The patient arrived at the emergency unit with a history of acute myocardial infarction, for which she was treated. Without improvement in the pain, the patient developed heart failure and underwent a hemodynamic study, which showed normal coronary arteries and extensive ventricular impairment. During evolution, the clinical findings improved and herpes zoster appeared on the right shoulder. In a few months the clinical findings subsided, and the findings of the electrocardiogram, chest X-ray, and ventricular function were normal. The patient is currently asymptomatic.Clinical manifestation of myocarditis may vary from an asymptomatic state secondary to focal infection to severe heart failure. In some cases, clinical manifestations may simulate myocardial infarction 1 , as electrocardiographic and laboratory findings do. Approximately 25 viruses may be associated with myocarditis, including the varicella-zoster virus. Myocardial involvement during infection by herpes zoster virus is rare, and when it occurs, it is usually asymptomatic or manifests as heart failure 2 . We report the case of a patient with clinical findings of myocardial infarction and infection by herpes zoster virus.
Case ReportThe patient is a white 68-year-old female, who arrived at the emergency unit complaining of precordial pain that irradiated to the left upper limb and was accompanied by sweating and weakness for 3 hours. The patient reported malaise in the previous 2 days, and a continuous discomfort in her right shoulder with no alleviating or worsening factors. The patient was hypertensive and had been using 20mg of enalapril for the last 5 years. She also reported having a family history of longevity.On physical examination the patient was restless, pale, sweating, and dyspneic. Her blood pressure was 134/80m-mHg in both upper limbs, her heart rate was 116bpm, the lungs showed no rales, and the peripheral pulses were palpable.The clinical hypothesis of myocardial infarction led the patient to immediately undergo electrocardiography ( fig. 1), which confirmed the diagnosis. A thrombolytic (streptokinase) was started, and hypotension occurred during infusion; therefore, the dripping was decreased, dopamine was started followed by dobutamine. After infusion, the patient remained restless, more dyspneic, and still complained of pain. On pulmonary auscultation, crepitant rales could be heard in the inferior 2/3 of the lungs. The patient was given sodium nitroprusside and a diuretic. The chest X-ray ( fig. 2) showed the classical pattern of pulmonary edema. As the pain persisted after 4 hours of thrombolytic infusion, the patient underwent coronary angiography, which revealed normal coronary arteries and an increase in left ventricular end-systolic volume due to an extensive anterior and inferior akinetic area, and also apical dyskinesia ( fig. 3). Table I shows the levels of the cardiac enzymes.The echocardiogram of 3/12/96 revealed an ejection fraction of 45%, mild mitral insufficiency, a deficit in left ventricular relaxation, middle api...