Cardiovascular Disease |

A Case of Severe HIV-Associated Cardiomyopathy: Highlighting Susceptibility, Despite a Reassuring CD4 FREE TO VIEW

Marjan Islam, MD; Belinda Velasquez, MD
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Mount Sinai Beth Israel, New York, NY

Chest. 2015;148(4_MeetingAbstracts):71A. doi:10.1378/chest.2275633
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SESSION TITLE: Cardiovascular Disease Student/Resident Case Report Posters

SESSION TYPE: Student/Resident Case Report Poster

PRESENTED ON: Tuesday, October 27, 2015 at 01:30 PM - 02:30 PM

INTRODUCTION: The human-immunodeficiency virus is increasingly being recognized as an important cause of cardiomyopathy. While the exact mechanism remains unclear, effects from direct viral burden may play a key role. We present a case of severe HIV-associated cardiomyopathy in a man with a normal CD4, but a high viral load.

CASE PRESENTATION: A 40 year-old male with HIV presented with bilateral lower-extremity swelling and right-calf pain. He was admitted with cellulitis, with course complicated by septic shock, requiring massive fluid resuscitation and broad-spectrum antibiotics. While the infection resolved, he developed severe dyspnea and worsening extremity edema. Chest x-ray showed pulmonary congestion and echocardiogram revealed severe 4-chamber dilated cardiomyopathy with ejection fraction of 27%. Cardiac catheterization revealed non-obstructive coronary arteries and cardiac MRI displayed findings consistent with prior myocarditis. CD4 count on admission was 604 cells/mm3, unchanged from 3 months prior, at which time he had a viral load of 100,000 RNA copies/mL. He was started on heart failure therapy and discharged. 6 months later, he remained off anti-retroviral therapy, with repeat viral load over 220,000 RNA copies/mL. Follow-up echocardiogram revealed worsening heart failure, with ejection fraction below 20%, requiring ICD placement.

DISCUSSION: HIV-associated cardiomyopathy presents a diagnostic challenge, as etiologies can range from co-infections by cardiotropic viruses, dysregulated inflammatory processes induced by HIV, or direct cardiomyocyte invasion by the virus itself. Expression of gp120 and other viral proteins from infected T-cells or marcophages have been shown to induce apoptosis in cardiac myocytes, while increased inflammatory cytokines like TNFα have been reported in the myocardium of patients with HIV cardiomyopathy (1). HIV may also cause defects in antigen-specific immunoglobulin production through poor B-cell activation from infected effector T-cells, further leading to immune dysfunction (2).

CONCLUSIONS: Our case highlights the importance of HAART therapy, both in maintaining appropriate CD4 counts but also in the suppression of high viral loads. We highlight the unique risk present in the HIV population, where immune dysfunction may be present beyond the threat of just opportunistic infections. We illustrate the need to firmly contain viral replication, as high viral loads may be a key player in HIV-associated cardiomyopathy.

Reference #1: Fiala et al. HIV-1 induces cardiomyopathy by cardiomyocyte invasion and gp120, Tat, and cytokine apoptotic signaling. Cardiovascular Toxicology. 2004; 4(2): 97.

Reference #2: Kelly et al. Diastolic dysfunction is associated with myocardial viral load in simian immunodeficiency virus-infected macaques. AIDS 2012, 26(815-823).

DISCLOSURE: The following authors have nothing to disclose: Marjan Islam, Belinda Velasquez

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