Author + information
- Received March 19, 2018
- Revision received April 27, 2018
- Accepted April 30, 2018
- Published online July 23, 2018.
- Raza M. Alvi, MDa,b,c,
- Anne M. Neilan, MD, MPHd,
- Noor Tariq, MDe,
- Magid Awadalla, MDa,
- Maryam Afshar, MDb,
- Dahlia Banerji, MDa,
- Adam Rokicki, BSa,c,
- Connor Mulligan, BAa,
- Virginia A. Triant, MD, MPHf,
- Markella V. Zanni, MDg and
- Tomas G. Neilan, MD, MPHa,c,∗ (, )@OfficialMGH
- aCardiac MR PET CT Program, Department of Radiology and Division of Cardiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
- bDivision of Cardiology, Department of Internal Medicine, Bronx-Lebanon Hospital Center of Icahn School of Medicine at Mount Sinai, Bronx, New York
- cDivision of Cardiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
- dDivision of Infectious Diseases, Department of Medicine and Department of Pediatrics, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
- eYale New-Haven Hospital of Yale University School of Medicine, New Haven, Connecticut
- fDivisions of Infectious Diseases and General Internal Medicine, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
- gProgram in Nutritional Metabolism, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
- ↵∗Address for correspondence:
Dr. Tomas G. Neilan, Cardiac MR/PET/CT Program, Massachusetts General Hospital, 165 Cambridge Street, Suite 400, Boston, Massachusetts 02114.
Background Incident heart failure (HF) is increased in persons with human immunodeficiency virus (PHIV). Protease inhibitors (PIs) are associated with adverse cardiac remodeling and vascular events; however, there are no data on the use of PIs in PHIV with HF.
Objectives This study sought to compare characteristics, cardiac structure, and outcomes in PHIV with HF who were receiving PI-based versus non-PI (NPI) therapy.
Methods This was a retrospective single-center study of all 394 antiretroviral therapy–treated PHIV who were hospitalized with HF in 2011, stratified by PI and NPI. The primary outcome was cardiovascular (CV) mortality, and the secondary outcome was 30-day HF readmission rate.
Results Of the 394 PHIV with HF (47% female, mean age 60 ± 9.5 years, CD4 count 292 ± 206 cells/mm3), 145 (37%) were prescribed a PI, whereas 249 (63%) were prescribed NPI regimens. All PI-based antiretroviral therapy contained boosted-dose ritonavir. PHIV who were receiving a PI had higher rates of hyperlipidemia, diabetes mellitus, and coronary artery disease (CAD); higher pulmonary artery systolic pressure (PASP); and lower left ventricular ejection fraction. In follow-up, PI use was associated with increased CV mortality (35% vs. 17%; p < 0.001) and 30-day HF readmission (68% vs. 34%; p < 0.001), effects seen in all HF types. Predictors of CV mortality included PI use, CAD, PASP, and immunosuppression. Overall, PIs were associated with a 2-fold increased risk of CV mortality.
Conclusions PI-based regimens in PHIV with HF are associated with dyslipidemia, diabetes, CAD, a lower left ventricular ejection fraction, and a higher PASP. In follow-up, PHIV with HF who are receiving a PI have increased CV mortality and 30-day HF readmission.
Dr. Alvi was supported by the National Institutes of Health/National Heart, Lung, and Blood Institute (5T32HL076136). Dr. Zanni was supported in part through the National Institutes of Health/National Heart, Lung, and Blood Institute (1R01HL137562-01A1), the National Institutes of Health/Harvard Center for AIDS Research (P30-AI060354), and the Nutrition Obesity Research Center at Harvard (P30-DK040561). Dr. A.M. Neilan was supported by the Eleanor and Miles Shore Scholars in Medicine Fellowship, the Harvard University Center for AIDS Research (P30AI060354), and the International Maternal Pediatric AIDS Clinical Trials Network Early Investigator Award (UM1AI068632). Dr. Triant was supported in part through the National Institutes of Health/National Heart, Lung, and Blood Institute (1R01HL132786-01A1). Dr. T.G. Neilan was supported in part through the Kohlberg Foundation, an American Heart Association Fellow to Faculty Award (12FTF12060588), the National Institutes of Health/National Heart, Lung, and Blood Institute (1R01HL130539-01A1; 1R01HL137562-01A1; K24HL113128-06), and the National Institutes of Health/Harvard Center for AIDS Research (P30 AI060354); and has served on the advisory board for Takeda. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received March 19, 2018.
- Revision received April 27, 2018.
- Accepted April 30, 2018.
- 2018 American College of Cardiology Foundation
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