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GW24-e3709 Relation between adipokines and coronary flow reserve in patients with chest pain and angiographically normal arteries
  1. Zhang Mo,
  2. Li Dan,
  3. Li Wei-hong,
  4. Li Cui-ping,
  5. Feng Xin-heng,
  6. Gao Wei,
  7. Li Zhao-ping
  1. Department of Cardiology, Peking University Third Hospital

Abstract

Objectives Adipokines have been shown to play an important role in coronary heart disease (CAD). Anti-inflammatory adipokines like adiponectin and omentin protect the vessels from plaque formation. On the other hand, release of pro-inflammatory adipokines like leptin will accelerate plaque formation and lead to coronary atherosclerosis. However, the impact of these adipokines on coronary microvascular dysfunction is not clear. Coronary flow reserve (CFR) is a marker of microvascular dysfunction. CFR < 3 suggests involvement of microvascular dysfunction. We sought to assess whether adipokines which included leptin, adiponectin and omentin, could be associated with CFR.

Methods We enrolled 61 nondiabetic patients who underwent computed tomography angiography or invasive coronary angiography and had no obstructive coronary artery disease (coronary stenosis < 50%). Data about classical risk factors, such as gender, age were obtained. CFR was measured by transthoracic doppler echocardiography (TTDE). Serum leptin, adiponectin and omentin were measured by enzyme-linked immunosorbent assay.

Results

  1. 61 patients (23 men and 38 women) with a mean age of 59 ± 10 years were enrolled. The mean CFR is 2.98 ± 0.67. 34 patients (56%) had reduced CFR (CFR < 3, mean 2.52 ± 0.32) suggestive of microvascular dysfunction and 27 patients (44%) had normal CFR (CFR ≥ 3, mean 3.56 ± 0.52). Classical risk factors of atherosclerosis such as body mass index (BMI), blood cholesterol, blood glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR) and family history of coronary heart disease showed no difference between two groups.

  2. Serum omentin was significantly decreased in patients with microvascular dysfunction as compared with those without (198.77 ± 23.83 ng/ml vs. 213.50 ± 17.62 ng/ml, P = 0.010). And the same result was revealed in men and women respectively (men 186.98 ± 25.40 ng/ml vs. 212.29 ± 18.46 ng/ml, P = 0.026; women 199.33 ± 21.92 ng/ml vs. 217.76 ± 15.10 ng/ml, P = 0.021). Whether in men or women, serum leptin and adiponectin showed no difference between two groups.

  3. Serum omentin was positively related to CFR (r = 0.361, P = 0.006), and it showed the same result in men and women respectively (men r = 0.353, P = 0.007; women r = 0.458, P = 0.006). In addition, baseline systolic blood pressure is also related to CFR (r = -0.264, P = 0.042). There were no marked correlation between serum leptin, adiponectin and CFR.

  4. On logistic regression analysis, serum omentin was the independent predictor of coronary microvascular dysfunction (OR = 0.62, CI 95%: 0.40-0.96).

Conclusions

  1. Serum omentin was decreased in patients with coronary microvascular dysfunction. It is the independent predictor of coronary microvascular dysfunction.

    There are no marked correlation between serum leptin, adiponectin and CFR.

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