

Enteroviruses and Myocarditis: Viral Pathogenesis Through Replication, Cytokine Induction, and Immunopathogenicity

Publisher Summary Viruses—especially enteroviruses—are major etiological agents in clinical myocarditis and dilated cardiomyopathy. Indeed, presence of viral RNA in heart biopsies is a negative prognostic indicator, as mortality rates in these individuals are significantly higher than in patients having virus-negative biopsies. Most likely, many different methods of myocyte damage exist, with distinct pathogenic mechanisms dominating in various patients in accordance with their genetic constitution, and the genetic characteristics of the initiating pathogen. The difficulty for clinicians is in deciding how t o treat patients. Immunity—while often viewed as the culprit in the pathogenicity of myocarditis—is also necessary for virus control. Immunosuppression may inhibit autoimmune reactions, but could lead to persistent virus infections which could be equally damaging. Classical immunosuppressive therapy is of little benefit t o the majority of myocarditis and dilated cardiomyopathy patients. Recent preliminary trials with interferon- alpha suggest that attacking the virus infection directly may be therapeutic. Currently, a large multicenter trial for interferon therapy in patients with biopsy-proven cardiac infections is underway. This is instrumental in elucidating the pathogenicity of clinical inflammatory heart disease. However, because interferon therapy itself can cause cardiogenic shock and acute perimyocarditis, caution should be practiced in its use in heart disease.

Does CMV infection play a role in myocarditis? New aspects from in-situ hybridization.

Endomyocardial biopsies of 20 patients with active myocarditis, 15 with post-myocarditis and 22 with acute perimyocarditis were assayed for cytomegalovirus (CMV) DNA by in-situ hybridization with a biotinylated DNA-probe. Positive probes were found in 10% of the cases with acute myocarditis and in 7% of those with post-myocarditis; no CMV-positive patients were found in acute peri-myocarditis. The results were compared to anti-CMV antibodies from patients sera detected by ELISA technique.

Lyme borreliosis as a cause of myocarditis and heart muscle disease

Lyme borreliosis (LB) is a multisystem disorder that may cause self-limiting or chronic diseases of the skin, the nervous system, the joints, heart and other organs. The aetiological agent is the recently discovered Borrelia burgdorferi. In 1980, cardiac manifestations of LB were first described, including acute conduction disorders, atrioventricular block, transient left ventricular dysfunction and even cardiomegaly. Pathohistological examination showed spirochaetes in cases of acute perimyocarditis. Recently, we were able to cultivate Borrelia burgdorferi from the myocardium of a patient with long-standing dilated cardiomyopathy. In this study, we have examined 54 consecutive patients suffering from chronic heart failure for antibodies to Borrelia burgdorferi. On ELISA, 32.7% were clearly seropositive. The endomyocardial biopsy of another patient also revealed spirochaetes in the myocardium by a modified Steiner's silver stain technique. These findings give further evidence that LB is associated with chronic heart muscle disease.

Acute Nonrheumatic Perimyocarditis Complicating Streptococcal Tonsillitis

Streptococcal infection is a rarely recognized cause of nonrheumatic perimyocarditis. We report a case of a young patient who developed acute perimyocarditis as manifested by diffuse electrocardiogram changes, and markedly elevated cardiac enzymes, concurrently with streptococcal tonsillitis. Despite the dramatic presentation, the patient recovered uneventfully. We conclude that streptococci can involve the heart also directly by a bacterial component or toxin, and not only through a delayed immunologic mechanism as in rheumatic fever. Further studies are necessary to accurately determine the incidence of myocardial involvement during early stages of streptococcal infection.

Carditis Associated With Mycoplasma pneumoniae Infection

A 16-year-old boy with acute perimyocarditis had serological evidence of Mycoplasma pneumoniae infection. The endomyocardial biopsy specimen showed grade 2 active lymphocytic myocarditis. A T-cell study suggested a cell-mediated immune process in the pathogenesis of carditis. Mycoplasma pneumoniae needs to be considered as a possible cause of acute carditis, and histological findings may influence management.

Rickettsial perimyocarditis—A follow-up study

Sera and lymphocytes from a 37-year-old male patient with acute perimyocarditis during a Q-fever endemic were analyzed for antibody and cell-mediated immune reactions and followed up 28 months later. Circulating autoantibodies against myocardial tissue were assessed by indirect immunofluorescence. Cytolysis of vital contracting rat cardiocytes, by antimyolemmal antibodies and complement, and lymphocytotoxicity, with and without the patient's serum, were evaluated and compared with the results obtained in ten patients suffering from Q-fever without perimyocardial involvement and with 40 healthy subjects. Antimyolemmal antibodies (AMLA), a muscle-specific subtype of antisarcolemmal antibodies, were demonstrated by immunofluorescence in the one patient with Q-fever perimyocarditis in titers of up to 1:320 but not in the controls. AMLA induced cytolysis of myocytes in the presence of complement. Both AMLA and cytolytic serum activity could be absorbed in all sera of this patient by using Coxiella burnetii. Only marginal lymphocytotoxicity against heterologous cardiocytes was detected in the early phase and again during the follow-up 2 years later in the Q-fever myocarditis patient but not in any of the noncarditic Q-fever cases nor in controls. It is postulated that cross-reacting, complement-fixing, cytolytic autoantibodies against the cardiac myolemma are operative either as a cause of cardiac damage or a consequence, pointing to a secondary immunopathogenesis of chronic Q-fever perimyocarditis.

Immunologic regulator and effector functions in perimyocarditis, postmyocarditic heart muscle disease and dilated cardiomyopathy.

In acute perimyocarditis we found that OKIAI-positive cells were increased, and in dilated cardiomyopathy OKMI-positive cells were increased. No significant alteration in suppressor T cell activity was observed in our patients with either disease. The characteristic immunofluorescent pattern in carditis and postmyocarditic heart disease is the presence of antimyolemmal antibodies with intact rat and human cardiocytes in titers of 1:40-1:320 as antigens. The antimyolemmal fluorescence can be absorbed with the respective causative virus in Coxsackie B, influenza, mumps and EBV-myocarditis, indicating that the antibodies are a cross-reactive. AMLA-positive sera induce cytolysis of vital rat cardiocytes in vitro, suggesting that the antibodies are of pathogenetic relevance. Cytolytic serum activity could be absorbed out with the respective virus. Immunohistologic specimens obtained from patients with carditis demonstrate the fixation of IgG and IgM antibodies; IgG antibodies also occur in dilated cardiomyopathy and coronary artery disease. In dilated postmyocarditic heart disease both antimyolemmal fluorescence and cytolytic activity are preserved at a lower level when compared to carditis. These antibodies can also fix complement. In the acute phase of carditis circulating immune complexes can be demonstrated. Cellular effector mechanisms against vital cardiocytes were maintained or even slightly enhanced in carditis, postmyocarditic and primary dilated cardiomyopathy. In vitro NK cell activity against K 562, however, was decreased. This is compatible with a sustained target-specific cytotoxicity whereas reduced NK cell activity may indicate impairment of this effector organ.

Four years of experience in endomyocardial biopsy--an immunohistologic approach.

Left ventricular biopsies from 376 patients (including 78 patients undergoing bypass surgery) were analyzed by light microscopy (necrosis, infiltration with or without fibrosis) and by immunohistology (bound antibodies). Circulating antisarcolemmal antibodies (ASA) were determined at the time of biopsy using a double-sandwich technique. Circulating antimyolemmal antibodies were assessed in intact rat and human cardiocytes. Histologic findings, heart catheterization, and echocardiography together with the patient's history established the diagnosis of perimyocarditis, myocarditis, postmyocarditic dilated cardiomyopathy, healed myocarditis, and healed perimyocarditis. Both bound and circulating ASA were found in up to 100% of cases in acute inflammatory heart disease and postmyocarditic cardiomyopathy, indicating a secondary immunopathogenesis of the myocardial disease. Analysis of immunoglobulin subclasses revealed: IgG-binding does not discriminate between acute/healing/healed carditis and postmyocarditic dilated heart disease (61.1%-91.7% positive); IgM binding is diagnostic for acute or healing perimyocarditis but has a relatively low incidence (33.3%); IgA binding occurs in acute or healing myocarditis (45.5%), perimyocarditis (33.3%), and in postmyocarditic heart disease (39.4%), but not in controls; complement fixation was never seen in controls, but was seen in acute myocarditis (45.4%), perimyocarditis (25%), and postmyocarditic heart disease (46%). Pretreatment of cryostat sections with collagenase to avoid "nonspecific" binding of antibodies to collagen considerably reduced the sensitivity but increased the specificity. Thus, endomyocardial biopsy proved a safe and valuable method for the further analysis of patients with carditis and myocardial disease of unknown origin.

Myocardial catecholamines in hypertrophic and dilated (congestive) cardiomyopathy: A biopsy study

A high performance liquid chromatographic method was used to determine myocardial norepinephrine and epinephrine concentrations in 66 biopsy specimens obtained from the right or left ventricle during routine diagnostic cardiac catheterization of 45 patients with dilated (congestive) or hypertrophic cardiomyopathy, or with heart disease other than cardiomyopathy, such as acute perimyocarditis, postmyocarditis and constrictive pericarditis. The validity of catecholamine determination in a 2 to 6 mg biopsy specimen to assess overall ventricular myocardial catecholamines was demonstrated. Norepinephrine concentrations in the myocardium were inversely correlated with the grade of hypertrophy in patients with congestive cardiomyopathy or heart disease other than cardiomyopathy, but not in patients with hypertrophic cardiomyopathy. The fact that the myocardial norepinephrine concentration was always lower in the left than in the right ventricle of the same patient may be explained by the simple dilution of sympathetic nerve endings in the left ventricle. There were some cases of hypertrophic cardiomyopathy in which the concentration of myocardial norepinephrine was exceptionally high, although its mean value was not significantly higher than that in patients with other types of heart disease who served as a control group without cardiomyopathy. Some patients with dilated cardiomyopathy had lower levels of myocardial norepinephrine than would be expected for the degree of interstitial fibrosis and the severity of heart failure. The mean plasma norepinephrine and epinephrine levels were significantly elevated in patients with dilated cardiomyopathy.