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J Clin Lipidol. 2018 Jul - Aug;12(4):988-998.e5. doi: 10.1016/j.jacl.2018.03.082. Epub 2018 Mar 29.

Low-density lipoprotein cholesterol response after statin initiation among persons living with human immunodeficiency virus.

Author information

1
Department of Medicine, Division of Infectious Diseases, University of Alabama at Birmingham, Birmingham, AL, USA. Electronic address: gburkholder@uabmc.edu.
2
Department of Epidemiology, School of Public Health, University of Alabama at Birmingham, Birmingham, AL, USA.
3
Department of Medicine, Division of Infectious Diseases, University of Alabama at Birmingham, Birmingham, AL, USA.
4
Department of Health Care Organization and Policy, School of Public Health, University of Alabama at Birmingham, Birmingham, AL, USA.
5
Department of Medicine, University of Washington, Seattle, WA, USA.
6
Department of Medicine, Johns Hopkins University, Baltimore, MD, USA.
7
Department of Medicine, University of California San Diego, San Diego, CA, USA.
8
Department of Medicine, University of California San Francisco, San Francisco, CA, USA.
9
Department of Medicine, Harvard Medical School, Boston, MA, USA.
10
Department of Medicine, Division of Infectious Diseases, University of North Carolina School of Medicine, Chapel Hill, NC, USA.
11
Department of Medicine, Mount Sinai Icahn School of Medicine, New York, NY, USA.

Abstract

BACKGROUND:

Meta-analyses of general population studies report mean low-density lipoprotein cholesterol (LDL-C) reductions of 30% to <50% with moderate-intensity and ≥50% with high-intensity statins. Persons living with human immunodeficiency virus (PLWH) are at high risk for atherosclerotic cardiovascular disease (ASCVD), yet many have elevated LDL-C.

OBJECTIVE:

To evaluate LDL-C response after statin initiation among PLWH.

METHODS:

We conducted a retrospective cohort study of PLWH initiating statins between 2009 and 2013 (N = 706). Patients were categorized into mutually exclusive groups in the following hierarchy: history of coronary heart disease (CHD), diabetes, prestatin LDL-C ≥190 mg/dL, 10-year predicted ASCVD risk ≥7.5%, and none of the above (ie, unknown statin indication). The primary outcome was a ≥30% reduction in LDL-C after statin initiation.

RESULTS:

Among patients initiating statins, 5.8% had a history of CHD, 13.6% had diabetes, 6.2% had LDL-C ≥190 mg/dL, 35.4% had 10-year ASCVD risk ≥7.5%, and 39.0% had an unknown statin indication. Among patients with a history of CHD, 31.7% achieved a ≥30% LDL-C reduction compared with 25.0%, 59.1%, and 33.9% among those with diabetes, LDL-C ≥190 mg/dL, and 10-year ASCVD risk ≥7.5%, respectively. In multivariable adjusted analyses and compared to patients with an unknown statin indication, LDL-C ≥ 190 mg/dL was associated with a prevalence ratio for an LDL-C reduction ≥30% of 1.81 (95% confidence interval, 1.34-2.45), whereas no statistically significant association was present for history of CHD, diabetes, and 10-year ASCVD risk ≥7.5%.

CONCLUSION:

A low percentage of PLWH achieved the expected reductions in LDL-C after statin initiation, highlighting an unmet need for ASCVD risk reduction.

KEYWORDS:

Cardiovascular disease; Dyslipidemia; HIV infection; Low-density lipoprotein cholesterol; Statin

PMID:
29853312
DOI:
10.1016/j.jacl.2018.03.082

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