© 1997 by European Society of Cardiology
Copyright © 1997, European Society of Cardiology
Circulating transforming growth factor β1 and coronary artery disease
Department of Cardiovascular Medicine, University of New South Wales, Prince Henry/Prince of Wales Hospitals, Sydney, Australia
* Corresponding author. Department of Cardiovascular Medicine, Clinical Sciences Building, Prince Henry Hospital, Little Bay, NSW 2036, Australia. Tel.: +61 (2) 382 5026; fax: +61 (2) 382 5755; e-mail: x.l.wang@unsw.edu.au
Objective: Transforming growth factor β1 (TGF-β1), a multifunctional cytokine, is involved in many physiological and pathological processes and possibly in atherogenesis. Methods: We explored the association between circulating plasma TGF-β1 measured by ELISA and coronary artery disease (CAD) assessed angiographically in 371 Caucasian patients (269 men and 102 women) aged 
65 years. Results: While mean±s.e.m. total TGF-β1 was not different among patients with (56.9±1.5 ng/ml) or without (54.6±2.8 ng/ml) angiographically demonstrable CAD, naturally active TGF-β1 was significantly higher in CAD patients (1.74±0.18 vs 0.96±0.17 ng/ml, P<0.01). Active TGF-β1 increased with the number of major coronary arteries with more than 50% luminal obstruction (P<0.01), and patients with triple vessel disease had twice the level of those with no or mild vessel disease (2.15±0.46 vs 1.12±0.14 ng/ml, P<0.001). We found no relationship between TGF-β1 and Lp(a), but TGF-β1 was significantly correlated with circulating fibrinogen (r=0.178, P=0.005) and fasting glucose (r=0.177, P=0.007) levels. Conclusions: Our study identifies an increase in active TGF-β1 levels with both the occurrence and severity of CAD which is independent of standard CAD risk factors. This may reflect a ‘double-edged sword’ effect of TGF-β1 in that it may reduce atherogenesis by inhibiting smooth muscle cell proliferation but, when there is ongoing vessel wall injury, enhance it by promoting excessive extracellular matrix accumulation. The outcome could represent a complex balance between these two competing influences.
KEYWORDS TGF-β1; Coronary artery disease; Lipoprotein(a); Fibrinogen; Human
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