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Circulating Prolidase Activity in Patients with Myocardial Infarction.

ABSTRACT: Collagen is a major determinant of atherosclerotic plaque stability. Thus, identification of differences in enzymes that regulate collagen integrity could be useful for predicting susceptibility to atherothrombosis or for diagnosing plaque rupture. In this study, we sought to determine whether prolidase, the rate-limiting enzyme of collagen turnover, differs in human subjects with acute myocardial infarction (MI) versus those with stable coronary artery disease (CAD).We measured serum prolidase activity in 15 patients with stable CAD and 49 patients with acute MI, of which a subset had clearly defined thrombotic MI (n = 22) or non-thrombotic MI (n = 12). Prolidase activity was compared across study time points (at cardiac catheterization, T0; 6 h after presentation, T6; and at a quiescent follow-up, Tf/u) in acute MI and stable CAD subjects. We performed subgroup analyses to evaluate prolidase activity in subjects presenting with acute thrombotic versus non-thrombotic MI.Although prolidase activity was lower at T0 and T6 versus the quiescent phase in acute MI and stable CAD subjects (p < 0.0001), it was not significantly different between acute MI and stable CAD subjects at any time point (T0, T6, and Tf/u) or between thrombotic and non-thrombotic MI groups. Preliminary data from stratified analyses of a small number of diabetic subjects (n = 8) suggested lower prolidase activity in diabetic acute MI subjects compared with non-diabetic acute MI subjects (p = 0.02).Circulating prolidase is not significantly different between patients with acute MI and stable CAD or between patients with thrombotic and non-thrombotic MI. Further studies are required to determine if diabetes significantly affects prolidase activity and how this might relate to the risk of MI.

SUBMITTER: Sultan A

PROVIDER: S-EPMC5535509 | biostudies-other | 2017

REPOSITORIES: biostudies-other

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Project description:Long noncoding RNAs (lncRNAs) are non-protein coding transcripts regulating various critical physiological and pathological processes, yet limited information is available about lncRNAs expression in acute myocardial infarction (AMI). We aimed to identified differentially expressed lncRNAs in blood samples of patients with AMI to assess their diagnostic value. Differential expression of lncRNAs in peripheral blood mononuclear cells (PBMC) of patients with non-ST-elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI) was compared by RNA sequencing method and validated by real-time polymerase chain reaction (PCR). The area under the receiver operating characteristic curve (ROC) was used to evaluate diagnostic accuracy. Gene ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of lncRNA-coexpressed mRNAs were conducted to determine the related biological modules and pathological pathways. RNA sequencing data showed that 58 lncRNAs were differentially expressed between NSTEMI patients and STEMI patients, including 42 upregulated lncRNAs and 16 down-regulated lncRNAs. The ROC curves showed that ENST00000508020.2, LNC_001265, LNC_001526, and LNC_002674 could distinguish AMI patients with preferable sensitivity and specificity. GO enrichment analysis of lncRNA-coexpressed mRNAs indicated that the biological modules were correlated with cell adhesion, calcium ion homeostasis, complement receptor mediated signaling pathway, and immune system process. KEGG pathway analysis indicated that the lncRNAs-co-expressed mRNAs were involved in the regulation of peroxisome proliferators-activated receptors (PPAR) signaling pathway, mTOR signaling pathway, Insulin signaling pathway, HIF-1 signaling, and chemokin signaling pathway. Our results are in line with the previous findings, suggesting that differential expression of lncRNAs would be helpful to understand the molecular mechanism of AMI and might be useful biomarkers for noninvasive diagnostic application. Further studies are still needed to verify our findings and hypothesis.

Project description:ObjectiveThe purpose of this study was to examine the level of serum FGF21 in acute myocardial infarction (AMI) and to explore the association between serum FGF21 and major adverse cardiovascular events in AMI patients.MethodsA total of 238 Chinese patients were recruited for this study between January 2016 and June 2016, including 183 AMI patients and 55 patients without AMI were enrolled in this study. The level of serum FGF21 was measured by ELISA. Patients were followed-up after admission using a standardized protocol that included Outpatient follow-up and telephone contacts to record the Major Adverse Cardiovascular Events (MACEs). Finally, 165 patients were enrolled and followed up during the period of 24 months.ResultsCirculating FGF21 level was elevated in the AMI patients compared to control (P < 0.05). Multivariate linear regression analysis showed that cTnI (? = -0.001, 95% CI = 0.021-0.001, P = 0.002), fibrinogen (? = -0.055, 95% CI = 0.098-0.013, P = 0.011) and hyperlipidemia (? = 0.129, 95% CI = 0.014-0.243, P = 0.011) were the independent risk factors for the serum of FGF21 in AMI patients. After follow-up, A Kaplan-Meier analysis showed that the all-cause mortality rate was not significantly different between the two groups (P = 0.4146). Meanwhile the rate of cardiovascular events was significantly higher in the high-FGF21 group than in the low-FGF21 group (P = 0.0399). In the multivariate Cox proportional hazards regression model suggested that the predictive independent risk factors for the occurrence of MACEs were FGF21 ? cut-off (HR: 1.637; 95% CI: 1.357-3.647, P = 0.029) and D-Dimer (HR: 1.420; 95% CI: 1.069-3.014, P = 0.046).ConclusionCirculating FGF21 level is elevated in the AMI patients. In AMI patients, cTnI, fibrinogen and hyperlipidemia are the inde pendent risk factors for the serum of FGF21. Higher circulating FGF21 level is associated with increased MACEs rate. This study suggests that circulating FGF21 level may be a predictive marker of the clinical outcomes in AMI patients.

Project description:PurposeNitric oxide (NO) is constitutively produced and released from the endothelium and several blood cell types by the isoform 3 of the NO synthase (NOS3). We have shown that NO protects against myocardial ischemia/reperfusion (I/R) injury and that depletion of circulating NOS3 increases within 24 h of ischemia/reperfusion the size of myocardial infarction (MI) in chimeric mice devoid of circulating NOS3. In the current study we hypothesized that circulating NOS3 also affects remodeling of the left ventricle following reperfused MI.MethodsTo analyze the role of circulating NOS3 we transplanted bone marrow of NOS3-/- and wild type (WT) mice into WT mice, producing chimerae expressing NOS3 only in vascular endothelium (BC-/EC+) or in both, blood cells and vascular endothelium (BC+/EC+). Both groups underwent 60 min of coronary occlusion in a closed-chest model of reperfused MI. During the 3 weeks post MI, structural and functional LV remodeling was serially assessed (24 h, 4 d, 1 w, 2 w and 3 w) by echocardiography. At 72 hours post MI, gene expression of several extracellular matrix (ECM) modifying molecules was determined by quantitative RT-PCR analysis. At 3 weeks post MI, hemodynamics were obtained by pressure catheter, scar size and collagen content were quantified post mortem by Gomori's One-step trichrome staining.ResultsThree weeks post MI, LV end-systolic (53.2±5.9 μl; ***p≤0.001; n = 5) and end-diastolic volumes (82.7±5.6 μl; *p<0.05; n = 5) were significantly increased in BC-/EC+, along with decreased LV developed pressure (67.5±1.8 mm Hg; n = 18; ***p≤0.001) and increased scar size/left ventricle (19.5±1.5%; n = 13; **p≤0.01) compared to BC+/EC+ (ESV: 35.6±2.2 μl; EDV: 69.1±2.6 μl n = 8; LVDP: 83.2±3.2 mm Hg; n = 24; scar size/LV13.8±0.7%; n = 16). Myocardial scar of BC-/EC+ was characterized by increased total collagen content (20.2±0.8%; n = 13; ***p≤0.001) compared to BC+/EC+ (15.9±0.5; n = 16), and increased collagen type I and III subtypes.ConclusionCirculating NOS3 ameliorates maladaptive left ventricular remodeling following reperfused myocardial infarction.

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Circulating Prolidase Activity in Patients with Myocardial Infarction.

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