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Acute myocarditis: retrospective analysis in 28 patients
Dallo Matías, Lema Luis, Zelaya Félix, Pacheco Guillermo, Sambuelli Rubén, Conci Eduardo, Serra César.
Instituto Modelo de Cardiología - FUCCADIM
Universidad Católica de Córdoba
Córdoba - Argentina.
Material and Methods
Myocarditis is an acute or chronic disease, focal or diffuse, of the
cardiac muscle. Although multiple causes of myocarditis are recognised (infectious,
toxic-metabolic, autoimmune, etc), the most frequent ethiological agent is a viral
infection. The cardiotropic viruses most frequently implied are entero virus Coxachie B
and Echo, adenovirus, influenza virus, Epstein Barr, hepatitis C and the human immuno
deficiency virus (HIV).
The anatomopathologic evidence is confirmed by the presence of focal or difusse lesions in the tissues involved, obtained by Endomyocardical Biopsy (EMB) using the Dallas criteria:
A - Active Myocarditis: presence of inflammatory infiltrates associated to cellular necrosis (fig 1)
B - Borderline Myocarditis: presence of inflammatory infiltrates without proved necrosis.
C - Absence of myocarditis: without evidence of infiltrates or cellular necrosis.
1- To report the clinical forms of presentation and their connection
with the laboratory, ECG, echocadiogram and ventricular function.
2- To analyse the immediate and long term evolution.
Material and Methods:
From April 1991 to February 1999, 28 patients (p) were analysed
retrospectively with acute myocarditis diagnosis (AM) confirmed by (EMB). Twenty
patients were men (71,5%) and 8 were women (28,5%), average age 30 years (13-76). The
average window of time between the beginning of symptoms and the EMB was 28 days.
All the EMB were done through internal jugular or femoral vein using 6-7 French biotomes. Five samples of tissue per patient were taken, which were fixed in glutaraldehyde and sent for pathology analysis with optical, electronic microscopy and/or immunohistochemical techniques.
The ventricular function was assessed through echocardiography, radioisotopic ventriculography and/or ventriculography during catheterization. It was considered as a normal ejection fraction (EF) if it was > than 50%, mild dysfunction between 40-50%, moderate between 30-40% and severe if it was < than 30%.
The most frequent clinical presentation was heart failure (HF) in 14
patients (50%), followed by precordial pain (pp) in 10 patients (36%) and arrythmias in 4
patients (14%). Nineteen patients showed febrile syndrome. Patients were divided in two
groups: Group A (p with HF) and Group B (p with pp and arrythmias) (fig 2).
The laboratory findings were: Group A: leukocytosis (1p), elevated CK MB (10p) and none
with accelerated ESR; Group B: none presented leukocytosis, elevated CK MB (8p) and
accelerated ESR (5p) All the patients presented abnormal ECG when they entered, Group A
patients: ventricular repolarization disorder 5p, left bunddle brunch block (LBBB) 3p,
complete AV block (CAVB) 1p,VT 1p,AF 3p and with frequent VE 1p. In Group B:LBBB 1 p,CAVB
2 p,VT 1 p,AF 1 p, frequent VE 1 p, and 8 p with localized or generalized ST elevation.
All the echocardiograms were pathological. Group A: cavity dilatation and global
hypokinesia in 13 p, and pericardial effusion in 2 p. Group B: cavity dilatation 1 p,
global hypokinesia 5 p, pericardial effusion 1 p, and wall motion abnormality 7
p.Ventricular function:, 50% in Group A presented serious dysfunction of the left
ventricle (LV), 43% moderate dysfunction, and 7% mild dysfunction; none of them had normal
ventricular function (fig 3). In Group B, 29% presented normal
ventricular function, 29% mild deterioration and 42% moderate dysfunction (fig
All patients with ventricular dysfunction received conventional treatment (ACEI, digitalis , diuretics ) and 20 p received immunossuppresive treatment.
Twenty one p (75%) were followed for a mean of 36 months; 3 of them die (14%), 1 p during the hospitalization and 2 p during re-hospitalization. All the dead p presented refractory HF. Four p (19%) of Group A and 2 of Group B showed relapses with new EMB. Two p (10%) of Group A show at present a dilated cardiomyopathy with HF and 12 p (57%) are asymptomatic and free from events (fig 5).
Most of AM cases are asymptomatic. Just 40% of the patients report the
previous history of an infectious syndrome in the last month. The cardiac manifestations
vary from the oligosypmtomatic forms to sudden death. Autopsies performed on children and
young adults showed a 17% to 21% incidence of myocarditis.
In our experience, 50% of the patients presented HF, 36% with precordial pain and 14% with arrythmias. Moreover, 19 of them presented fever some time in the evolution, from the beginning of the symptoms up to the first day of hospitalization.
In order to perform an AM diagnosis, we can divide the methods in two groups: 1.- Myocarditis Presumptive Diagnosis. 2.- Myocarditis Definitive Diagnosis.
In the first group is the laboratory; which is generally normal or shows nonspecific alterations. In our group of cases, just one patient reported leukocytosis, 5 accelerated ESR and 18 had an elevation of the MB fraction of the CPK, as an expression of the myocardial damage. The troponin I dosage would be more sensitive than that of the CPK, but it was not done.
Though ECG and echocardiogram do not offer specific data for the AM
diagnosis, they are of great help as tools in the initial handling, as prognostic markers
and for the follow up of these patients. In our experience, in 100% of the cases, both
methods showed some abnormality. The radionucleide study with galium offers interesting
information, because it makes evident the presence of inflamatory infiltrates in the
myocardium. Provides evidence of during last years they were published many papers with
radionucleide study with antimyosin monoclonal antibodies marked with Indio 111. The
sensitivity and specificity of it are of 66% and 71% respectively.
Nuclear magnetic resonance, apart from being a valid method for the AM diagnosis, has been an important tool in the understanding of the pathophysiology of the inflammatory process, showing that the cellular infiltrates are initially focal and scattered, to become then diffuse.
Though there are no studies with a great number of patients, most of
them show a great sensitivity and specificity, which is about 90% when they are compared
wiht that of EMB.
For the definitive diagnosis of AM, the only available method is the EMB. Although it is an invasive method, it is rather safe in experimented hands, with a global incidence of complications between 1-1,7%, with a mortality of 0,003-0,005%.
Some studies which assess the diagnostic effectiveness of EMB, using
autopsy as gold standard, report that this technique has a 79% sensitivity and a 63%
specificity. This low sensitivity may be in part because of the focal distribution that
infiltrates adopt at the beginning.
The treatment includes general support measures and pharmacologic treatment. The former consist of a low sodium diet, alcohol interruption and physical restriction.
A lot of drugs have been experimentally used in laboratory animals for
viral AM: rivabirina, ACEI, ß blockers and calcium blockers have shown certain
effectiveness without a translation to human beings.
Even though there is no accepted consent about the indications of immunosupressors in the AM, there would be of usefulness in cases of progressive dysfunction of the LV in spite of the conventional therapy, persistent active myocarditis or fulminating myocarditis which does not get better during the first 24-72 hours of hemodynamic support.
Some variables behave like survival independent predictors in AM:
In our experience, those patients who did their debut with heart failure, had a greater inpatient and outpatient morbility and mortality.
1.- The most frequent clinical form of presentation was HF.
2.- The presentation with HF is correlated with a greater number of inpatient and outpatient events.
3.- All the patients reported abnormal ECHO and ECG.
4.- Acute myocarditis is a disorder with high late morbi mortality
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