This is part two of a three-part series to answer the question, “it is acceptable to order a single troponin in an elderly patient with dizziness, weakness, or a similarly vague anginal equivalent?” So far, we understand that troponin testing can be tricky, and while it’s common clinical practice to order a single troponin, only serial troponins are truly evidence-based in the risk stratification of ACS. Next, let’s take a look at the significance of anginal equivalents.
[spacer height=”20px”]
[spacer height=”20px”]
“Anginal equivalents” is catch-all term for atypical symptoms of myocardial ischemia. These include shortness of breath, weakness, nausea, syncope, and essentially any other presentation of an ACS patient other than classic anginal chest pain (constant pressure-like chest pain not affected by movement or respiration).
[spacer height=”20px”]
This is a confusing concept for several reasons. First of all, there is no clear consensus on what collection of symptoms comprise anginal equivalents, to what extent they predict or correlate with acute MI, what characterizes patients who experience atypical symptoms, or how the absence of chest pain affects clinical outcomes. Secondly, some groups (such as the WHO) still require the presence of angina to diagnose acute MI, which is contradictory to studies showing that up to 30% of patients with ACS do not experience ischemic chest pain.
[spacer height=”20px”]
A large multi-center study of over 10,000 patients (Coronado et al, 2004) attempted to address some of these issues by examining atypical presentations of acute MI more closely. They found that patients older than 65, women, diabetics, and those with prior infarctions were more likely to have painless presentations of ACS. Most importantly, they found that ACS patients with anginal equivalents are more likely to have poor hospital outcomes compared to patients who present with angina. Among other factors, ED physicians were significantly more likely to admit patients with angina to the ICU, compared to patients with anginal equivalents. The authors theorized that the latter may have worse outcomes due to late detection of acute MI or suboptimal treatment after hospital admission, and not simply due to the fact that these patients had preexisting multiple co-morbidities. This echoed the findings from other large studies in JAMA and Chest (Canto, 2000 and Brieger, 2004), which showed that patients without chest pain on presentation represented a surprisingly large segment of the acute MI population (especially the elderly segment), and were at increased risk of under-treatment and higher in-hospital mortality.
[spacer height=”20px”]
Another interesting finding from these studies is that patients with CHF are significantly more likely to experience painless acute MI, particularly if they are older than 40 years of age. This doesn’t seem to be because CHF predisposes patients to painless MI; rather, it seems that painless MIs predispose patients to CHF exacerbations once myocardial perfusion becomes sufficiently compromised. That is, CHF patients can deteriorate very quickly in the setting of acute MI, without necessarily presenting with or developing chest pain. In fact, painless shortness of breath is one of the most common presentations of acute MI in CHF patients.
[spacer height=”20px”]
This all goes to suggest that elderly patients with anginal equivalents, particularly those with painless shortness of breath, should be evaluated carefully and ACS should not be ruled out lightly. Syncope and weakness are close seconds for atypical presentations, and should also be treated carefully in the elderly population. Because of this, it may be prudent to obtain serial troponins on all these patients, particularly if there is no other clear explanation for their symptoms.
[spacer height=”20px”]
So far, it seems that serial troponins are the way to go, even if our elderly patients don’t present with typical chest pain symptoms. In fact, we may want to be even more vigilant when it comes to anginal equivalents. Is there any evidence to the contrary, or any basis for the single troponin in atypical chest pain? Stay tuned for Part Three…
[spacer height=”20px”]

1. Coronado BE1, Pope JH, Griffith JL, Beshansky JR, Selker HP. Clinical features, triage, and outcome of patients presenting to the ED with suspected acute coronarysyndromes but without pain: a multicenter study. Am J Emerg Med. 2004 Nov;22(7):568-74.

2. Canto JG, Shlipak MG, Rogers WJ, et al. Prevalence, Clinical Characteristics, and Mortality Among Patients With Myocardial Infarction Presenting Without Chest Pain. JAMA. 2000;283(24):3223-3229.
3. Brieger D, Eagle KA, Goodman SG, et al. Acute Coronary Syndromes Without Chest Pain, An Underdiagnosed And Undertreated High-Risk Group*: Insights From The Global Registry Of Acute Coronary Events. Chest. 2004;126(2):461-469.
June 2024