Validating a High-Sensitivity Troponin I Assay in Your Lab

My name is Alan Wu, and I'm a Professor of Laboratory Medicine at the University of California at San Francisco, and I am the Coal Core Laboratory Director for the Zuckerberg San Francisco General Hospital. We plan on implementing the high-sensitivity troponin I test in two phases. The first phase is an analytical phase.

We need to be able to demonstrate that the assay works according to manufacturer's specifications in our hands. This will include precision, verification of the cut-off concentration, and determining what the linearity where the upper reportable reference ranges are. In the second phase, we intend on conducting a clinical evaluation where we have to engage with our stakeholders, the people who will be using our test, and interpreting results.

These include the individuals from the emergency department and cardiology. In my mind, it is exceptionally important for them to understand that the high-sensitivity troponin I assay will detect more patients who have cardiac injury as opposed to myocardial infarction, which is just really one of the causes that somebody might have an elevated troponin value for.

I think a lab that will be implementing a high-sensitivity assay needs to be mindful that the cut-off concentrations will be lower than the current generation assays. This will require the use of different quality control materials that have lower concentrations that challenge the 99th percentile cut-off.

It may also be necessary for clinical laboratories to consider adopting a sex-specific reference intervals. Males have higher troponin values than females when using the high-sensitivity troponin I assay. The use of sex-specific cut-off concentrations will enable a more accurate diagnosis of acute myocardial infarction when the high-sensitivity troponin I assay is used.

It's important for emergency department staff and cardiologists to recognize that the high-sensitivity troponin I assay is not just a marker of acute myocardial infarction. That it is in fact, a marker of minor myocardial damage. Therefore, we will see more cases of positive results in a non-AMI setting.

Patients who have heart failure, who have renal failure, pulmonary emboli will have increased concentrations of troponin, and they need to be considered as true positive indicators of myocardial damage and not a false positive indicator of acute myocardial infarction.

I think the key benefit of implementing a high-sensitivity troponin I assay is in an earlier rule-out of acute myocardial infarction than what we can do with the conventional assay. In addition, it may be possible to rule in acute myocardial infarction sooner with the use of a high-sensitivity troponin I assay.

Our emergency department is overcrowded with patients. If we can do a more efficient job at triaging patients to receive the proper level of care and to discharge the patients who do not need to stay in the emergency department, this will have a tremendous economic advantage for our healthcare system.

At the same time, it can improve the quality of medical care for the patients who do have a heart attack.