1. ¹Department of Clinical Physiology and Nuclear Medicine, Glostrup Hospital, University of Copenhagen, Denmark
2. ²Department of Internal Medicine, Glostrup Hospital, University of Copenhagen, Denmark
3. ³Department of Cardiology and Endocrinology, Frederiksberg Hospital, University of Copenhagen, Denmark
4. ⁴Department of Cardiology, Ullevaal Hospital, University of Oslo, Norway
5. ⁵Department of Clinical Physiology and Nuclear Medicine, Frederiksberg Hospital, University of Copenhagen, Denmark
6. ⁶Department of Medicine, Department of Echocardiography, Weill Medical College of Cornell University, NY, USA

Correspondence: Dr MH Olsen, Department of Clinical Physiology and Nuclear Medicine, Glostrup Hospital, University of Copenhagen, Ringvejen, DK-2600 Glostrup, Denmark. E-mail: mho@dadlnet.dk

Received 30 October 2004; Revised 16 November 2004; Accepted 16 November 2004; Published online 13 January 2005.

Abstract

Cardiac fibrosis and high levels of circulating collagen markers has been associated with left ventricular (LV) hypertrophy. However, the relationship to vascular hypertrophy and blood pressure (BP) load is unclear. In 204 patients with essential hypertension and electrocardiographic LV hypertrophy, we measured sitting BP, serum collagen type I carboxy-terminal telopeptide (ICTP) reflecting degradation, procollagen type I carboxy-terminal propeptide (PICP) reflecting synthesis and LV mass by echocardiography after 2 weeks of placebo treatment and after 1 year of antihypertensive treatment with a losartan- or an atenolol-based regimen. Furthermore, we measured intima–media thickness of the common carotid arteries (IMT), minimal forearm vascular resistance (MFVR) by plethysmography and ambulatory 24-h BP in around half of the patients. At baseline, PICP/ICTP was positively related to IMT (r=0.24, P<0.05), MFVR_men (r=0.35, P<0.01), 24-h systolic BP (r=0.24, P<0.05) and 24-h diastolic BP (r=0.22, P<0.05), but not to LV mass. After 1 year of treatment with reduction in systolic BP (17515 vs 15117 mmHg, P<0.001) and diastolic BP (998 vs 889 mmHg, P<0.001), ICTP was unchanged (3.71.4 vs 3.81.4 g/l, NS) while PICP (12139 vs 10229 g/l, P<0.001) decreased. The reduction in PICP/ICTP was related to the reduction in sitting diastolic BP (r=0.31, P<0.01) and regression of IMT (r=0.37, P<0.05) in patients receiving atenolol and to reduction in heart rate in patients receiving losartan (r=0.30, P<0.01). In conclusion, collagen markers reflecting net synthesis of type I collagen were positively related to vascular hypertrophy and BP load, suggesting that collagen synthesis in the vascular wall is increased in relation to high haemodynamic load in a reversible manner.