Treatment of dyslipidemia in non-insulin-dependent diabetes mellitus with lovastatin

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Abstract

Coronary artery disease (CAD) is the leading cause of death among whites with non-insulin-dependent diabetes mellitus (NIDDM). Several risk factors-dyslipidemia induced by NIDDM, obesity, hypertension and hyperglycemia-likely contribute to accelerated atherosclerosis. The dyslipidemia in NIDDM is characterized by abnormalities in composition and metabolism of very low density lipoproteins, low-density lipoproteins (LDL) and high-density lipoproteins (HDL). However, because of the lack of long-term prospective epidemiologic studies, the relative importance of lipoprotein risk factors in the causation of CAD in diabetic patients is not clear. The World Health Organization Multinational Study of vascular disease in diabetics observed increased prevalence of CAD in diabetic populations with relatively high levels of plasma cholesterol and supports the concept that lowering cholesterol levels may significantly reduce coronary risk in NIDDM. To determine the effectiveness of lovastatin, an inhibitor of HMG CoA reductase, for lowering cholesterol levels, 16 patients with NIDDM and mild to moderate increases in plasma cholesterol were given lovastatin (20 mg twice daily) in a randomized, double-blind, placebo-controlled manner for 4 weeks. Compared with the placebo, lovastatin reduced concentrations of total cholesterol (233 ± 10 vs 172 ± 7 mg/dl [standard error of the mean], p < 0.001), LDL cholesterol (140 ± 9 vs 101 ± 6 mg/dl, p < 0.001), and LDL apolipoprotein-B (108 ± 16 vs 80 ± 16 mg/dl, p < 0.001). Plasma triglycerides and very low density lipoprotein cholesterol levels also decreased by 31 and 42%, respectively. Although HDL cholesterol levels did not increase, the total cholesterol/HDL cholesterol ratio decreased significantly with lovastatin therapy. No adverse effects were noted and glycemic control was well-maintained. If HMG CoA reductase inhibitors such as lovastatin continue to be devoid of serious toxicity, they could reduce the prevalence of CAD in NIDDM.

Original languageEnglish (US)
JournalThe American Journal of Cardiology
Volume62
Issue number15
DOIs
StatePublished - Nov 11 1988

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Lovastatin
Dyslipidemias
Type 2 Diabetes Mellitus
Cholesterol
Coronary Artery Disease
Hydroxymethylglutaryl-CoA Reductase Inhibitors
LDL Lipoproteins
HDL Cholesterol
Therapeutics
Placebos
Diabetic Angiopathies
VLDL Cholesterol
VLDL Lipoproteins
Apolipoproteins B
HDL Lipoproteins
Hypercholesterolemia
Hyperglycemia
Causality
LDL Cholesterol
Lipoproteins

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

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title = "Treatment of dyslipidemia in non-insulin-dependent diabetes mellitus with lovastatin",
abstract = "Coronary artery disease (CAD) is the leading cause of death among whites with non-insulin-dependent diabetes mellitus (NIDDM). Several risk factors-dyslipidemia induced by NIDDM, obesity, hypertension and hyperglycemia-likely contribute to accelerated atherosclerosis. The dyslipidemia in NIDDM is characterized by abnormalities in composition and metabolism of very low density lipoproteins, low-density lipoproteins (LDL) and high-density lipoproteins (HDL). However, because of the lack of long-term prospective epidemiologic studies, the relative importance of lipoprotein risk factors in the causation of CAD in diabetic patients is not clear. The World Health Organization Multinational Study of vascular disease in diabetics observed increased prevalence of CAD in diabetic populations with relatively high levels of plasma cholesterol and supports the concept that lowering cholesterol levels may significantly reduce coronary risk in NIDDM. To determine the effectiveness of lovastatin, an inhibitor of HMG CoA reductase, for lowering cholesterol levels, 16 patients with NIDDM and mild to moderate increases in plasma cholesterol were given lovastatin (20 mg twice daily) in a randomized, double-blind, placebo-controlled manner for 4 weeks. Compared with the placebo, lovastatin reduced concentrations of total cholesterol (233 ± 10 vs 172 ± 7 mg/dl [standard error of the mean], p < 0.001), LDL cholesterol (140 ± 9 vs 101 ± 6 mg/dl, p < 0.001), and LDL apolipoprotein-B (108 ± 16 vs 80 ± 16 mg/dl, p < 0.001). Plasma triglycerides and very low density lipoprotein cholesterol levels also decreased by 31 and 42{\%}, respectively. Although HDL cholesterol levels did not increase, the total cholesterol/HDL cholesterol ratio decreased significantly with lovastatin therapy. No adverse effects were noted and glycemic control was well-maintained. If HMG CoA reductase inhibitors such as lovastatin continue to be devoid of serious toxicity, they could reduce the prevalence of CAD in NIDDM.",
author = "Abhimanyu Garg and Grundy, {Scott M}",
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T1 - Treatment of dyslipidemia in non-insulin-dependent diabetes mellitus with lovastatin

AU - Garg, Abhimanyu

AU - Grundy, Scott M

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N2 - Coronary artery disease (CAD) is the leading cause of death among whites with non-insulin-dependent diabetes mellitus (NIDDM). Several risk factors-dyslipidemia induced by NIDDM, obesity, hypertension and hyperglycemia-likely contribute to accelerated atherosclerosis. The dyslipidemia in NIDDM is characterized by abnormalities in composition and metabolism of very low density lipoproteins, low-density lipoproteins (LDL) and high-density lipoproteins (HDL). However, because of the lack of long-term prospective epidemiologic studies, the relative importance of lipoprotein risk factors in the causation of CAD in diabetic patients is not clear. The World Health Organization Multinational Study of vascular disease in diabetics observed increased prevalence of CAD in diabetic populations with relatively high levels of plasma cholesterol and supports the concept that lowering cholesterol levels may significantly reduce coronary risk in NIDDM. To determine the effectiveness of lovastatin, an inhibitor of HMG CoA reductase, for lowering cholesterol levels, 16 patients with NIDDM and mild to moderate increases in plasma cholesterol were given lovastatin (20 mg twice daily) in a randomized, double-blind, placebo-controlled manner for 4 weeks. Compared with the placebo, lovastatin reduced concentrations of total cholesterol (233 ± 10 vs 172 ± 7 mg/dl [standard error of the mean], p < 0.001), LDL cholesterol (140 ± 9 vs 101 ± 6 mg/dl, p < 0.001), and LDL apolipoprotein-B (108 ± 16 vs 80 ± 16 mg/dl, p < 0.001). Plasma triglycerides and very low density lipoprotein cholesterol levels also decreased by 31 and 42%, respectively. Although HDL cholesterol levels did not increase, the total cholesterol/HDL cholesterol ratio decreased significantly with lovastatin therapy. No adverse effects were noted and glycemic control was well-maintained. If HMG CoA reductase inhibitors such as lovastatin continue to be devoid of serious toxicity, they could reduce the prevalence of CAD in NIDDM.

AB - Coronary artery disease (CAD) is the leading cause of death among whites with non-insulin-dependent diabetes mellitus (NIDDM). Several risk factors-dyslipidemia induced by NIDDM, obesity, hypertension and hyperglycemia-likely contribute to accelerated atherosclerosis. The dyslipidemia in NIDDM is characterized by abnormalities in composition and metabolism of very low density lipoproteins, low-density lipoproteins (LDL) and high-density lipoproteins (HDL). However, because of the lack of long-term prospective epidemiologic studies, the relative importance of lipoprotein risk factors in the causation of CAD in diabetic patients is not clear. The World Health Organization Multinational Study of vascular disease in diabetics observed increased prevalence of CAD in diabetic populations with relatively high levels of plasma cholesterol and supports the concept that lowering cholesterol levels may significantly reduce coronary risk in NIDDM. To determine the effectiveness of lovastatin, an inhibitor of HMG CoA reductase, for lowering cholesterol levels, 16 patients with NIDDM and mild to moderate increases in plasma cholesterol were given lovastatin (20 mg twice daily) in a randomized, double-blind, placebo-controlled manner for 4 weeks. Compared with the placebo, lovastatin reduced concentrations of total cholesterol (233 ± 10 vs 172 ± 7 mg/dl [standard error of the mean], p < 0.001), LDL cholesterol (140 ± 9 vs 101 ± 6 mg/dl, p < 0.001), and LDL apolipoprotein-B (108 ± 16 vs 80 ± 16 mg/dl, p < 0.001). Plasma triglycerides and very low density lipoprotein cholesterol levels also decreased by 31 and 42%, respectively. Although HDL cholesterol levels did not increase, the total cholesterol/HDL cholesterol ratio decreased significantly with lovastatin therapy. No adverse effects were noted and glycemic control was well-maintained. If HMG CoA reductase inhibitors such as lovastatin continue to be devoid of serious toxicity, they could reduce the prevalence of CAD in NIDDM.

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