ADVERSE EVENTS – CARDIOVASCULAR
P25
Late gadolinium enhancement and subclinical cardiac dysfunction on cardiac MRI in asymptomatic HIV-positive men Loy, A*; Morgan, R; O’Dea, S; Takacs, E; Daly, C; Mulcahy, F (Dublin, Ireland)
P26
Nevirapine vs efavirenz in virologically suppressed patients: differences in lipoprotein subclasses and inflammatory biomarkers Estrada, V*; Gómez-Garre, M; Santos, J; Gutiérrez, F; Labarga, P; Palacios, R; Masiá, M; López-Vázquez, M; Isernia, V; Vispo, E; Fernández-Cruz, A (Madrid, Spain)
P27
Too old too soon? Heart age compared with actual age in HIV-positive individuals Davies, T*; May, M; Gompels, M (Bristol, UK)
P28
Carotid intima media thickness changes, endothelial activation and inflammatory markers in advanced naïve HIV patients starting antiretroviral therapy Bellacosa, C; Maggi, P*; Leone, A; Altizio, S; Ladisa, N; Uglietti, A; Zanaboni, D; Maserati, R; Viglietti, R; Chirianni, A; Abbrescia, N; De Rosa, A; Sofia, S; Celesia, M; Angarano, G (Bari, Italy)
P29
Role of maraviroc in a dyslipidemic murine model of atherosclerosis RTV-induced Cipriani, S; Mencarelli, A; Francisci, D; Renga, B; Renga, B; Schiaroli, E; D’Amore, C; Fiorucci, S; Balbelli, F* (Perugia, Italy)
P30
HIV-infected patients show functionally defective high-density lipoprotein (HDL) paralleled with changes in HDL-associated proteins Estrada, V*; Gómez-Garre, M; Ortega-Hernandez, A; Muñoz-Pacheco, P; Serrano-Vilar, S; Sainz-Costa, T; Carranza, M; Rodrigo, M; Fernández-Cruz, A (Madrid, Spain)
P31
Incidence and risk factors of major cardiovascular events in a multicentre HIV cohort Carenzi, L; Meraviglia, P; Menzaghi, B; Valsecchi, L; Capetti, A*; Rizzardini, G (Milan, Italy)
P32
SCORE underestimates cardiovascular risk (CVR) of HIV+ patients Ramírez, R*; Márquez, J; Tasias, M; Ruiz, S; Delegido, A; Díaz, A; Araújo, O; Hernández, S; Tikhomirova, L; Creus, C; Alonso-Villaverde, C; Pedrol, E (Tarragona, Spain)
P33
Effectiveness of antihypertensive therapy in HIV-positive patients: evaluation to 144 weeks Falasca, K*; Ucciferri, C; Vignale, K; Ripani, P; Pizzigallo, E; Vecchiet, J (Chieti, Italy)
*Indicates presenting author.
Late Gadolinium Enhancement and Subclinical Cardiac Dysfunction on Cardiac MRI in Asymptomatic HIV Positive Men AUTHORS/INSTITUTION: A.M. Loy, R.B. Morgan, S. O' Dea, A. Takacs, C.A Daly, F. Mulcahy. St. James's Hospital, Dublin, IRELAND.
INTRODUCTION HIV infected individuals are at an increased risk of cardiovascular disease (CVD)1-4. Early detection of cardiovascular abnormalities is key to understanding and modifying the processes involved. Cardiac Magnetic Resonance Imaging (CMR) can identify multiple forms of cardiac pathology even in the absence of overt clinical manifestations5. CMR is also capable of detecting and quantifying subtle changes in systolic and diastolic function. Isolated diastolic dysfunction (DD) may be the first indication of underlying cardiac disease and an early marker of coronary artery disease.
METHODS 131 asymptomatic virally suppressed HIV positive men on ART compared to 33 matched controls were prospectively recruited to this observational cohort study. Baseline demographics, HIV parameters,12 lead ECG, routine biochemistry, and traditional cardiovascular risk factors were recorded. Images were acquired on a 3T Achieva Philips MRI scanner with 5 channel phase array cardiac coil and weight based IV gadolinium was administered. Data was analysed using SPSS software.
RESULTS Of 131 HIV positive patients 6 had late gadolinium enhancement on CMR, of these 2 were consistent with previous myocardial infarction and 4/6 had a pattern consistent with prior myocarditis despite no previous symptoms. On logistic regression analysis the number of pack years smoking was the only significant contributing factor (p=0.01). Diastolic dysfunction was significantly higher in cases than controls, as demonstrated by the E:A ratio (1.28 vs 1.47 p=0.045). On logistic regression analysis significant contributors were age (p14mm, in the range of moderate to severe LVH. On multiple regression analysis contributing factors were BMI p=0.01and family history of cardiac disease p=0.032.
RESULTS CASES (N=131)
CONTROLS (N=33)
P VALUE
AGE(mean, yrs)
47
43
0.875
SMOKING PK YRS
14
5
*0.006
FRAMINGHAM RISK
8.1
7.4
0.939
KNOWN HTN
25
3
0.173
COCAINE USE(ever)
60
2
*0.03
FHX PCAD
37
10
0.916
LVEF(%)
65.9
66.4
0.688
LVMI(g/m2)
59.2
57.1
0.323
E/A Reversal
30
3
0.085
E/A Ratio(mean)
1.28
1.47
*0.045
Anteroseptal Wall Thickness (mean, mm)
10.89
9.78
*0.004
Posterolateral Wall Thickness (mean, mm)
8.27
8.40
0.64
Presence of Late Gad enhancement(LGE)
6
0
0.21
PATIENT/CMR FINDINGS
CONCLUSION Despite HIV viral suppression with ART, early functional cardiac changes have been detected with CMR in asymptomatic HIV positive men. The prevalence of previously undetected MI was 1.5% and the prevalence of previously undiagnosed myocarditis was 3%. Given the prognostic importance of LGE in other clinical settings this will have important implications for this cohort. Significantly higher rates of diastolic dysfunction and increased anteroseptal wall thickness in HIV positive men appears strongly linked to age, waist:hip ratio, family hx of cardiac disease, length of years since HIV diagnosis and BMI. Traditional cardiovascular risk factors eg framingham risk did not predict early cardiovascular disease.
REFERENCES 1. Friis-Moller N, Smieja M, Klein D. Antiretroviral therapy as a cardiovascular disease risk factor: fact or fiction? A review of clinical and surrogate outcome studies. Curr Opin HIV AIDS 2008;3(3):220-5. 2. Friis-Moller N, Thiebaut R, Reiss P, et al. Predicting the risk of cardiovascular disease in HIV-infected patients: the data collection on adverse effects of anti-HIV drugs study. Eur J Cardiovasc Prev Rehabil;17(5):491-501. 3. Currier JS. Update on cardiovascular complications in HIV infection. Top HIV Med 2009;17(3):98-103. 4. Lang S, Mary-Krause M, Simon A, Partisani M, Gilquin J, Cotte L, et al. HIV Replication and Immune Status Are Independent Predictors of the Risk of Myocardial Infarction in HIV-Infected Individuals. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America 2012.4 5 Hendel RC, Patel MR, Kramer CM, et al. Appropriateness criteria for cardiac computed tomography and cardiac magnetic resonance imaging. J Am Coll Cardiol 2006;48(7):1475-97
Funding: AVEC (Abbott Virology External Collaborations)
P026
Glasgow, 11-15 Nov 2012
Nevirapine vs Efavirenz in virollogically supressed patients: differences in lipoprotein subclasses and inflammatory biomarkers Authors: Estrada V; Gómez‐Garre, M; Santos, J; Gutiérrez, F; Labarga, P; Palacios, R; Masiá, M; López‐Vázquez, M; Isernia, V; Vispo, E; Fernández‐Cruz, A. Hospital Clínico San Carlos, Madrid; Hospital Virgen de la Victoria, Málaga; Hospital Universitario Elche, Alicante; Hospital Carlos III, Madrid; Spain Background: Lipid disturbances are common in HIV-infected patients, in particular high triglyceride and low HDL-cholesterol levels. Chronic inflammation may be responsible of some HIV-related complications as cardiovascular, renal or bone disease. The source for this chronic inflammation has not been fully elucidated and a chronic bacterial translocation from the gut is considered to be a potential source. The interaction between lipid disturbances and inflammatory markers is not well known in patients on ART. NNRTIs are considered as a family of drugs with a good lipid profile, and NVP is ussually associated with a better lipid profile than EFV, in particular lower levels of TG and HDL-C. Aim of the study: 1. To investigate the relationships between lipid profiles, lipoprotein subclasses and inflammatory biomarkers in HIV-infected patients on NNRTI-based therapy; and 2. To explore whether there are differences in inflammatory biomarkers among patients on EFV or NVP-based treatments, as presenting lipid profile is often different. Methods: Clinically stable HIV-infected patients, with HIV-1 RNA EFV AIDS (%) 24 NS BMI (kg/m2) 23.8 kg/m2 (SD 2.7) NS Smokers (%) 36% NS Lymphocyte CD4 count (cels/µL) 550/µL (324) NS Time since HIV diagnosis (months) 96 (102)* NVP > EFV Accumulated time on ART (months) 50 (101)* NVP > EFV Accumulated time on NRTI (months) 70 (109)* NVP > EFV Accumulated time on NNRTI (months) 65 (87)* NVP > EFV Lipid profile No differences but HDL-C, apoA1, apoA1/apoB ratio Lipoprotein particles & subclasses and Inflammatory biomarkers No significant differences No relationships between inflammatory biomarkers and lipid profile
65
HDL particles by RMN
165
0,75
apoA1
HDL-c
95% IC apo-B/apo-A1 ratio
155
95% IC ApoA1
95% IC HDL_C
40
0,70
* p=0,007
150
7 42
6
160
60
55
apoB/apoA1 ratio
* p=0,002
5 38
34
0,65
145
50
3
EFV
NVP
EFV
NVP
23 16
22
21 14
0,60
140
4
36
20
19
12
18
17
10
45
0,55
135
EFV
NNRTI
NVP
EFV
NNRTI
NVP
16
EFV
NNRTI
NVP
EFV
NNRTI
NVP
EFV
NVP
Conclusions: Patients with prolonged viral suppression on NVP present significantly higher HDL and apoA1 levels and reduced apoB/apoA1 ratios than those on EFV, but no differences were found in lipoprotein particles nor inflammatory biomarkers. Relationships between lipid parameters and inflammatory biomarkers in NNRTI‐treated patients are complex and do not show a linear relationship in this study.
Poster No: P027 Email:
[email protected]
Too old too soon? Heart age compared with actual age in HIV positive individuals T-L Davies1, M Gompels2 and M T May1 1School of Social and Community Medicine, University of Bristol. 2North Bristol NHS Trust, HIV Service, Bristol, UK
Introduction
HIV+ individuals are now living to much older ages and therefore may be at high risk of cardiovascular disease (CVD). Communication of CVD risk to HIV patients is extremely important, particularly the impact of modifiable risk factors, such as smoking. Recently the British Heart Foundation has promoted the use of ‘heart age’ derived from the 10-year Framingham risk equations for general CVD (1). Here we investigate how ‘heart age’ compares to actual age in the Bristol cohort of HIV+ individuals.
Objectives To assess heart age deviation (heart age – actual age) in HIV+ individuals using Framingham CVD risk scores To identify clinical and demographic variables that predict heart age deviation To promote the use of heart age deviation as a tool for communicating CVD risk to HIV+ individuals
Methods
AGE GROUP (YRS)
Sex-specific 10-year Framingham risk equation for CVD
Calculate heart age deviation: heart age – real age
HEART AGE HEART MEAN HEART HEART AGE AGE REAL AGE NON- DEVIATION DEVIATION AGE SMOKERS NON-SMOKERS SMOKERS SMOKERS (YRS) (YRS) (YRS) (YRS) (YRS) (95% CI) (95% CI) 34 35 1.3 (0.6,2.1) 43 9.8 (8.8,10.7) 45 48 3.3 (2.2,4.5) 60 15.0 (13.5,16.5)
184 (37%) 182 (36%)
50-59
91 (18%)
53
60
6.1 (3.9,8.4)
74
20.4 (17.6,23.2)
60-
46 (9%)
66
73
6.8 (2.2,11.4)
90
23.3 (18.3,28.3)
total
503 (100%)
44
48
3.4 (2.6,4.2)
59
14.8 (13.8,15.8)
16-39
126 (51%)
33
32
-1.4 (-2.9,0.0)
40
6.8 (4.9,8.6)
40-49
83 (34%)
44
47
3.0 (-0.1,6.1)
59
15.0 (11.2,18.9)
50-59
27 (11%)
55
63
7.7 (1.5,13.9)
79
23.7 (15.8,31.6)
60-
10 (4%)
66
82
16.3 (0.1,32.5)
100
33.9 (16.8,51.0)
246 (100%)
41
42
1.8 (0.1,3.4)
53
12.5 (10.4,14.6)
total
Table 1: Real age, heart age and heart age deviation by smoking status
Results 2: Predictors of Heart Age Deviation
Table 2 shows differences in heart age deviation by patient characteristics mutually adjusted for sex, age (years), CD4 count (mm3), viral load (ml)/treatment status and period of starting ART. Heart age Deviation (years)
CD4 VIRAL LOAD & TREATMENT STATUS
Of the 749 patients in the study, 67% were male and 82% were treated with ART. The median age was 42 years (IQR: 49-35). The figure shows heart age deviation increases with real age and is much higher for smokers eg for males aged 50, the heart age deviation is around 18 years in smokers and around 5 years in nonsmokers. At younger ages, females have better heart age deviation than males, although this crosses over in the late forties. Table 1 shows estimated heart age and heart age deviation compared with real age.
N (%)
16-39 40-49
AGE
Results 1: Heart Age vs. Actual Age
FEMALES
Trace the risk score back to sex-specific “heart age”
MALES
HIV+ individuals attending the Bristol HIV clinic up to November 2011 contributed data on Framingham risk factors, CD4 count and viral load. We used the latest available measurements, within a 6 month time window. We calculated the Framingham risk and traced back to ‘heart age’: the age of an individual with the same score but ideal risk factor values (nonsmoker, non-diabetic, untreated SBP 125 mmHg, total cholesterol 180 mg/dL, HDL 45 mg/dL (1)). Smoking status was not available therefore analyses were conducted twice assuming all were 1) smokers 2) non-smokers. Heart age deviation (heart age - real age) was calculated for each individual for each smoking assumption. Fractional polynomial regression was used to show the relationship between heart age deviation and actual age. We used linear regression to estimate crude and mutually adjusted associations between heart age deviation and gender, age, CD4 count, viral load/treatment status and period of starting ART.
Figure: Fractional polynomial regression - 95% CI shown shaded
16-39 40 -49 50-59 60