CROI 2015 Program and Abstracts

Abstract Listing

Poster Abstracts

730 Angiographic Restenosis After PTCA in HIV-Infected Patients: Incidence and Predictors Dominik Promny 3 ; Christoph D. Spinner 1 ; Salvatore Cassese 2 ; Isabell Bernlochner 3 ; Christian Bradaric 3 ; Karl-Ludwig Laugwitz 3 ; Adnan Kastrati 2 ; Simon Schneider 3 1 University Hospital Klinikum Rechts der Isar, Munich, Germany; 2 Deutsches HerzzentrumMuenchen, Munich, Germany; 3 University Hospital Klinikum Rechts der Isar, Munich, Germany Background: Patients infected with human immunodeficiency virus (HIV) are at risk of accelerated coronary arteriopathy. With the success of combinded antiretroviral therapy, HIV infection has become a chronic condition and percutaneous coronary intervention (PCI) in HIV-infected patients has become an important treatment option. However, dedicated angiographic follow-up studies examining anti-restenotic efficacy in PCI-treated HIV-infected patients are lacking. Methods: Patients with HIV infection who underwent coronary stenting at our center were enrolled in a dedicated registry. Clinical and laboratory data were prospectively collected in an online database. Angiographic follow-up was scheduled at 6-8 months and predictors of restenosis were evaluated. To investigate individualls with multiple interventions in different segments, generalized estimating equation (GEE) models were employed to consider for repeated measurements (lesions) per subject within the analysis of group differences. Results: A total of 47 HIV-infected patients were treated for de-novo lesions and prospectively enrolled. Angiographic follow-up was available in 41 patients (87%) with 131 lesions. Overall 103 (78%) lesions were treated with drug eluting stents (DES), 14 (11%) lesions with bare metal stents (BMS) and 14 (11%) lesions with percutaneus coronary intervention (PTCA) balloon alone. Intraprocedural success rate was 100%. The total rate of binary angiographic restenosis was 24%with DES: 19% (p 0.032). We observed an independent association of binary angiographic restenosis with an elevated CD-8 T cell count (p=0.001), a reduced CD4/CD8 ratio (p=0.036) or an elevated viral load (p=0.001). In GEE analysis, commonly known predictors for restenosis like diabetes or small vessel size are not associated. Conclusions: The rate of angiographic in-stent restenosis in HIV-infected patients is considerably elevated. CD8 and CD4/CD8-ratio as HIV-specific inflammatory markers are independent predictors of elevated coronary restenosis, while in GEE analysis, commonly known predictors for restenosis like diabetes or small vessel size are not associated.

WEDNESDAY, FEBRUARY 25, 2015 Session P-P2 Poster Session

Poster Hall

2:30 pm– 4:00 pm Dyslipidemia: Mediators and Treatment 731 PCSK9 Is Elevated in HIV+ Patients and May Mediate HIV-Associated Dyslipidemia Payal Kohli 1 ; Peter Ganz 1 ;Yifei Ma 1 ; Rebecca Scherzer 1 ; Kristinalisa Maka 1 ; ScottWasserman 2 ; Rob Scott 2 ; Priscilla Hsue 1 1 University of California San Francisco, San Francisco, CA, US; 2 Amgen, Thousand Oaks, CA, US

Background: Proprotein convertase subtilisin kexin 9 (PCSK9) is induced by inflammation and leads to elevated levels of LDL cholesterol, increasing cardiovascular risk. Increased PCSK9 might explain the dyslipidemia observed in HIV-infected individuals, which has been previously attributed to HIV medication, HIV disease, and/or chronic inflammation. We aimed to compare PCSK9 levels in HIV-infected individuals and uninfected controls and to identify predictors of elevated PCSK9 in HIV disease. Methods: We measured PCSK9 levels in 567 participants (495 HIV, 72 controls) from an outpatient cohort in San Francisco using a high affinity ELISA assay. Generalized linear models with log link function were used to determine factors associated with PCSK9. Results: The median age of participants was 50 years (IQR 43-55) and 89%were male, 34% smokers, 25% hypertensive; the median LDL was 103 mg/dL (IQR 80-127), and 21% were on statins. HIV-infected individuals and controls were similar in age, gender, and had similar rates of traditional risk factors except for prior CAD, which was more common among those with HIV (7% vs. 0%). Most (56%) percent of HIV subjects were treated and suppressed on antiretroviral medication with a median HIV duration of 14.5 years, median CD4+ count of 527 (IQR 346-732) cells/mm 3 and nadir CD4+ count of 240 (IQR 96-394) cells/mm 3 . Unadjusted PCSK9 levels were 11% higher in HIV subjects vs. controls [mean 430 ng/ml (SD 166) vs. 386 ng/ml (SD134), p=0.015]; in addition, of the patients with extremely elevated PCSK9 levels (>800 ng/ml, n=20), 95%were HIV-infected. After adjustment for demographic factors (age, gender, race) and statin use, HIV remained independently associated with 10% higher PCSK9 levels (p=0.03); results were similar in the treated and suppressed cohort. In addition, older age, other race (comprised of mixed ethnicities, Middle Eastern and Pacific Islanders), statin use, Hepatitis C (HCV), higher triglycerides, current smoking and Lp(a)>90 nmol/L were all independently associated with higher PCSK9 levels in adjusted analysis. In contrast, neither inflammatory markers (IL-6, hs-CRP) nor CD4 + count or HIV viral load were associated with higher PCSK9.

Poster Abstracts

PCSK9 is 10% higher (9% CI 2-22%) (after adjustment for demographics, statin use and cardiovascular risk factors) in HIV-Infected compared with uninfected persons. Note that there are many HIV+ patients having very high PCSK9 levels (>800 ng/mL), suggesting that PCSK9 inhibition may prove to be an attractive target for treating HIV-associated dyslipidemia.

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CROI 2015