scholarly journals Sensitive detection of cardiac biomarkers using a magnetic microbead immunoassay

2015 ◽  
Vol 7 (20) ◽  
pp. 8632-8639 ◽  
Author(s):  
Christine F. Woolley ◽  
Mark A. Hayes
Keyword(s):  
Myocardial Infarction ◽  
Magnetic Bead ◽  
Cardiac Biomarkers ◽  
Sensitive Detection ◽  
Magnetic Microbead

A novel magnetic bead-based microimmunoassay achieves superior quantitation abilities for three cardiac biomarkers used in the diagnosis of myocardial infarction.

Abstract P372: Evaluation of International Classification of Disease-Ninth Edition (ICD-9) codes for Determining Subclasses and Anatomic Location of Myocardial Infarction in the Community

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Wayne D Rosamond ◽  
Rachel Kloss ◽  
Natalia Petruski-ivleva ◽  
Lisa Wruck ◽  
Erin Michos ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Biomarkers ◽  
General Category ◽  
Atherosclerosis Risk In Communities ◽  
International Classification Of Disease ◽  
Anatomic Location ◽  
St Segment ◽  
Definition Of ◽  
Anatomic Locations ◽  
Epidemiology Studies

Background: Epidemiology studies of acute myocardial infarction (MI) often rely on hospital discharge codes or claims data to identify events. The fourth digit of ICD-9 code 410 is meant to identify anatomic location of an MI. Although the validity of ICD-9 410 codes to identify the general category of MI has been studied, far less is known about the validity of ICD codes to identify ST segment MI (STEMI) and non-STEMI (NSTEMI) and to identify anatomic location of STEMI infarcts. Methods: From 1987 to 2010 we evaluated random samples of hospitalizations with ICD-9 discharge codes 410-414, 402, 427, 428, or 518.4 among men and women age 35-74 years from hospitals serving the 4 communities of the Atherosclerosis Risk in Communities (ARIC) Study (400,000 base population in 2010). Trained staff abstracted medical records and copied up to three 12-lead electrocardiograms (ECG) that were coded by Minnesota Code. A standardized algorithm was applied to data on chest pain, cardiac biomarkers, and ECG evidence to determine MI diagnosis. Validated MI events with abnormal biomarkers were further classified by ECGs as STEMI or NSTEMI. ICD-9 codes 410.0-410.6 and 410.8 were used to define STEMI while codes 410.7 or 410.9 defined NSTEMI. STEMI infarct location was assessed by ECG and categorized as anterior, inferior, lateral, or multi-location. We determined the validity of code-based definitions using the ARIC algorithm and ECG evidence as referent standards. All analyses were weighted to account for sampling. Results: Between 1987 and 2010, 208,920 (weighted) hospitalizations with discharge codes suggestive of MI occurred in the 4 ARIC communities. Of these, 19% (38,729/208,920) were validated as MI. The positive predictive value (PPV) of an ICD-9 410 code to identify a validated MI was 72% (22218/30652). This PPV declined slightly from 78% (862/1111) in 1987 to 71% (1031/1462) in 2010. Center differences by community were seen (range 63% (197/315) to 78% (173/222) in 2010). Sensitivity of a 410 code to identify validated MIs remained stable from 1987 to 2010 at about 57% (22218/38,729). The PPV of the ICD-9 code-based STEMI definition improved after 2005 but remained moderate at 41% (175/430) in 2010. The PPV of the ICD-9 code based definition of NSTEMI was 63% (599/945) in 2010 and was stable over time. The PPV of codes to identify anterior and inferior infarctions were high (66% (1145/1741) and 78% (1956/2518), respectively). However codes for lateral and multiple site infarctions had lower PPV (53% (327/619) and 21% (153/727), respectively). Conclusions: The PPV of an ICD-9 code 410 to identify MI remained stable over the past 2 decades, but geographic differences persist. ICD-9 codes are better at correctly identifying NSTEMI than STEMI and better at identifying inferior infarcts than other anatomic locations. These data suggest caution in interpreting studies of MI trends based solely on ICD-9 codes.

Unstable Angina and Other Acute Coronary Syndromes

2013 ◽  
Author(s):  
R Scott Wright ◽  
Joseph G Murphy
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Risk Stratification ◽  
Unstable Angina ◽  
The United States ◽  
Cardiac Biomarkers ◽  
St Segment Elevation ◽  
Coronary Syndrome ◽  
Segment Elevation Myocardial Infarction ◽  
St Segment

Patients with coronary artery disease (CAD) present clinically when their disease enters an unstable phase known as an acute coronary syndrome (ACS), in which the cap of a previously stable atheromatous coronary plaque ruptures or erodes, which in turn activates a thrombotic cascade that may lead to coronary artery occlusion, myocardial infarction (MI), cardiogenic shock, and patient death. There are nearly 2 million episodes of ACS in the United States annually; it is the most common reason for hospitalization with CAD and is the leading cause of death in the developed world. ACS patients include those with unstable angina (UA), non–ST segment elevation myocardial infarction (non-STEMI), and ST segment elevation myocardial infarction (STEMI) and patients who die suddenly of an arrhythmia precipitated by coronary occlusion. The distinction among various ACS subgroups reflects varying characteristics of clinical presentation (presence or absence of elevated cardiac biomarkers) and the type of electrocardiographic (ECG) changes manifested on the initial ECG at the time of hospitalization. This chapter focuses on UA and non-STEMI. A graph outlines mortality risks faced by patients with varying degrees of renal insufficiency. An algorithm describes the suggested management of patients admitted with UA or non-STEMI. Tables describe the risk stratification of the patient with chest pain, categories of Killip class, examination findings of a patient with high-risk ACS, diagnosis of MI, causes of troponin elevation other than ischemic heart disease, initial risk stratification of ACS patients, and long-term medical therapies and goals in ACS patients. This review contains 2 highly rendered figures, 11 tables, and 76 references.

scholarly journals CURRENT PHARMACOLOGICAL STATUS OF CARDIOPROTECTIVE PLANTS AGAINST ISOPROTERENOL INDUCED MYOCARDIAL INFARCTION

2018 ◽  
Vol 11 (4) ◽  
pp. 17
Author(s):  
Syeda Nishat Fathima ◽  
Vasudeva Murthy S
Keyword(s):  
Myocardial Infarction ◽  
Lifestyle Modification ◽  
Treatment Options ◽  
Surgical Techniques ◽  
Cardiac Biomarkers ◽  
Therapeutic Interventions ◽  
Current Status ◽  
Plant Parts ◽  
Heart Muscle Cells ◽  
Modern Era

 Objective: Cardiovascular diseases are the major cause of morbidity and mortality in the modern era. Myocardial infarction is a condition where there is a significant decrease or block in the blood (oxygen) supply to the part of heart, leading to degeneration of a portion of the myocardium which triggers a cascade of cellular, inflammatory and biochemical events, leading eventually to the irreversible death (necrosis) of heart muscle cells. Various therapeutic interventions, including lifestyle modification, pharmacological treatment options, and surgical techniques are available. The present review focus on the plants that have been evaluated for cardioprotective activity against isoproterenol-induced myocardial infarction.Method: The current status of Cardioprotective plants was obtained from a literature search of electronic databases such as Google Scholar, Pubmed and Scopus up to 2017 for publications on medicinal plants used against isoproterenol-induced myocardial infarction. Isoproterenol, Isoprenaline, myocardial infarction, cardioprotective were used as keywords for the searching.Result: A total of 117 different plant parts and their extracts have till now been published to possess cardioprotection against isoproterenol-induced myocardial infarction. Isoproterenol a beta-adrenergic receptors agonist causes severe stress in myocardium resulting in the infarct-like lesion and produced cardiotoxic effects by elevating the levels of cardiac biomarkers and causing changes in ECG. Plant-based medicines with their antioxidant, antiapoptotic, antihyperlipidemic, platelet antiaggregatory, anti-lipid peroxidation property provide substantial evidence for the management of Ischemia.Conclusion: This review, therefore, provides a useful resource to enable a thorough assessment of the profile of plants that have cardioprotective activity against isoproterenol-induced myocardial infarction.

scholarly journals Postoperative ‘STEMI’ in Intracerebral Hemorrhage due to Arteriovenous Malformation: A Case Report and Review of Literature

2019 ◽  
Vol 2019 ◽  
pp. 1-5
Author(s):  
Ravinder Datt Bhanot ◽  
Jasleen Kaur ◽  
Shitiz Sriwastawa ◽  
Kendall Bell ◽  
Kushak Suchdev
Keyword(s):  
Myocardial Infarction ◽  
Intracerebral Hemorrhage ◽  
Arteriovenous Malformation ◽  
Cardiac Biomarkers ◽  
Review Of Literature ◽  
Fibrinolytic Agents ◽  
Intraparenchymal Hemorrhage ◽  
Ecg Changes ◽  
St Segment ◽  
Electrocardiogram Ecg

Electrocardiogram (ECG) changes suggestive of cardiac ischemia are frequently demonstrated in patients with ischemic stroke and subarachnoid hemorrhage. However, little is known of such changes particularly acute ST segment myocardial infarction (STEMI) in patients with intracerebral hemorrhage (ICH), especially after neurosurgery. We present a patient with intraparenchymal hemorrhage due to cerebral arteriovenous malformation (AVM) who exhibited acute STEMI after neurosurgery. Serial cardiac biomarkers and echocardiograms were performed which did not reveal any evidence of acute myocardial infarction. The patient was managed conservatively from cardiac stand point with no employment of anticoagulants, antiplatelet therapy, fibrinolytic agents, or angioplasty and recovered well with minimal neurological deficit. This case highlights that diffuse cardiac ischemic signs on the ECG can occur in the setting of an ICH after neurosurgery, potentially posing a difficult diagnostic and management conundrum.

scholarly journals Hypertensive Emergency and Type 2 Myocardial Infarction Resulting From Pheochromocytoma and Concurrent Capnocytophaga Canimorsus Infection

2014 ◽  
Vol 8 (1) ◽  
pp. 43-47 ◽  
Author(s):  
Graham J Fent ◽  
Hazlyna Kamaruddin ◽  
Pankaj Garg ◽  
Ahmed Iqbal ◽  
Nicholas F Kelland ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Clinical Presentation ◽  
Plaque Rupture ◽  
Interesting Case ◽  
Hypertensive Emergency ◽  
Cardiac Biomarkers ◽  
Dog Bite ◽  
Capnocytophaga Canimorsus ◽  
Review Current

A diagnosis of myocardial infarction is made using a combination of clinical presentation, electrocardiogram and cardiac biomarkers. However, myocardial infarction can be caused by factors other than coronary artery plaque rupture and thrombosis. We describe an interesting case presenting with hypertensive emergency and type 2 myocardial infarction resulting from Pheochromocytoma associated with Capnocytophaga canimorsus infection from a dog bite. We also review current literature on the management of hypertensive emergency and Pheochromocytoma.

Amplified suspension magnetic bead-based assay for sensitive detection of anti-glycan antibodies as potential cancer biomarkers

2022 ◽  
pp. 339444
Author(s):  
Anna Blsakova ◽  
Filip Květoň ◽  
Lenka Lorencová ◽  
Ola Blixt ◽  
Alica Vikartovska ◽  
...  
Keyword(s):  
Cancer Biomarkers ◽  
Magnetic Bead ◽  
Sensitive Detection ◽  
Potential Cancer

Abstract 2832: Which Cardiac Marker is Most Useful to Predict Final Infarct Size and Cardiac Function Following Primary Percutaneous Coronary Intervention For Acute Myocardial Infarction?

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Stanley Chia ◽  
O. Christopher Raffel ◽  
Faisal Merchant ◽  
Frans J Wackers ◽  
Fred Senatore ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Troponin I ◽  
Troponin T ◽  
Coronary Intervention ◽  
Left Ventricular ◽  
Cardiac Biomarkers ◽  
Primary Pci ◽  
Percutaneous Coronary

Background: Assessment of cardiac biomarker release has been traditionally used to estimate the size of myocardial damage after acute myocardial infarction (AMI). However, the significance of cardiac biomarkers in the setting of primary percutaneous coronary intervention (PCI) has not been systematically studied in a large patient cohort. We evaluated the usefulness of serial and single time-point measures of various cardiac biomarkers (creatine kinase (CK), CK-MB, troponin T and I) in predicting infarct size and left ventricular ejection fraction (LVEF) after primary PCI. Methods: EVOLVE (Evaluation of MCC-135 for Left Ventricular Salvage in AMI) was a randomized double-blind, placebo-controlled trial comparing the efficacy of intracellular calcium modulator as an adjunct to primary PCI in patients with first large AMI. Levels of cardiac biomarkers (CK, CK-MB mass, troponin T and I) were determined in 375 patients at baseline before PCI and 2, 4, 12, 24, 48 and 72 hours thereafter. Single photon emission computed tomography imaging was performed to measure infarct size and LVEF on day 5. Results: Area under curve and peak concentrations of all cardiac markers: CK, CK-MB mass, troponin T and troponin I were significantly correlated with myocardial infarct size and LVEF determined on day 5 (Spearman correlation, all P< 0.001; Table ). Troponin I, however provided the best predictor and a single measure at 72 hr was a strong indicator of both infarct size and LVEF. Using receiver operator characteristics curve, troponin I cutoff value of >55 pg/mL at 72 hr has 90% sensitivity and 70% specificity for detection of large infarct size≥10% ( c =0.88; P< 0.001). Conclusions: Plasma levels of CK, CK-MB, troponin T and troponin I remain useful predictors of infarct size and cardiac function in the era of primary PCI for AMI. A single measurement of circulating troponin I at 72 hours can provide an effective and convenient indicator of infarct size and LVEF in clinical practice. Correlation of cardiac biomarkers with Day 5 SPECT determined infarct size and LVEF

Activation of the Nitric Oxide Pathway and Acute Myocardial Infarction Complicated by Acute Kidney Injury

2020 ◽  
Vol 10 (2) ◽  
pp. 85-96 ◽  
Author(s):  
Jiri Parenica ◽  
Petr Kala ◽  
Alexandre Mebazaa ◽  
Simona Littnerova ◽  
Klara Benesova ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Myocardial Infarction ◽  
Acute Kidney Injury ◽  
Uric Acid ◽  
Predictive Value ◽  
Kidney Injury ◽  
Cardiac Biomarkers ◽  
Receiver Operating Curve ◽  
Circulating Biomarkers ◽  
Clinical Model

Background/Aims: The pathophysiology of acute kidney injury (AKI) in ST-elevation myocardial infarction (STEMI) patients remains poorly explored. The involvement of the nitric oxide (NO) pathway has been demonstrated in experimental ischemic AKI. The aim of this study was to assess the predictive value of circulating biomarkers of the NO pathway for AKI in STEMI patients. Methods: Four hundred and twenty-seven STEMI patients treated with primary percutaneous coronary intervention were included. The primary end point was AKI. Biomarkers of the NO pathway (plasma superoxide dismutase [SOD], uric acid, nitrite/nitrate [NOx], neopterin) as well as cardiac biomarkers (B-type natriuretic peptide [BNP] and troponin) were sampled 12 h after admission. The predictive value of circulating biomarkers was evaluated in addition to the multivariate clinical model. Results: AKI developed in 8.9% of patients. The 3-month mortality was significantly higher in patients with AKI (34.2 vs. 4.1%; p < 0.001). SOD, uric acid, NOx, neopterin, BNP and troponin were significantly associated with the development of AKI (area under curve [AUC]-receiver operating curve [ROC] ranging between 0.70 and 0.81). In multivariate analysis cardiogenic shock, neopterin, NOx and troponin were independent predictors of AKI. AUC-ROC of the association of multibiomarkers and clinical model was 0.90 and outperformed the predictive value of the clinical model alone. OR of NOx ≥45 µmol/L was 8.0 (95% CI 3.1–20.6) for AKI. Conclusion: Biomarkers of the NO pathway are associated with the development of AKI in STEMI patients. These results provide insights into the pathophysiology of AKI and may serve at developing preventing strategies for AKI targeting this pathway.

Long-term prognostic value of late gadolinium enhancement and periprocedural myocardial infarction after uncomplicated revascularization: MASS-V follow-up

2020 ◽  
Author(s):  
Jaime Linhares-Filho ◽  
Whady Hueb ◽  
Eduardo Lima ◽  
Paulo Rezende ◽  
Diogo Azevedo ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Primary Endpoint ◽  
Prognostic Value ◽  
Independent Predictor ◽  
Cardiac Biomarkers ◽  
Gadolinium Enhancement ◽  
Periprocedural Myocardial Infarction ◽  
Lge Cmr

Abstract Aims Cardiac biomarkers elevation is common after revascularization, even in absence of periprocedural myocardial infarction (PMI) detection by imaging methods. Thus, late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) may be useful on PMI diagnosis and prognosis. We sought to evaluate long-term prognostic value of PMI and new LGE after revascularization. Methods and results Two hundred and two patients with multivessel coronary disease and preserved ventricular function who underwent elective revascularization were included, of whom 136 (67.3%) underwent coronary artery bypass grafting and 66 (32.7%) percutaneous coronary intervention. The median follow-up was 5 years (4.8–5.8 years). Cardiac biomarkers measurement and LGE-CMR were performed before and after procedures. The Society for Cardiovascular Angiography and Interventions definition was used to assess PMI. Primary endpoint was composed of death, infarction, additional revascularization, or cardiac hospitalization. Primary endpoint was observed in 29 (14.3%) patients, of whom 13 (14.9%) had PMI and 16 (13.9%) did not (P = 0.93). Thirty-six (17.8%) patients had new LGE. Twenty (12.0%) events occurred in patients without new LGE and 9 (25.2%) in patients with it (P = 0.045). LGE was also associated to increased mortality, with 4 (2.4%) and 4 (11.1%) deaths in subjects without and with it (P = 0.02). LGE was the only independent predictor of primary endpoint and mortality (P = 0.03 and P = 0.02). Median LGE mass was estimated at 4.6 g. Patients with new LGE had a greater biomarkers release (median troponin: 8.9 ng/mL vs. 1.8 ng/mL and median creatine kinase-MB: 38.0 ng/mL vs. 12.3 ng/mL; P &lt; 0.001 in both comparisons). Conclusions New LGE was shown to be better prognostic predictor than biomarker-only PMI definition after uncomplicated revascularization. Furthermore, new LGE was the only independent predictor of cardiovascular events and mortality. Clinical trial registration http://www.controlled-trials.com/ISRCTN09454308.

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