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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2002-5-13
pubmed:abstractText
Cardiovascular disease is the most important cause of morbidity and mortality in patients with type 2 diabetes. Endothelial dysfunction predicts cardiovascular outcome. Type 2 diabetes is characterized by endothelial dysfunction, which may be caused by dyslipidemia. Statin therapy restores endothelial function in hyperlipidemic patients. Therefore, we hypothesize a beneficial effect of atorvastatin on NO-dependent vasodilation in patients with type 2 diabetes and mild dyslipidemia (low density lipoproteins >4.0 mmol/L and/or triglycerides >1.8 mmol/L). We evaluated the effect of intensive lipid lowering (4 weeks of 80 mg atorvastatin once daily) on vasoreactivity in 23 patients with type 2 diabetes by using venous occlusion plethysmography. Twenty-one control subjects were matched for age, sex, body mass index, blood pressure, and smoking habits. The ratio of blood flows in the infused (measurement [M]) and noninfused (control [C]) arm was calculated for each recording (M/C ratio), and M/C% indicates the percentage change from the baseline M/C ratio. Serotonin-induced NO-dependent vasodilation was significantly blunted (52+/-30 versus 102+/-66 M/C%, P<0.005), and nitroprusside-induced endothelium-independent vasodilation was modestly reduced (275+/-146 versus 391+/-203 M/C%, P<0.05) in patients with type 2 diabetes compared with control subjects. Despite significant reduction of total cholesterol, low density lipoproteins, and triglycerides (5.8+/-1.0 to 3.2+/-0.6 [P<0.0001], 4.1+/-1.1 to 1.8+/-0.7 [P<0.0001], and 2.2+/-1.3 to 1.4+/-0.5 [P<0.05] mmol/L, respectively), no effect on NO-dependent (59+/-44 M/C%) and endothelium-independent (292+/-202 M/C%) vasodilation was demonstrated. These data suggest that intensive lipid lowering by atorvastatin has no effect on NO availability in forearm resistance arteries in type 2 diabetic patients. Other factors, such as hyperglycemia, may be a more important contributing factor regarding impaired vasoreactivity in this patient group.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1524-4636
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
799-804
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:12006393-Anticholesteremic Agents, pubmed-meshheading:12006393-Diabetes Mellitus, Type 2, pubmed-meshheading:12006393-Drug Administration Schedule, pubmed-meshheading:12006393-Endothelium, Vascular, pubmed-meshheading:12006393-Female, pubmed-meshheading:12006393-Forearm, pubmed-meshheading:12006393-Heptanoic Acids, pubmed-meshheading:12006393-Humans, pubmed-meshheading:12006393-Hyperlipidemias, pubmed-meshheading:12006393-Hypolipidemic Agents, pubmed-meshheading:12006393-Male, pubmed-meshheading:12006393-Microcirculation, pubmed-meshheading:12006393-Middle Aged, pubmed-meshheading:12006393-Nitric Oxide, pubmed-meshheading:12006393-Nitroprusside, pubmed-meshheading:12006393-Plethysmography, pubmed-meshheading:12006393-Prospective Studies, pubmed-meshheading:12006393-Pyrroles, pubmed-meshheading:12006393-Serotonin, pubmed-meshheading:12006393-Vasodilation
pubmed:year
2002
pubmed:articleTitle
Intensive lipid lowering by statin therapy does not improve vasoreactivity in patients with type 2 diabetes.
pubmed:affiliation
Department of Vascular Medicine and Diabetes, University Medical Center, Utrecht, the Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't