By Dr. Payal Kohli, MD, FACC
It was a Saturday morning at a hospital in San Francisco during my final year of cardiology fellowship. With the backdrop of one of the most stunning vistas in San Francisco, I sat down to complete my least favorite task of the day: the "troponin rounds." The troponin rounds were hardly rounds in the traditional sense of standing at a patient's bedside—they involved sitting at a computer and reviewing the chart of every single patient seen in the hospital, admitted or discharged, who had a positive troponin value or elevated troponin in the past 24 hours.
Once a patient's ECG, clinical history, and other chart specifics were reviewed, it was determined whether a formal cardiology consultation was warranted for the troponin elevation. In the majority of cases, the troponin was nonspecifically elevated due to a type 2 NSTEMI (a supply-demand mismatch event) rather than a type 1 NSTEMI tied to a plaque rupture.
When I did the troponin rounds, it was clear to me that the use of troponin is such a sensitive marker for myocardial injury that, paradoxically, it's an incredibly insensitive marker for myocardial infarction. The advent of high-sensitivity troponin tests has miraculously streamlined the work-up of chest pain in the emergency room. These assays have been developed to improve detection of MI, and because they are able to pick up much lower concentrations of troponin, they have shortened the interval to detection of myocardial injury. However, as the University of Michigan notes, because of their increased sensitivity, up to 50 percent of patients can have detectable levels of hs-troponin without having an acute coronary syndrome.1
What are Normal Troponin Levels? Context is Everything
A clinical conundrum occurs when troponin is nonspecifically elevated, and there is a long list of conditions that can elevate hs-troponin in the absence of an acute coronary syndrome, including:
- Anemia
- Ventricular tachycardia
- Heart failure
- Kidney disease
- Hypotension/shock
- Pulmonary embolism
- Myocarditis
- Hypoxemia
Therefore, the clinical context of elevated troponin is critical to interpreting the results. That's where ECG becomes so important, as it can help establish the diagnostic and prognostic context of a troponin elevation. In fact, guidelines on the fourth universal definition of MI include new ischemic ECG changes as additional criteria needed for an MI diagnosis.2
Using this simple bedside tool should be the first step in triaging the clinical presentation of chest pain, which could range from an acute coronary syndrome to musculoskeletal pain. For this reason, it's no surprise that many emergency rooms obtain the ECG first, within a few minutes of presentation, long before the troponin is drawn. Although hs-troponin has increased the sensitivity for detection of even low levels of myocardial injury, biomarkers of myocardial damage can lag behind ECG changes suggestive of ischemia. This discrepancy is why many emergency room protocols assess serial levels of biomarkers.
ECG and Troponin: Clinical and Prognostic Implications
The combination of ECG and troponin level testing is valuable for risk stratification in the first six hours of presentation. In multivariate analysis, both ST segment monitoring and troponin T were independent predictors of cardiac death or MI.3 When ECG results and troponin levels are used together, patients can be divided into low-, intermediate-, or high-risk groups.
Following the evolution of troponin levels and ECG results over time can also provide important information regarding the disease course. I remember the case of one STEMI patient who presented with troponin values far above the upper limit of detection. He was quickly revascularized with resolution of his chest pain. However, once his troponin was so substantially elevated due to myocardial injury, following troponins serially over time was no longer clinically useful.
On the other hand, later serial ECGs in this patient after revascularization provided useful information about his clinical presentation. When his ST-segments nearly normalized following revascularization and then elevated again one day later in the setting of chest pain, his in-stent thrombosis was quickly diagnosed using the ECG. The troponin had started to come down, but it remained significantly elevated and therefore lacked diagnostic utility so soon after an MI. The ECG evolution following an acute MI, on the other hand, can provide clinical as well as prognostic information.4
As I look back on all of the Saturday mornings when I did the troponin rounds, it's clear that the ECG was one of the most important parts of the patient charts I reviewed for determining the clinical context of troponin elevation and how to address each patient's myocardial injury. Even now, in my day-to-day practice as a noninvasive cardiologist, when a patient presents with chest pain, my first question is always, "can I take a look at the ECG?"
References:
1. High-sensitivity troponin T: What you need to know. Michigan Medicine. https://www.med.umich.edu/clinical/Troponin%20T%20Assay%20Educational%20Presentation.pdf. Last accessed August 2021.
2. Thygesen K et al. Fourth universal definition of myocardial infarction (2018). Journal of the American College of Cardiology. Oct 2018; vol. 72 (iss.18): 2231-2264. https://pubmed.ncbi.nlm.nih.gov/30153967/.
3. Jernberg J et al. The combination of a continuous 12-lead ECG and troponin T; a valuable tool for risk stratification during the first 6 hours in patients with chest pain and a non-diagnostic ECG. European Heart Journal. Sept 2000; vol. 21 (iss. 17): 1464-1472. https://academic.oup.com/eurheartj/article/21/17/1464/478743.
4. Nable J V and Brady W. The evolution of electrocardiographic changes in ST-segment elevation myocardial infarction. American Journal of Emergency Medicine. Jul 2009; vol. 27 (iss. 6): 734-746. https://pubmed.ncbi.nlm.nih.gov/19751632/.
Dr. Payal Kohli, MD, FACC is a top graduate of MIT and Harvard Medical School (magna cum laude) and, as a practicing noninvasive cardiologist, is the managing partner of Cherry Creek Heart in Denver, Colorado.
The opinions, beliefs and viewpoints expressed in this article are solely those of the author and do not necessarily reflect the opinions, beliefs and viewpoints of GE Healthcare. The author is a paid consultant for GE Healthcare and was compensated for creation of this article.
