Comparison of matrix metalloproteinase 9 and brain natriuretic peptide as clinical biomarkers in chronic heart failure

Vorovich, Esther; Chuai, Shaokun; Li, Mingyao; Averna, Justin; Marwin, Victor; Wolfe, David J.; Reilly, Muredach P.; Cappola, Thomas P.

doi:10.1016/j.ahj.2008.01.007

Cited by 25 publications

(24 citation statements)

References 25 publications

(19 reference statements)

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“…The group of 442 ACS patients went on to have 90 end point events, and follow-up measurements were based on 51 events in 338 patients, which represents a relatively low power for the study and we cannot discount the possibility of type II errors. Nevertheless, our results on baseline associations of adiponectin with age and the female gender [36], as well as with BNP [10][11][12][13][14][15][17][18][19], and the link to end points [19,23,37], is consistent with the literature and suggest the results are externally valid. Further larger studies with serial measurements are required to confirm and expand on the potential mechanistic relationships of adiponectin, BNP and cardiac stress.…”

Section: Discussionsupporting

confidence: 93%

Serial changes in adiponectin and BNP in ACS patients: paradoxical associations with each other and with prognosis

et al. 2009

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Plasma adiponectin is inversely associated with the risk of coronary heart disease in healthy people. However, adiponectin and BNP (B-type natriuretic peptide) are both known to be positively associated with a risk of poor outcome, and with each other, in ACS (acute coronary syndrome) patients. Serial changes in plasma adiponectin and BNP following ACS have not been assessed previously, and may clarify these apparently paradoxical associations. In the present study, adiponectin, BNP, classical risk markers and clinical parameters were measured in plasma from 442 consecutive ACS patients in an urban teaching hospital, with repeat measures at 7 weeks (n=338). Patients were followed-up for 10 months. Poor outcome was defined as mortality or readmission for ACS or congestive heart failure (n=90). In unadjusted analysis, the change in adiponectin (but not baseline or 7-week adiponectin) was significantly associated with the risk of an adverse outcome {odds ratio (OR), 5.42 [95% CI (confidence interval), 2.78-10.55]}. This association persisted after adjusting for classical risk factors and clinical markers, but was fully attenuated by adjusting for the 7-week BNP measurement [OR, 1.13 (95% CI, 0.27-4.92)], which itself remained associated with risk [OR, 5.86 (95% CI, 1.04-32.94)]. Adiponectin and BNP positively correlated at baseline and 7 weeks, and the change in both parameters over 7 weeks also correlated (r=0.39, P<0.001). In conclusion, increases in plasma adiponectin (rather than absolute levels) after ACS are related to the risk of an adverse outcome, but this relationship is not independent of BNP levels. The results of the present study allude to a potential direct or indirect relationship between adiponectin and BNP post-ACS which requires further investigation.

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Section: Discussionsupporting

confidence: 93%

Serial changes in adiponectin and BNP in ACS patients: paradoxical associations with each other and with prognosis

et al. 2009

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“…Recent community based studies demonstrated an approximately 2-fold increased risk of hypertension progression in subjects with elevated MMP-9 levels. 46-49 Moreover, these elevated MMP-9 plasma levels were associated with higher PIIINP levels. In the present study, both PIIINP and MMP-9 were important components of the multi-biomarker prediction modeling for LVH.…”

Section: Discussionmentioning

confidence: 93%

“…55-57 The biomarkers measured in the present study fulfill this requirement. In addition, it is clear that no single biomarker is optimal for screening, diagnosis and potentially disease management and therefore the multivariable modeling utilized in the present study addressed this issue 23,38,40,47-49,55-57 . Finally, the current study clearly fulfilled the recommended first “phase of evaluation” outlined by the AHA.…”

Section: Discussionmentioning

confidence: 99%

Plasma Biomarkers That Reflect Determinants of Matrix Composition Identify the Presence of Left Ventricular Hypertrophy and Diastolic Heart Failure

Zile

DeSantis

Baicu

et al. 2011

Circ: Heart Failure

188

176

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Background Chronic pressure overload (such as arterial hypertension) may cause left ventricular (LV) remodeling, alterations in cardiac function, and the development of diastolic heart failure. Changes in the composition of the myocardial extracellular matrix (ECM) may contribute to the development of pressure-overload (PO) induced LV remodeling. We hypothesized that a specific pattern of plasma biomarker expression that reflected changes in these pathophysiologic mechanisms would have diagnostic application to identify: 1-patients who have developed LV hypertrophy and 2-patients with LV hypertrophy who have developed diastolic heart failure. Methods and Results Plasma concentration of 17 biomarkers (MMP-1, 2, 3, 7, 8, 9, TIMP-1, 2, 3, 4, NT-proBNP, cardiotrophin, osteopontin, sRAGE, CITP, PINP, PIIINP), an echocardiogram, and 6-minute hall walk were performed on 241 referent control subjects, 144 patients with LV hypertrophy (LVH) but no evidence of heart failure, and 61 patients with LV hypertrophy and diastolic heart failure (DHF). A plasma multi-biomarker panel consisting of increased MMP-7, MMP-9, TIMP-1, PIIINP, and NT-proBNP predicted the presence of LVH with an AUC of 0.80. A plasma multi-biomarker panel consisting of increased MMP-2, TIMP-4, PIIINP and decreased MMP-8 predicted the presence of DHF with an AUC of 0.79. These multi-biomarkers panels performed better than any single biomarker including NT-proBNP, and better than using clinical co-variates alone (AUC = 0.73 for LVH, 0.68 for DHF). Conclusions Plasma biomarkers reflecting changes in ECM fibrillar collagen homeostasis, combined into a multi-biomarker panel, have discriminative value in identifying the presence of structural remodeling (LVH) and clinical disease (DHF).

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“…(Creemers et al 2001; Wilson et al 2002; Sundstrom et al 2004; Wagner et al 2006; Yan et al 2006; Moe et al 2008; Zhao et al 2009; Buralli et al 2010; Dini et al 2010; Yang et al 2010). However, recent studies have found no significant association between plasma levels of MMP-9 and increased risk for myocardial infarction as well as other forms of heart failure (Vorovich et al 2008; Welsh et al 2008; Eldrup et al 2012). The apparent difference could be due to variations in the study population and (or) gene polymorphisms (Mizon-Gerard et al 2004; Shevchenko et al 2010).…”

Section: Mitochondria In Heart Diseasementioning

confidence: 96%

Dysregulation of Mfn2 and Drp-1 proteins in heart failure

Givvimani

Pushpakumar

Veeranki

et al. 2014

Can. J. Physiol. Pharmacol.

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Therapeutic approaches for cardiac regenerative mechanisms have been explored over the past decade to target various cardiovascular diseases (CVD). Structural and functional aberrations of mitochondria have been observed in CVD. The significance of mitochondrial maturation and function in cardiomyocytes is distinguished by their attribution to embryonic stem cell differentiation into adult cardiomyocytes. An abnormal fission process has been implicated in heart failure, and treatment with mitochondrial division inhibitor 1 (Mdivi-1), a specific inhibitor of dynamin related protein-1 (Drp-1), has been shown to improve cardiac function. We recently observed that the ratio of mitofusin 2 (Mfn2; a fusion protein) and Drp-1 (a fission protein) was decreased during heart failure, suggesting increased mitophagy. Treatment with Mdivi-1 improved cardiac function by normalizing this ratio. Aberrant mitophagy and enhanced oxidative stress in the mitochondria contribute to abnormal activation of MMP-9, leading to degradation of the important gap junction protein connexin-43 (Cx-43) in the ventricular myocardium. Reduced Cx-43 levels were associated with increased fibrosis and ventricular dysfunction in heart failure. Treatment with Mdivi-1 restored MMP-9 and Cx-43 expression towards normal. In this review, we discuss mitochondrial dynamics, its relation to MMP-9 and Cx-43, and the therapeutic role of fission inhibition in heart failure.

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Comparison of matrix metalloproteinase 9 and brain natriuretic peptide as clinical biomarkers in chronic heart failure

Abstract: Compared to BNP, MMP-9 is a poor clinical biomarker of remodeling and outcome in patients with systolic heart failure derived from clinical practice.

Cited by 25 publications

References 25 publications

Serial changes in adiponectin and BNP in ACS patients: paradoxical associations with each other and with prognosis

Serial changes in adiponectin and BNP in ACS patients: paradoxical associations with each other and with prognosis

Plasma Biomarkers That Reflect Determinants of Matrix Composition Identify the Presence of Left Ventricular Hypertrophy and Diastolic Heart Failure

Dysregulation of Mfn2 and Drp-1 proteins in heart failure

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