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P. M. Timms, V. Srikanthan, S. Campbell, F. G. Dunn, N. Prasad, P-517: Plasma tissue inhibitor of metalloproteinase-1 and pro-collagen III N peptide are elevated in left ventricular hypertrophy, American Journal of Hypertension, Volume 14, Issue S1, April 2001, Pages 204A–205A, https://doi.org/10.1016/S0895-7061(01)01782-4
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Abstract
Essential hypertension (EH) aortic stenosis (AS) and hypertrophic obstructive cardiomyopathy (HOCM) can cause left ventricular hypertrophy (LVH). LVH is associated with increased collagen concentrations in the heart but the mechanisms causing LVH in EH, AS and HOCM are different. Collagen synthesis (fibrogenesis) can be monitored by measurement of pro-collagen III N peptide (PIIINP) which measures synthesis of mature collagen III. Inhibition of degradation was assessed by plasma tissue inhibitor of metalloproteinase -1 (TIMP-1) which inhibits the activity of metalloproteinases. We investigated levels of TIMP-1 and PIIINP in patients with the three types of LVH. Patients with EH had never been treated or had been off treatment for one month and patients with AS had blood samples taken preoperatively for PIIINP and TIMP-1. The results for the EH, AS and HOCM groups were compared with seventeen normotensive controls. Heparinised plasma was used in the assays for TIMP-1 and PIIINP which were measured by ELISA and RIA respectively. (See Table)
LVH . | No patients . | Median PIIINP U/ml 95% limits . | Median TIMP-1 ng/ml 95%limits . |
---|---|---|---|
Control | 17 | 0.53 (0.34-0.70) | 178 (99-330) |
EH | 31 | 0.59 (0.33-0.78) | 380 (161-1356)* |
AS | 27 | 0.78 (0.53-1.32)* | 270 (132-648) |
HCOM | 12 | 0.72 (0.58-0.89)* | 258 (160-351) |
LVH . | No patients . | Median PIIINP U/ml 95% limits . | Median TIMP-1 ng/ml 95%limits . |
---|---|---|---|
Control | 17 | 0.53 (0.34-0.70) | 178 (99-330) |
EH | 31 | 0.59 (0.33-0.78) | 380 (161-1356)* |
AS | 27 | 0.78 (0.53-1.32)* | 270 (132-648) |
HCOM | 12 | 0.72 (0.58-0.89)* | 258 (160-351) |
p<0.05 in comparison to controls
LVH . | No patients . | Median PIIINP U/ml 95% limits . | Median TIMP-1 ng/ml 95%limits . |
---|---|---|---|
Control | 17 | 0.53 (0.34-0.70) | 178 (99-330) |
EH | 31 | 0.59 (0.33-0.78) | 380 (161-1356)* |
AS | 27 | 0.78 (0.53-1.32)* | 270 (132-648) |
HCOM | 12 | 0.72 (0.58-0.89)* | 258 (160-351) |
LVH . | No patients . | Median PIIINP U/ml 95% limits . | Median TIMP-1 ng/ml 95%limits . |
---|---|---|---|
Control | 17 | 0.53 (0.34-0.70) | 178 (99-330) |
EH | 31 | 0.59 (0.33-0.78) | 380 (161-1356)* |
AS | 27 | 0.78 (0.53-1.32)* | 270 (132-648) |
HCOM | 12 | 0.72 (0.58-0.89)* | 258 (160-351) |
p<0.05 in comparison to controls
Elevated levels of collagen in the left ventricule in EH arise from both increased collagen synthesis as well as decreased collagen degradation whereas in AO and HOCM the increased heart collagen is associated with increased collagen III synthesis. This suggests that LVH can arise by different biochemical mechanisms.
- aortic valve stenosis
- hypertrophic cardiomyopathy
- enzyme-linked immunosorbent assay
- hypertension, essential
- left ventricular hypertrophy
- collagen
- metalloproteases
- peptides
- plasma
- tissue inhibitor of metalloproteinases
- tissue-inhibitor of metalloproteinase-1
- heart
- procollagen type iii-n-terminal peptide
- collagen synthesis
- catabolism