Cardiac consequences of prolonged exposure to an isolated increase in aortic stiffness

In elderly patients, aortic stiffness is a major determinant of increased e nd-systolic stress leading to left ventricular (LV) hypertrophy with impair ed cardiac performance. However, in a rat model of aortic elastocalcinosis (induced by vitamin D-3-nicotine [VDN] treatment), brief exposure (1 month) to increased aortic stiffness modified neither cardiac function nor cardia c structure. Here we report the impact of longer exposure (3 months) to aor tic stiffness. Three months after induction of aortic stiffness, aortic cha racteristic impedance was. measured in awake rats, 8 control and 10 VDN. St roke volume was measured (electromagnetic probe) at baseline and after acut e volume overload. LV weight/body weight ratio, collagen, and myosin heavy chain (MHC) contents were determined. Although aortic characteristic impeda nce increased (controls, 32 +/- 2; VDN rats, 50 +/- 8 10(3) dyne.s/cm(5); P =0.0248), stroke volume was maintained in VDN rats at baseline (controls, 2 23 +/- 18; VDN, 211 +/- 13 mu L) and after volume overload (controls, 378 /- 14; VDN, 338 +/- 15 mu L). However, LV weight/body weight ratio (control s, 1.54 +/- 0.07; VDN, 1.73 +/- 0.05 g/kg, P = 0.0397) and LV collagen cont ent (controls, 31 +/- 4; VDN, 52 +/- 4 mu g/g dry wt; P = 0.0192) increased . A shift from alpha-MHC (controls, 82 +/- 2%; VDN, 69 +/- 3%; P = 0.0056) to beta-MHC (controls, 18 +/- 2%; VDN, 31 +/- 3%; P = 0.0056) was also obse rved. Three months' exposure to increased aortic stiffness in VDN rats indu ced LV hypertrophy with moderate interstitial fibrosis and a shift in the M HC-isoform pattern. Such structural adaptation maintains LV performance.