Impact of the metabolic syndrome on subcutaneous microcirculation in obese patients.
OBJECTIVE
Patients with the metabolic syndrome are at increased cardiovascular risk and display an augmented wall stiffness of the large-sized and medium-sized arteries, coupled with an endothelial dysfunction. Whether this is the case also for the small resistance arteries is unknown, however. It is also unknown whether and to what extent the hypothesized microvascular alterations are greater for magnitude than the ones characterizing obesity, that is the most common component of the metabolic syndrome.


METHODS
In 14 lean healthy controls (age 48.7 +/- 2.4 years, mean +/- SEM), 13 obese participants and 12 individuals with the metabolic syndrome (Adult Treatment Panel III criteria), all age-matched with healthy controls, we assessed the small resistance arteries dissected from the abdominal subcutaneous tissue on a pressurized myograph.


RESULTS
The media thickness, media cross-sectional area (CSA) and media-to-lumen ratio (M/L) of the small resistance arteries were markedly and significantly greater in metabolic syndrome than in controls (media thickness: 28.3 +/- 0.7 vs. 17.5 +/- 0.3 microm; CSA: 24 760.8 +/- 1459 vs. 16 170.7 +/- 843.6 microm and M/L: 0.12 +/- 0.01 vs. 0.064 +/- 0.002 a.u., respectively, P < 0.01 for all). Acetylcholine-induced relaxation was impaired in the vessels from metabolic syndrome participants compared with the lean healthy individuals (-48.8%, P < 0.01), whereas endothelium-independent vasorelaxation was similar in the two groups. The structural and functional microvascular alterations seen in metabolic syndrome were slightly, although not significantly, greater than the ones seen in uncomplicated obese participants. Stiffness of small arteries, as assessed by the stress/strain relationship, was also similar in the three groups of participants.


CONCLUSIONS
Thus, metabolic syndrome is characterized by marked alterations in the structural and functional patterns of the small resistance arteries. These alterations, which are only slightly greater than the ones seen in obesity, may be responsible for the increased incidence of coronary and cerebrovascular events reported in metabolic syndrome.
Grassi
Guido
G
Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie, Università Milano-Bicocca, Ospedale San Gerardo, Clinica Medica, Monza, Italy. guido.grassi@unimib.it
Seravalle
Gino
G
Brambilla
Gianmaria
G
Facchetti
Rita
R
Bolla
Gianbattista
G
Mozzi
Enrico
E
Mancia
Giuseppe
G
D000005:Abdomen; D000109:Acetylcholine / Q000494:pharmacology; D000328:Adult; D001158:Arteries / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology; D001837:Body Weights and Measures; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008297:Male; D024821:Metabolic Syndrome / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D008833:Microcirculation; D008875:Middle Aged; D009126:Muscle Relaxation / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D009213:Myography; D009599:Nitroprusside / Q000494:pharmacology; D009765:Obesity / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D040521:Subcutaneous Tissue / Q000098:blood supply*; D017540:Tunica Media / Q000000981:diagnostic imaging / Q000473:pathology; D014463:Ultrasonography
D009599:Nitroprusside; D000109:Acetylcholine