- Email: [email protected]
W16-O-005 Efficacy and safety of statin therapy in children with familial hypercholesterolemia
Workshops WI 6 Treatment of atherosclerosis risk
100
Conclusion: RSV 40 nag was well tolerated and enabled the majority of pts to be at their LDL-C goal after 48 wks of treatment, while providing additional significant increases in HDL-C and apt A-I.
W16-O-004 ] COMPARISON OF APOLIPOPROTEIN B AND PLASMA LIPIDS AS TARGETS FOR LIPID LOWERING TREATMENT H. Vaverkov~i1, j. Frohlich 2, D. Jackuliakovlt 1, D. Novotn~ 3 . 13rd Dept. of
Internal Medicine, Medical Faculty of Palacloj University Olomouc, Czech Republic," 2Dept of Pathol. and Lab. Medicine, St.Paul's Hospita~ Vancouver, B.C., Canada; ~Dept. of Consolidated Laboratories, University Hospital Olomouc, Czech Republic
Objective:
Numerous prospective studies confirmed that apolipoprotein (apt) B is a better marker of CHD risk than LDL-cholesterol and nonHDL-cholesterol. Many intervention studies questioned the importance of LDL-cholesterol as a risk marker in the course of hypolipidemic therapy and proved that the risk remained high at the concentration of ape B>0.9 g/L. The aim of the present study was to investigate whether the patients on lipid lowering therapy achieving the target lipid levels also reach non-risk concentrations of apo B<0.9 g/L. Methods: We evaluated 499 examinations of lipid parameters performed during one year in 224 patients treated with hypolipidemic drugs. The patients were divided into two groups: Group I (182 patients whose triglyceride levels were _>1.7 mmol/L or who had impaired fasting glucose or type 2 diabetes) and the Group II (42 patients with triglycerides <1.7 mmol/L and normal glucose homeostasis). Results: In the group I, 46% of the patients who reached the high risk LDL-C target of <2.5 mmol/L did not reach apo B<0.9 g/L, compared with only 19% in the group II. Similar results were obtained for TC and non-HDL-C. Conclusions: Our findings confirm that, in the presence of hypertriglyceridemia or impaired glucose homeostasis, LDL-C is a poor guide to lipid lowering treatment.
The study was supported by the grant VVZ-M,~ 151100005
I W16-P-001 I A CASE O F A C U T E PANCREATITIS POSSIBLY ASSOCIATED W I T H COMBINED SALICYLATE AND SIMVASTATIN TREATMENT S. Antonopoulos, S. Mikros, S. Kokkoris, K. Filioti, G. Lepeniotis, G.R. Giannoulis. 2nd Department of Internal Medicine, Tzaneion General
Hospita~ Piraeus, Greece Objective: To report a case of acute onset pancreatitis associated with simvastatin and acetylsalicylic aciduse. Case summary: A 58-year-old male with a history of coronary heart disease and hypercholesterolemia, under treatment with acetylsalicylic acid for 6 years and simvastatin for 2 months, presented at the emergency department of our hospital with epigastric and right upper abdominal pain, vomiting and diarrhea that had started 24 hours ago. The clinical and laboratory investigation led to the diagnosis of acute pancreatitis, which met 3 criteria according to Ranson. Conservative and rich in fluids treatment resulted in clinical and laboratory amelioration and the patient was discha~ed at day 15, after full restoration of his health. Discussion: Drag-induced acute pancreatitis is a rather rare clinical entity. Several cases have been reported from time to time, in which statins or salicylate have been incriminated in the development of acute pancreatitis. There is only one report, which implies the involvement of both drugs in pancreatic inflammation. In our patient, all possible common causes of acute pancreatitis were excluded. Thus, it is a rational assumption to connect this case with the co-administration of simvastatin and salicylate. However, the pathophysiological mechanism behind the onset of acute pancreatitis due to a statin, or, even more, due to its combination with salicylate, remains vague. Conclusions: Simvastatin and acetylsalicylic acid are a common combination treatment in patients with a history of coronary heart disease. The report on the possible harmful effect of their co-administration and their involvement in acute pancreatitis should raise the clinician's level of suspicion for this, sometimes fatal, adverse reaction.
I W16-P-002 I PHYSICIAN PERCEIVED BARRIERS TO OPTIMAL MANAGEMENT OF HYFERLIPIDEMIA i
W16-O-005 1 EFFICACY AND SAFETY OF STATIN THERAPY IN CHILDREN W I T H FAMILIAL HYPERCHOLESTEROLEMIA J
A. Wiegman 1, B.A. Hutten 3, E. de Groot 2, J. Rodenburg 2, H.D. Bakker 1, H.R. Buller 2, E.J.G. Sijbrands4, J.J.P. Kastelein 2 . JPediatrics, Academic
Medical Center, Amsterdam, the Netherlands; 2Vascular Medicine, Academic Medical Center, Amsterdam, the Netherlands; ~Clinical Epidemiology and Biostatistics, Academic Medical Center, Amsterdam, the Netherlands; 4Internal Medicine, Erasmus Medical Center, Rotterdam, the Netherlands Children with familial hypercholesterolemia (FH) have increased carotid intima-media thickness (IMT). Long-term efficacy and safety of cholesterollowering medication has not been investigated in children. Methods: Randomized, double-blind, placebo-controlled trial in 214 consecutive children with FH (8-18yr) from one academic referral center, to determine 2-year efficacy and safety of pravastatin (20-40mg). Primary efficacy outcome was defined as change from baseline in mean carotid IMT between two groups over two years, whereas principal safety outcome was measurement of growth, maturation and hormone levels over two years as well as changes of levels of muscle and liver enzymes. Remits: Compared to baseline, carotid IMT showed a trend towards regression on pravastatin (A IMT: -0.010+0.048 mm: p=0.049), whereas a trend towards progression was observed in the placebo group (A IMT: +0.005±0.044 mm: p=0.280). Predefined primary efficacy outcome, namely change of IMT between two groups (0.014-t-0.046 mm) did differ significantly (p=0.019). Also, pravastatin significantly reduced mean LDL-C levels compared to placebo (-24.1% versus +0.3%, respectively: p<0.0001). No differences were observed for growth, muscle or liver enzymes, endocrine function parameters, Tanner scores, onset of menses or in testicular volume between both groups. Conclusions: Two years of pravastatin induced a significant regression of carotid atherosclerosis in FH children with no adverse effects on growth, sexual maturation, hormone levels, liver or muscle tissue.
A. Bakhai 1, S. Allan 1, G.M. Davies 2, E. Alemao 2, K. Thilo 3, L. Parker 3 , D. Yin 2, M. Drummond 4. 1Barrier General Hospital & AMOREgroup,
UK, 2Merck & Co., Inc, New Jersey, USA, 3Rertwdica, London, UK, 4University of York, New York, USA Objective: Many hyperlipidemia patients in the UK are not managed optimally and do not reach target cholesterol levels. The objective of this study was to determine the main barriers to patients reaching target cholesterol levels amongst prescribers in UK. Methods: A cross-sectional study of 72 randomly selected (450 invited) primary care physicians was undertaken using a structured questionnaire adapted from a previously validated instrument. Prior to starting the questionnaire physicians were asked to identify and rank three major barriers to attaining target cholesterol levels. In addition, for each physician, 9 barrier categories were ranked in order of relevance to patients reaching target cholesterol levels, and mean ranks were averaged across all physicians. Results: On average, physicians had practiced for 22 years (SD 7), 44% were in the age group of 41-50 years and 32% in the age group >50 years and 19% were in a single partner practice and the median practice population was approximately 7500 patients. Overall compliance was ranked as one of the three major barriers 67% of the time followed by statin associated AE's (46%) and lack of time and resources (35%), lack of efficacious medication (22%) and diet (22%). Initial physician identified barrier's correlate well with the the ranking of the perceived barriers to patients reaching target cholesterol levels (Table 1). Table 1. Bardess to patients reaching target cholesterol levels Barrier categories (construct) Patient compliance Drug efficacy/dosing Ttming and Resources Adverse effects Adjusting Statin Therapy
GuidanceJtargcts Too many co-therapies Cost therapies Lifestyle changes
75th EAS Congress, 23-26 April 2005, Prague, Czech Republic
Mean (SD) Rankingof barriers
Rank
2.5 (2.0) 3.9 (2.4) 4.1 (2.4) 5.0 (2.4) 5.5 (2.2) 5.7 (2.0) 5.8 (2.0) 5.9 (2.5) 6.5 (2.4)
1 2 3 4 5 6 7 8 9
100
Conclusion: RSV 40 nag was well tolerated and enabled the majority of pts to be at their LDL-C goal after 48 wks of treatment, while providing additional significant increases in HDL-C and apt A-I.
W16-O-004 ] COMPARISON OF APOLIPOPROTEIN B AND PLASMA LIPIDS AS TARGETS FOR LIPID LOWERING TREATMENT H. Vaverkov~i1, j. Frohlich 2, D. Jackuliakovlt 1, D. Novotn~ 3 . 13rd Dept. of
Internal Medicine, Medical Faculty of Palacloj University Olomouc, Czech Republic," 2Dept of Pathol. and Lab. Medicine, St.Paul's Hospita~ Vancouver, B.C., Canada; ~Dept. of Consolidated Laboratories, University Hospital Olomouc, Czech Republic
Objective:
Numerous prospective studies confirmed that apolipoprotein (apt) B is a better marker of CHD risk than LDL-cholesterol and nonHDL-cholesterol. Many intervention studies questioned the importance of LDL-cholesterol as a risk marker in the course of hypolipidemic therapy and proved that the risk remained high at the concentration of ape B>0.9 g/L. The aim of the present study was to investigate whether the patients on lipid lowering therapy achieving the target lipid levels also reach non-risk concentrations of apo B<0.9 g/L. Methods: We evaluated 499 examinations of lipid parameters performed during one year in 224 patients treated with hypolipidemic drugs. The patients were divided into two groups: Group I (182 patients whose triglyceride levels were _>1.7 mmol/L or who had impaired fasting glucose or type 2 diabetes) and the Group II (42 patients with triglycerides <1.7 mmol/L and normal glucose homeostasis). Results: In the group I, 46% of the patients who reached the high risk LDL-C target of <2.5 mmol/L did not reach apo B<0.9 g/L, compared with only 19% in the group II. Similar results were obtained for TC and non-HDL-C. Conclusions: Our findings confirm that, in the presence of hypertriglyceridemia or impaired glucose homeostasis, LDL-C is a poor guide to lipid lowering treatment.
The study was supported by the grant VVZ-M,~ 151100005
I W16-P-001 I A CASE O F A C U T E PANCREATITIS POSSIBLY ASSOCIATED W I T H COMBINED SALICYLATE AND SIMVASTATIN TREATMENT S. Antonopoulos, S. Mikros, S. Kokkoris, K. Filioti, G. Lepeniotis, G.R. Giannoulis. 2nd Department of Internal Medicine, Tzaneion General
Hospita~ Piraeus, Greece Objective: To report a case of acute onset pancreatitis associated with simvastatin and acetylsalicylic aciduse. Case summary: A 58-year-old male with a history of coronary heart disease and hypercholesterolemia, under treatment with acetylsalicylic acid for 6 years and simvastatin for 2 months, presented at the emergency department of our hospital with epigastric and right upper abdominal pain, vomiting and diarrhea that had started 24 hours ago. The clinical and laboratory investigation led to the diagnosis of acute pancreatitis, which met 3 criteria according to Ranson. Conservative and rich in fluids treatment resulted in clinical and laboratory amelioration and the patient was discha~ed at day 15, after full restoration of his health. Discussion: Drag-induced acute pancreatitis is a rather rare clinical entity. Several cases have been reported from time to time, in which statins or salicylate have been incriminated in the development of acute pancreatitis. There is only one report, which implies the involvement of both drugs in pancreatic inflammation. In our patient, all possible common causes of acute pancreatitis were excluded. Thus, it is a rational assumption to connect this case with the co-administration of simvastatin and salicylate. However, the pathophysiological mechanism behind the onset of acute pancreatitis due to a statin, or, even more, due to its combination with salicylate, remains vague. Conclusions: Simvastatin and acetylsalicylic acid are a common combination treatment in patients with a history of coronary heart disease. The report on the possible harmful effect of their co-administration and their involvement in acute pancreatitis should raise the clinician's level of suspicion for this, sometimes fatal, adverse reaction.
I W16-P-002 I PHYSICIAN PERCEIVED BARRIERS TO OPTIMAL MANAGEMENT OF HYFERLIPIDEMIA i
W16-O-005 1 EFFICACY AND SAFETY OF STATIN THERAPY IN CHILDREN W I T H FAMILIAL HYPERCHOLESTEROLEMIA J
A. Wiegman 1, B.A. Hutten 3, E. de Groot 2, J. Rodenburg 2, H.D. Bakker 1, H.R. Buller 2, E.J.G. Sijbrands4, J.J.P. Kastelein 2 . JPediatrics, Academic
Medical Center, Amsterdam, the Netherlands; 2Vascular Medicine, Academic Medical Center, Amsterdam, the Netherlands; ~Clinical Epidemiology and Biostatistics, Academic Medical Center, Amsterdam, the Netherlands; 4Internal Medicine, Erasmus Medical Center, Rotterdam, the Netherlands Children with familial hypercholesterolemia (FH) have increased carotid intima-media thickness (IMT). Long-term efficacy and safety of cholesterollowering medication has not been investigated in children. Methods: Randomized, double-blind, placebo-controlled trial in 214 consecutive children with FH (8-18yr) from one academic referral center, to determine 2-year efficacy and safety of pravastatin (20-40mg). Primary efficacy outcome was defined as change from baseline in mean carotid IMT between two groups over two years, whereas principal safety outcome was measurement of growth, maturation and hormone levels over two years as well as changes of levels of muscle and liver enzymes. Remits: Compared to baseline, carotid IMT showed a trend towards regression on pravastatin (A IMT: -0.010+0.048 mm: p=0.049), whereas a trend towards progression was observed in the placebo group (A IMT: +0.005±0.044 mm: p=0.280). Predefined primary efficacy outcome, namely change of IMT between two groups (0.014-t-0.046 mm) did differ significantly (p=0.019). Also, pravastatin significantly reduced mean LDL-C levels compared to placebo (-24.1% versus +0.3%, respectively: p<0.0001). No differences were observed for growth, muscle or liver enzymes, endocrine function parameters, Tanner scores, onset of menses or in testicular volume between both groups. Conclusions: Two years of pravastatin induced a significant regression of carotid atherosclerosis in FH children with no adverse effects on growth, sexual maturation, hormone levels, liver or muscle tissue.
A. Bakhai 1, S. Allan 1, G.M. Davies 2, E. Alemao 2, K. Thilo 3, L. Parker 3 , D. Yin 2, M. Drummond 4. 1Barrier General Hospital & AMOREgroup,
UK, 2Merck & Co., Inc, New Jersey, USA, 3Rertwdica, London, UK, 4University of York, New York, USA Objective: Many hyperlipidemia patients in the UK are not managed optimally and do not reach target cholesterol levels. The objective of this study was to determine the main barriers to patients reaching target cholesterol levels amongst prescribers in UK. Methods: A cross-sectional study of 72 randomly selected (450 invited) primary care physicians was undertaken using a structured questionnaire adapted from a previously validated instrument. Prior to starting the questionnaire physicians were asked to identify and rank three major barriers to attaining target cholesterol levels. In addition, for each physician, 9 barrier categories were ranked in order of relevance to patients reaching target cholesterol levels, and mean ranks were averaged across all physicians. Results: On average, physicians had practiced for 22 years (SD 7), 44% were in the age group of 41-50 years and 32% in the age group >50 years and 19% were in a single partner practice and the median practice population was approximately 7500 patients. Overall compliance was ranked as one of the three major barriers 67% of the time followed by statin associated AE's (46%) and lack of time and resources (35%), lack of efficacious medication (22%) and diet (22%). Initial physician identified barrier's correlate well with the the ranking of the perceived barriers to patients reaching target cholesterol levels (Table 1). Table 1. Bardess to patients reaching target cholesterol levels Barrier categories (construct) Patient compliance Drug efficacy/dosing Ttming and Resources Adverse effects Adjusting Statin Therapy
GuidanceJtargcts Too many co-therapies Cost therapies Lifestyle changes
75th EAS Congress, 23-26 April 2005, Prague, Czech Republic
Mean (SD) Rankingof barriers
Rank
2.5 (2.0) 3.9 (2.4) 4.1 (2.4) 5.0 (2.4) 5.5 (2.2) 5.7 (2.0) 5.8 (2.0) 5.9 (2.5) 6.5 (2.4)
1 2 3 4 5 6 7 8 9