Paradoxical preservation of vascular function in severe obesity.
BACKGROUND
Obesity is associated with a high risk of coronary artery disease morbidity and mortality. Yet, postmortem studies have shown that severely obese subjects exhibit smooth coronary arteries, thus suggesting that they may be protected from atherosclerosis. We assessed vascular function and its possible determinants in a cohort of normal-weight to severely obese insulin-sensitive subjects (body mass index [BMI] 23.2-49 kg/m(2)).


METHODS
Seventy-one healthy, insulin-sensitive subjects (Homeostasis Model Assessment of Insulin Resistance index <2.5), divided into normal-weight (n = 13; BMI = 23.2 +/- 1.6), obese (n = 35; BMI=32.6+/-2.5), and severely obese (n=23; BMI=49.0+/-7.9) groups, were enrolled. Vascular function was evaluated by flow-mediated dilation and carotid intima-media thickness. High-sensitivity C-reactive protein, leptin, adiponectin, vascular growth factors, and CD34+KDR+/CD133+ endothelial progenitor cells, known markers of vascular health/protection, also were measured.


RESULTS
Flow-mediated dilation was higher in severely obese than in obese and normal-weight individuals (P=.019 and P=.011 respectively). Intima-media thickness was consistently lower in severely obese than in obese individuals (P=.040) and similar in severely obese and normal-weight individuals (P >.99). Levels of high-sensitivity C-reactive protein and leptin were higher in severely obese than in obese and normal-weight individuals (high-sensitivity C-reactive protein: P=.018 and P=.05, respectively; leptin: P <.001 for both comparisons). CD34+KDR+ endothelial progenitor cells were significantly higher in severely obese versus obese individuals (P=.039).


CONCLUSIONS
Our study demonstrates that vascular function is paradoxically better in severely obese than in obese subjects and similar to that found in normal-weight subjects. Despite higher levels of high-sensitivity C-reactive protein and leptin, severely obese individuals may be partially protected from atherosclerosis, possibly by a greater mobilization of endothelial progenitor cells.
Biasucci
Luigi Marzio
LM
Institute of Cardiology, Catholic University of the Sacred Heart, Rome, Italy. lmarzio.biasucci@rm.unicatt.it
Graziani
Francesca
F
Rizzello
Vittoria
V
Liuzzo
Giovanna
G
Guidone
Caterina
C
De Caterina
Alberto Ranieri
AR
Brugaletta
Salvatore
S
Mingrone
Gertrude
G
Crea
Filippo
F
D000328:Adult; D015992:Body Mass Index; D001916:Brachial Artery / Q000000981:diagnostic imaging; D002097:C-Reactive Protein / Q000032:analysis; D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000502:physiology; D004730:Endothelium, Vascular / Q000166:cytology / Q000503:physiopathology*; D005260:Female; D006801:Humans; D020738:Leptin / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000097:blood / Q000473:pathology / Q000503:physiopathology*; D013234:Stem Cells / Q000502:physiology; D017539:Tunica Intima / Q000473:pathology; D017540:Tunica Media / Q000473:pathology; D014463:Ultrasonography; D014664:Vasodilation / Q000502:physiology
D020738:Leptin; D002097:C-Reactive Protein