It's estimated that cardiac involvement is present in up to 1% of cardiotropic virus infections (in viral infection from Coxsackie B up to 4%). The actual frequency is relatively higher, since most cases have a mild or asymptomatic course.
Infectious myocarditis recognize the
following pathogens as causes:
-virus (50% of cases): Coxsackie B (frequent and dangerous), influenza viruses,
adenoviruses, echoviruses and others.
- Infections from bacteria that are determined.
- in septic states, especially during a staph infection and enterococcus, and
that causes bacterial endocarditis, for example in valvulopathies.
- in the course of Beta A hemolytic streptococcus infection of group A (tonsillar
angina, scarlet fever, eresipela)
- in the course of infection with Borrelia burgdorferi (Lyme disease)
- diphtheria, this is now almost unknown.
Again, but more rarely, except in non-EU patients who come from the Eastern
countries and Sri Lanka, other causes of myocarditis are salmonella typhoid
infection, Tuberculosis, lue, etc.
Mushrooms, especially in immunodefied patients, can give myocarditis, for
example in people with AIDS,
- Still you can have myocarditis from protozoa, from toxoplasma, Cbagas disease
(Trypanosoma cruzi / South America.
- parasitic infections: trichinelle, echinococcus and others.
However, even non-infectious conditions are at the basis of myocarditis, for
example in collagenopathies, in vasculitis, during radiotherapy:
Causes of non-infectious myocarditis:
- rheumatoid arthritis, collagenopathies, vasculitis
- mediastinal irradiation myocarditis
- idiopathic myocarditis from FiedIer.
Why is myocarditis, that is, the inflammation of specific myocardial tissue?
Myocarditis on viral etiopathogenesis is determined because antibody movement is
performed against antigens present in viruses (such as missiles against targets!),
But antibodies to the mechanism of cross-reactivity, including viral antigens
and myocardial antigens, are also directed against the myocardium itself. For
this reason, in the acute myocarditis, the following findings, which usually
regress clinical improvement, are present in 70-80% of cases:
- lMM type anti-myolemic antibodies
- anti-sarcolemma type lgM antibodies
- deposits of lgM and C, in myocardial biopsy.
fibrosi cardiaca
Dallas criteria.
Myocarditis from the histological point of view can be framed in types:
1. "active" myocarditis, if the presence of lymphocyte infiltrate with myocytolysis is shown with or without fibrosis and interstitial edema and if possibly viral RNA is shown, and lgM and C3 antibodies
2. "borderline myocarditis", ie border myocarditis, with poorly pronounced
infiltrate, therefore it is necessary to perform a biopsy of control.
With the control biopsy the following diagnoses are possible:
3. Persistent ('ongoing') myocarditis; the presence of myocardial fibrosis and
hypertrophy of the fibers worsens the prognosis
4. Myocarditis undergoing resolution (reduction of lymphocyte infiltrate,
demonstration of repair changes)
5. resolved myocarditis ("resolved") (absence of inflammatory cells, absence of
necrosis).
Additional findings are the possible demonstration of viral DNA in the
myocardium, and the demonstration of self-reactive phenomena (immunohistology).
Special histological forms: rheumatic myocarditis (Aschoff's nodules), FiedIer
idiopathic myocarditis (lymph-plasmacellular infiltrate + giant cells).
The patient with myocarditis has a very varied symptomatology, which clinical
course of myocarditis is very variable and ranges from asymptomatic or mild
forms that constitute the majority of cases to fulminant forms with an
inauspicious outcome (rare).
Chronic courses with evolution to dilated cardiomyopathy are possible. In
infectious myocarditis the symptoms related to the infection are represented by
asthenia, fatigue, palpitations up to serious and dangerous rhythm disturbances,
especially extra-strokes, tachyarrhythmias and signs of acute heart failure.
At the auscultation there are puffs due to the dilatation of the cardiac
chambers and possibly signs of heart failure, with a rhythm of galappo or III
added tone.
The laboratory supports clinical diagnosis for the verification of:
• increase of CPK / CPK-MB
• any signs of inflammation (ESR, PCR, high ferritin etc.)
• cultural examinations, possibly positive but not always positive blood
cultures, and special bacteriological / virological serodiagnosis
• The most advanced laboratories demonstrate the presence in the patient's serum
of anti-myolemic and anti-sarcolemma antibodies.
All 'ECG appear alterations consist of rhythm disorders ranging from sinus
tachycardia to arrhythmias, but especially extrasystoles in diphtheria and Lyme
disease, or more often conduction disorders (eg AV block).
If the subendocardial is damaged, an ST sub-segmentation appears, but
differential diagnosis with the digital effect (to "mustache of Salvador D'Ali)
and with acute coronary syndrome, flat or negative T waves (differential
diagnosis: regression stage after heart attack or pericardite).
If then there is a concomitant pericarditis, some authors speak of "myopericarditis")
eventually appear single-phase alterations of ST-tract from subepicardial
suffering (differential diagnosis with myocardial infarction, in myocarditis no
reduction of amplitude of the R wave and no Q wave ). Finally, it should be
noted that the QRS complexes may be of low voltage, but also in this case we
need to think about pericardial dissection.
Therefore it is necessary to proceed with further investigations, among which
the main one is the echocardiographic survey. Often the echocardiographic
finding is normal, with the exception of any. regional kinetic disorders, a
pericardial effusion in the case of pericarditis and, if a heart failure occurs,
the ejection fraction appears with an expansion of dilatation of the cardiac
chambers.
At the chest X-ray, we will have signs of lung stasis, "wet lung image" or signs
of multiple thickening. In limited cases it may be necessary to proceed with
invasive diagnostics: left heart catheterization with endomyocardial biopsy to
diagnose suspected special forms of endocarditis.
1) Causal: eg. treatment with penicillin if rheumatic carditis is suspected,
diphtheria or Lyme disease therapy, nifurtimax in the case of Chagas disease,
etc.
In progressive viral myocarditis with demonstration of viral RNA in myocardial
biopsy, antiviral therapy may be indicated (experimental therapy in controlled
studies).
2) Symptomatic:
- physical rest until normalization of the ECG (in the first weeks bed rest)
- prophylaxis of thromboembolism during the period of stay in bed
- complication therapy (heart failure, heart rhythm disorders)
3) "Ultima ratio" in terminal heart failure: cardiac transplantation.
• In most cases healing
• Often persistence of non-threatening arrhythmias (eg extrasystolic)
• Rarely due to acute complications (rhythm disturbances, conduction disorders,
heart failure). Frequent complications occur among others in Coxsackie type B
infections (especially in the newborn), diphtheria and Chagas disease.
• Chronic course with development of dilated cardiomyopathy and heart failure
(in particular in viral myocarditis).