Is the process of stabilization of carotid plaque more dynamic than expected? a high-resolution 3D-CMR statin-naive huma

  • PDF / 150,944 Bytes
  • 1 Pages / 595.276 x 793.701 pts Page_size
  • 79 Downloads / 132 Views

DOWNLOAD

REPORT


ORAL PRESENTATION

Open Access

Is the process of stabilization of carotid plaque more dynamic than expected? a high-resolution 3D-CMR statin-naive human study Robert WW Biederman1*, David R Neff1, Saundra B Grant1, Ronald B Williams1, Geetha Rayarao1, June A Yamrozik1, George Angheloiu1, Sobhan Kodali1, Vikas K Rathi2, Mark Doyle1 From 2011 SCMR/Euro CMR Joint Scientific Sessions Nice, France. 3-6 February 2011 Introduction Atherosclerosis is a dynamic process thought to stabilize with statin therapy. However, the uniformity of plaque stabilization and subsequent regression when examined under high-resolution 3D CMR is unknown. We hypothesize that plaque characteristics illustrate marked heterogeneity with both plaque regression and progression as lipid lowering therapy is instituted. Purpose Methods

Via CMR (1.5T GE), 707-two mm contiguous in vivo slices of advanced carotid disease (>50%; mean 64±21 ) representing 42 complete bilateral human plaques (age 68±15yrs) were analyzed for 2D/3D extent of vascular wall: lipid pool, fibrous cap, outer wall area (OWA), vessel wall area (VWA), lumen area (LA) and lipid pool (LP). All were related to fasting lipids relative to %stenosis via QPlaque (Medis). Plaque morphology was determined by CMR (T1/T2/PD) at baseline and one year following lipid lowering agent (simvastatin or simva/ ezetimibe). Plaque progression was defined as LP pre/LP post < 1 while plaque regression was defined as LP pre/ LP post >1.

Results 39/42 in vivo plaques in statin naïve pts were successfully imaged. Resolution: 1x1x2mm. Pre therapy, mg/dL range of LDLC was 60-189 (mean 142), HDLC: 23-71 and TG: 80-214. LP represented 30±4% and fibrous laque 9±22% of total vessel wall. Post therapy, LDL was

66±31mg/dL. In 707 slices, 378 (53.5%) demonstrated progression while 329 (46.5%) showed regression. In those plaques that regressed there was significant decrease in both OWA, VWA and fibrous plaque as well as a paradoxical decrease in LA (p