The report by Wolfe and Edelman [1] prompted us to describe a similar patient who developed severe left ventricular systolic dysfunction in the setting of cardiac tamponade and who recovered completely in 3 weeks.

A 27-year-old woman presented on 14 July 1993 with a history of pleuritic chest pain, dyspnea on exertion, low-grade fever, abdominal swelling, and edema developing over 3 weeks. Thirteen years before, she had a successful secundum atrial septal defect repair. Examination showed a blood pressure of 90/60 mm Hg with a pulsus paradoxus of 20 mm Hg, a heart rate of 130 beats/min, and a respiratory rate of 32/min. The patient's jugular pressure was markedly elevated and heart sounds were distant. An electrocardiogram showed sinus tachycardia and low voltage. An echocardiogram showed a large pericardial effusion with right atrial and right ventricular compression. Pericardiocentesis yielded 500 mL of straw-colored fluid. Because of a pericardial effusion and right atrial compression, she was transferred to Barnes Hospital.

An echocardiogram documented a large pericardial effusion with normal left ventricular size; biventricular function was markedly impaired with an estimated left ventricular ejection fraction of 20%. She had a surgical pericardial window procedure, with removal of 1000 mL of pericardial fluid. After this procedure, she developed hypotension and a low output state that required dobutamine. A third heart sound was present. Antinuclear antibody, rheumatoid factor, Coxsackie virus, and mycoplasma titers, cultures, and results of cytologic examination for cancer were all negative. A purified protein derivative skin test was nonreactive. The creatine kinase MB fraction was not elevated. A pericardial biopsy specimen showed acute and chronic inflammation. An endomyocardial biopsy (five specimens) showed diffuse mild hypertrophic changes and rare scattered mononuclear cells but no evidence of myocyte necrosis or acute myocarditis.

The patient was begun on captopril and digoxin; dobutamine was subsequently discontinued. An echocardiogram done 5 days after admission showed severe left ventricular dysfunction (ejection fraction, 25%) and a tiny pericardial effusion; 4 days later, there was improvement in left ventricular function with an ejection fraction of 45%. The patient was discharged to her home. A follow-up echocardiogram on 12 August showed normal left ventricular function. The patient has regained her baseline functional status and has discontinued therapy with all medications.

We were unable to define a cause for the pericarditis. The time course of illness and recovery is consistent with that of the two patients described by Wolfe and Edelman [1] and suggests that cardiac tamponade was responsible for the severe ventricular dysfunction seen in our patient. Unlike their patients, our patient had left ventricular dysfunction at a time when a hemodynamically significant pericardial effusion was still present. Decreased left ventricular contractility has been described in experimental cardiac tamponade because of diminished coronary perfusion pressure [2]. Diminished coronary flow may have led to a degree of myocardial stunning and hibernation that contributed to the patient's transient systolic dysfunction.