Intracoronary microparticles and microvascular obstruction in patients with ST elevation myocardial infarction undergoing primary percutaneous intervention (original) (raw)
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Archives of Medical Research, 2012
Background and Aims. Elevated levels of circulating microparticles (MPs) have been reported in patients with acute myocardial infarction (AMI) and coronary artery disease. Platelet activation and inflammation have been recognized during AMI and stable angina (SA). We hypothesize that the origin and count of MPs in AMI and SA patients are related to markers of inflammation and platelet activation. Methods. Platelet, monocytes and endothelial MPs and surface P-selectin were determined in 12 AMI patients, 10 SA patients and 9 controls by flow cytometry. Plasma P-selectin, CD40 ligand (sCD40L) and interleukin 6 (IL-6) levels were evaluated by ELISA methods. Results. The total MP count was compared in control subjects, AMI, and SA patients: 12,765 (8465) vs. 38,750 (11,931) vs. 29,715 (12,072) counts/ml (p 5 0.01), respectively. Patients with AMI displayed higher levels of total and platelet origin-tissue factorpositive (CD42/CD142) MPs than patients with SA: 72.8 (6.2) vs. 56.2 (6.4) %, p 5 0.001. Levels of soluble P-selectin were significantly elevated in patients with AMI as compared to SA patients: 146 (6.5) vs. 107 (2.7) ng/mL, p 5 0.005; significant correlation between total MP count and relative number of CD34, CD51, CD42-positive MPs, and the P-selectin expression was observed in patients with AMI. Conclusions. Platelet activation in AMI is associated with increased generation of MPs not only from platelets, but also monocytes and endothelial cells. It suggests that interactions between platelets, monocytes and endothelial cells play an important role in the pathogenesis of myocardial ischemia.
Endothelial microparticles correlate with high-risk angiographic lesions in acute coronary syndromes
International Journal of Cardiology, 2004
Background: Endothelial Microparticles (EMP) are small fragments of endothelial cell membrane shed during apoptosis or activation. Our group has previously reported elevations of EMP in patients with coronary artery disease (CAD), thrombotic thrombocytopenic purpura (TTP), pre-eclampsia, multiple sclerosis (MS), and severe hypertension (HTN). In the present study, we evaluate the possible relationship between EMP levels and the angiographic severity and characteristics of coronary obstructive lesions. Methods: We studied a total of 43 patients undergoing coronary angiography. Fifteen had presented with acute myocardial infarction (MI), 20 with unstable anginas (UA), 5 with stable angina (SA) and 3 with congestive heart failure. Coronary angiography was reviewed and coronary lesions were classified using the Ambrose classification. Coronary stenoses were classified as high and low risk. High-risk included lesions with eccentric appearance (type II), presence of thrombi, or multiple irregularities. Low-risk lesions were defined as concentric or type I. Lesions were also analyzed by degree of stenosis and history of acute coronary syndrome (ACS). EMP in plasma was assayed by flow cytometry. Results: EMP in eccentric type II or multiple irregular lesions (high-risk) were 2.5-fold higher than in type I or concentric (low-risk) lesions, p < 0.05. Lesions with thrombi had three-fold higher EMP than those without ( p = 0.05). Mild stenosis (>20% -< 45%) had three-fold higher EMP than more severe (>45%), and five-fold higher than those without stenosis ( p < 0.01). Among patients with type II lesions, those with first ACS episode had four-fold higher EMP levels than those with recurrent ACS ( p < 0.01). Conclusion: High EMP was associated with high-risk angiographic lesions including eccentric type II, multiple irregular, and lesions with thrombi. Mild to moderate stenosis was associated with higher EMP levels than severe stenosis. EMP may be a useful marker in detecting endothelial injury and risk of ACS as defined by angiography.
Differences in Microparticle Release in Patients With Acute Coronary Syndrome and Stable Angina
Circulation Journal, 2012
Background: Microparticles (MP) are vesicles released from activated or apoptotic cells. Endothelial MP (EMP) are derived from injured endothelium, platelet MP (PMP) from activated platelets, and Annexin V positive MP (AMP) from apoptotic endothelial cells. The aim was to assess the release of MP and its association with inflammation and atherosclerotic burden.
Archives of Medical Science, 2016
A b s t r a c t Introduction: Activated platelets generate microparticles. Increased platelet microparticles occur in acute myocardial infarction (AMI) and contribute to intracoronary thrombosis and subsequent myocardial injury. This study aimed to investigate the impact of platelet microparticles on intracoronary thrombosis by assessing the relationship between platelet microparticles and the extent of myocardial damage in AMI. Material and methods: This was a cross sectional study. The subjects were patients with acute coronary syndrome (ACS). Forty-one consecutive subjects with ACS admitted to intensive cardiovascular care unit were enrolled. The clinical spectrum of ACS comprised AMI (n = 26), both ST-elevation AMI (STEMI) and non-ST-elevation AMI (NSTEMI), and unstable angina (n = 15). Platelet microparticles were isolated from peripheral venous blood and detected with anti-CD42b-PE by the flow cytometry method. The extent of myocardial damage was determined by measuring the peak level of serial cardiac enzymes within 24 h of admission. Results: Subjects with AMI had a significantly higher number of platelet microparticles than those with unstable angina (4855 ±4509/μl vs. 2181 ±1923/μl respectively; p = 0.036). Subjects with STEMI had the highest number of platelet microparticles, but no significant difference was detected as compared to those with NSTEMI (5775 ±5680/μl vs. 3601 ±1632/μl). The number of platelet microparticles in AMI was positively associated with the extent of myocardial damage (peak CK-MB: r = 0.408, p = 0.019 and peak GOT: r = 0.384, p = 0.026). Conclusions: The number of platelet microparticles was increased in AMI as compared to unstable angina and associated with the extent of myocardial damage.
International Journal of Cardiology, 2018
Background: Cardiogenic shock (CS) is the leading cause of death in patients admitted for acute myocardial infarction (MI). Despite the recent advances in reperfusion and medical treatment mortality remains unacceptably high. Whether cells of the blood compartment in CS-patients are activated and release microparticles (cMPs) that may be both messengers and biomarkers of cell damage is not known. We aimed to investigate the cMP subtypes and parental activated cells of ST-elevation MI (STEMI)-patients complicated by CS and that of non-CS STEMI-patients (non-CS) in order to identify a cMP signature that could aid CS patient's risk stratification. Methods: Clinically-characterized STEMI-patients with and without CS (36/group) were included. Treatment was delivered according to guidelines and included primary percutaneous coronary intervention. cMPs were characterized by triple-labeling flow cytometry using Annexin V and cell surface-specific monoclonal antibodies. Results: Increased levels of leukocyte-derived (neutrophil and granulocyte origin) and platelet-derived cMPs were detected in CS compared to non-CS patients. A signature of cMPs derived from platelets, leukocytes, and endothelium discriminated CS-patients (AUC of 0.743 ± 0.059 [95% CI: 0.628-0.859], P b 0.0001) and predicted mortality in CS (AUC of 0.869 ± 0.06 [95% CI: 0.750-0.988], P b 0.0001). In CS-patients, a higher number of platelet-and monocyte-cMPs and of tissue factor-rich cMPs associated to worse myocardial blush grade and thrombolysis in myocardial infarction flow. Conclusions: cMPs derived from proinflammatory and prothrombotic cells were found to be elevated in CS-patients. In treated as per guidelines CS patients, granulocytes and neutrophils remained activated and actively shed cMPs. These cMPs were biomarkers of adverse prognosis in CS. Translational aspect: Increased levels of leukocyte and platelet-derived circulating microparticles (cMPs) are found in cardiogenic shock (CS) patients as compared to non-CS patients. In CS-patients, a higher number of platelet-and monocyte-cMPs and a higher number of tissue factor-rich cMPs were associated to worse myocardial reperfusion. A specific prothrombotic and proinflammatory cMPs signature in cardiogenic shock (CS) patients is a potential discriminator and survival prognostic biomarker for CS, which could aid management and improve clinical outcomes.
International Journal of Cardiology, 2012
Objectives: We sought to assess the relation of late microvascular obstruction (l-MVO) size as quantified by cardiac magnetic resonance (CMR) imaging with cardiac and inflammatory marker concentrations after acute myocardial infarction (AMI). Methods: CMR was performed in 118 consecutive patients within 8 days after successful interventional reperfused first acute ST-elevation AMI. Infarct volumes and l-MVO sizes were calculated from late enhancement (LE) sequences and functional parameters were determined from short-axis cine MR sequences. Creatine kinase (CK) and cardiac troponin T (cTnT), high-sensitivity C-reactive protein (hs-CRP) as well as lactate dehydrogenase (LD) concentrations were determined serially from day 1 to day 4 after symptom onset. Results: L-MVO was detected in 66/118 patients (55.9%) and comprised 18.2 ± 10% of infarct size and 4.7 ± 3% of left ventricle myocardial mass. Each single-point, peak and cumulative release concentration of cTnT (r = 0.44 to 0.73, p b 0.0001), CK (r = 0.21 to 0.76, p b 0.0001), LD (r = 0.36 to 0.82, all p b 0.0001) as well as hs-CRP single-point values as assessed from day 1 to day 4 and its peak and cumulative release concentrations (r = 0.24 to 0.49, p b 0.003) significantly correlated with l-MVO size. Receiver operating curve (ROC) analysis indicated a cut-off value of 4.7 μg/l cTnT to best identify the presence of l-MVO (area under the curve (AUC) 0.904; 95% CI: 0.85-0.95; p b 0.0001). Conclusion: L-MVO sizes significantly correlate with cardiac and inflammatory marker concentrations as determined early after AMI. cTnT concentration of N 4.7 μg/l could help to identify patients in whom l-MVO is present.
Cardiovascular revascularization medicine : including molecular interventions, 2018
In this prospective study, we compared the invasive measures of microvascular function in two subsets: patients with pharmacoinvasive thrombolysis for STEMI, and patients undergoing percutaneous coronary intervention (PCI) for NSTEMI. The study consisted of 17 patients with STEMI referred for cardiac catheterisation post thrombolysis, and 20 patients with NSTEMI. Coronary physiological indexes were measured in each patient before and after PCI. The median pre-PCI index of microcirculatory function (IMR) at baseline was significantly higher in the STEMI group than the NSTEMI group (26 units vs. 15 units, p = 0.02). Following PCI, IMR decreased in both groups (STEMI 20 units vs. NSTEMI 14 units, p = 0.10). There was an inverse correlation between post PCI IMR and left ventricular ejection fraction (LVEF) (r = -0.52, p = 0.001). Furthermore, post PCI IMR was an independent predictor of index admission LVEF in the total population (β = -0.388, p = 0.02). Invasive measures of microvascul...
Could mean platelet volume be a predictive marker for acute myocardial infarction?
Medical Science Monitor International Medical Journal of Experimental and Clinical Research, 2005
Platelets play an important role in developing intravascular thrombus, the major cause of acute coronary syndromes. We investigated the clinical value of mean platelet volume (MPV) in coronary atherosclerosis and its possibility of being an independent risk factor for acute myocardial infarction (MI). Two hundred patients who underwent coronary angiography were included in the study. Thirty-five patients were randomly selected for each of the four study groups of stable (SAP) and unstable (USAP) angina pectoris and MI with and without ST-segment elevation. Sixty patients with chest pain having normal coronary angiograms were controls. The groups were compared regarding age, sex, smoking, diabetes, hypertension, positive family history, number of diseased vessels, lipid profile, complete blood count, creatine kinase (CK)-MB, Troponin-I, and MPV. MPV was found to be elevated in MI patients compared with controls (p&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.001) and SAP (p&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.05) and patients with two- (p&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.001) and three-vessel (p&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.001) disease. We observed a significant association between MI and higher MPV (&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt; or = 12 fl). High MPV (p&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.001) and WBC (p&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.001) were independent risk factors, among others. CK-MB, Troponin-I, and higher MPV demonstrate MI risk with 87%, 70%, and 87% specificity, respectively, while higher MPV only demonstrates coronary artery disease with 98% specificity. Our study shows high MPV is an independent risk factor for coronary atherosclerosis and MI. Because this is a simple, economic, and practical method, we suggest MPV be considered with other conventional risk factors.
Cardiology Research and Practice
Introduction. Platelet-derived microparticles (PDMPs) measurement adds prognostic implication for ST-elevation acute myocardial infarction (STEMI). The long-term implication of PDMPs in STEMI needs to be corroborated. Methods. The research design was a cohort study. Subjects were STEMI patients and were enrolled consecutively. The PDMPs were defined as microparticles bearing CD41(+) and CD62P(+) markers detected with flow cytometry. The PDMPs were measured on hospital admission and 30 days after discharge. The outcomes were major adverse cardiac events (MACE), i.e., a composite of cardiac death, heart failure, cardiogenic shock, reinfarction, and resuscitated ventricular arrhythmia, occurring from hospitalization until 1 year after discharge. Results. We enrolled 101 subjects with STEMI. During hospitalization, 17 subjects (16.8%) developed MACE. The PDMPs were not different between subjects with MACE and those without (median (IQR): 3305.0/μL (2370.0–14690.5/μL) vs. 4452.0/μL (2024...