An ST-segment myocardial infarction is diagnosed when 1 mm or more of ST-segment elevation is present in two or more contiguous leads, or 2 mm in one lead, except for V1–V2. However, there are several different ECG presentations where the patient may not have the classic ST-segment elevation in two or more contiguous leads with reciprocal changes seen on the 12-lead ECG. These are the patterns we call STEMI equivalents, and we should treat them in the same manner as we would a STEMI.
EMS providers play an invaluable role in the early management of STEMI patients. EMS crews provide early recognition of STEMI, transmit the ECG to a PCI center, activate the cardiac catheterization lab, and expedite patients’ triage, transport, and ultimately timely treatment.1 According to the American Heart Association, delivering the patient with STEMI-related chest pain to a PCI center within 90 minutes of first medical contact is a Class I (its strongest level of evidentiary support) intervention.
The first of the STEMI equivalents is a specific ECG pattern known as de Winter T-waves. It indicates a possible left anterior descending coronary artery (LAD) occlusion.2 In this pattern the morphology presents with a concave upward sloping of a least 1 mm in the depressed ST segment. It starts at the J-point with uniform tall and remarkable T-waves, normally in leads V1–V4; however, they can be present in V5 and V6 as well.2 Notably, with this pattern there is no ST-segment elevation in the concomitant leads. However, they may develop later with serial ECGs.
The significance of the de Winter T-wave pattern is that it provides evidence of an obstruction of flow to the left anterior descending coronary artery.3 This pattern may not present as often as other STEMI patterns, as it is only present in about 2% of proximal LAD occlusions.2,3
Wellens syndrome is identified by a gradually evolving deep, developed T-wave inversion in leads V1–V4. T-waves that are deep, wide, and inverted are consistent with myocardial ischemia. Angiographic studies on patients with Wellens syndrome found 20% of them had 100% occlusion of the LAD with collateral flow present.4 It is believed 75% will progress to having an AMI within one week of identification if not treated.4
Normal progression of the R-wave will remain to be seen with these patients.4 Anterior wall myocardial infarcts will result in loss of developing R-waves; that means Wellens syndrome is not present and the patient has progressed to complete anterior wall vessel occlusion.4
Isolated ST-segment depression of at least 0.5 mm in leads V1–V3 is the primary observational finding of an AMI within the inferior and basal portion of the heart, often coinciding with the left circumflex region.1 The depression in this area can occur due to right coronary artery occlusions, reflecting ischemia in the location being provided by the diseased artery.5 Place chest leads posteriorly V7–V9, and ST-segment elevation of 0.5 mm or more, when detected, is consistent with inferior and basal wall myocardial infarction.1 Treat these ECG findings as a STEMI.
ST-segment depression of 1 mm or more on eight surface leads, combined with ST-segment elevation of at least 1 mm in aVR and/or V1, indicates an obstructed left main coronary artery, or three-vessel disease.1 ST-segment depression is a sign of myocardial ischemia resulting in insufficient blood flow to the coronary circulation. Lead aVR reflects the electrical activity from the right upper portion of the myocardium, which includes right ventricular outflow, along with the basal portion of the intraventricular septum.6 The basal septum’s blood supply comes from the first perforator artery, located in the very proximal branch of the LAD. Involvement of the basal septum by ischemia or infarct would involve the proximal LAD or left main circumflex artery.6 ST-segment elevation in aVR will have reciprocal ST-depression changes in leads I, II, aVL, V4, V5, and V6 because they are electrically opposite, being left-side leads. An ST-segment elevation in aVR that’s greater than that in V1 can distinguish LMCA from LAD occlusion.6
When a ventricle becomes hypertrophied, the result is a thickened myocardium, potentially causing a reduction in cardiac blood supply. This can cause the subendocardial surface wall to become ischemic. Subendocardial ischemia in this case will produce changes to the ST segment and T-waves to appear in a strain pattern.7 Recognize a strain pattern by the downward-sloped ST segment accompanied by asymmetrical inversion of the T-wave.7 Subendocardial non-Q-wave infarcts are also classified as non-ST-segment elevation myocardial infarcts (NSTEMIs). This means the damage is limited within the subendocardial region. Treat these as STEMI equivalents because myocardial damage can be minimized with early intervention.
Prinzmetal’s angina occurs without exertion or even while at rest, usually at night or in the early morning. It is caused by coronary vessel spasms with reduction in vessel lumen size, characteristically seen within a single diseased vessel but possible in the normal vessel. ST-segment elevation will be present on the 12-lead during these episodes of pain but will subside when the patient is pain-free.8
Angina in this case is the direct result of an insufficient oxygen supply that does not supersede demand. Since the oxygen supply is not being entirely interrupted by cessation of flow, the underlying cardiac muscle will not suffer tissue death.9 Narrowing of these coronary vessels makes the arteries more vulnerable to complete occlusion when plaque ruptures and a thrombus develops.9 This is an ominous sign of increased coronary artery disease, placing the patient at higher risk for myocardial infarction. Life-threatening arrythmias can occur when the vessel spasm occurs to the epicardial surface of the affected left ventricle.8
Notable ST-segment depression in the anteroseptal leads, with accompanying tall R-waves and upright T-waves in leads V1–V3, indicates a true posterior wall myocardial infarction.7 The ST depression here will be the reciprocal changes on the opposite-facing leads from where a STEMI is occurring.5 Full-thickness myocardial infarction is related, with partial depolarization of the ischemic location and ST-segment elevation in the leads superimposing the area being affected.5 Placement of leads on the posterior side V7–V9 will confirm the diagnosis, and ST-segment elevation will be noted here.7 This ECG presentation is a true STEMI, not just an equivalent, but without further examination will not likely be discovered until a great deal of myocardial damage has occurred.
These STEMI equivalents can occur in patients with active, intermittent, or no chest pain at all. Observation of these patterns may come from a routine evaluation where the 12-lead was obtained for some other presenting symptom.
Symptoms such as unexplained dyspnea, weakness, nausea, or indigestion can be enough for practitioners to evaluate things a little more in depth and obtain an ECG tracing. Diabetics, women, and the elderly can also present with vague symptoms or other forms of atypical pain that would warrant obtaining one.
1. Ibanez B, James S, Agewall S, et al; ESC Scientific Document Group. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The task force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology. Eur Heart J, 2018 Jan 7; 39(2): 119–77.
2. De Winter RJ, Verouden NJ, Wellens HJ, Wilde AA; Interventional Cardiology Group of the Academic Medical Center. A new ECG sign of proximal LAD occlusion. N Engl J Med, 2008 Nov 6; 359(19): 2,071–3.
4. Geiter HB Jr. Critical Care: Wellens’ syndrome subtle clues to big trouble. Nursing2020, 2004 Jun; 34(6): 32cc1–32cc4.
5. Vaidya GN, Antoine S, Imam SH, et al. Reciprocal ST-segment changes in myocardial infarction: Ischemia at distance versus mirror reflection of ST-elevation. Am J Med Sci, 2018 Feb; 355(2): 162–7.
6. Kossaify A. ST segment elevation in aVR: clinical significance in acute coronary syndrome. Clin Med Insights Case Rep, 2013; 6: 41–5.
7. American Academy of Orthopaedic Surgeons. Critical Care Transport. Jones & Bartlett, 2017.
8. Keller KB, Lemberg L. Prinzmetal’s angina. Am J Crit Care, 2004 Jul; 13(4): 350–4.
9. Shaban R. Paramedic field care: A complaint-based approach. Austral J Paramed, 2004; 2(3): 401–17.
Roger L. Layell, FP-C, CCP-C, CCEMT-P, NRP is a flight and critical care paramedic at Wake Forest Baptist Health AirCare in Winston-Salem, N.C. He has 15 years of experience in the field as a paramedic and 10 of critical care experience in the HEMS environment.