Cell-free DNA and Microvascular Damage in ST-segment Elevation Myocardial Infarction Treated With Primary Percutaneous Coronary Intervention (original) (raw)
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Cell free DNA detected by a novel method in acute ST-elevation myocardial infarction patients
Acute Cardiac Care, 2010
Background: High levels of circulating cell free DNA (CFD) have been associated with poor prognosis in various diseases. Data pertaining to CFD in acute myocardial infarction (MI) are scarce. The available data have been obtained by either electrophoresis or polymerase chain reaction. We evaluated a novel method for the detection of CFD in patients with ST elevation myocardial infarction (STEMI) and examined its correlation with established markers of necrosis and ventricular function. Methods: Serum concentrations of CFD, troponin-T and creatine kinase (CK) were measured simultaneously in 16 randomly selected acute STEMI patients upon admission and at three more time points. 47 healthy subjects served as a control group. CFD was quantifi ed by a novel rapid fl uorometric assay. Ejection fraction (EF) was assessed by echocardiography. Results: Peak CFD levels were signifi cantly higher in patients compared with controls ( P ϭ 0.001) and correlated with peak levels of CK and troponin-T (R ϭ 0.79, P Ͻ 0.001); R ϭ 0.65, P ϭ 0.006, respectively). Peak CFD levels tended to be associated with lower EF ( P ϭ 0.075). Conclusion: With this method, CFD levels correlated with the levels of established markers of myocardial necrosis but not with EF. The kinetic pattern of CFD release after STEMI and its prognostic value require further investigation.
Prognostic value of culprit artery double-stranded DNA in ST-segment elevated myocardial infarction
Scientific reports, 2018
The double-stranded DNA (dsDNA) which is scaffold of neutrophil extracellular traps (NETs) has been reported to be associated with the occurrence of major adverse cardiovascular events (MACEs) in patients with coronary atherosclerosis. However, the relationship between the dsDNA and the occurrence of MACEs in patients with ST-segment elevated myocardial infarction (STEMI) remains unclear. In this study, 142 consecutive STEMI patients were admitted to medical institutions. Blood from the infarct-related coronary artery (ICA) and peripheral artery (PA) were obtained during percutaneous coronary intervention. Clinical follow-up was performed to analyze the occurrence of MACEs. Patients were divided into low ds-DNA group and high dsDNA group according to the cut-off value of ICA dsDNA. Mean follow-up time was 24.52 months in low dsDNA group and 25.71 months in high dsDNA group. dsDNA in the ICA was significantly higher than in the PA (p = 0.038) and Spearman's correlation analysis s...
Cell-free DNA for diagnosing myocardial infarction: not ready for prime time
Clinical chemistry and laboratory medicine : CCLM / FESCC, 2015
A modest amount of cell-free DNA is constantly present in human blood, originating from programmed cell death, apoptosis and rupture of blood cells or pathogens. Acute or chronic cell injury contributes to enhance the pool of circulating nucleic acids, so that their assessment may be regarded as an appealing perspective for diagnosing myocardial ischemia. We performed a search in Medline, Web of Science and Scopus to identify clinical studies that investigated the concentration of cell-free DNA in patients with myocardial ischemia. Overall, eight case-control studies could be detected and reviewed. Although the concentration of cell-free DNA was found to be higher in the diseased than in the healthy population, the scenario was inconclusive due to the fact that the overall number of subjects studied was modest, the populations were unclearly defined, cases and controls were not adequately matched, the methodology for measuring the reference cardiac biomarkers was inadequately descri...
Circulation Research, 2014
A cute coronary syndrome (ACS) is among the leading causes of death. 1 However, precise pathomechanisms of acute coronary occlusion and atherothrombosis are still not well understood. Circulating leukocytes, particularly monocytes, play a central role in atherothrombosis. 2,3 The role of neutrophils (polymorphonuclear cells [PMNs]) in coronary thrombosis is less explored, although systemic PMN counts are among the most robust predictors of acute coronary events 4 and impact outcomes. We have previously shown PMN accumulation in coronary thrombi, and PMNs have been described in thrombi recovered during surgical thrombectomies and open repair of abdominal aortic aneurysms. 7 PMNs hold powerful effector mechanisms, particularly by the formation of neutrophil extracellular traps (NETs). On activation, PMNs release their nuclear content into the extracellular space to engulf and isolate pathogens. 8 NETs are composed of chromatin, which consists of DNA segments wound in sequence around 8 histone protein cores, and other granule proteins, exerting potent proinflammatory, cytotoxic, and prothrombotic effects. 9,10 Rationale: Mechanisms of coronary occlusion in ST-elevation acute coronary syndrome are poorly understood. We
Kardiologia Polska, 2006
Background: In a large group of patients with myocardial infarction, lack of tissue reperfusion following successful recanalisation of the infarct-related epicardial artery is seen. Blood flow in the microcirculation depends not only on structural changes in the microvasculature but also on rheological features of the blood itself. Aim: To investigate the association between baseline fibrinogen concentration and myocardial reperfusion following successful coronary angioplasty. Methodology: In 105 patients with acute ST-segment elevation myocardial infarction, baseline fibrinogen concentration was compared between patients with successful tissue reperfusion (n=79) and with no myocardial reperfusion (n=26) measured as the degree of ST-segment normalisation after successful recanalisation of the infarct-related artery. Results: Baseline fibrinogen concentration was significantly higher in the no-reperfusion group than in the reperfusion group (523±198.02 mg/dl vs 395.56±144.98 mg/dl, p...
European Heart Journal, 2006
Aims The aim of this study was to correlate total and differential leucocyte (WBC) count with myocardial blush, peak CK levels, and left ventricular (LV) functional recovery at 6 months in 238 consecutive acute myocardial infarction (MI) patients treated with successful primary coronary angioplasty (PCI). Methods and results Total and differential WBC counts were measured on admission and every 24 h for at least 4 days after PCI. ST-segment resolution and myocardial blush were evaluated immediately after successful primary PCI. LV functional recovery (defined as improvement involving at least two segments, or at least one segment, when only two were asynergic on the basal examination) was obtained through echocardiographic evaluation of LV wall motion at the baseline and at 6 months. Basal CK (P , 0.001) and increased neutrophil levels (P , 0.001) were the only independent factors related to peak CK, whereas neutrophils and monocytes peaks were related to ST-segment resolution as well as to myocardial blush grade (MBG) 2-3. MBG 2-3 and monocytes number (both as continuous values as well as percentile values) were the only variables independently associated with 6-month LV functional recovery. Conclusion The present study shows that neutrophils and monocytes counts on the first days after acute MI treated with primary PCI are related to markers of effective myocardial reperfusion such as MBG 2-3 and ST-segment resolution. However, only monocytes and MBG are significantly and independently associated with contractile recovery of the infarcted area at 6 months.
SpringerPlus, 2015
The frequency and profile of lymphocyte subsets within the culprit coronary artery were investigated in 33 patients with myocardial infarction and compared to their systemic circulating counterparts. T cell subsets including CD4 + CD28null, activated and regulatory T-cells, TH1/TH2/TH17 phenotypes, NK and B-cells were studied in intracoronary (IC) and arterial peripheral blood (PB) samples. CD4 + CD28null T-lymphocytes were significantly increased in IC compared to PB (3.7 vs. 2.9 %, p < 0.0001). Moreover, patients with more than 6 h of evolution of STEMI exhibited higher levels of CD4 + CD28null T-cells suggesting that this subset may be associated with more intense myocardial damage. The rare NK subpopulation CD3 − CD16 + CD56 − was also increased in IC samples (5.6 vs. 3.9 %, p = 0.006). CD4 + CD28null T-cells and CD3 − CD16 + CD56 − NK subpopulations were also associated with higher CK levels. Additionally, IFN-γ and IL10 were significantly higher in IC CD4 + lymphocytes. Particular immune cell populations with a pro-inflammatory profile at the site of onset were increased relative to their circulating counterparts suggesting a pathophysiological role of these cells in plaque instability, thrombi and myocardial damage.
The American Journal of Cardiology, 2010
Myeloperoxidase (MPO) is associated with risk in acute coronary syndromes. However, the precise role it plays in ST-elevation myocardial infarction (STEMI) remains unclear. In this study we tested the hypothesis that levels of MPO in plasma after a myocardial infarction are affected by its ability to bind to the endothelium and there is local release of the enzyme at the culprit lesion. We measured plasma MPO in systemic circulation and throughout the coronary circulation in patients with STEMI undergoing primary percutaneous coronary intervention (PCI). MPO levels at the femoral artery were higher (p <0.001) in patients with STEMI (n ؍ 67, median 45 ng/ml, interquartile range 34 to 83) compared to control patients (n ؍ 12, 25 ng/ml, 19 to 30) with chronic stable angina undergoing elective PCI. After administration of the anticoagulant bivalirudin in 13 patients with STEMI, plasma MPO was increased only at the culprit coronary artery lesion before PCI (178 ng/ml, 91 to 245) versus all other sites (femoral artery 86 ng/ml, 54 to 139, p ؍ 0.019). Administration of heparin caused a marked increase of plasma MPO. Even so, it was still possible to detect an increase of plasma MPO at culprit lesion in patients with STEMI (n ؍ 54, 171 ng/ml, 122 to 230) versus controls (n ؍ 12, 136 ng/ml, 109 to 151, p <0.05) after heparin and before PCI. MPO levels were higher at the culprit lesion in patients with STEMI who presented early and in those with restricted flow (p <0.05). In conclusion, our results demonstrate that, in addition to a systemic increase of MPO in patients presenting early with STEMI, levels of this leukocyte enzyme are increased at the culprit coronary lesion before PCI.
Coronary Artery Disease, 2015
The aim of this study was to investigate the relationship between lymphocyte to monocyte ratio (LMR) and the severity of coronary artery disease (CAD) by using Gensini score. A total of 199 patients, who had undergone coronary angiography, were included in the study and retrospectively analyzed. Among them, 49 patients who had normal coronary arteries were selected as the control group. Patients with CAD were divided into 2 groups, those with low Gensini score (40) and those with high Gensini score (≥40). Our results showed that LMR in the severe atherosclerosis group was significantly lower than those of the mild atherosclerosis group and the control group. There was a closely significant correlation between the Gensini score and LMR (r = À0.362, P < .001). Furthermore, multivariate logistic regression analysis demonstrated that LMR (odds ratio, 0.715; 95% confidence interval [CI], 0.551-0.927; P = .012) was independent predictors of severe atherosclerosis. Using an optimal LMR cutoff value of 5.06, LMR predicted severe atherosclerosis with a sensitivity of 57.1% and specificity of 69.7% (area under curve = 0.634; 95% CI, 0.545-0.724; P = .005). Then patients with CAD group was divided into 2 groups according to the LMR value of 5.06. Patients with LMR 5.06 had worse prognosis, with a higher rate of cardiovascular events during up to 1 year follow-up. Our study demonstrated that LMR was independently and positively associated with the severity of coronary atherosclerosis, providing a new insight in the application of inflammation index evaluating the severity of CAD. And LMR may be a useful predictor of future cardiovascular events in patients with CAD. Abbreviations: ACEI = angiotensin-converting enzyme inhibitor, ARB = angiotensin II receptor blocker, CAD = coronary artery disease, CI = confidence interval, Cr = creatinine, GLU = glucose, HDL-C = high-density lipoprotein cholesterol, LDL-C = lowdensity lipoprotein cholesterol, LMR = lymphocyte to monocyte ratio, LVEF = left ventricular ejection fraction, NLR = neutrophil to lymphocyte ratio, OR = odds ratio, RR = relative risk, TC = total cholesterol, TG = triglyceride, WBC = white blood cell.