BACKGROUND: Although progressive chronic congestive heart failure (CHF) is associated with elevated systemic vascular resistance and increased impedance to ventricular outflow, the contribution of changes in large artery function has not been well documented in humans. METHODS AND RESULTS: We studied 45 patients with a broad range of clinical severity of CHF and compared noninvasive measurements of brachial artery diameter, flow, and pulse wave velocity with 22 normal controls of similar age. In CHF, mean arterial pressure was lower than in controls (85 +/- 1 versus 93 +/- 2 mm Hg, p less than 0.001), as were brachial artery diameter (4.07 +/- 0.10 versus 4.53 +/- 0.09 mm, p less than 0.001), flow (40.9 +/- 4.1 versus 70.9 +/- 11.5 ml.min-1, p less than 0.02), compliance (1.29 +/- 0.12 versus 2.00 +/- 0.18 cm4.dyne-1.10(-7), p less than 0.002), and conductance (0.49 +/- 0.05 versus 0.76 +/- 0.13 units, p = 0.06). Limb vascular resistance (40.2 +/- 5.0 versus 20.5 +/- 3.1 units, p less than 0.001) and pulse wave velocity (10.6 +/- 0.5 versus 9.2 +/- 0.4 m.sec-1, p less than 0.03) were higher than in controls. Brachial artery diameter was progressively lower than in controls as severity of CHF increased (New York Heart Association class II, 4.47 +/- 0.23 mm, p = NS; class III, 4.05 +/- 0.10 mm, p less than 0.05; class IV, 3.71 +/- 0.28 mm, p less than 0.05). Similar changes were observed for arterial compliance (class II, 1.76 +/- 0.32 cm4.dyne-1.10(-7), p = NS; class III, 1.21 +/- 0.13 cm4.dyne-1.10(-7), p less than 0.05; class IV, 0.95 +/- 0.10 cm4.dyne-1.10(-7), p less than 0.05). While the lower arterial pressure and flow might be expected to passively reduce arterial diameter, this would be associated with a reduced pulse wave velocity and improved arterial compliance, yet the opposite was observed. Differences in large artery function were not likely caused by underlying atherosclerosis alone, because patients with dilated cardiomyopathy and patients with ischemic heart disease of the same sex, age, left ventricular ejection fraction, and exercise treadmill duration had similar changes in large artery function. CONCLUSIONS: We conclude that alterations in brachial artery function are present in patients with moderate and severe CHF. The observed reduction in arterial compliance, if present diffusely throughout the arterial tree, could increase left ventricular end-systolic stress directly and through increased velocity of reflected pressure waves from the periphery.
BACKGROUND: Although progressive chronic congestive heart failure (CHF) is associated with elevated systemic vascular resistance and increased impedance to ventricular outflow, the contribution of changes in large artery function has not been well documented in humans. METHODS AND RESULTS: We studied 45 patients with a broad range of clinical severity of CHF and compared noninvasive measurements of brachial artery diameter, flow, and pulse wave velocity with 22 normal controls of similar age. In CHF, mean arterial pressure was lower than in controls (85 +/- 1 versus 93 +/- 2 mm Hg, p less than 0.001), as were brachial artery diameter (4.07 +/- 0.10 versus 4.53 +/- 0.09 mm, p less than 0.001), flow (40.9 +/- 4.1 versus 70.9 +/- 11.5 ml.min-1, p less than 0.02), compliance (1.29 +/- 0.12 versus 2.00 +/- 0.18 cm4.dyne-1.10(-7), p less than 0.002), and conductance (0.49 +/- 0.05 versus 0.76 +/- 0.13 units, p = 0.06). Limb vascular resistance (40.2 +/- 5.0 versus 20.5 +/- 3.1 units, p less than 0.001) and pulse wave velocity (10.6 +/- 0.5 versus 9.2 +/- 0.4 m.sec-1, p less than 0.03) were higher than in controls. Brachial artery diameter was progressively lower than in controls as severity of CHF increased (New York Heart Association class II, 4.47 +/- 0.23 mm, p = NS; class III, 4.05 +/- 0.10 mm, p less than 0.05; class IV, 3.71 +/- 0.28 mm, p less than 0.05). Similar changes were observed for arterial compliance (class II, 1.76 +/- 0.32 cm4.dyne-1.10(-7), p = NS; class III, 1.21 +/- 0.13 cm4.dyne-1.10(-7), p less than 0.05; class IV, 0.95 +/- 0.10 cm4.dyne-1.10(-7), p less than 0.05). While the lower arterial pressure and flow might be expected to passively reduce arterial diameter, this would be associated with a reduced pulse wave velocity and improved arterial compliance, yet the opposite was observed. Differences in large artery function were not likely caused by underlying atherosclerosis alone, because patients with dilated cardiomyopathy and patients with ischemic heart disease of the same sex, age, left ventricular ejection fraction, and exercise treadmill duration had similar changes in large artery function. CONCLUSIONS: We conclude that alterations in brachial artery function are present in patients with moderate and severe CHF. The observed reduction in arterial compliance, if present diffusely throughout the arterial tree, could increase left ventricular end-systolic stress directly and through increased velocity of reflected pressure waves from the periphery.
Authors: Daniel R Wagner; Norbert Roesch; Patrick Harpes; Heinrich Körtke; Pierre Plumer; Amir Saberin; Viviane Chakoutio; Denis Oundjede; Charles Delagardelle; Jean Beissel; Georges Gilson; Ingrid Kindermann; Michael Böhm Journal: Clin Res Cardiol Date: 2010-05-16 Impact factor: 5.460
Authors: Patrick F McArdle; Brian W Whitcomb; Keith Tanner; Braxton D Mitchell; Alan R Shuldiner; Afshin Parsa Journal: BMC Cardiovasc Disord Date: 2012-03-14 Impact factor: 2.298
Authors: John C Murphy; Katherine Morrison; James McLaughlin; Ganesh Manoharan; Aa Jennifer Adgey Journal: J Clin Hypertens (Greenwich) Date: 2011-03-04 Impact factor: 3.738