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<Case
presentation>
A 55-year-old man was admitted to the hospital because of
progressive dyspnea for one month.
The patient had been considered well until
a scheduled transurethral resection of the prostate gland
at another hospital 3 years ago. No definite abnormal findings in
chest X –way and ECG were noted at that time. One episode
of general malaise, low-grade fever and productive cough
was experienced for one week after the surgery. He complained
of progressive dyspnea and leg edema one year later. He came to
a local doctor several times and the symptoms
improved after medication including diuretics. He stopped drugs use
for 6 months because he felt better. However,
the symptoms progressed rapidly in recent one month. Then he visited our
outpatient clinic for help.
The patient was a businessman. He had a 10-pack-year
history of cigarette smoking but had discontinued smoking 10
years before admission. He drank alcohol occasionally. He had
a slightly elevated cholesterol level. At the time of
deterioration of exercise tolerance, he had begun to have
constant substernal “heaviness” without radiation, especially
after rapid climbing of a hill or flight of stairs. The
discomfort was accompanied by prominent exertional dyspnea and
was not relieved by nitrate medication. The patient took an
antacid, which provided slight relief of the sensation of
heaviness.
The patient had no history of diabetes mellitus,
hypertension, previous chest discomfort or intravenous
injection of drugs. His father had had a myocardial infarction
at the age of 52 years, and a male of cousin had had some kind
of heart disease and expired at the age of 35 years.
The temperature was 36.9℃, the pulse was 100 and irregular,
and the respirations were 30. The blood pressure was 125/80
mmHg.
On physical examination, the patient appeared acute ill
looking. There was no rash or lymphadenopathy. The jugular
veins were engorged. The carotid pulses were ＋＋ and equal.
There was a systolic precordial murmur of grade 1 to 2.
Bilateral basal crackles were heard. The abdomen, arms were
normal and pitting edema was noted at bilateral pedal regions
and ankles. An electrocardiogram obtained at admission showed
atrial fibrillation with rapid ventricular rate (HR 102 /min)
and diffuse, nonspecific ST segment and T-wave
abnormalities.
On a posteroanterior radiograph of the
chest that obtained at the admission, bilateral pleural
effusions and increased lung markings were noted, and the
cardiomegaly was also seen. A cardiac ultrasonographic study
revealed four-chamber dilatation, poor systolic LV function
(ejection fraction of 22%) with global hypokinesia. There were
no definite vegetations while moderate-severe tricuspid
regurgitation was detected by Doppler ultrasonography.
Laboratory tests including CBC and BCS were within normal
limits.
After stabilization, the patient
underwent the catheterization, which revealed the patent
coronary artery. Endomyocardial biopsy showed scant
mononuclear-cell infiltrates composed of lymphocytes around
the microvasculature and marked myocardial loss and fibrosis.
The findings were consistent with the presence of chronic
myocarditis, but nonspecific. The bacterial, fungal and viral
culture and serology tests were negative.
Under the impression of dilated
cardiomyopathy, medical therapy started, and patient was
referred for pre-heart transplantation evaluation. The
symptoms improved after aggressive medical therapy, and he was
discharged and followed at our OPD.
<Case
discussion>
Myocarditis is defined as clinically
as inflammation of the heart muscle, and it is an insidious
disease with various clinical presentations. The causes of
myocarditis include a large variety of infections, systemic
diseases, drugs and toxins. Recent studies have identified
several important features in patients with idiopathic dilated
cardiomyopathy that support the infectious-immune hypothesis.
Some patients may present with a history of a recent flu-like
syndrome. The endomyocardial biopsy remains the gold standard
for the diagnosis, despite of limited sensitivity and
specificity. The supportive therapy is the first line of
treatment. The use of coronary angiography in patients with
heart failure is indicated only in patients has risks and with
the evidence of myocardial ischemia. The medication of CHF
should include diuretics to lower ventricular filling
pressures, ACE inhibitor to decrease vascular resistance, and
beta-blocker when patient is stabilized. In patients with
severe symptoms, inotropic therapy or implantation of
ventricular assist device could be
used.
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Case Discussion
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