title: Clinical impact of insulin resistance syndrome in cardiovascular diseases and its therapeutic approach.
abstract: In subjects with coronary artery diseases (obstructive and vasospastic angina pectoris (AP)) who have no diabetes, hypertension, obesity and physical inactivity, insulin sensitivity was significantly reduced with compensated hyperinsulinemia on OGTT. Insulin resistance significantly correlated with coronary atherosclerosis score. In vasospastic AP (VAP), those who fulfilled more than 3 risk factors out of 5 (hyperinsulinemia, obesity, glucose intolerance, hypertension, dyslipidemia) consist of 70 and 40% for smokers and nonsmokers respectively. Insulin resistance syndrome who fulfilled all the criteria was 9-10% for VAP. In atherothrombotic brain infarction (ATTI) with the same exclusion criteria, the similar insulin resistance and hyperinsulinemia have been observed, but not in embolic (cardiac origin) or lacunar infarction. In ATTI, high TG and apo B with low HDL-chol were noted in blood. In essential hypertension without diabetes and obesity, hyperinsulinemia was noted in 25-35% and insulin resistance in 56-88%. Reduction of blood pressure with alpha blocker (bunazosin), ACE inhibitor (cilazapril), long-acting Ca++ blocker (amlodipine) significantly improved lowered insulin sensitivity. Insulin resistance rather than hyperinsulinemia is more closely associated with blood pressure. Cardiovascular diseases (vasospastic and obstructive AP, brain cortical artery diseases) are prone to develop diabetes because of insulin resistance and also promote the generation of cumulative risk factors resulting in a vicious cycle. Efforts to alleviate insulin resistance is crucial for the primary and secondary prevention of cardiovascular diseases.
authors.affiliation: Department of Medicine, National Cardiovascular Center, Suita, Osaka, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Harano
authors.forename: M
authors.initials: M
authors.lastname: Suzuki
authors.forename: K
authors.initials: K
authors.lastname: Shinozaki
authors.forename: Y
authors.initials: Y
authors.lastname: Hara
authors.forename: K
authors.initials: K
authors.lastname: Ryomoto
authors.forename: A
authors.initials: A
authors.lastname: Kanazawa
authors.forename: Y
authors.initials: Y
authors.lastname: Nishioheda
authors.forename: M
authors.initials: M
authors.lastname: Tsushima
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000627:therapeutic use; D000328:Adult; D000368:Aged; D017311:Amlodipine / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000503:physiopathology*; D017315:Cilazapril / Q000627:therapeutic use; D006801:Humans; D007333:Insulin Resistance; D008875:Middle Aged; D011799:Quinazolines / Q000627:therapeutic use
chemical_list: D000317:Adrenergic alpha-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D002121:Calcium Channel Blockers; D011799:Quinazolines; D017315:Cilazapril; D017311:Amlodipine; C018176:bunazosin