December 2, 2011Journal of Hypertension109 citations
View Full PaperPlasma levels of matrix metalloproteinases and their inhibitors in hypertension
Key Result
Hypertensive patients had significantly higher plasma levels of MMP-9 (SMD 1.95; P<0.05) and TIMP-1 (SMD 1.92; P<0.01) compared to normotensive controls.
Study Design
Type
Meta-Analysis
Structured PICO
Are plasma levels of MMPs and TIMPs elevated in hypertension and associated with cardiovascular remodeling?
P
Population
Meta-analysis of studies evaluating plasma levels of matrix metalloproteinases and their inhibitors in hypertensive patients versus normotensive controls.
C
Comparator
Normotensive controls or hypertensive patients without cardiovascular remodeling (LV hypertrophy or diastolic HF)
O
Outcome
Plasma levels of MMPs (MMP-2, MMP-9) and TIMPs (TIMP-1)surrogate
Plasma levels of MMP-2, MMP-9, and TIMP-1 are elevated in hypertension and associated with cardiovascular remodeling, suggesting potential utility as biomarkers for risk stratification.
Main Result
Standardized Mean Difference: 1.95
p-value: p=<0.05
Limitations
- High heterogeneity among studies
Abstract
BACKGROUND: Hypertension is a major cause of cardiovascular remodeling. In the cardiovascular system, the remodeling of the extracellular matrix is controlled by the matrix metalloproteinases (MMPs) and the tissue inhibitors of MMPs (TIMPs). The aim of this meta-analysis is to elucidate the behavior of plasma MMP and TIMP levels in hypertension and their relationship to cardiovascular remodeling. METHODS: MEDLINE and EMBASE databases were searched up to July 2011. Studies were considered eligible if they provided values of plasma MMPs and TIMPs in hypertensive patients. Given the high variability of the plasma biomarker values among studies, the standardized mean difference (SMD) was calculated. RESULTS: Ten studies provided plasma MMP-9; the SMD between 778 hypertensive patients and 669 controls was 1.95 units (P < 0.05). Thirteen studies provided plasma TIMP-1; the SMD between 851 hypertensive patients and 646 normotensive individuals was 1.92 units (P < 0.01). Three studies investigated whether plasma TIMP-1 predicted left ventricular (LV) remodeling; the SMD between 92 hypertensive patients with and 88 hypertensive patients without LV hypertrophy was 5.81 units (P < 0.05). As for diastolic heart failure (HF), five studies provided data for plasma MMP-2; the SMD between 321 hypertensive patients with and 334 hypertensive patients without HF was 2.36 units (P < 0.01). The heterogeneity among studies was high. CONCLUSIONS: These results suggest that MMP-2, MMP-9 and TIMP-1 may have a role as biomarkers of cardiovascular remodeling in hypertension. If these results are confirmed in prospective clinical studies, they could provide new tools to stratify cardiovascular risk in hypertensive patients.