Abstract 12594: Mmp9 but not Diastolic Function Parameters, Reflect Early Adaptive Cardiac Response in the Metabolic Syndrome
Introduction: Metabolic syndrome is defined as a combination of several risk factors that are associated with cardiovascular disease. Whether myocardial changes in this syndrome are adaptive consequences of the systemic effects and/ or are direct myocardial effects via related specific mechanisms is unclear.
Hypothesis: Diastolic function measured by echocardiography could reflect early cardiac adaptive responses related to Metabolic Syndrome, together with a set of biomarkers representing extracellular matrix activity [ECM], inflammation and cardiac hemodynamic stress.
Methods: In a cross-sectional study, we enrolled subjects aged 30-55 years in two groups: metabolic syndrome (n=76) and healthy volunteers (n=30). We performed a clinical exam, evaluated diastolic function by echocardiography, and measured the plasma levels of metalloproteinase-9 (MMP9), plasma tissue inhibitor of metalloproteinase-1 (TIMP1), ultrasensitive-reactive-C-Protein (us-CRP), insulin resistance (HOMA-IR) and natriuretic peptide (NT-proBNP).
Results: The metabolic syndrome group showed increased peak mitral A wave velocities (63.4±14.0 cm/s vs. 53.1±8.9 cm/s; P<0.001), E/E’ ratios (8.0±2.2 vs. 6.3±1.2; P<0.001), MMP9 (502.9±237.1 ng/mL vs. 330.4±162.69 ng/mL; P<0.001), us-CRP (P=0.001) and HOMA-IR (P<0.001), but not TIMP1 (P=0.41) or NT-proBNP (P=0.19). In multivariable analysis, only MMP9 was independently associated with the metabolic syndrome.
Conclusion: Patients with the metabolic syndrome showed subtle differences in echocardiographic measures of diastolic function, in ECM activity measured by MMP9, and in us-CRP and HOMA-IR. However, only MMP9 was independently associated with the metabolic syndrome. These findings suggest that although the syndrome may exert early effects on extracellular matrix activity, its early morphologic consequences on the heart cannot be adequately tracked with routine Doppler measurements.
- © 2012 by American Heart Association, Inc.