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Cardiovascular risk assessment in HIV-infected patients attending a designated lipid clinic
4
Abstracts / Atherosclerosis xxx (2008) xxx–xxx
Cardiovascular risk assessment in HIV-infected patients attending a designated lipid clinic Monika Dham Kohli a , Sandra Parra b , Raimon Ferre b , Carlos Alonso-Villaverde b , Mike Youle a , Margaret Johnson a , Devaki Nair a a
Royal Free Hospital Hampstead NHS Trust, London NW3 2QG, UK b Hospital Universitari Sant Joan de Reus, Spain
Introduction: Metabolic complications related to HIV infection or therapy increase the risk for cardiovascular disease (CVD). The management of HIV together with their CVD risk factors is complex. The effectiveness of a designated lipid clinic in improving CVD risk factors was assessed. Methods: Data from 217 patients were included. As part of their routine care all patients underwent a cardiovascular risk assessment. Results: The mean age was 49.2(8.2) years; 26.7% were current smokers. 17.1% were referred for secondary prevention and 82.9% for primary prevention. The Framingham score for CVD in 10.6% of the patients was >20%; 29.5% had a score between 10 and 20% and 53.9% had a score of <10%. For primary prevention 54.5% patients reached the recommended target according to JBS2 guidelines of BP <140/85 mm, 58.8% reached the LDL target of<3 mmol/l, 46.9% reached the target of TC <5 mmol/l and 61.8% have TG <2.3 mmol/l. For secondary prevention, 56.8% of patients reached the recommended BP target of <130/80 mmHg, 47.1% reached the LDL target of <2 mmol/l, 37.8% reached the target of TC <4 mmol/l and 52.8% had TG <2.3 mmol/l. Conclusion: A high proportion of HIV infected patients on anti-retroviral treatment have an increased risk for CVD and the management of CVD risk is mandatory. However our study shows difficulty in achieving the targets for both blood pressure and lipids. The reasons for difficulties in optimal management of CVD risk in these patients should be explored. doi:10.1016/j.atherosclerosis.2008.04.029
Mutation detection rate and spectrum in definite (DFH) and possible (PFH) patients from the department of health (DH) pilot project S.E. Humphries a , A. Taylor b , D. Wang b , R. Whittall a , D. Neely c , D. Nair d , M. Barbir e , S. Egan f , Y. Lolin g , G. Hadfield a , G. Norbury b a
Centre for Cardiovascular Genetics, BHF Labs, RF&UCL Medical School, London, UK b Regional Molecular Genetics Laboratory, Great Ormond Street Hospital for Children, London, UK c Lipid and Metabolic Clinic, Royal Victoria Infirmary, Newcastle upon Tyne, London, UK d Royal Free Hampstead NHS Trust, London, UK e Royal Brompton & Harefield NHS Trust, Middlesex, UK f The Royal Bournemouth & Christchurch Hospitals NHS Trust, Castle Lane East, Bournemouth, UK g Maidstone & Tunbridge Wells NHS Trust, Kent, UK Background: DH funding covered FH DNA testing to compare the detection rate and mutation spectrum in DFH vs. PFH patients. Methods: Patients were recruited from five UK clinics. A commercial ARMS kit for 11 LDLR mutations plus APOB R3527Q and PCSK9 D374Y were used as an initial screen, followed by an MLPA kit to determine deletions and duplications. Samples with no mutation detected were screened in all exons using dHPLC. Results: 536 patients were collected. In 162 DFH patients, the detection rate was 59%, and in the 329 PFH patients the rate was 31% (p > 0.00001). For 45 patients there was inadequate information to determine PFH/DFH status, and in this (UFH) group the detection date was 22% (p = 0.2 vs. PFH). Of the 209 patients with detected mutations (101 different), the ARMS kit detected 71 (34%) and MLPA kit 9 (4.3%). Compared to PFH, there was suggestive evidence (p = 0.06) for a higher prevalence in DFH of “severe” (functional null alleles and mis-sense in exon 3/4) compared to “mild” (mis-sense outside exons3/4) mutations (68% vs. 46%). Conclusion: The high detection rate in UFH patients suggests that even in subjects with a low clinical suspicion of FH mutation testing will be useful. Overall, the detection rate compares favourably with the 20–30% seen in BRCA1/2 in familial breast cancer. Acknowledgements Work was funded by a grant from the DH to the IDEAS GKP. We thank the nurses for patient recruitment. doi:10.1016/j.atherosclerosis.2008.04.030
ATH 10385 1–6
Abstracts / Atherosclerosis xxx (2008) xxx–xxx
Cardiovascular risk assessment in HIV-infected patients attending a designated lipid clinic Monika Dham Kohli a , Sandra Parra b , Raimon Ferre b , Carlos Alonso-Villaverde b , Mike Youle a , Margaret Johnson a , Devaki Nair a a
Royal Free Hospital Hampstead NHS Trust, London NW3 2QG, UK b Hospital Universitari Sant Joan de Reus, Spain
Introduction: Metabolic complications related to HIV infection or therapy increase the risk for cardiovascular disease (CVD). The management of HIV together with their CVD risk factors is complex. The effectiveness of a designated lipid clinic in improving CVD risk factors was assessed. Methods: Data from 217 patients were included. As part of their routine care all patients underwent a cardiovascular risk assessment. Results: The mean age was 49.2(8.2) years; 26.7% were current smokers. 17.1% were referred for secondary prevention and 82.9% for primary prevention. The Framingham score for CVD in 10.6% of the patients was >20%; 29.5% had a score between 10 and 20% and 53.9% had a score of <10%. For primary prevention 54.5% patients reached the recommended target according to JBS2 guidelines of BP <140/85 mm, 58.8% reached the LDL target of<3 mmol/l, 46.9% reached the target of TC <5 mmol/l and 61.8% have TG <2.3 mmol/l. For secondary prevention, 56.8% of patients reached the recommended BP target of <130/80 mmHg, 47.1% reached the LDL target of <2 mmol/l, 37.8% reached the target of TC <4 mmol/l and 52.8% had TG <2.3 mmol/l. Conclusion: A high proportion of HIV infected patients on anti-retroviral treatment have an increased risk for CVD and the management of CVD risk is mandatory. However our study shows difficulty in achieving the targets for both blood pressure and lipids. The reasons for difficulties in optimal management of CVD risk in these patients should be explored. doi:10.1016/j.atherosclerosis.2008.04.029
Mutation detection rate and spectrum in definite (DFH) and possible (PFH) patients from the department of health (DH) pilot project S.E. Humphries a , A. Taylor b , D. Wang b , R. Whittall a , D. Neely c , D. Nair d , M. Barbir e , S. Egan f , Y. Lolin g , G. Hadfield a , G. Norbury b a
Centre for Cardiovascular Genetics, BHF Labs, RF&UCL Medical School, London, UK b Regional Molecular Genetics Laboratory, Great Ormond Street Hospital for Children, London, UK c Lipid and Metabolic Clinic, Royal Victoria Infirmary, Newcastle upon Tyne, London, UK d Royal Free Hampstead NHS Trust, London, UK e Royal Brompton & Harefield NHS Trust, Middlesex, UK f The Royal Bournemouth & Christchurch Hospitals NHS Trust, Castle Lane East, Bournemouth, UK g Maidstone & Tunbridge Wells NHS Trust, Kent, UK Background: DH funding covered FH DNA testing to compare the detection rate and mutation spectrum in DFH vs. PFH patients. Methods: Patients were recruited from five UK clinics. A commercial ARMS kit for 11 LDLR mutations plus APOB R3527Q and PCSK9 D374Y were used as an initial screen, followed by an MLPA kit to determine deletions and duplications. Samples with no mutation detected were screened in all exons using dHPLC. Results: 536 patients were collected. In 162 DFH patients, the detection rate was 59%, and in the 329 PFH patients the rate was 31% (p > 0.00001). For 45 patients there was inadequate information to determine PFH/DFH status, and in this (UFH) group the detection date was 22% (p = 0.2 vs. PFH). Of the 209 patients with detected mutations (101 different), the ARMS kit detected 71 (34%) and MLPA kit 9 (4.3%). Compared to PFH, there was suggestive evidence (p = 0.06) for a higher prevalence in DFH of “severe” (functional null alleles and mis-sense in exon 3/4) compared to “mild” (mis-sense outside exons3/4) mutations (68% vs. 46%). Conclusion: The high detection rate in UFH patients suggests that even in subjects with a low clinical suspicion of FH mutation testing will be useful. Overall, the detection rate compares favourably with the 20–30% seen in BRCA1/2 in familial breast cancer. Acknowledgements Work was funded by a grant from the DH to the IDEAS GKP. We thank the nurses for patient recruitment. doi:10.1016/j.atherosclerosis.2008.04.030
ATH 10385 1–6