International Journal of Cardiology 88 (2003) 313–314 www.elsevier.com / locate / ijcard
Letter to the Editor
Cardiac tamponade in acquired immunodeficiency syndrome a b, a a Ramesh M. Gowda , Ijaz A. Khan *, Terrence J. Sacchi , Balendu C. Vasavada, b
a Division of Cardiology, Long Island College Hospital, Brooklyn, NY, USA Division of Cardiology, Creighton University School of Medicine, Omaha, NE, USA
Received 19 May 2002; accepted 2 June 2002
Keywords: Human immunodeficiency virus; HIV; Acquired immune deficiency syndrome; AIDS; Pericardial effusion; Cardiac tamponade
A 26-year-old female with human immunodeficiency virus infection and advanced acquired immunodeficiency syndrome, diagnosed 1 year ago, was admitted with generalized weakness, left-sided chest discomfort, and progressive dyspnea of 2 weeks duration. She had been empirically treated with antibiotics, but without any improvement. She had suffered from chronic sinusitis, perianal herpes, oral candidiasis, and pneumocystis carinii pneumonia. The patient had a strong family history of human immunodeficiency virus disease, including in husband, mother, stepfather, and three children. She weighed 76 pounds. Her temperature was 98.4 8F, blood pressure 90 / 40 mmHg, pulse rate 116 beats / min, and respiratory rate 40 / min. She had jugular venous distension, and pulsus paradoxus of 18 mmHg. Heart sounds were muffled. Chest examination revealed decreased breath sounds at both lung bases. The CD4 / CD8 cell count ratio was 0.006. Electrocardiogram revealed sinus tachycardia at 116 beats / min, low voltage QRS complexes, and diffuse T-wave abnormalities. Echocardiogram showed a large pericardial effusion with mild collapse of the left ventricle during diastole suggestive of cardiac tamponade. Patient underwent emergency pericardiocen*Correspondence author. Creighton University Cardiac Center, 3006 Webster Street, Omaha, NE 68131, USA. Tel.: 11-402-280-4573; fax: 11-402-280-4938. E-mail address:
[email protected] (I.A. Khan).
tesis. About 1000 ml of serosanguinous fluid was aspirated. After pericardiocentesis, the blood pressure improved to 110 / 70 mmHg. Soon afterwards, while arrangements were being made for pericardial window and biopsy, her shortness of breath worsened and she went into cardiac arrest. Advanced Cardiac Life Support protocol was performed, but she could not be revived. The autopsy revealed 350 ml of residual pericardial effusion, focal fibrinous pericarditis, multiple microgranulomas in lungs and liver, and generalized acquired immunodeficiency syndrome related lymphadenopathy. The heart weighed 240 g, and cardiac chambers, valves, cut sections of the myocardium, and coronary arteries were unremarkable. Microscopic sections showed accumulation of plasma cells and lymphocytes admixed with fibrous tissue in the pericardium. Pericardial fluid cytology and cultures for bacteria, mycobacteria, virus, and fungus were negative. The cause of death in this patient was attributed to pericardial effusion with cardiac tamponade. The cause of the pericardial effusion remained unknown but was likely related to acquired immunodeficiency syndrome. Because of a number of coexistent morbidities, the symptoms of cardiac tamponade may not be obvious in patients with advanced acquired immunodeficiency syndrome. Particularly, the shortness of breath in these patients could be caused by a myriad of conditions, which may result in an unintentional
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delay in the clinical suspicion and diagnosis of cardiac tamponade [1]. Most of the reported cases of cardiac tamponade in human immunodeficiency virus patients had hypotension, tachycardia, tachypnea, jugular venous distention, pulsus paradoxus, and distant heart sounds [2]. However, the typical clinical signs of cardiac tamponade may be absent, especially in those with low-pressure tamponade, which tends to occur in patients with tuberculosis and neoplastic pericarditis complicated with severe dehydration, cachexia, and wasting states associated with the advanced acquired immunodeficiency syndrome [2]. A small amount of pericardial effusion may lead to cardiac tamponade in these already critical ill patients [3]. Echocardiography is of particular help in these situations, and an echo free space consistent with fluid around the heart with right atrial, right ventricular or left ventricular diastolic collapse, inferior vena cava plethora with blunted response to inspiration, and respiratory variation of mitral and tricuspid inflow velocities would point toward a possibility of cardiac tamponade [4]. The value of pericardial fluid analysis in human immunodeficiency virus associated pericardial effusions is controversial with diagnostic yields ranging from none to 100% [5]. Pericardial effusion with cardiac tamponade in human immunodeficiency virus patients may be a marker of end-
stage infection as it is associated with a low CD4 cell count and is often caused by opportunistic infections and malignant neoplasms associated with the advanced acquired immunodeficiency syndrome. Although opportunistic infections and malignant neoplasms, along with the advanced acquired immunodeficiency syndrome, could be a contributory factor in the high mortality in these patients, a high index of suspicion for cardiac tamponade in those with cardiac symptoms might result in an early and proper management of cardiac tamponade.
References [1] Kwan T, Karve MM, Emerole O. Cardiac tamponade in patients infected with HIV: a report from an inner-city hospital. Chest 1993;104:1059–62. [2] Karve MM, Murali MR, Shah HM, Phelps KR. Rapid evolution of cardiac tamponade due to bacterial pericarditis in two patients with HIV-1 infection. Chest 1992;101:1461–3. [3] Turco M, Seneff M, McGrath BJ, Hsia J. Cardiac tamponade in the acquired immunodeficiency syndrome. Am Heart J 1990;120:1467– 8. [4] D’Cruz IA, Calderon E, Kuri K, Shearin S. Left ventricular diastolic compression in acquired immunodeficiency syndrome with large, non-loculated pericardial effusion. Am Heart J 1997;133:383–4. [5] Hsia J, Ross AM. Pericardial effusion and pericardiocentesis in human immunodeficiency virus infection. Am J Cardiol 1994;74:94–5.
