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Effects of atorvastatin on plasma lipids and urinary microalbumin in niddm patients
71st EAS Meeting Abstracts accepted for presentation in the abstract book
198
LIPID INTERVENTION STRATEGIES IN ACUTE CORONARY SYNDROMES: A RANDOMISED T R I A L W I T H SIMVASTATIN
Atorvastatin Baseline Final
T.R, Pcdersen, K. Eide Jahnsen, S. Vain, A.G. Semb, E Konmy, A. Zalmai,
T. Nerdrum. Aker Universi O, Hospital, Oslo, Norway We randomly allocated 151 patients aged <75 years with acute myocardial infarction (n = 112) or unstable angina (n = 39) and LDL-cholesterol (LDL-C) > 3.0 mmol/L to two strategies of lipid intervention. Both groups received individual dietary counselling while in hospital. One group also received simvastatin (S) 40 mg daily from the day of randomisation, while the other group started S after 3 months if LDL-C was still >3,0 mmol/L. The objectives were to investigate whether patients adherence to therapy and advice would differ with the strategies and result in different lipid levels after 6 months and to study the success rate of bringing patients to the therapeutic target (LDL-C < 3.0 mmol/L) with either strategy. Lipids were measured fasting on the day after admission and the average of two measurements with 1-2 weeks intervals after 3 and 6 months was calculated. The number of patients with lipid measurements after 3 months was 68 in the group with immediate S treatment and 73 in the group with deferred treatment. After 6 months the numbers were 66 and 73, respectively. In the deferred treatment group, 5 (7%) reached the target of LDL-C < 3.0 mmol/L on diet alone, one of these increased to 3.6 mmol/L at 6 months and was then given S. The remaining 68 patients were given S 40 mg daily at the 3 month visit. At 6 months 60 (82%) patients had reached the target. In the immediate treatment group 61 (90%) of the patients had reached the target after 3 months, with a mean LDL-C reduction of 50% from baseline, at 6 months the same 61 remained with LDL-C < 3.0 mmol/L (the difference in proportion of patients at target at 6 months was not statistically significant). Mean lipid levels were:
S Immediate
S Deferred
Total C (retool/L) LDL-C(mmol/L) TotalC (mmol/l.) LDL-C (mmol/L)
Baseline 3 Months 6 months
6+55±1.01 4. I 14-0.64 4.214-I. 17
4.544-0.93 2.284-0.53 2.284-0.62
6.49 0± I.1 6.484-I. 1 4.434-0.82
4J94-0.89 4.40:t-0.9I 2.454-0.66
Conclusions: Few patients with acute coronary syndromes reached the target of LDL-C < 3.0 mmol/L with dietary advice alone. Almost all patients (90%) reached the target with S 40 mg daily combined with dietary advice. Such therapy can successfully and safely be started during the initial hospitalisation.
% Change
Placebo Baseline
Final
%
Change
TC TG HDL-C
273 14. 23) 202 t± 11) -26 ° 295 (4- 88) 224 (4- 471 -24" 35 (4- 4) 38 (4- 3) +9"
271 14. 22) 263 (:t: 23) -3 NS 288 14- 93) 302 (4- 65) +5 NS 36 (4- 5) 35 (4- 41 -3 NS
LDL-C
179(4-55)
120(4-32)
-33"
175(4-59)
166(4-45)
-5NS
MU
145 15:
136 (4.
-6 NS
132 (4.
141 (4.
+7 NS
112)
102)
lOg}
115)
"p < 0.0~5
P E C U L I A R I T Y OF BLOOD COAGULATION AND LIPIDS T R A N S P O T IN PATIENTS W I T H MILD HYPERTENSION A. Olferiev, M. Mamedov, L. Ramirova, A. Britov, N. Perova. National
Center from Preoentive Medicine, Moscow Russia The peculiarities o f blood coagulation and lipids transport in 122 Moscow men (35-66 years old) with mild hypertension were examined. Cholesterol (Ch), triglycerides (Tg) HDL and LDL Ch, glucose (Glu), insulin (Ins). fibrinogen (F), VII coagulation factors activity (VII F), antithrombine III (AT III), euglobulin fraction lysis time (EFLT), plasminogen (P) were determined in fasting plasma. BP, BMI, waist to hip ratio (W/H) have been also studied. Patients were divided to 2 groups according to TG levels: I) Tg < 1.71 mM, 2) Tg >_ 1.71 mM. Fifty (41%) patients (group 2) had hypertriglyceridemia and higher DBP, BMI and W/H ratio than the patients from the first group. Some biochemical parameters were higher in the second group than in the first group: Tg (3.074- 0.22 mmol/l vs. 1.064-0.04), Ch 16.454-0.19 mmol,q vs. 5.33+0.10), Ins (17.2+1.8 mU/ml vs.8.3+0.9), Glu - (5.32+0.24 mmol/1 vs. 4.72+0.13). F (3.0+0.1 g/I vs. 2.8 + 0.1), VII F (139.6+10.7% vs. 120.6+7.9), AT Ill (86.3+3.8% vs. 78.4+2.6), and EFLT (280.9-1-6.7 rain vs. 253.84-6.3). HDL Ch in the second groups was less than in first on 16%. Thus, hypertriglyceridemia in the patients with mild hypertension is associated with insulinresistents and atherogenity disturbances of lipids transport and blood coagulation.
RELATION OF L E F T ATRIAL E J E C T I O N F O R C E TO L E F T V E N T R I C U L A R FUNCTION IN A R T E R I A L HYPERTENSION EFFECTS OF ATORVASTATIN ON PLASMA LIPIDS AND URINARY MICROALBUMIN IN NIDDM PATIENTS
S. Qirko, T. Goda, LI. Rroku. Department of Cardiology. UniversiO' Hospital Center. 7~rana, Albania
S. Bottazzo, G. Severi, M.G. Leperdi. Medical Department, Umberto I
Hospital, Venice, ltaly NIDDM is often associated with high plasma levels o f Total Cholesterol (TC) and Triglycerides (TG) combined with low levels of HDL-Cholesterol (HDL-C). Clinical and experimental data have shown that lipid abnormalities in diabetes could contribute to nephron damage and influence the onset and the progression of diabetic nephropathy. Microalbuminuria (MU) is considered a predictor of clinical nephropathy in diabetes. The aim of this study was to determine the efficacy and safety of low doses of Atorvastatin (A), a new HMG-CoA reductase inhibitor, on lipid plasma levels of NIDDM patients and to evaluate UM before and after lipid lowering therapy. Thirty hyperlipidemic NIDDM patients 118 m and 12 f, aged 574-8 ys) were randomized to receive 10 mg of A or placebo (P) once daily for three months. Serum lipids were determined in fasting blood samples. MU was measured by nephelometric method in the first spot urine collected in the early morning. Plasma lipid levels (mg/dl, mean+SD) and MU (mg/L, mean+SD) before and after treatment are shown in the Table. In NIDDM patients treated with A we observed a significant decrease of TC, LDL-C, TG associated with an increase of HDL-C No significant modification of MU was seen in the two groups of patients. No adverse effects were complained during the treatment period. Conclusions: In NIDDM patients with hyperlipidemia, low doses of A are safety and effective in improving lipid plasma levels. These lipid modifications are not associated with significant reductions in urinary albumin excretion.
The left atrial ejection function (LAEF), defined as that force exerted by the left atrium (LA) to accelerate the blood into the left venticle during atrial systole, is well accepted for the evaluation of LA systolic function. The aim of this study is determine whether LAEF is a precursor of the impairment of LV systolic function in patients with arterial hypertension (HTN). For that purpose we studied LAEF in 36 patients with HTN (av. age 58+8 yrs.) with LV hypertrophy (Lvmi > 134 g/m 2 for men and >110 g/m 2 for women). LV systolic function estimated by the fiactional shortening (FSh) was 35+4% (28 to 44). 32 normal subjects (NS) were also analyzed. All subjects were submitted to echo and doppler examinations. Methods: LAEF was obtained by the formula: I/3 x MVA x (A-vel) 2, Where MVA is mitral valve area measured by 2D echo while A-vel. is the late diastolic (atrial) mitral velocity. Results: I) LAEF increased significantly with age in NS (r = 0.78) (p < 0.05). Age corrected LAEF was calculated as % LAEF = (actual LAEF/normal LAEF) x 100. 2) Compared to NS, % LAEF was lower in HTN 178-t-25%). 3) There was a significant inverse correlation between LAEF and LV wall thickness (r = 0.46) (p < 0.05). 4) % LAEF was 664-31% in patients with FSh < 33% and 794- 25% in those with FSh > 33%. (p < 0.05). 5) In HTN with the duration > 15 years, % LAEF was lower than in patients with <15 years (624-25 vs 764-24) (p < 0.05). Conclusions: I) LAEF is decreased in more advanced stages of HTN. 2) This impairment is related to LV hypertrophy and to the duration of the disease. 3) LAEF is a sensitive precursor for LV systolic deterioration in patients with hypertension.
71st EAS Congress and Satellite Symposia
198
LIPID INTERVENTION STRATEGIES IN ACUTE CORONARY SYNDROMES: A RANDOMISED T R I A L W I T H SIMVASTATIN
Atorvastatin Baseline Final
T.R, Pcdersen, K. Eide Jahnsen, S. Vain, A.G. Semb, E Konmy, A. Zalmai,
T. Nerdrum. Aker Universi O, Hospital, Oslo, Norway We randomly allocated 151 patients aged <75 years with acute myocardial infarction (n = 112) or unstable angina (n = 39) and LDL-cholesterol (LDL-C) > 3.0 mmol/L to two strategies of lipid intervention. Both groups received individual dietary counselling while in hospital. One group also received simvastatin (S) 40 mg daily from the day of randomisation, while the other group started S after 3 months if LDL-C was still >3,0 mmol/L. The objectives were to investigate whether patients adherence to therapy and advice would differ with the strategies and result in different lipid levels after 6 months and to study the success rate of bringing patients to the therapeutic target (LDL-C < 3.0 mmol/L) with either strategy. Lipids were measured fasting on the day after admission and the average of two measurements with 1-2 weeks intervals after 3 and 6 months was calculated. The number of patients with lipid measurements after 3 months was 68 in the group with immediate S treatment and 73 in the group with deferred treatment. After 6 months the numbers were 66 and 73, respectively. In the deferred treatment group, 5 (7%) reached the target of LDL-C < 3.0 mmol/L on diet alone, one of these increased to 3.6 mmol/L at 6 months and was then given S. The remaining 68 patients were given S 40 mg daily at the 3 month visit. At 6 months 60 (82%) patients had reached the target. In the immediate treatment group 61 (90%) of the patients had reached the target after 3 months, with a mean LDL-C reduction of 50% from baseline, at 6 months the same 61 remained with LDL-C < 3.0 mmol/L (the difference in proportion of patients at target at 6 months was not statistically significant). Mean lipid levels were:
S Immediate
S Deferred
Total C (retool/L) LDL-C(mmol/L) TotalC (mmol/l.) LDL-C (mmol/L)
Baseline 3 Months 6 months
6+55±1.01 4. I 14-0.64 4.214-I. 17
4.544-0.93 2.284-0.53 2.284-0.62
6.49 0± I.1 6.484-I. 1 4.434-0.82
4J94-0.89 4.40:t-0.9I 2.454-0.66
Conclusions: Few patients with acute coronary syndromes reached the target of LDL-C < 3.0 mmol/L with dietary advice alone. Almost all patients (90%) reached the target with S 40 mg daily combined with dietary advice. Such therapy can successfully and safely be started during the initial hospitalisation.
% Change
Placebo Baseline
Final
%
Change
TC TG HDL-C
273 14. 23) 202 t± 11) -26 ° 295 (4- 88) 224 (4- 471 -24" 35 (4- 4) 38 (4- 3) +9"
271 14. 22) 263 (:t: 23) -3 NS 288 14- 93) 302 (4- 65) +5 NS 36 (4- 5) 35 (4- 41 -3 NS
LDL-C
179(4-55)
120(4-32)
-33"
175(4-59)
166(4-45)
-5NS
MU
145 15:
136 (4.
-6 NS
132 (4.
141 (4.
+7 NS
112)
102)
lOg}
115)
"p < 0.0~5
P E C U L I A R I T Y OF BLOOD COAGULATION AND LIPIDS T R A N S P O T IN PATIENTS W I T H MILD HYPERTENSION A. Olferiev, M. Mamedov, L. Ramirova, A. Britov, N. Perova. National
Center from Preoentive Medicine, Moscow Russia The peculiarities o f blood coagulation and lipids transport in 122 Moscow men (35-66 years old) with mild hypertension were examined. Cholesterol (Ch), triglycerides (Tg) HDL and LDL Ch, glucose (Glu), insulin (Ins). fibrinogen (F), VII coagulation factors activity (VII F), antithrombine III (AT III), euglobulin fraction lysis time (EFLT), plasminogen (P) were determined in fasting plasma. BP, BMI, waist to hip ratio (W/H) have been also studied. Patients were divided to 2 groups according to TG levels: I) Tg < 1.71 mM, 2) Tg >_ 1.71 mM. Fifty (41%) patients (group 2) had hypertriglyceridemia and higher DBP, BMI and W/H ratio than the patients from the first group. Some biochemical parameters were higher in the second group than in the first group: Tg (3.074- 0.22 mmol/l vs. 1.064-0.04), Ch 16.454-0.19 mmol,q vs. 5.33+0.10), Ins (17.2+1.8 mU/ml vs.8.3+0.9), Glu - (5.32+0.24 mmol/1 vs. 4.72+0.13). F (3.0+0.1 g/I vs. 2.8 + 0.1), VII F (139.6+10.7% vs. 120.6+7.9), AT Ill (86.3+3.8% vs. 78.4+2.6), and EFLT (280.9-1-6.7 rain vs. 253.84-6.3). HDL Ch in the second groups was less than in first on 16%. Thus, hypertriglyceridemia in the patients with mild hypertension is associated with insulinresistents and atherogenity disturbances of lipids transport and blood coagulation.
RELATION OF L E F T ATRIAL E J E C T I O N F O R C E TO L E F T V E N T R I C U L A R FUNCTION IN A R T E R I A L HYPERTENSION EFFECTS OF ATORVASTATIN ON PLASMA LIPIDS AND URINARY MICROALBUMIN IN NIDDM PATIENTS
S. Qirko, T. Goda, LI. Rroku. Department of Cardiology. UniversiO' Hospital Center. 7~rana, Albania
S. Bottazzo, G. Severi, M.G. Leperdi. Medical Department, Umberto I
Hospital, Venice, ltaly NIDDM is often associated with high plasma levels o f Total Cholesterol (TC) and Triglycerides (TG) combined with low levels of HDL-Cholesterol (HDL-C). Clinical and experimental data have shown that lipid abnormalities in diabetes could contribute to nephron damage and influence the onset and the progression of diabetic nephropathy. Microalbuminuria (MU) is considered a predictor of clinical nephropathy in diabetes. The aim of this study was to determine the efficacy and safety of low doses of Atorvastatin (A), a new HMG-CoA reductase inhibitor, on lipid plasma levels of NIDDM patients and to evaluate UM before and after lipid lowering therapy. Thirty hyperlipidemic NIDDM patients 118 m and 12 f, aged 574-8 ys) were randomized to receive 10 mg of A or placebo (P) once daily for three months. Serum lipids were determined in fasting blood samples. MU was measured by nephelometric method in the first spot urine collected in the early morning. Plasma lipid levels (mg/dl, mean+SD) and MU (mg/L, mean+SD) before and after treatment are shown in the Table. In NIDDM patients treated with A we observed a significant decrease of TC, LDL-C, TG associated with an increase of HDL-C No significant modification of MU was seen in the two groups of patients. No adverse effects were complained during the treatment period. Conclusions: In NIDDM patients with hyperlipidemia, low doses of A are safety and effective in improving lipid plasma levels. These lipid modifications are not associated with significant reductions in urinary albumin excretion.
The left atrial ejection function (LAEF), defined as that force exerted by the left atrium (LA) to accelerate the blood into the left venticle during atrial systole, is well accepted for the evaluation of LA systolic function. The aim of this study is determine whether LAEF is a precursor of the impairment of LV systolic function in patients with arterial hypertension (HTN). For that purpose we studied LAEF in 36 patients with HTN (av. age 58+8 yrs.) with LV hypertrophy (Lvmi > 134 g/m 2 for men and >110 g/m 2 for women). LV systolic function estimated by the fiactional shortening (FSh) was 35+4% (28 to 44). 32 normal subjects (NS) were also analyzed. All subjects were submitted to echo and doppler examinations. Methods: LAEF was obtained by the formula: I/3 x MVA x (A-vel) 2, Where MVA is mitral valve area measured by 2D echo while A-vel. is the late diastolic (atrial) mitral velocity. Results: I) LAEF increased significantly with age in NS (r = 0.78) (p < 0.05). Age corrected LAEF was calculated as % LAEF = (actual LAEF/normal LAEF) x 100. 2) Compared to NS, % LAEF was lower in HTN 178-t-25%). 3) There was a significant inverse correlation between LAEF and LV wall thickness (r = 0.46) (p < 0.05). 4) % LAEF was 664-31% in patients with FSh < 33% and 794- 25% in those with FSh > 33%. (p < 0.05). 5) In HTN with the duration > 15 years, % LAEF was lower than in patients with <15 years (624-25 vs 764-24) (p < 0.05). Conclusions: I) LAEF is decreased in more advanced stages of HTN. 2) This impairment is related to LV hypertrophy and to the duration of the disease. 3) LAEF is a sensitive precursor for LV systolic deterioration in patients with hypertension.
71st EAS Congress and Satellite Symposia