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Effects of long-term lipid lowering therapy on lipids and apolipoprotein B and A-I
$94
Poster session abstracts / Atherosclerosis 115 ( SuppL ) (1995) $45-S129 P12 Medical Treatment o f Hyperlipidaemia
3511
352
EFFICIENCY OF PROLONGED MEVACOR T R E A T M E N T IN PATIENTS W I T H ISCHEMIC H E A R T DISEASE AND TYPE I1 HYPERLIPIDEMIA B.M. Lipovetsk¥ Institute of the Human Brain, St. Petersburg. Russia
THE C H A N G E S OF SERUM HDL C H O L E S T E R O L IN T H E TREAFMI-NTS WITH SIMVASTATIN AND ONLY W I T H DIET N Salto', F Ootsuji . A Kuchiba and T Kannagi ~ IDepartmenl of Geriatrics. Kochi Medical University, Kochi 783. Japan, -'Shiga Prefectural College. Shiga. ~Kyoto Women University, Kvot~. 'Kvoto Medical Prevention Center. Kyoto. Japan
The purpose of the study is to evaluate the clinical and hypolipidemic effects of 3-year mevacor treatment in patients suffering from ischemic heart disease and type IIa or llb hyperlipidemia. Two groups of patients were compared: 26 took 20-40 mg/d mevacor (Merck) for 3 yr along with nitrates and nifidipin (group 1) while 20 similar patients received the same treatment without hypolipidemie drug (group 2). There were 42 men of 46 patients, the age: 5 2 ± 1.7 (1) and 5 3 + 1 . 4 (2). Patients with angina (functional classes 1I-1II) without arrhythmia or heart failure had been selected. Blood cholesterol levels in group I fell by 36%, triglycerides - by 17 % while those in group 2 remained unchanged. No death or acute myocardial infarction (MI) occurred in group 1 during 3 yr follow up, whereas in the 2-nd group 5 patients died and l had MI. The stable improvement was observed in 27 % patients of group 1 only. The improvement in the first line can be explained by better micro-circulation and tissue oxygen diffusion due to hypolipidemic effect of mevacor.
This ~,tud; i~, aimed It) citriC\ tire change of serum HDL cholesterol in the treatlllel/lS wilh siii2vastatln and only with diet. In diet treatment 207 outpaticnls with diabetic type. which was determined by oral 75g GTT. were recruited In simvastatin treatment 24 diabetic outpatient,, received oral 5rag ot slmvastatin daily for 3 to 26 months Fasting blood sample was obtained ii1 the early morning for measuring serum lipids and lipoprotetns In diet treatment maird', witll diet energy restriction, serum total cholesterol tTC). triglyceride (TG). apolipoprotein B (apo B) and HDL cholesterol /HDL-Ci decreased, if a great change of either bod} wcigln or TG was not plesenl, ha Slmvastatin treatment, TC. LDL-C. apo B, renlnant like particle cholesterol (HDL-C) and atberogemc index decreased, and TG decreased slightly, when HDLC did not change significantly However. HDL--C tended to increase ( p < ( ! 11 Concerning the correlations between prevalues and the changed ~.aluer, ot HDL C there were lound about 40 mgldl in diet treatnlent alld approxinlatel,. 61/ ing/dl ii2 sunvastatin treatment as the crhical polHls lhe sanle tendenc? was observed in 13 individual patients uho received diet old\ and then simvastatin. The stop of SilllVastatlll adlnillisnatit)n resulted in elevation of TC and decrement of HDI. C As a ~ummar\ there was a difference of HDL-C change betwecll diel al}d silIn, astaitll [reaHiicnts
351
353
EFFECTS OF L O N G - T E R M LIPID L O W E R I N G T H E R A P Y ON LIPIDS AND APOL1POPROTEIN B AND A-I I. Reiber. ,/~. G6gl 1st Department of Internal Medicine. Szent Gyorgy Hospital, 8000 Sz6kesfeh6rv~ir, Sereg61yesi u 3
SIMVASTATIN VS. MICRONIZED FENOFIBRATE IN PATIENTS WITH PRIMARY HYPERCHOLESTEROLEMIA M. Chell'¢ On behalf of the French Study Group
The aim of the study was to investigate the drugs affecting changes of lipids and lipoproteins in patients (pts) with hyperlipidemia in a Hungarian County Fej6r. Subjects and methods: 273 pts (146 males and 127 females) were studied; 117 with hypercholesterolemia (HCH), 20 with hypertriglyceridemia (HTG) and 136 with combined hyperlipidemia (CHL). The mean age ( + S D ) of pts was 49,9 (10 2) years. The pts were treated with HMG-CoA R] (Iovastatin or fluvastatin, n = l 1 4 } or fibrate (fend-, bezafibrate, gemfibrnzil, n = 7 0 ) or nicotinic acid derivate (acipimox, n=32). The duration of continuous therapy ranged 3-38 months ( m e a n + S D : 1 0 . 6 ± 9 ) Total-cholesterol (TC), HDL-C and LDL-C, triglycerides (TG) and apolipoprotein B and A-I were determined regularly Results: Statins reduced plasma levels of TC. LDL-C, apoB and TG vs baseline by -23.5 %. -30.1%, -24 % (p < .001), -11.3 % (p < .05) and increased HDL-C and apo A-I by 3.5% and 7.1%. The effects of f i b r a t e - 2 1 . 5 % . - 2 2 . 1 % . - 3 7 . 8 % . - 6 0 . 1 % ( p < . 0 0 I ) a n d 15.7% (p < .05) and 8 1% respectively The ratio TC to HDL-C and apoB to A-I decreased by -19 % and -23.4% in HCH pts and by - 2 2 1 % and -39% in CHL patients. All drugs were well tolerated No cases of myopathy appeared in this series of pts Conclusions: These lipid lowering drugs favorably altered plasma lipid and lipoprotein levels in suitably selected hyperlipidemic population.
The efficacy and safety of once daily evening treatment with simvastatin and micronized fenofibrate were compared in a muhicenter, randomized, double-blind trial conducted among patients with primary hypercholesterolemia, with or without coronary heart disease. The study consisted of a 6week screening period during which patients were started or continued on a standard lipid-lowering diet followed by a 4-week, placebo baseline period. Patients continuing to demonstrate elevated total cholesterol levels (>6.5 mmol/1) were then randomized to treatment with simvastatin 20 rag/day (N=II1) or micronized fenofibrate 200 mg/day ( N = I I 6 ) for 8 weeks. Treatment with simvastatin 20 mg/day was associated with significantly (p< 0.001) larger reductions in plasma levels of total and low density lipoprotein (LDL) cholesterol than was treatment with mieronized fenofibrate 200 mg/day (-23 vs. -17% and -32% vs. -22%, respectively). Both drugs were associated with significant (p_< 0.001), comparable elevations in plasma levels of high density lipoprotein cholesterol (7-8%) and apolipoprorein AI (5-6%); however, simvastatin treatment increased Lp-AI levels by 7 %, while treatment with fenofibrate decreased levels of this lipoprotein by 12% (p < 0.001). Plasma levels of apolipoprotein B and triglycerides were significantly reduced by both treatments (p< 0.001), although the reduction in triglycerides was more pronounced in the micronized fenofibrate group (p = 0.042). Simvastatin and micronized fenofibrate were equally welltolerated in this study, with few patients reporting drug-related adverse events or exhibiting clinically meaningful laboratory changes. The results of this trial demonstrate the superiority of simvastatin 20 rag/day over micronized fenofibrate 200 mg/day in lowering plasma levels of the principle atherogenic lipoprotein, LDL cholesterol.
Poster session abstracts / Atherosclerosis 115 ( SuppL ) (1995) $45-S129 P12 Medical Treatment o f Hyperlipidaemia
3511
352
EFFICIENCY OF PROLONGED MEVACOR T R E A T M E N T IN PATIENTS W I T H ISCHEMIC H E A R T DISEASE AND TYPE I1 HYPERLIPIDEMIA B.M. Lipovetsk¥ Institute of the Human Brain, St. Petersburg. Russia
THE C H A N G E S OF SERUM HDL C H O L E S T E R O L IN T H E TREAFMI-NTS WITH SIMVASTATIN AND ONLY W I T H DIET N Salto', F Ootsuji . A Kuchiba and T Kannagi ~ IDepartmenl of Geriatrics. Kochi Medical University, Kochi 783. Japan, -'Shiga Prefectural College. Shiga. ~Kyoto Women University, Kvot~. 'Kvoto Medical Prevention Center. Kyoto. Japan
The purpose of the study is to evaluate the clinical and hypolipidemic effects of 3-year mevacor treatment in patients suffering from ischemic heart disease and type IIa or llb hyperlipidemia. Two groups of patients were compared: 26 took 20-40 mg/d mevacor (Merck) for 3 yr along with nitrates and nifidipin (group 1) while 20 similar patients received the same treatment without hypolipidemie drug (group 2). There were 42 men of 46 patients, the age: 5 2 ± 1.7 (1) and 5 3 + 1 . 4 (2). Patients with angina (functional classes 1I-1II) without arrhythmia or heart failure had been selected. Blood cholesterol levels in group I fell by 36%, triglycerides - by 17 % while those in group 2 remained unchanged. No death or acute myocardial infarction (MI) occurred in group 1 during 3 yr follow up, whereas in the 2-nd group 5 patients died and l had MI. The stable improvement was observed in 27 % patients of group 1 only. The improvement in the first line can be explained by better micro-circulation and tissue oxygen diffusion due to hypolipidemic effect of mevacor.
This ~,tud; i~, aimed It) citriC\ tire change of serum HDL cholesterol in the treatlllel/lS wilh siii2vastatln and only with diet. In diet treatment 207 outpaticnls with diabetic type. which was determined by oral 75g GTT. were recruited In simvastatin treatment 24 diabetic outpatient,, received oral 5rag ot slmvastatin daily for 3 to 26 months Fasting blood sample was obtained ii1 the early morning for measuring serum lipids and lipoprotetns In diet treatment maird', witll diet energy restriction, serum total cholesterol tTC). triglyceride (TG). apolipoprotein B (apo B) and HDL cholesterol /HDL-Ci decreased, if a great change of either bod} wcigln or TG was not plesenl, ha Slmvastatin treatment, TC. LDL-C. apo B, renlnant like particle cholesterol (HDL-C) and atberogemc index decreased, and TG decreased slightly, when HDLC did not change significantly However. HDL--C tended to increase ( p < ( ! 11 Concerning the correlations between prevalues and the changed ~.aluer, ot HDL C there were lound about 40 mgldl in diet treatnlent alld approxinlatel,. 61/ ing/dl ii2 sunvastatin treatment as the crhical polHls lhe sanle tendenc? was observed in 13 individual patients uho received diet old\ and then simvastatin. The stop of SilllVastatlll adlnillisnatit)n resulted in elevation of TC and decrement of HDI. C As a ~ummar\ there was a difference of HDL-C change betwecll diel al}d silIn, astaitll [reaHiicnts
351
353
EFFECTS OF L O N G - T E R M LIPID L O W E R I N G T H E R A P Y ON LIPIDS AND APOL1POPROTEIN B AND A-I I. Reiber. ,/~. G6gl 1st Department of Internal Medicine. Szent Gyorgy Hospital, 8000 Sz6kesfeh6rv~ir, Sereg61yesi u 3
SIMVASTATIN VS. MICRONIZED FENOFIBRATE IN PATIENTS WITH PRIMARY HYPERCHOLESTEROLEMIA M. Chell'¢ On behalf of the French Study Group
The aim of the study was to investigate the drugs affecting changes of lipids and lipoproteins in patients (pts) with hyperlipidemia in a Hungarian County Fej6r. Subjects and methods: 273 pts (146 males and 127 females) were studied; 117 with hypercholesterolemia (HCH), 20 with hypertriglyceridemia (HTG) and 136 with combined hyperlipidemia (CHL). The mean age ( + S D ) of pts was 49,9 (10 2) years. The pts were treated with HMG-CoA R] (Iovastatin or fluvastatin, n = l 1 4 } or fibrate (fend-, bezafibrate, gemfibrnzil, n = 7 0 ) or nicotinic acid derivate (acipimox, n=32). The duration of continuous therapy ranged 3-38 months ( m e a n + S D : 1 0 . 6 ± 9 ) Total-cholesterol (TC), HDL-C and LDL-C, triglycerides (TG) and apolipoprotein B and A-I were determined regularly Results: Statins reduced plasma levels of TC. LDL-C, apoB and TG vs baseline by -23.5 %. -30.1%, -24 % (p < .001), -11.3 % (p < .05) and increased HDL-C and apo A-I by 3.5% and 7.1%. The effects of f i b r a t e - 2 1 . 5 % . - 2 2 . 1 % . - 3 7 . 8 % . - 6 0 . 1 % ( p < . 0 0 I ) a n d 15.7% (p < .05) and 8 1% respectively The ratio TC to HDL-C and apoB to A-I decreased by -19 % and -23.4% in HCH pts and by - 2 2 1 % and -39% in CHL patients. All drugs were well tolerated No cases of myopathy appeared in this series of pts Conclusions: These lipid lowering drugs favorably altered plasma lipid and lipoprotein levels in suitably selected hyperlipidemic population.
The efficacy and safety of once daily evening treatment with simvastatin and micronized fenofibrate were compared in a muhicenter, randomized, double-blind trial conducted among patients with primary hypercholesterolemia, with or without coronary heart disease. The study consisted of a 6week screening period during which patients were started or continued on a standard lipid-lowering diet followed by a 4-week, placebo baseline period. Patients continuing to demonstrate elevated total cholesterol levels (>6.5 mmol/1) were then randomized to treatment with simvastatin 20 rag/day (N=II1) or micronized fenofibrate 200 mg/day ( N = I I 6 ) for 8 weeks. Treatment with simvastatin 20 mg/day was associated with significantly (p< 0.001) larger reductions in plasma levels of total and low density lipoprotein (LDL) cholesterol than was treatment with mieronized fenofibrate 200 mg/day (-23 vs. -17% and -32% vs. -22%, respectively). Both drugs were associated with significant (p_< 0.001), comparable elevations in plasma levels of high density lipoprotein cholesterol (7-8%) and apolipoprorein AI (5-6%); however, simvastatin treatment increased Lp-AI levels by 7 %, while treatment with fenofibrate decreased levels of this lipoprotein by 12% (p < 0.001). Plasma levels of apolipoprotein B and triglycerides were significantly reduced by both treatments (p< 0.001), although the reduction in triglycerides was more pronounced in the micronized fenofibrate group (p = 0.042). Simvastatin and micronized fenofibrate were equally welltolerated in this study, with few patients reporting drug-related adverse events or exhibiting clinically meaningful laboratory changes. The results of this trial demonstrate the superiority of simvastatin 20 rag/day over micronized fenofibrate 200 mg/day in lowering plasma levels of the principle atherogenic lipoprotein, LDL cholesterol.