They’re countingon you.

Make sure you havethe biomarkers you need.

ED Visits for Influenza-like Illness Are Predictive of CVD Mortality1

ED Census Influences Triage Decision-making11

When They Have Trouble Breathing

Three For the Crowd

Patients commonly present to the emergency department (ED) with breathing difficulties.2
These signs and symptoms may reflect several respiratory and cardiac etiologies.3,4Patients with COVID-19 infection have been shown to present with a greater than 20%
incidence of dyspnea and a series of cardiovascular abnormalities.5,6

In the U.S., the demand for ED services has increased rapidly.12 Past influenza outbreaks
and the ongoing pandemic have created great challenges for emergency departments.
ED crowding has been shown to negatively impact patient outcomes, patient satisfaction,and patient safety.13-15 Increased ED occupancy has been found to be associated with morepatients classified as higher acuity and result in higher hospital admission rates.11

Influenza can also precipitate cardiac events. This is thought
to be due to a range of factors including inflammatory releaseof cytokines, disruption of atherosclerotic plaques, andthrombogenesis.7
ED visits for influenza-like illness have been associated withand predictive of cardiovascular disease (CVD) mortality.1
Older patients with influenza infection and those with prevalent
CVD risk factors, have been shown to be especially prone tomyocardial infarction.8,9 Influenza infection has also been associated with increased in-hospitalmorbidity and mortality in patients with heart failure (HF).10

With all this added pressure on the ED, it is now more important than ever to adopt efficiencies
which allow for a more rapid diagnosis.
Quidel’s Triage® array of tests provide important data to assist with an expedient diagnosis
and proper course of treatment.

When they have trouble breathing, it is important to rapidly determine the cause and identify
existing and potential sequelae whether cardiac or viral in origin.

Quidel Triage products are not indicated for use in testing for SARS-CoV-2 or influenza.

D-dimer Levels in COVID-19 and Influenza Patients Are Prognostic16,17

The Quidel Triage D-Dimer Test is a rapid, quantitative, immunoassay
to aid in assessing and evaluating patients with suspecteddisseminated intravascular coagulation and thromboembolic events
including pulmonary embolism (PE) and deep venous thrombosis (DVT).18

DVT and PE are associated with significant morbidity and mortality.19,20 The clinical diagnosis
can be difficult as signs and symptoms overlap with many other conditions including shortnessof breath.21
The fibrinolytic degradation products of cross-linked fibrin are D-dimers.22 A negative D-dimer
assay can be effectively used to exclude PE.23
Early predictors of clinical outcome in COVID-19 patients are needed and D-dimer has beenshown to effectively predict in-hospital mortality rates.16 Increased D-dimer levels are common
in influenza cases and have been associated with disease progression and prognostication.17

Knowing Troponin Levels Earlier Can Prevent Cardiac Damage.24,25

Troponin is the preferred biomarker for aiding in the diagnosis of acute myocardial infarction by
providing early detection to prevent myocardial injury and further cardiovascular damage.24,25
For patients with underlying CVD, viral illness can further damage myocardial cells throughseveral mechanisms including direct damage by the virus, systemic inflammatory responses,
destabilized coronary plaque, and aggravated hypoxia.26-28
The Quidel Triage Cardiac Panel is a fluorescence immunoassay to be used with the Quidel
Triage Meter for the quantitative determination of creatine kinase MB (CK-MB), myoglobin,
and troponin I in EDTA anticoagulated whole blood or plasma specimens.29
Point-of-care (POC) troponin testing has been shown to decrease patient length of stay, turnaround time, and potentially decrease overall costs.30

The Triage BNP Test Is Powerful31

BNP From the Beginning
A B-type natriuretic peptide (BNP) level on admission has been found to be an independentand powerful marker of early and late cardiac mortality in patients with acute chest pain without
ST-segment elevation. It is suggested that BNP be measured upon arrival at the ED.31

The Triage BNP Test Can Assist With a Rapid Rule Out32

Natriuretic peptide testing is now recommended for the prevention, diagnosis, and prognosis
of HF.33
The newest guideline recommends that the measurement of baseline levels of natriureticpeptide biomarkers and/or cardiac troponin on admission are useful in establishinga prognosis in acute decompensated heart failure.33
The evidence is strong. When you need to know, you need a BNP.

Mortality in Acute Coronary Syndrome (ACS) by BNP Level
1 Month30

1 YearMortality (%)

RR = 5.3,
P < 0.0000001
20RR = 13.0,
P < 0.00003

100

15.4.04
BNP > 101

2.9
BNP ≤ 101

BNP > 101

Cardiac mortality in patients with acute chest pain without ST-segment elevationaccording to the receiver-operating characteristic curve-generated best prognostic
BNP cut-off level (in pg/mL).
RR = relative risk

ClassLevel of Evidence

DiagnosisIA

Pre-discharge Risk Assessment

IIa

B-NRPrognosis

Prevent Onset of Heart Failure

IIIaA

B-R

NR = non randomized R = randomized

5.4

BNP ≤ 101

Indication

A single measurement of BNP in the ED is associatedwith greater diagnostic accuracy and its use
decreases time to discharge and cost of stay.34

The Quidel Triage BNP Test is a rapid, POC fluorescence immunoassay used with theQuidel Triage MeterPro. The test is used to measure BNP in EDTA anticoagulated whole bloodor plasma specimens. The Triage BNP Test is the first rapid BNP immunoassay indicated for risk
stratification for both ACS and HF.35

References
1. Nguyen JL, Yang W, Ito K, et al. Seasonal influenza infections and cardiovascular disease mortality. JAMA Cardiol.
2016;1(3):274-281.
2. Centers for Disease Control and Prevention. National Hospital Ambulatory Medical Care Survey: 2017 Emergency
Department Summary Tables. 2020. https://www.cdc.gov/nchs/data/nhamcs/web_tables/2017_ed_web_tables-508.pdf.
Accessed 29 July 2020.

18. Triage D-Dimer Test [package insert]. San Diego, CA: Quidel Cardiovascular Inc., 2018.
19. Anderson FA Jr, Wheeler HB, Goldberg RJ, et al. A population-based perspective of the hospital incidence andcase-fatality rates of deep vein thrombosis and pulmonary embolism. The Worcester DVT Study. Arch Intern Med.
1991;151(5):933-938.

3. Collins S, Storrow AB, Kirk JD, et al. Beyond pulmonary edema: diagnostic, risk stratification, and treatment challengesof acute heart failure management in the emergency department. Ann Emerg Med. 2008;51:45-57.

20. Ozaki A, Bartholomew JR. Venous thromboembolism (deep venous thrombosis & pulmonary embolism). December 2012.
http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/venous-thromboembolism/.
Accessed 29 July 2020.

4. Liteplo AS, Marill KA, Villen T, et al. Emergency thoracic ultrasound in the differentiation of the etiology of shortnessof breath (ETUDES): sonographic B-lines and N-terminal pro-brain-type natriuretic peptide in diagnosing congestive
heart failure. Acad Emerg Med. 2009;16:201-210.

21. Le Gal G, Righini M. Controversies in the diagnosis of venous thromboembolism. J Thromb Haemost. 2015;13(Suppl 1):S259-S265.

5. Li LQ, Huang T, Wang YQ, et al. COVID-19 patients’ clinical characteristics, discharge rate, and fatality rate of metaanalysis. J Med Virol. 2020;92(6):577-583.
6. Wu L, O’Kane A, Peng H, et al. SARS-CoV-2 and cardiovascular complications: from molecular mechanisms topharmaceutical management. Biochem Pharmacol. 2020;178:114114. https://www.sciencedirect.com/science/article/pii/S0006295220303506?via%3Dihub. Accessed 18 August 2020.

22. Kesieme E, Kesieme C, Jebbin N, et al. Deep vein thrombosis: a clinical review. J Blood Med. 2011;2:59-69.
23. Fesmire FM, Brown MD, Espinosa JA, et al. Critical issues in the evaluation and management of adult patients
presenting to the emergency department with suspected pulmonary embolism. Ann Emerg Med. 2011;57(6):628-652.
24. Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. Eur Heart J. 2012;33:2551-2567.

7. MacIntyre CR, Mahimbo A, Moa Am, et al. Influenza vaccine as a coronary intervention for prevention of myocardial
infarction. Heart. 2016;102(24):1953-1956.

25. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for the Management of Patients withNon-ST-Elevation Acute Coronary Syndromes: a Report of the American College of Cardiology/American Heart Association
Task Force on Practice Guidelines. J Am Coll Cardiol. 2014;64:e139-e228.

8. Ludwig A, Lucero-Obusan C, Schirmer P, et al. Acute cardiac injury events ≤30 days after laboratory-confirmed
influenza virus infection among U.S. veterans, 2010-2012. BMC Cardiovasc Disord. 2015;15:109.

26. Guo T, Fan Y, Chen M, et al. Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019
(COVID-19). JAMA Cardiol. 2020;5(7):1-8.

9. Barnes M, Heywood AE, Mahimbo A, et al. Acute myocardial infarction and influenza: a meta-analysis of case-control
studies. Heart. 2015;101(21):1738-1747.

27. Zheng YY, Ma YT, Zhang JY, et al. COVID-19 and the cardiovascular system. Nature Reviews Cardiology. 2020;5:1-2.

10. Panhwar MS, Kalra A, Gupta T, et al. Effect of influenza on outcomes in patients with heart failure. JACC Heart Fail.
2019;7(2):112-117.
11. Chen W, Linthicum B, Argon NT, et al. The effects of emergency department crowding on triage and hospital admission
decisions. Am J Emerg Med. 2020;38(4):774-779.
12. Bellow AA, Gillepsie GL. The evolution of ED crowding. J Emerg Nurs. 2014;40(2):153-160.
13. Pines JM, Hollander JE. Emergency department crowding is associated with poor care for patients with severe pain.
Ann Emerg Med. 2008;51(1):1-5.
14. Bursch B, Beezy J, Shaw R. Emergency department satisfaction: what matters most? Ann Emerg Med. 1993;22(3):586-591.
15. Trzeciak S, Rivers EP. Emergency department overcrowding in the United States: an emerging threat to patient safety
and public health. Emerg Med J. 2003;20(5):402-405.
16. Wang ZF, Su F, Lin XJ, et al. Serum D-dimer changes and prognostic implication in 2009 novel influenza A(H1N1).
Thromb Res. 2011;127(3):198-201.
17. Zhang L, Yan X, Fan Q, et al. D-dimer levels on admission to predict in-hospital mortality in patients with Covid-19.
Thromb Haemost. 2020;18(6):1324-1329.

28. American College of Cardiology. Troponin and BNP use in COVID-19. https://www.acc.org/latest-in-cardiology/
articles/2020/03/18/15/25/troponin-and-bnp-use-in-covid19. Accessed 17 August 2020.
29. Triage Cardiac Panel [package insert]. San Diego, CA: Quidel Cardiovascular Inc., 2018.
30. Koehler J, Flarity K, Hertner G, et al. Effect of troponin I point-of-care testing on emergency department throughput
measures and staff satisfaction. Adv Emerg Nurs J. 2013;35(3):270-277.
31. Bassan R, Tura BR, Maisel AS. B-type natriuretic peptide: a strong predictor of early and late mortality in patients withacute chest pain without ST-segment elevation in the emergency department. Coron Artery Dis. 2009;20(2):143-149.
32. Harrison A, Amundson S. Evaluation and management of the acutely dyspneic patient: the role of biomarkers.
Am J Emerg Med. 2005;23(3):371-378.
33. Yancy CW, Jessup M, Bozkurt B, et al. 2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for theManagement of Heart Failure: Report of the American College of Cardiology/American Heart Association Task Forceon Clinical Practice Guidelines and the Heart Failure Society of America. Circulation. 2017;136(6):e137-e161.
34. Mueller C, Scholler A, Laule-Kilian K. Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea.
N Engl J Med. 2004;350(7):647-654.
35. Triage BNP Test [package insert]. San Diego, CA: Quidel Cardiovascular Inc., 2018.

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