title: Differential impacts of blood pressure and lipid lowering on regression of ventricular and arterial mass: the Stop Atherosclerosis in Native Diabetics Trial.
abstract: The relative impacts of lowering blood pressure versus lowering low-density lipoprotein (LDL) cholesterol on regression of ventricular and arterial mass have not been systematically examined. Changes in left ventricular mass and arterial mass (common carotid artery cross-sectional area) after 36 months of simultaneous lowering of systolic blood pressure and LDL cholesterol were examined in the Stop Atherosclerosis in Native Diabetics Trial of standard versus aggressive LDL cholesterol and blood pressure targets in American Indians with type 2 diabetes mellitus. The 2 treatment groups were combined to examine changes in left ventricular and arterial mass over a spectrum of achieved blood pressure and lipid levels. Among the combined group of 413 Stop Atherosclerosis in Native Diabetics Trials participants, systolic blood pressure, LDL cholesterol, and left ventricular mass were all significantly reduced, whereas arterial mass significantly increased, after 36 months of therapy (P<0.001 for all). In linear regression models, a decrease in arterial mass was significantly related to achieved systolic blood pressure and, to a lesser extent, achieved LDL cholesterol, after adjustment for important covariates. Left ventricular mass progressively decreased with lower achieved levels of systolic blood pressure, independent of baseline levels of left ventricular mass. In conclusion, achieved levels of systolic blood pressure are important determinants of the extent of regression of arterial and ventricular mass during prolonged therapy in diabetic individuals. Achieved levels of LDL cholesterol influence regression of arterial but not ventricular mass. Our findings suggest that there is no threshold of systolic blood pressure below which regression of cardiovascular target organ damage cannot be achieved.
authors.affiliation: Division of Cardiology, Weill Cornell Medical College, 525 East 68th St, New York, NY 10021, USA. mroman@med.cornell.edu
authors.forename: Mary J
authors.initials: MJ
authors.lastname: Roman
authors.forename: Barbara V
authors.initials: BV
authors.lastname: Howard
authors.forename: Wm James
authors.initials: WJ
authors.lastname: Howard
authors.forename: Mihriye
authors.initials: M
authors.lastname: Mete
authors.forename: Jerome L
authors.initials: JL
authors.lastname: Fleg
authors.forename: Elisa T
authors.initials: ET
authors.lastname: Lee
authors.forename: Richard B
authors.initials: RB
authors.lastname: Devereux
mesh_terms: D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D050197:Atherosclerosis / Q000097:blood / Q000503:physiopathology / Q000517:prevention & control; D001794:Blood Pressure / Q000187:drug effects*; D017536:Carotid Artery, Common / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D008078:Cholesterol, LDL / Q000097:blood*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000503:physiopathology / Q000517:prevention & control; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D006973:Hypertension / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D007198:Indians, North American; D016014:Linear Models; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D016896:Treatment Outcome; D017539:Tunica Intima / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D017540:Tunica Media / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology
chemical_list: D000959:Antihypertensive Agents; D008078:Cholesterol, LDL; D000960:Hypolipidemic Agents; D008055:Lipids