Biosite® Inc. Web Site -- Profiler Shortness of Breath

By: Alere  09-12-2011

Triage® Profiler Shortness of Breath Panel

The Triage® Profiler Shortness of Breath Panel provides rapid risk assessment and differential diagnosis of patients presenting to the emergency department with shortness of breath and risk assessment of patients with acute coronary syndromes. The Panel gives physicians the ability to distinguish between the many causes of shortness of breath in approximately 15 minutes. By evaluating the symptom, physicians are able to quickly, economically and effectively determine the appropriate care pathway. The Triage Profiler Shortness of Breath Panel is a new approach in diagnosis for physicians.

THE PANEL APPROACH
Symptom panels are diagnostics, employing multiple markers intended to help physicians determine the cause of a particular symptom that is common to a variety of diseases and conditions. The Triage Profiler Shortness of Breath Panel is a symptom panel that enables physicians to more efficiently diagnose shortness of breath patients, provide a better understanding of the event and reduce the time-to-diagnose.Differential diagnosis, or having the ability to rule out an ailment, is often equally as valuable to a physician as identifying an actual disease. With the Triage Profiler Shortness of Breath Panel, physicians can easily obtain the measurements of five markers without sacrificing accuracy. Troponin I, CK-MB, myoglobin, BNP and D-dimer each provide unique clinical information, and the panel approach maximizes the strengths of each marker.

DIAGNOSTIC CHALLENGES OF SHORTNESS OF BREATH
The challenge in diagnosing shortness of breath or dyspnea lies in the numerous potential causes. Heart failure and pulmonary embolism patients can present with the same nonspecific, overlapping symptom. Shortness of breath is a subjective symptom of a variety of different diseases and disorders, commonly associated with diseases of the heart or lungs.Shortness of breath is a common symptom and is one of the top 10 reasons patients visit hospital emergency departments in the United States.6 The time interval between the onset of shortness of breath and presentation to the emergency department is a challenging variable for physicians. Because no single marker can diagnose the cause of shortness of breath, a rapid, multi-marker strategy best overcomes this issue.

More than 4 million patients present to emergency departments in the U.S. with shortness of breath or dyspnea each year.6

ABOUT THE TRIAGE PROFILER SHORTNESS OF BREATH PANEL
The Triage Profiler Shortness of Breath Panel provides quantitative information on three primary cardiac necrosis markers, plus brain-type natriuretic peptide (BNP) and D-dimer. The test uses whole blood or plasma, and has built-in, lot-specific calibration and internal quality controls to ensure accuracy. The Triage Profiler Shortness of Breath Panel:

  • Allows for the rapid, simultaneous assessment of shortness of breath patients for acute coronary syndrome and heart failure.
  • Allows for the rapid assessment and evaluation of patients suspected of having disseminated intravascular coagulation and thromboembolic events including pulmonary embolism.

BENEFITS OF RAPID DIAGNOSIS

  • Rapid treatment decisions may lead to better outcomes and lower costs.
  • New treatments that require early administration are driving the need for early diagnosis.
  • By streamlining the diagnostic process, rapid testing may contribute to improved efficiency in emergency departments.
  • A better experience for the patient with fewer uncomfortable tests and a shorter time to wait.

THE POWER OF FIVE MARKERS

  • CK-MB the historical “gold standard” remains a frequently ordered marker. Its presence, however, is not specific to damaged heart muscle. CK-MB usually rises within the first four to six hours after AMI onset, but remains elevated for only a short period of time.
  • Myoglobin is not specific to the heart muscle, but is highly sensitive and has been shown to be useful in ruling-out AMI.1 It is the earliest marker to rise in cases of AMI (<2 hours) and also usually drops first. Myoglobin is under-utilized in the U.S., but is used more frequently in Europe.
  • Troponin I and troponin I complexes are highly specific to the heart muscle and has recently emerged as a valued marker with widespread acceptance. Troponin is currently the most frequently ordered marker. It is not an “early” marker but stays elevated longer than other markers. Because troponin stays in a patient’s system for up to one week, it is also useful for retrospective diagnosis of AMI. Elevated Troponin I levels also convey prognostic information and have been shown to identify patients with increased risk of death.
  • BNP is a naturally occurring protein in the body, that when elevated is an indicator of congestive heart failure. When the heart is unable to pump blood efficiently, BNP is produced to ease its workload. Testing BNP levels aids in the diagnosis and assessment of heart failure severity, and risk stratification in patients with acute coronary syndromes. Research suggests that BNP has a number of physiologic effects, which work in concert on the vessels, heart and kidney to decrease the fluid load on the heart, thus allowing the heart to function better, improving cardiac performance.
  • D-dimer is a protein arising directly from the body’s natural mechanism to break down blood clots. Elevated levels of D-dimer in a patient’s blood are indicative of abnormal rates of clotting. Published studies suggest the absence of circulating D-dimer can aid in the diagnosis of disseminated intravascular coagulation and thromboembolic events including pulmonary embolism (PE).

THE CHALLENGES OF PULMONARY EMBOLISM

  • Approximately 60% of patients who die in the hospital have PE; the diagnosis is missed in 70% of cases.5
  • Approximately 10% of patients in whom acute PE is diagnosed die within the first 60 minutes.5

THE IMPACT OF AMI

  • In 2004, the estimated direct and indirect cost of coronary heart disease in the United States is $133.2 billion. Of this, $66.3 billion is for direct medical costs.2
  • Coronary Heart Disease is the No. 1 killer of both men and women in the United States. In 2003, more than 500,000 Americans died of heart attacks caused by CHD.6

THE TOLL OF HEART FAILURE

  • In 2004, the estimated direct and indirect cost of CHF in the United States will be $28.8 billion.3
  • CHF affected more than 15 million people worldwide in 2001, and approximately 4.8 million in the United States alone.1
  • About 4.9 million new cases of CHF were diagnosed in the United States in 2001, and CHF contributes to 287,000 deaths each year.1

1McCord J, Nowak, et al. Ninety-minute exclusion of acute myocardial infarction by use of quantitative point-of-care testing of myoglobin and troponin I. Circulation. 2001; 104:1483-1488
22004 Heart and Stroke Statistical Update: American Heart Association
32002 Heart and Stroke Statistical Update: American Heart Association
4Mayo Foundation for Medical Education and Research [MFMER], 2003
5Feied C, Handler JA. Pulmonary Embolism. Available at:
6National Hospital Ambulatory Medical Survey: 2001 Emergency Dept. Summary, June 2003

The information in this article was current at 06 Dec 2011


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