1.
Statins Reduce Epicardial Adipose Tissue Attenuation Independent of Lipid Lowering: A Potential Pleiotropic Effect.
Raggi, P, Gadiyaram, V, Zhang, C, Chen, Z, Lopaschuk, G, Stillman, AE
Journal of the American Heart Association. 2019;(12):e013104
Abstract
Background High epicardial adipose tissue (EAT) attenuation (Hounsfield units [ HUs] ) on computed tomography is considered a marker of inflammation and is associated with an increased risk of cardiovascular events. Statins reduce the volume of EAT , but it is unknown whether they affect EAT HUs . Methods and Results We reviewed the chest computed tomographic scans of 420 postmenopausal women randomized to either 80 mg of atorvastatin or 40 mg of pravastatin daily and rescanned after 1 year to measure change in coronary artery calcium score. EAT HUs were measured near the proximal right coronary artery and remote from any area of coronary artery calcium. Computed tomographic images were also queried for subcutaneous adipose tissue (SubQ) attenuation ( HUs ) change over time. The mean patients' age was 65±6 years. The baseline EAT HU value was higher than the SubQ HU value (-89.4±24.0 HU versus -123.3±30.4 HU ; P<0.001). The EAT HU value decreased significantly in the entire cohort (-5.4±29.7 HU [-6% change]; P<0.001), but equally in the patients given atorvastatin and pravastatin (-6.35+31 HU and -4.55+28 HU ; P=0.55). EAT HU change was not associated with change in total cholesterol, low-density lipoprotein cholesterol, coronary artery calcium, and EAT volume (all P=not significant). Change in high-density lipoprotein cholesterol was marginally associated with EAT HU change ( P=0.07). Statin treatment did not induce a change in SubQ HUs . Conclusions Statins induced a decrease in EAT HUs over time, independent of intensity of low-density lipoprotein cholesterol lowering. The positive effect on EAT and the neutral effect on SubQ suggest that statins induced a decrease in metabolic activity in EAT by reduction in cellularity, vascularity, or inflammation. The clinical significance of the observed change in EAT HUs remains to be demonstrated.
2.
Pathologic Intimal Thickening Plaque Phenotype: Not as Innocent as Previously Thought. A Serial 3D Intravascular Ultrasound Virtual Histology Study.
Kovarnik, T, Chen, Z, Wahle, A, Zhang, L, Skalicka, H, Kral, A, Lopez, JJ, Horak, J, Sonka, M, Linhart, A
Revista espanola de cardiologia (English ed.). 2017;(1):25-33
Abstract
INTRODUCTION AND OBJECTIVES Pathologic intimal thickening (PIT) has been considered a benign plaque phenotype. We report plaque phenotypic changes in a baseline/follow-up intravascular ultrasound-based virtual histology study. METHODS A total of 61 patients with stable coronary artery disease were analyzed from the HEAVEN trial (89 patients randomized between routine statin therapy vs atorvastatin 80mg and ezetimibe 10mg) with serial intravascular ultrasound imaging of nonculprit vessels. We compared changes in 693 baseline and follow-up 5-mm long segments in a novel risk score, Liverpool Active Plaque Score (LAPS), plaque parameters, and plaque composition. RESULTS The PIT showed the highest increase of risk score and, with fibrous plaque, also the LAPS. Necrotic core (NC) abutting to the lumen increased in PIT (22 ± 51.7; P = .0001) and in fibrous plaque (17.9 ± 42.6; P = .004) but decreased in thin cap fibroatheroma (TCFA) (15.14 ± 52.2; P = .001). The PIT was the most likely of all nonthin cap fibroatheroma plaque types to transform into TCFA at follow-up (11% of all TCFA found during follow-up and 35.9% of newly-developed TCFA), but showed (together with fibrous plaque) the lowest stability during lipid-lowering therapy (24.7% of PIT remained PIT and 24.5% of fibrous plaque remained fibrous plaque). CONCLUSIONS Over the 1-year follow-up, PIT was the most dynamic of the plaque phenotypes and was associated with an increase of risk score and LAPS (together with fibrous plaque), NC percentage (together with fibrous plaque) and NC abutting to the lumen, despite a small reduction of plaque volume during lipid-lowering therapy. The PIT was the main source for new TCFA segments.