title: Relationship between aortic stiffness and the development of coronary collateral in patients with coronary artery disease.
abstract: Large artery stiffness is an independent predictor of cardiovascular mortality and a major determinant of pulse pressure. The stiff aorta may result in greater systolic, lower diastolic, and wider pulse pressures, which may decrease coronary artery perfusion. Shear stress has been implicated in the development of coronary collateral. Decreased coronary perfusion may reduce shear stress and thus collateral formation. The goal of this study was to assess the relationship between the development of coronary collateral and aortic stiffness in patients with coronary artery disease. In 106 patients with at least one coronary artery stenosis of 90% or greater, collateral vessels were assessed angiographically by the Rentrop grading (grade 0-3), establishing two groups: 50 patients with poor collateral vessels (Rentrop grade 0 or 1), and 56 patients with good collateral vessels (Rentrop grade 2 or 3). Internal aortic root diameters were measured at 3 cm above the aortic valve by use of two-dimensional guided M-mode transthoracic echocardiography, and arterial pressure was measured simultaneously at the brachial artery by sphygmomanometry. Two indexes of the aortic elastic properties were measured: aortic distensibility index was calculated by use of the formula: 2 x (systolic diameter - diastolic diameter)/(diastolic diameter) x (pulse pressure) in cm(- 2)dyn(-1)10(-6). The aortic stiffness index was calculated by: (systolic blood pressure/diastolic blood pressure)/pulsatile change in diameter/diastolic diameter. The aortic distensibility index and the aortic stiffness index were not significantly different between the patients with poor collateral vessels and those with good collateral vessels (5.1 +/-2.3 vs 5.7 +/-3.3 cm(-2)dyn( -1)10(-6), p = 0.31; 4.02 +/-2.3 vs 4.43 +/-3.7, p = 0.49, respectively). There were no significant differences regarding the aortic elastic properties between the patients with poor collateral vessels and those with good collateral vessels, suggesting that collateral formation is a complex phenomenon consisting of several distinct processes.
authors.affiliation: KTU Faculty of Medicine, Department of Cardiology, Trabzon, Turkey. scelik@meds.ktu.edu.tr
authors.forename: Sükrü
authors.initials: S
authors.lastname: Celik
authors.forename: Sahin
authors.initials: S
authors.lastname: Kaplan
authors.forename: Remzi
authors.initials: R
authors.lastname: Yilmaz
authors.forename: Turan
authors.initials: T
authors.lastname: Erdogan
authors.forename: Abdulkadir
authors.initials: A
authors.lastname: Kiris
mesh_terms: D000368:Aged; D001011:Aorta / Q000000981:diagnostic imaging / Q000503:physiopathology*; D001794:Blood Pressure; D001795:Blood Pressure Determination / Q000295:instrumentation; D001916:Brachial Artery / Q000503:physiopathology; D003097:Collateral Circulation; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000503:physiopathology*; D003326:Coronary Circulation; D004548:Elasticity; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011673:Pulsatile Flow; D012107:Research Design; D019722:Sphygmomanometers; D013314:Stress, Mechanical; D014463:Ultrasonography