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PubMed2000

MRI changes in myocarditis--evaluation with spin echo, cine MR angiography and contrast enhanced spin echo imaging.

AIM: Myocarditis is probably under-diagnosed with clinical criteria generally used for diagnosis. Magnetic resonance imaging (MRI) has shown promise in detecting heart muscle disorders and we set out to assess the role of cine magnetic resonance angiography (MRA) and contrast enhancement in myocarditis, as there is a need for a non-invasive tool that can aid prognosis and follow-up. MATERIALS AND METHODS: Twenty patients were evaluated with T1 SE pre- and post-gadolinium enhancement and cine MRA. Four patients were histologically proven to have myocarditis, eight others were diagnosed as having myocarditis by clinical criteria and eight did not have myocarditis. Images were evaluated in a blinded fashion for regional wall motion abnormality and contrast enhancement pattern. Analysis of contrast enhancement by signal intensity measurement was also performed. RESULTS: Focal myocardial enhancement with associated regional wall motion abnormality correlated with myocarditis in 10 out of 12 patients, two patients with abnormal focal enhancement alone also clinically had myocarditis. None of the non-myocarditis patients showed abnormal focal enhancement. Enhancement analysis suggests that focal corrected myocardial enhancement of > 40% is abnormal. CONCLUSION: In the correct clinical context, focal myocardial enhancement on spin echo MRI strongly supports a diagnosis of myocarditis, especially when associated with regional wall motion abnormality.Roditi, G. H. (2000). Clinical Radiology55, 752-758.

Adult↗
PubMed2006

[Diagnosis of myocarditis: description and assessment of available methods].

Myocarditis is a common disease in all age groups. Correct diagnosis of myocarditis is difficult, but of clinical and scientific importance. It is the aim of this review to describe and evaluate diagnostic possibilities. It is not possible to make a definitive diagnosis of myocarditis by electrocardiography, laboratory tests or echocardiography. Nor can techniques of nuclear medicine or coronary angiography provide an unequivocal diagnosis of myocarditis. Myocarditis can be diagnosed with certainty only by endomyocardial biopsy, which must be examined by histological, immunohistological and molecular techniques to obtain maximal sensitivity. But optimal diagnosis of a biopsy is subject to the problem of sampling error. Furthermore, myocardial biopsy is in practice used only rarely, despite a low complication rate. Thus the diagnosis of myocarditis is often based merely on suspicion. The limitations of standard methods employed so far have made cardiac magnetic resonance imaging (CMR) a valuable new additional test when there is the clinical suspicion of myocarditis. A myocardial biopsy will often reveal myocarditis in patients with cardiac symptoms and CMRI findings typical of myocarditis, especially if the biopsy was obtained near the area of contrast enhancement in the CMRI. CMRI can also be used for noninvasive and low-risk follow-up of functional parameters and tissue damage.

Biopsy↗
PubMedDate not supplied

Survival outcomes of patients with giant cell myocarditis bridged by ventricular assist devices.

Giant cell myocarditis is a highly lethal disorder characterized by rapidly progressive congestive heart failure. The aim of this study was to describe the clinical course of patients with giant cell myocarditis who received a ventricular assist device. Patients with giant cell myocarditis were identified from the Multicenter Giant cell Myocarditis Registry. Bridging to cardiac transplantation in the giant cell myocarditis patients who received a ventricular assist device was compared with bridging in the general population of heart failure patients, as reported in the literature. Median posttransplantation survival for patients with giant cell myocarditis who received and did not receive ventricular assist devices was calculated by the Kaplan-Meier method and compared with use of the log-rank test. Nine patients with giant cell myocarditis who received ventricular assist devices were identified. Seven patients survived to transplantation, four were alive 30 days posttransplantation, and two survived to 1 year. The rate of successful bridging to transplantation in seven of nine patients (78%) is similar to that reported for other ventricular assist device recipients. Posttransplantation survival of 57% (4 of 7) at 30 days and 29% (2 of 7) at 1 year was significantly lower compared with 93% 1-year survival of the 30 patients with giant cell myocarditis who did not receive ventricular assist devices before transplantation (p<0.001). Ventricular assist devices can be an effective bridge to transplantation for patients with heart failure caused by giant cell myocarditis. Although their posttransplantation survival was poor in our series, a few patients had long-term survival.

Adolescent↗
PubMed1982

Evaluation of mild acute infectious myocarditis.

The diagnosis of acute mild myocarditis in vaguely defined. Therefore we studied 185 consecutive young men in military service with electrocardiographic changes arousing a suspicion of myocarditis in connection with an acute infectious disease. It was possible to classify 160 patients into seven electrocardiographic groups; definite or probable myocarditis was observed in 104 patients. The electrocardiographic patterns considered characteristic for acute myocarditis were: ST segment elevations followed by T wave inversions; gradually changing T wave inversions not corrected by beta blockade; and ventricular extrasystoles more than 10 per minute triggered by acute infection. Thirty-nine subjects without myocarditis had "functional" T wave abnormalities completely normalised by beta blockade, or stable T wave inversion. The leading symptoms in acute myocarditis were fatigue and chest pains; loud S3 gallop, paradoxical cardiac pulsation, pericardial friction rub, or enlargement of the heart were noted altogether in 50% of the patients. Echocardiography disclosed segmental wall motion abnormalities related to the T wave inversions. Serum creatine kinase MB fraction increased in 70% of the acute myopericarditis patients during the ST segment elevation stage. In the non-myocarditis groups the clinical and pertinent laboratory findings remained normal. Thus, we noted in clinically mild acute infectious myocarditis clear-cut and early signs of myocardial dysfunction, suggesting that the direct and often local viral invasion of the myocardium is the basic pathogenetic mechanism. The present electrocardiographic classification based on serial tracings and beta blockade proved useful in the evaluation of patients suspected of having mild acute myocarditis.

Acute Disease↗
PubMed2004

Immunoglobulin treatment suppressed adoptively transferred autoimmune myocarditis in severe combined immunodeficient mice.

We investigated the suppressive effects of immunoglobulin (Ig) on effector T cells in autoimmune myocarditis. Treatment with Ig reduced production of the so-called T-helper type 1 (Th1) cytokines stimulated by concanavalin A or cardiac myosin in cultured lymph node (LN) cells from rats with myocarditis. The cytotoxic activities of LN cells from rats immunized with myosin and treated with Ig were reduced against cardiomyocytes and F-2 cells compared with those treated without Ig. The adoptive transfer of myocarditis from LN cells of Lewis rats with myocarditis to severe combined immunodeficient (SCID) recipients was successfully achieved. Treatment with Ig, but not with F(ab')2 fragments of Ig, reduced the mortality and severity of myocarditis in SCID recipient mice. Decreased ability of LN cells of Ig-treated rats, but not rats treated with F(ab')2 fragments, to transfer autoimmune myocarditis was also demonstrated. The findings of the present study suggest that autoimmune myocarditis was successfully transferred to SCID mice and that treatment with Ig ameliorated autoimmune myocarditis by inducing selective myosin unresponsiveness via the Fc portion, resulting in suppression of Th1 cytokine production and cytotoxic activities of LN cells, which operated together in the development of autoimmune myocarditis.

Adoptive Transfer↗
PubMed1991

Giant cell versus lymphocytic myocarditis. A comparison of their clinical features and long-term outcomes.

BACKGROUND: Giant cell myocarditis has rarely been diagnosed premortem, and little is known about its natural history. In addition, no comparative studies with lymphocytic myocarditis exist. METHODS AND RESULTS: The clinical features, serial change in left ventricular fraction (LVEF), and outcomes of all patients with histologically verified myocarditis were retrospectively evaluated. Ten patients (22%) were found to have giant cell myocarditis (group 1), whereas the remaining 36 (78%) had lymphocytic myocarditis (group 2). Age at presentation, gender distribution, duration of symptoms, initial LVEF, and resting hemodynamics did not differ between groups. Ventricular tachycardia was detected in 90% of group 1 patients compared with only 25% of group 2 (p = 0.0007). Atrioventricular block that required pacemaker insertion was also more common in group 1 (60%) than in group 2 (8.3%) (p = 0.001). Left ventricular systolic function declined during follow-up in group 1 patients (LVEF, 0.43 +/- 0.07-0.26 +/- 0.05, p = 0.11) but increased in group 2 patients (LVEF, 0.33 +/- 0.03-0.41 +/- 0.03, p = 0.02). When the net change between initial and final LVEF was assessed, a significant difference was evident (giant cell group, -0.17 +/- 0.06; lymphocytic group, +0.07 +/- 0.03; p = 0.0008). Although a greater proportion of patients in group 1 died or required transplantation (seven of 10 versus 11 of 36, p = 0.03), actuarial survival over 4 years was not different for the giant cell group (50%) than for the lymphocytic group (62%). CONCLUSION: Giant cell myocarditis was more prevalent than previously recognized and highly associated with both ventricular tachycardia and pacemaker requirement. The likelihood of an adverse event, either cardiovascular mortality or cardiac transplantation, was significantly greater for patients with giant cell myocarditis than for those with lymphocytic myocarditis, perhaps because of the progressive decline in left ventricular systolic function that was observed in those with giant cell myocarditis.

Adult↗
PubMed1992

In vivo lymphocyte-mediated myocardial injuries demonstrated by adoptive transfer of experimental autoimmune myocarditis.

BACKGROUND: To elucidate the mechanisms of immune-related myocardial injuries, we examined whether autoimmune myocarditis was passively transferable by use of humoral or cellular factors. METHODS AND RESULTS: Active myocarditis was elicited in Lewis rats by immunization with human cardiac myosin fraction in complete Freund's adjuvant. This experimental myocarditis was characterized by macroscopic features such as pericardial effusion, enlargement of the heart, and gray discoloration of the cardiac surface. Histologically, extensive myocardial necrosis and numerous inflammatory cell infiltrations were observed. Interestingly, multinucleated giant cells were frequently observed in the lesions. Transfer of the disease by the humoral factor was examined by use of fresh sera and immunoglobulin fraction of pooled sera from rats with severe myocarditis, and transfer by the cellular factor was tested by use of spleen cells and lymph node cells from the diseased rats. When naive Lewis rats were given 15.75 mg of immunoglobulin fraction, no particular change was observed in the hearts. Fresh sera also could not elicit myocarditis in recipient rats. In contrast, intravenous injection of spleen cells or lymph node cells that were cultured for 3 days in the presence of 1 microgram/ml of concanavalin A elicited severe myocarditis. The macroscopic and microscopic findings of passively transferred myocarditis are essentially the same as those found in actively induced myocarditis. Multinucleated giant cells were also observed in the lesions of transferred myocarditis. CONCLUSIONS: This study demonstrates direct evidence for in vivo lymphocyte-mediated myocardial injuries.

Animals↗
PubMed1995

Serum cardiac troponin T and creatine kinase-MB elevations in murine autoimmune myocarditis.

BACKGROUND: We used a murine model of autoimmune myocarditis to investigate systematically whether serum markers of myocardial cell injury, that is, cardiac troponin T (TnT) and the MB isoenzyme of creatine kinase (CK-MB) are useful for the diagnosis of inflammatory heart disease. METHODS AND RESULTS: Fifty-two A.SW mice were immunized with cardiac myosin to induce myocarditis. The disease was evident on day 12 after the initial immunization in 14 of 22 immunized mice, on day 16 in 7 of 10 mice, on day 19 in 6 of 10 mice, and on day 23 in 5 of 10. The severity of myocarditis increased between days 12 and 16 and remained constant thereafter. TnT was elevated in a considerable number of mice with myocarditis, resulting in a diagnostic sensitivity (number of marker elevations per number of mice with myocarditis) of 0.43 on day 12, 0.71 on day 16, and 0.50 on day 19. CK-MB elevations were not seen on day 12 but resulted in a diagnostic sensitivity of 0.71 on day 16 and of 0.33 on day 19. No elevations of CK-MB or TnT were observed on day 23. All elevations were specific for the disease, as none of the mice lacking myocarditis showed increased markers. CONCLUSIONS: In murine autoimmune myocarditis, TnT is a more sensitive marker for the disease than CK-MB. Elevations clearly indicate myocarditis, but negative test results do not exclude the presence of the disease. These data suggest that the determination of CK-MB and, in particular, of TnT, can be useful for the diagnostic evaluation of patients with suspected myocarditis.

Animals↗
PubMed1989

Myocarditis and arrhythmia: a clinico-pathological study of conduction system based on serial section in 65 cases.

We studied the conduction system of 65 cases of proven active or healed myocarditis and related diseases among 7120 autopsy samples. For this purpose, we prepared serial sections by Lev's method. The pathological diagnoses were idiopathic acute myocarditis (5), giant cell myocarditis (3), chronic myocarditis (13), healed myocarditis (22), sarcoidosis (4), collagen or autoimmune disease (13) and complication of cachexia (5). Among all the autopsy cases, Fiedler's myocarditis was found in only one case, but myocarditis was revealed in 19 out of 30 cases of dilated cardiomyopathy, and 15 out of 25 cases of sick sinus syndrome. Conduction system lesions were divided into two groups. In older cases manifesting mainly arrhythmia, the SA node, atrial muscle and AV node were involved concomitantly with perimyocarditis. In younger cases mainly showing heart failure, the RBB, LBB and Purkinje fibers were damaged by endomyocarditis. Histologically, interstitial myocarditis was observed in the former group and parenchymatous myocarditis in the latter.

Adolescent↗
PubMed1998

A new scoring system to predict the efficacy of steroid therapy for patients with active myocarditis--a retrospective study.

The efficacy of steroid therapy for active myocarditis is controversial, so a new scoring system was constructed based on 6 clinical parameters: (1) the mode of onset of the disease; (2) complications of immune-related systemic disorders; (3) evidence of viral infection; (4) the population of infiltrating inflammatory cells; (5) the appearance of multinucleated giant cells in endomyocardial biopsy specimens; and (6) the duration of active myocarditis. Points from -2 to +2 were assigned to each parameter and the total score was calculated from the 6 parameters. Twenty-one patients with clinically suspected myocarditis, who had been admitted to hospital from 1987, were retrospectively analyzed by this scoring system. Sixteen patients were treated without corticosteroids at presentation, and 5 patients were treated by conventional methods with adjunctive use of corticosteroids. In 10 patients of the non-steroid group myocarditis improved and their mean score was -4.8 at presentation. In 6 patients of the non-steroid group, myocarditis and cardiac symptoms persisted after initial therapy, and their score at presentation was -0.8. In 2 patients of the steroid group myocarditis improved after initial therapy and their score was +2. In 2 other patients of the steroid group, myocarditis and cardiac symptoms persisted and their score was +3. Another patient of the steroid group died from congestive heart failure and his score was -5 at presentation. In 8 of 9 patients with persistent myocarditis, the secondary phase therapy was challenged. Seven patients were treated with corticosteroids and 6 patients improved. Their score at the secondary phase was +2.5. Overall, non-steroid conventional treatment was successful in patients with the scores from -5 to -4, and steroid therapy succeeded in patients with scores from 0 to +6. Although this is a retrospective study, this scoring system is able to predict the efficacy of steroid therapy in patients with clinically suspected active myocarditis.

Acute Disease↗
PubMed1999

Detection and evaluation of asymptomatic myocarditis in schoolchildren: report of four cases.

STUDY OBJECTIVE: Data on the prevalence of myocarditis in children are limited. Autopsy studies have shown that myocarditis is often undiagnosed. We attempted to investigate the clinical features of asymptomatic myocarditis in four schoolchildren detected during a mass ECG screening in schoolchildren. DESIGN AND SETTING: To evaluate asymptomatic myocarditis, we clinically examined 12 schoolchildren who were referred to Shiga University of Medical Science Hospital, Otsu, Japan, because of abnormal ST or T waves detected during ECG screening. None of the 12 children had experienced any episodes suggesting cardiac disease or Kawasaki disease. Cardiac function and myocardial viability were assessed by two-dimensional echocardiography (2-DE), thallium-201 (201Tl) myocardial scintigraphy, and cardiac catheterization. Endomyocardial biopsy specimens were examined histologically. PATIENTS: Endomyocardial biopsy specimens revealed histologic evidence of myocarditis in 4 of the 12 children with abnormal ST or T waves. RESULTS: Abnormal tracer perfusion was observed on 201Tl myocardial scintigrams in these four children, but the results of coronary arteriography were normal. 2-DE showed left ventricular hypokinesis in one child and left ventricular enlargement in one of the four children with histologic evidence of myocarditis. A second endomyocardial biopsy specimen was obtained in two of four children, showing persistent myocarditis in one child. CONCLUSIONS: This type of screening program and indepth evaluation using 2-DE and 201Tl myocardial scintigraphy appear to be helpful in identifying children with myocarditis. The present histologic investigations suggested that even asymptomatic myocarditis might result in persistent heart damage.

Biopsy↗
PubMedDate not supplied

Frequency of myocarditis in cases of fatal meningococcal infection in children: observations on 31 cases studied at autopsy.

The frequency of myocarditis associated with meningococcal disease in children was reported only in two autopsied series (United States and South Africa). Here we report the frequency of associated myocarditis in 31 children who died of meningococcal infection at Hospital Infantile N.S. da Glória in Vitória, Espirito Santo State, Brazil. The diagnosis was confirmed by isolation of Neisseria meningitidis. At least three sections of fragments of both atria and ventricles were studied using the Dallas Criteria for the morphologic diagnosis of myocarditis. The mean age was 47.6 +/- 39.8 months and the mean survival time after the onset of symptoms was 46.1 +/- 26.5 h (12-112 h). Myocarditis was present in 13 (41.9%) patients, being of minimal severity in 11 cases and of moderate severity in 2 cases. There were no cases with severe diffuse myocarditis. The frequency of myocarditis was not influenced by sex, presence of meningitis, survival time after the onset of symptoms or use of vasoactive drugs. The frequency of myocarditis reported here was intermediate between the values reported in the only two case series published in the literature (57% in the United States and 27% in South Africa). Although our data confirm the high frequency of myocarditis in meningococcal disease, further investigations are necessary to elucidate the contribution of myocarditis to myocardial dysfunction observed in cases of meningococcal infection in children.

Autopsy↗
PubMed2003

Risks versus benefits of NSAIDs including aspirin in myocarditis: a review of the evidence from animal studies.

NSAIDs, including aspirin (acetylsalicylic acid), are frequently used and effective in a broad variety of inflammatory diseases, i.e. rheumatic carditis and pericarditis. Myocarditis may constitute another suitable indication for NSAIDs in order to relieve the symptoms of the presumed viral infection or because pericardial effusion is often associated with this condition. However, concerns have been raised about their indiscriminate use in myocarditis. To clarify this issue, we conducted a systematic review of the literature concerning myocarditis, aspirin and NSAIDs. We examined five animal studies of NSAIDs (indomethacin and ibuprofen) and aspirin in coxsackievirus B3- and B4-induced myocarditis. These studies indicated a deleterious effect of NSAIDs and aspirin in this setting, demonstrating a 2- to 3-fold increase in inflammation, myocytes necrosis and even mortality when compared with placebo. This possible deleterious effect was more predominant when NSAIDs or aspirin were administered during the acute and subacute phases of myocarditis; however, it was still noted when NSAIDs were administered during the late phase of the disease (the effect of aspirin was not evaluated in late phase studies). According to these animal studies, such effect might be attributed to decreased viral clearance (possibly via interferon inhibition) and/or exaggerated cytotoxic response (via interleukin-2 or inhibition of suppressor cells factors) and/or coronary artery spasm. We found one animal study looking at autoimmune myocarditis and it did not demonstrate any beneficial or detrimental effect of aspirin. Moreover, recent data suggest that aspirin and NSAIDs may counteract part of the efficacy of ACE inhibitors and be deleterious in chronic heart failure. Taken together, these studies point to a possible deleterious effect of aspirin and NSAIDs in human myocarditis. In view of these animal studies and in the absence of controlled studies of aspirin or NSAIDs in human myocarditis, we do not recommend indiscriminate treatment with NSAIDs or high-dose aspirin in patients with myocarditis where there is no or minimal associated pericarditis.

Animals↗
PubMed1999

Morphometrical and stereological analysis of myocardial mast cells in myocarditis and dilated cardiomyopathy.

Mast cells play a certain role in inflammation and immunological reactions. Cardiac mast cells, shown by sodium sulfate-alcian blue staining, were evaluated in endomyocardial biopsy specimens in patients with unexplained congestive heart failure. The results of histopathological analysis were consistent with active myocarditis according to the Dallas criteria in 10 patients (15%), borderline myocarditis in 9 (13.8%), and dilated cardiomyopathy in 25 patients (38.5%); these results were compared with a control group of 10 traffic accident victims. The highest numerical areal density of mast cells was found in active myocarditis (3.92 counts/mm2, SD = 1.84), followed by borderline myocarditis (2.76 counts/mm2, SD = 1.66), dilated cardiomyopathy (1.56 counts/mm2, SD = 0.45) and control group (0.77 counts/mm2, SD = 0.19). Degranulation involved 27% (SD = 3.6) of mast cells in active myocarditis, 18% (SD = 4.5) of mast cells in borderline myocarditis, 10.8% (SD = 3.12) of mast cells in dilated cardiomyopathy and 4% (SD = 2.0) of mast cells from autopsy tissue. The differences among the four groups were statistically significant (P <0.001). The increased number of mast cells and the higher degree of their degranulation in myocarditis compared to dilated cardiomyopathy and to control group indicate that they were activated. The mast cells could be involved in modulation of fibrous response, since they tended to be associated with areas of fibrosis. Likewise, numerical areal density and degree of degranulation of mast cells could also be used as additional diagnostic criteria for acute myocarditis, since a higher numerical areal density and degree of degranulation were present in myocarditis vs. dilated cardiomyopathy and control group.

Adolescent↗
PubMed1989

[Immunosuppressive therapy in myocarditis and dilated cardiomyopathy--a critical analysis].

Clinical and experimental examinations suggest that autoimmunological mechanisms may play an important role in the pathogenesis of postmyocarditic cardiomyopathy. These may be due to the viral infection itself or may be induced by the viral persistence. Following these ideas an immunosuppressive therapy to prevent the progression of myocarditis to dilative cardiomyopathy is discussed. Since the introduction of endomyocardial biopsies in the diagnosis of myocarditis several papers reported trials of an immunosuppressive therapy in histologically proven myocarditis. But all of these studies were not randomized and only a limited number of patients were treated. Both the primary diagnosis, "myocarditis", as well as the histological findings to evaluate the course of the disease are not well defined and therefore were used differently in the studies published so far. Moreover, the regimens used for immunosuppressive therapy until now were not standardized, thus making it impossible to compare the various studies. Another important problem is the often observed spontaneous remission of histologically proven myocarditis. It may be that it is due to these factors that the results published so far report quite different success rates for the immunosuppressive therapy in myocarditis. Recent scientific findings indicate that the combination of virological, histological, immunohistological and immunological examinations will allow a marked improvement in the finding of the diagnosis and the further control of the course of myocarditis in the near future. But as long as no significant results about the clinical advantage of immunosuppressive therapy in myocarditis exist a general use of immunosuppressive therapy should be avoided. It is to be hoped that the doubleblind-randomized multicenter studies now in progress will provide definite results about the use of immunosuppressive therapy in myocarditis.

Autoimmune Diseases↗
PubMed1985

[Histologically detectable myocarditis in patients with impaired left ventricular function].

In patients with impaired left ventricular function in whom dilated cardiomyopathy is initially suspected after performance of comprehensive diagnostic studies, histologic evidence of myocarditis or status-post myocarditis is being documented with increasing frequency since the systematic use of endomyocardial biopsy has been incorporated into the work-up. This investigation was undertaken to analyze the histologic, clinical, hemodynamic and immunologic findings in these patients to delineate possible relationships between histologically-documented myocarditis and dilated cardiomyopathy. Incidence of histologically-documented myocarditis. In our patient population, 41 of 150 patients with impaired left ventricular function, the etiology of which had been unknown, histologic evidence of myocarditis was documented. In seven of eight in whom active myocarditis was diagnosed at initial biopsy, after a mean follow-up period of two years the histologic findings were consistent with dilated cardiomyopathy. In similar groups of patients comparable incidences of myocarditis have been reported by Parrillo et al. in 19 of 100 (19%) and Fenoglio et al. in 34 of 135 patients (25%). A higher incidence has been reported by Zee-Cheng et al. in 22 of 35 patients (63%). Accordingly, pooled data indicate that the overall incidence of histologically-documented myocarditis was 30% in 528 patients initially suspected to have dilated cardiomyopathy. The variances in the incidence reported by the respective authors may be attributable to differences in the histologic definition of myocarditis, number of biopsies obtained, size of the patient population and the epidemiologically-related incidence of viral disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Autoantibodies↗
PubMed1994

[Myocarditis. Epidemiology, etiology and clinical aspects].

The term myocarditis covers a diversity of pathological conditions. Aetiologically, the best documented is acute infective myocarditis, predominantly caused by enteroviruses, particularly Coxsackie B. However, there are many possible sources of infection, and the management of immunosuppressed patients requires careful deliberation. Research into the pathogenesis of viral myocarditis has made formidable advances and provided detailed knowledge of the mechanisms responsible for myocardial damage. Microbiological techniques have yielded evidence of the involvement of Coxsackie viruses in the development of dilated cardiomyopathy. Nowadays, the term myocarditis has a strictly histopathological definition which is clinically applicable only in the few cases where endomyocardial biopsy is performed. The diagnosis, acute infective myocarditis, can usually be made with reasonable certainty on the basis of ECG findings and the serum concentrations of biochemical markers. Physical diagnostic procedures, particularly echocardiography, can provide useful supporting evidence. Prognosis is generally good in cases of acute infective myocarditis, whereas that in other forms of myocarditis varies from case to case. To date, antiviral agents have no established place in the treatment of viral myocarditis. Where diagnosis is based upon endomyocardial biopsy (e.g., in lymphocytic myocarditis), immunosuppressive therapy generally has no significant effect.

Acute Disease↗
PubMed1998

Ambiguity of morphological criteria of myocarditis in cardiac biopsy specimens.

Myocarditis is diagnosed when leukocytic infiltrate is accompanied by myocyte degeneration or necrosis. Endomyocardial biopsy is evaluated as the main diagnostic method. The purpose of the present study was to examine the individual elements of a histological picture and specify morphological criteria of diagnosing myocarditis in cardiac biopsy. The Dallas criteria were the point of reference. In the cardiobiopsies from 70 patients with clinically suspected myocarditis or congestive cardiomyopathy an active myocarditis was found in 19 cases, significantly more frequently in the group clinically classified as having myocarditis. Contraction bands, endocardial changes and vasculopathy were more frequent in cases histologically classified as active myocarditis than in borderline myocarditis. In our opinion the Dallas criteria include certain ambiguities concerning mainly differences of individual types and phases of myocarditis as well as their relations to congestive cardiomyopathy. The sensitivity and specificity of the diagnosis are related both to methodological limitations (material selection) and difficulties occurring mainly at the level of perception, evaluation and interpretation of changes. It is possible to improve the efficacy of cardiac biopsy in diagnosing myocarditis if a new techniques better revealing myocyte damage and more unequivocally determining the cellular composition of the stroma have been developed.

Adolescent↗