scholarly journals The assessment of acute chest pain in New Zealand rural hospitals utilising point-of-care troponin

2018 ◽  
Vol 10 (1) ◽  
pp. 90 ◽  
Author(s):  
Rory Miller ◽  
Garry Nixon
Keyword(s):  
New Zealand ◽  
Chest Pain ◽  
Point Of Care ◽  
Acute Chest Pain ◽  
Rural Hospitals

scholarly journals Study protocol for an observational study to evaluate an accelerated chest pain pathway using point-of-care troponin in New Zealand rural and primary care populations

2020 ◽  
Vol 12 (2) ◽  
pp. 129
Author(s):  
Rory Miller ◽  
Joanna Young ◽  
Garry Nixon ◽  
John W. Pickering ◽  
Tim Stokes ◽  
...  
Keyword(s):  
General Practice ◽  
New Zealand ◽  
Chest Pain ◽  
Point Of Care ◽  
Rural Hospitals ◽  
Low Risk ◽  
Rural Settings ◽  
Pain Pathway ◽  
Risk Patients ◽  
General Practices

ABSTRACT INTRODUCTIONAccelerated diagnostic chest pain pathways are used widely in urban New Zealand hospitals. These pathways use laboratory-based troponin assays with good analytical precision. Widespread implementation has not occurred in many of New Zealand’s rural hospitals and general practices as they are reliant on point-of-care troponin assays, which are less sensitive and precise. An accelerated chest pain pathway using point-of-care troponin has been adapted for use in rural settings. A pilot study in a low-risk rural population showed no major adverse cardiac events at 30 days. A larger study is required to be confident that the pathway is safe. AIMSTo assess the safety and effectiveness of an accelerated chest pain pathway adapted for rural settings and general practice using point-of-care troponin to identify low-risk patients and allow early discharge. METHODSThis is a prospective observational study of an accelerated chest pain pathway using point-of-care troponin in rural hospitals and general practices in New Zealand. A total of 1000 patients, of whom we estimate 400 will be low risk, will be enrolled in the study. OUTCOME MEASURESThe primary outcome is the proportion of patients identified by the pathway as low risk for a 30-day major adverse cardiac event. Secondary outcomes include the proportion of low-risk patients who were discharged directly from general practice or rural hospitals, the proportion of patients reclassified as having acute myocardial infarction by the pathway and the proportion of patients with low and intermediate risk safely managed in the rural hospital.

scholarly journals Pericarditis masking a localised thoracic aorta dissection: Making a point for point-of-care ultrasound

2020 ◽  
pp. 201010582097866
Author(s):  
Raja Ezman Raja Shariff ◽  
Ahmad Farook ◽  
Chiao Wen Lim ◽  
Sazzli Kasim
Keyword(s):  
Chest Pain ◽  
Aortic Root ◽  
Point Of Care ◽  
Acute Chest Pain ◽  
High Sensitivity ◽  
Sudden Onset ◽  
Initial Assessment ◽  
Point Of Care Ultrasound ◽  
Persistent Symptoms ◽  
Start Up

Early detection of aortic dissection (AD) remains essential due to high mortality rates. We report a case of localised thoracic AD initially misdiagnosed as pericarditis, but subsequently diagnosed through point-of-care ultrasound (POCUS). A 35-year-old gentleman presented with sudden-onset jaw and chest pain. An initial electrocardiogram revealed changes consistent with pericarditis, and high-sensitive troponin levels on admission were not raised. An initial diagnosis of pericarditis was made. However, due to persistent symptoms despite treatment, an urgent POCUS was performed, revealing a prominently dilated aortic root, with evidence of an intimal flap near the coronary cusps. Computed tomography imaging revealed a focal aortic root dissection confined within the sinus of Valsalva, with no involvement of coronary arteries or descending thoracic or abdominal aorta. This case highlights how commonly a misdiagnosis of AD can occur and how concurrent pericarditis can often mask AD. Our report highlights the need for better incorporation of POCUS in the initial assessment of acute chest pain, as studies have shown both high sensitivity and specificity in diagnosing AD, with no additional burden on treatment start-up time and mortality.

scholarly journals Evaluation of a Rapid Whole Blood ELISA for Quantification of Troponin I in Patients with Acute Chest Pain

1999 ◽  
Vol 45 (10) ◽  
pp. 1789-1796 ◽  
Author(s):  
Christopher Heeschen ◽  
Britta U Goldmann ◽  
Lukas Langenbrink ◽  
Guido Matschuck ◽  
Christian W Hamm
Keyword(s):  
Chest Pain ◽  
Whole Blood ◽  
Troponin I ◽  
Point Of Care ◽  
Acute Chest Pain ◽  
Test System ◽  
Healthy Population ◽  
Roc Curve Analysis ◽  
Prognostic Information ◽  
Point Of Care Test

Abstract Background: Troponin I (cTnI) provides important prognostic information in patients with chest pain. We wished to evaluate a rapid, whole-blood analyzer for quantitative point-of-care testing. Methods: A quantitative point-of-care test system (Stratus CS®; Dade-Behring) for cTnI with an incorporated centrifuge was evaluated in 412 patients with chest pain less than 12 h. Results: Results were available within 15 min. CVs were 4.5% at 0.1 μg/L, 4.2% at 0.25 μg/L, and 6.5% at 0.82 μg/L. The detection limit was 0.01 μg/L. The 97.5% percentile in a healthy population was 0.08 μg/L. Based on ROC curve analysis, a threshold of 0.15 μg/L was calculated for the detection of acute myocardial infarction (AMI). With it, sensitivity for the detection of patients with AMI (n = 62) was 63% at arrival and 98% after 4 h (Stratus II®, 48% and 85%, respectively; P <0.01). In 42% of patients with unstable angina (n = 121), cTnI was ≥0.08 μg/L (Stratus II, 28%; P <0.01). During 30 days, death or AMI occurred in 25.5% of these cTnI-positive vs 2.9% of cTnI-negative patients (Stratus II, 29.4% vs 5.8%). Conclusion: The Stratus CS provided better analytical performance and comparable or better prognostic information than the Stratus II.

scholarly journals Soluble urokinase plasminogen activator receptor (suPAR) predicts 2-year cardiovascular events in patients after acute chest pain

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J Chew-Harris ◽  
S Appleby ◽  
R.W Troughton ◽  
A.M Richards ◽  
C.J Pemberton
Keyword(s):  
Heart Failure ◽  
Logistic Regression ◽  
New Zealand ◽  
Chest Pain ◽  
Plasminogen Activator ◽  
Acute Chest Pain ◽  
Funding Source ◽  
Urokinase Plasminogen Activator Receptor ◽  
Prognostic Performance ◽  
Plasminogen Activator Receptor

Abstract Background Soluble urokinase plasminogen activator receptor (suPAR) is an emerging biomarker of sub-inflammation related to plaque instability. Its modulation may reflect on immune dysfunction related to cardiovascular (CVD) outcomes. We assessed the prognostic performance of suPAR to predict 2-year clinical outcomes in patients with acute chest pain, suspicious of acute coronary syndromes. Methods A total of 812 patients presenting to the emergency department with the primary complaint of acute chest pain were prospectively recruited. Baseline suPAR concentrations were measured at presentation using the ViroGates CE-marked ELISA. Standard cardiac markers including hsTnT and NT-proBNP (both Roche) were also measured. Data for all biomarkers were treated as continuous and expressed as median [interquartile range (IQR)]. Statistical assessment was made using SPSS v25 (IBM). Groups were compared by Mann-Whitney U test/Spearman's rho. Prognostic performance of suPAR in comparison with hsTnT and NT-proBNP to predict the primary outcomes of new myocardial infarction (MI), new heart failure (HF), all cause readmission, and the composite of major adverse cardiac events (MACE) were assessed using binary logistic regression after the adjustment of traditional risk factors. Results In the entire chest pain cohort [median age: 63 yrs (IQR: 54–74), 34% female], 156/812 of patients had adjudicated AMI [STEMI (n=22)/NSTEMI (n=134)]. suPAR concentrations were found to be lower in males (Spearman's Rho, r=−0.17, P<0.0001) and in those with eGFR ≥60mL/min/1.73m2 (n=439) (r=−0.40, P<0.0001), but elevated in those older than 65 years (n=372) (r=0.55, P<0.0001). During the 2-year follow-up period, there were 54 fatalities, 287 recorded as having new CVD events, 46 diagnosed with new heart failure, 71 with new MI (66 NSTEMI/5 STEMI), 54 with new unstable angina, 126 patients classified with MACE and 190 patients who were readmitted into hospital within 1-year from presentation. In logistic regression analyses, the odds ratio (OR) of suPAR; 8.5 (95% CI:1.8–40.9) to predict a 2-year event (for example new total CVD events) was stronger than hsTnT; OR: 1.2 (95% CI: 0.9–1.5) and NT-proBNP; OR: 0.8 (95% CI:0.8–1.3) (P<0.0001) (Figure). Further, incorporation of baseline suPAR values into multivariate models for predicting events, such as MACE at 2-years (adjusted for age, gender and eGFR), resulted in an improvement in the C-statistic from 0.72 to 0.76. Conclusion In this acute chest pain cohort, suPAR concentrations are independent predictors of cardiovascular outcomes at 2 years. suPAR may add value in the risk assessment of patients with acute chest pain. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): Health Research Council of New Zealand, National Heart Foundation of New Zealand

P3408The signal peptide of CNP is a novel predictor of MI, MACE and bleeding risk in chest pain patients

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C J Pemberton ◽  
J A Lee ◽  
S Aldous ◽  
S Appleby ◽  
J Chew-Harris ◽  
...  
Keyword(s):  
New Zealand ◽  
Chest Pain ◽  
Signal Peptide ◽  
Predictive Ability ◽  
Acute Chest Pain ◽  
Bleeding Risk ◽  
Protective Role ◽  
Continuous Variables ◽  
St Depression ◽  
Health Research Council

Abstract Aim CNP is an important vascular and cardiac derived member of the natriuretic peptide family. We have previously provided the first reports that the signal peptide of CNP (CNPsp) is present in the human circulation and is elevated in those with chest pain suspicious of ACS. Here, show that CNPsp levels are highly predictive of new MI, MACE and post-index bleeding in patients presenting with potential ACS. Methods We prospectively recruited 493 patients presenting with the primary complaint of acute chest pain to our hospital ED. Patients were adjudicated as ACS by 2 independent cardiologists in accordance with ESC guidelines with hsTnI as biomarker. Plasma EDTA samples taken at presentation and 2 hours after were interrogated for CNPsp measurements using our validated, specific assay. Clinical data/variables, standard biochemistry analytes, hsTnT and NT-proBNP (both Roche Cobas e411) were also measured. Statistical assessments were made using SPSS v23. Data for all biomarkers were treated as continuous variables and are presented as median (interquartile range, (IQR)). Statistical assessment of the comparative abilities of CNPsp, hsTnT, NT-proBNP and hsTnI (log values) to predict new MACE, MI, bleeding and mortality within 2 yrs of index presentation was undertaken using a logistic regression base model (95% CI) that included all clinical variables and hsTnI and hsTnT and NT-proBNP, with CNPsp added to into the multivariate analyses. Results Of the 493 recruited patients (median age 63 (IQR: 54–73, 35% female), 148 were adjudicated to have ACS (30%, 109 MI, 39 UAP). Presentation CNPsp levels were not higher in those with adjudicated ACS versus non-ACS (51, (45–65) vs. 50, (42–63) pmol/L, P=0.412), did not correlate with hsTnI, hsTnT or NT-proBNP, but were significantly lower in those with a history of MI (49, (42–59) vs. 51, (43–64) pmol/L, P=0.044). In contrast, they were significantly higher in those with ECG ST-depression (56, (47–85) vs. 50 (42–62) pmol/L, P=0.038). In the multivariate regression model of all 493 patients, lower values of CNPsp were a significant multivariate predictor of new MI (n=37, 95% CI: 0.06–0.89, P=0.038), MACE (n=64, 95% CI: 0.08–0.81, P=0.020) and new bleeding (n=40, 95% CI: 0.05–0.63, P=0.005) within 2 years of presentation. This predictive ability was additive and independent from NT-proBNP and troponin. Conclusion This is the first report that CNPsp measurement provides meaningful and independent risk assessment of important outcomes in ACS patients. In particular, the fact that lower levels of CNPsp are predictive of negative MI, MACE and bleeding outcomes suggests that CNPsp may have an unappreciated protective role in the cardiovascular system. Acknowledgement/Funding Health Research Council of New Zealand; Heart Foundation of New Zealand

scholarly journals Biomarker Diagnostics in Acute Cardiac and Noncardiac Dyspnea: Is There a Role for Point-of-Care Testing?

2013 ◽  
Vol 2013 ◽  
pp. 1-4
Author(s):  
Dirk Peetz
Keyword(s):  
Chest Pain ◽  
Laboratory Testing ◽  
Limit Of Detection ◽  
Point Of Care ◽  
Acute Chest Pain ◽  
Central Laboratory ◽  
Point Of Care Testing ◽  
Test Quality ◽  
Relevant Effect ◽  
Few Data

The use of biomarkers in acute chest pain and dyspnea is well established and point-of-care testing (POCT) is increasingly used in emergency departments and chest pain units for this purpose. However, few data give evidence that POCT has advantages for the patient or the medical process over central laboratory testing. Especially for troponin testing in patients with myocardial infarction, the newest guidelines define prerequisites on diagnostic test quality which most POC assays do not fulfill. Additionally, no data are available showing that POCT has relevant effect on a change of physician’s diagnostic and therapeutic thinking compared to laboratory testing. Regarding patient outcomes and societal costs, central laboratory testing seems to be even superior to POCT. The main limit of currently available POC troponin assays is the higher limit of detection and higher imprecision compared to the new high sensitive laboratory assays. However, new upcoming POC technologies may perform comparable to today’s laboratory analyzers.

Rapid-access cardiology services: can these reduce the burden of acute chest pain on Australian and New Zealand health services?

2017 ◽  
Vol 47 (9) ◽  
pp. 986-991 ◽  
Author(s):  
Harry Klimis ◽  
Aravinda Thiagalingam ◽  
Mikhail Altman ◽  
Emily Atkins ◽  
Gemma Figtree ◽  
...  
Keyword(s):  
New Zealand ◽  
Chest Pain ◽  
Health Services ◽  
Acute Chest Pain ◽  
Rapid Access

Plasma Fibrinopeptide A and Beta-Thromboglobulin in Patients with Chest Pain

1983 ◽  
Vol 50 (02) ◽  
pp. 541-542 ◽  
Author(s):  
J T Douglas ◽  
G D O Lowe ◽  
C D Forbes ◽  
C R M Prentice
Keyword(s):  
Myocardial Infarction ◽  
Chest Pain ◽  
Unstable Angina ◽  
Plasma Levels ◽  
Thrombin Generation ◽  
Acute Chest Pain ◽  
Fibrinopeptide A ◽  
Control Hospital ◽  
Hospital Patients ◽  
Platelet Release

SummaryPlasma levels of β-thromboglobulin (BTG) and fibrinopeptide A (FPA), markers of platelet release and thrombin generation respectively, were measured in 48 patients within 3 days of admission to hospital for acute chest pain. Twenty-one patients had a confirmed myocardial infarction (MI); 15 had unstable angina without infarction; and 12 had chest pain due to noncardiac causes. FPA and BTG were also measured in 23 control hospital patients of similar age. Mean plasma BTG levels were not significantly different in the 4 groups. Mean plasma FPA levels were significantly higher in all 3 groups with acute chest pain when compared to the control subjects (p < 0.01), but there were no significant differences between the 3 groups. Increased FPA levels in patients with acute chest pain are not specific for myocardial infarction, nor for ischaemic chest pain.

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