Acute Myocarditis Mimicking Acute Myocardial Infarction miocardial infarction

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Acute Myocarditis Mimicking Acute Myocardial Infarction miocardial infarction Powered By Docstoc
					                                           CASE REPORT

Editor: Rachel Hajar, MD

                               Acute Myocarditis Mimicking
                                Acute Myocardial Infarction
                         Mohammed El-Dessouky, MSc., Ali Ashraf Abbas, MSc.

   The clinical manifestations of acute myocarditis    15-20), and CPK 880 IU/L (normal 35-232); CK-
ranges from an asymptomatic condition to               MB 62 ng/ml (normal <5ng). BUN, electrolytes,
progressive cardiac dysfunction or sudden              cholesterol, and triglycerides were within normal
unexpected death. Myocarditis can mimic acute          limits.
myocardial infraction (AMI) with chest pain,              He was treated with morphine, IV nitrates, rTPA,
electrocardiographic abnormalities, serum              and heparin. Aspirin 300 mg daily was also started.
creatinine kinase elevation, and hemodynamic           The chest pain did not resolve completely.
instability (1-3).                                        Six hours following admission, he had another
   We present a case of myocarditis treated            severe attack of chest pain. Emergency coronary
inappropriately with thrombolysis due to clinical      angiography was performed. The coronary arteries
features suggestive of AMI.                            were normal. A bedside transthoracic
                                                       echocardiogram showed no segmental wall motion
                                                       abnormality, normal ejection fraction, and minimal
Case presentation                                      pericardial effusion.
                                                          Twelve hours following admission, temperature
    A 19-year-old male student was admitted to the     was noted to be 39 0C and fluctuated from 37.6 to
CCU because of retrosternal chest pain. The pain       38.6 0C for three days (Fig.2). The WBC count
occurred at rest two hours before admission and        went down to 8,000 two days after admission, but
persisted up to the time of admission. He described    the ESR went up to 73. C-reactive protein was
the pain as heaviness, which was associated with       positive. Serum troponin T (cTnT) was 4.40ng/ml
profuse sweating and nausea; there was no              (normal 0-0.1). Brucellosis antibody was negative.
associated vomiting or shortness of breath. The        On the third hospital day, a pericardial rub was
pain was non-radiating and non-exertional. He has      heard. The CPK and CK-MB remained in the range
had recurrent, similar episodes for 3 days before      of 700-800 IU/L and 60-78 ng/ml, respectively
admission. The patient has no history of diabetes      (Fig.3a and 3b). The ST-segment elevation on the
or hypertension; he is a non-smoker. He denied         ECG persisted for several days with gradual return
any history of cocaine abuse. He has a family          to near baseline and no Q waves developed. Blood
history of diabetes mellitus and coronary artery       cultures and tuberculin tests were negative.
disease. He denied any history of recent infectious       He was treated with analgesics. Aspirin was
illness, but his father and brothers have recently     increased to 300 mg BID and NSAID was started
been found to have brucellosis. The patient drinks     on the third hospital day. The chest pain and fever
raw camel’s milk                                       resolved and he was discharged.
    Physical examination revealed a moderately
obese young man, distressed with pain.                 Discussion
Temperature was 36.4 0C; PR was 94/min, regular;
BP 140/90. The rest of his physical examination           The clinical features that strongly suggest
was unremarkable. ECG on admission (Fig 1)             myocarditis in our patient are the young age, the
showed sinus rhythm, normal axis, ST elevation         paucity of risk factors, failure of symptoms to
in V2-V6, leads 1 and aVL and ST depression in         resolve with nitrates and thrombolysis, and the
leads III, aVF and V1. Chest x-ray was normal.         normal coronary arteries. Additional supportive
Laboratory examination showed WBC 11,800               evidence for myocarditis includes the prolonged
(normal 4,800 to 10,800), ESR 46 mm/hr (normal         CK-rise and absence of segmental wall motion
                                                       abnormalities on echocardiography. Most
From the Department of Cardiology and Cardiovascular   important, the cTnT was elevated which, in the
Surgery, Hamad Medical Corporation, Doha, Qatar
Correspondence to Dr. Mohammed El-Dessouky
                                                       absence of AMI or acute ischemia, has recently
P. O. Box 3050, Doha, Qatar,   been shown to be a sensitive marker for

HEART VIEWS VOL. 1 NO. 3 MARCH / MAY 1999: 77-9
                                               CASE REPORT

     Fig.1. ECG on admission shows ST-segment elevation in leads 1,II, and AVL, V2-V6, and ST-depression in leads
     III, AVF and V1.

     Fig.2. Graph showing temperature course, therapeutic and diagnostic interventions. Spike in temperature is evident
     12 hours after admission and remained slightly elevated for 3 days.

     Abbrev.: C. Angio = Coronary Angiogarm; NSAID = Non-Steroidal Anti-Inflamatory drug; ECHO = Echocardiogarm

     HEART VIEWS VOL. 1 NO. 3 MARCH / MAY 1999: 77-9
                                                 CASE REPORT

Fig.3a. (left panel) show CPK graph and Fig.3b. (right panel) shows CK-MB graph. The graphs demonstrate
elevated levels, with prolonged duration of the creatinine kinase levels.
myocarditis (4). Although endomyocardial biopsy                       The frequency of this uncommon presentation
remains the diagnostic standard in myocarditis,                    is unknown. The incidence of normal coronary
its usefulness remains controversial because of                    arteries in all patients who present with AMI has
the morbidity associated with the procedure and                    been estimated to be < 3%. This figure rises
the potential for sampling error (5).                              dramatically to 17% to 20% when only patients
    A subset of patients with acute myocarditis may                <35 years old are considered (10-12). It is likely
have chest pain and ECG findings suggestive of                     that the majority of patients admitted with signs
AMI (6). Myocarditis may mimic myocardial                          and symptoms highly suggestive of AMI will be
infarction in that the histologic changes are                      treated with thrombolytic therapy, as was the case
typically focal or multifocal in distribution.                     in our patient.
Segmental wall motion abnormalities may be                             Myocarditis should be strongly considered in
present (7) and associated myocyte necrosis often                  the differential diagnosis of patients with pain
leads to elevation of serum creatine kinase (8).                   admitted to the CCU whose symptoms fail to
Myocyte injury and necrosis associated with                        resolve after aggressive anti-ischemic therapy and
inflammation may produce repolarization changes                    thrombolytic therapy. Such patients will certainly
as well as temporary or permanent abnormal Q                       represent only a tiny minority of patients admitted
waves (3,9).                                                       with suspected AMI.


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