Article Text

Metabolic syndrome is a key determinant of coronary microvascular function in patients with stable coronary disease and optimal low-density lipoprotein cholesterol levels undergoing percutaneous coronary intervention
  1. N Melikian1,
  2. A Shah1,
  3. J Byrne1,
  4. M Thomas2,
  5. R Sherwood1,
  6. R Dworakowsk1,
  7. M Kearney3,
  8. P MacCarthy1
  1. 1King’s College Hospital, London, UK
  2. 2St Thomas Hospital, London, UK
  3. 3University of Leeds, Leeds, UK


Objective To examine the influence of the metabolic syndrome (MS; defined by ATP-III criteria) on coronary microvascular function (CMF) in patients on optimal therapy with statins undergoing percutaenous coronary intervention (PCI).

Background CMF determines cardiovascular prognosis. However, there are limited data on the influence of the MS, a major risk factor for vascular disease, on CMF.

Methods and Results 54 patients with stable coronary disease undergoing PCI were divided into two groups according to the presence/absence of MS (mean age (years), MS (n  =  20): 61 ± 11; no MS (n  =  34): 66 ± 8, p = 0.10). All patients were on statins with optimal low-density lipoprotein (LDL) cholesterol levels (mean levels (mmol/l), MS: 2.0 ± 1.0; no MS: 2.1 ± 0.6, p = 0.79). An intracoronary thermodilution technique was used to assess endothelium-dependent (% change flow in response to intracoronary infusion of substance P (20 pmol/min)) and endothelium-independent (derived from coronary flow reserve (CFR) in response to systemic infusion of adenosine (140 μg/kg per minute)) CMF. Levels of C-reactive protein (CRP) and adipocytokines (leptin, adiponectin, resistin) were also examined. Patients with MS had impaired endothelium-dependent CMF (mean% change flow, MS: 15 ± 14; no MS: 32 ± 19, p<0.001). There was no difference in endothelium-independent CMF (CFR, MS: 3.0 ± 1.2; no MS: 3.4 ± 1.8, p = 0.31). Levels of CRP (p = 0.79), leptin (p = 0.48), adiponectin (p = 0.64) and resistin (p = 0.39) were also similar between the two groups. The association between diagnostic ATP-III criteria for MS and CMF was examined. Systolic (r  =  −0.51, p<0.01) and diastolic (r  =  −0.47, p<0.01) blood pressure were the only correlates of endothelium-dependent CMF. In addition, one way analysis of variance showed a linear negative trend between endothelium-dependent CMF and the number of ATP-III diagnostic features in each subject (F  =  4.63, p<0.01). There was a similar trend after the removal of blood pressure as a variable (F  =  3.21, p = 0.04) confirming that non-blood pressure ATP-III diagnostic ATP-III criteria also influence CMF. There was no association between ATP-III diagnostic criteria and endothelium-independent CMF. Similarly, there was no correlation between other continuous variables (age, LDL-cholesterol, CRP and adipocytokines) and endothelium-dependent/-independent CMF. On multivariate regression analysis the presence/absence of MS (β  =  −0.40; p = 0.04) was the only independent determinant of endothelium-dependent CMF (other covariates: age, gender, smoking, LDL-cholesterol, CRP, leptin, adiponectin, resistin). MS and the other covariates used in the multivariate analysis did not independently influence endothelium-independent CMF (β for MS −0.12; p = 0.36).

Conclusion In patients with stable coronary artery disease and optimal LDL levels, MS was an independent determinant of endothelium-dependent CMF. MS had no influence on endothelium-independent CMF.

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