Case:
A 40-year-old woman with a history of CAD and prior RCA stent presents to the emergency department with chest pain for one day. Her triage vitals are BP 100/60, HR 60, T 98.7, RR 20, O2 99%. You examine that patient, noticing her holding her chest in pain with diaphoresis. The technician brings you the following ECG:
The ECG does not meet “STEMI” criteria however you are concerned that there may be an occlusion myocardial infarction (OMI) based on the patient’s history and exam, and call your cardiologist. Upon hearing the case the fellow asks “what does the echo show?” Puzzled, you admit you haven’t performed a bedside ultrasound, but think to yourself “will this change management?”
When to assess regional wall motion abnormalities in the ED?
2011 society guidelines report it is appropriate to use transthoracic echocardiogram (TTE) for “acute chest pain with suspected MI and non-diagnostic ECG when a resting echocardiogram can be performed during pain.” [1]. Examples listed of difficult or uninterpretable ECGs include patients with resting ST depressions, complete LBBB (consider using Sgarbossa or Smith), pre-excitation syndrome (WPW) or paced rhythms. [1] They also suggested TTE may be appropriate for “evaluation of a patient without chest pain but with other features of an ischemic equivalent or laboratory markers indicative of ongoing MI.” While typically you would not think to send troponin or ECG if they don’t have any anginal symptoms, it could be reasonable if you have an intubated or nonverbal patient.
What is regional wall motion abnormality and how do I do it?
Regional wall motion abnormalities are described as focal areas of impaired myocardial contraction. In the setting of OMI, occlusion of coronary blood flow results in regional wall motion abnormalities that correlate with the affected vascular territory. Wall motion abnormalities are described as hypokinesis, dyskinesis, or akinesis.[2]
While the heart can be divided into 17 different regions, a simplified approach breaks down the myocardium based on the 3 main coronary territories: left anterior descending, circumflex, and right coronary artery.[2,3,4]
For further explanation, watch this short, helpful video:
TIP: When looking for regional wall motion abnormalities, look for shortening and thickening of the myocardium
Why are we even talking about ultrasound for MI: What are the early changes in acute coronary occlusion?
Animal and human studies have demonstrated regional wall motion abnormalities to be early and sensitive markers of acute coronary occlusion. A 1986 study of 14 patients with isolated proximal LAD stenosis underwent angiography and angioplasty for treatment of angina.[5] All patients underwent continuous TTE and electrocardiography. 14 out of 14 patients (100%) had regional left ventricular dysfunction on TTE within 20 seconds from balloon occlusion, with a range of 5 to 20 seconds. Unsurprisingly, the degree of dysmotility increased with the duration of balloon occlusion with 100% having severe hypokinesia or akinesia by 40 seconds of occlusion. After deflation of the balloon, 100% had complete recovery by 70 seconds with a mean of 43 seconds. Electrocardiographic changes were less sensitive, with only 9/14 patients and 12/14 having ECG changes at 20 and 60 seconds. Why do I bring up this study? This was obviously a controlled experiment on a small population and therefore is not directly generalizable to patients presenting to the ED with chest pain. However, if you believe the patient has an occlusion MI, this study provides at least theoretical evidence that regional wall motion abnormalities reliably exist early and may precede ECG changes.
This is essentially the basis of the echo stress test. Theoretically, a patient with coronary artery disease (but not OMI), will not have ischemic chest pain at rest. However, when demands are increased (either by treadmill or pharmacologically), the patient will begin to have ischemic symptoms if the oxygen demand surpasses coronary blood supply. Regional wall motion abnormalities (as demonstrated by the earlier study) are an early finding that precedes ECG changes, with anginal pain being a late finding. This is depicted in the below figure.
As the rate-perfusion product (heart rate multiplied by systolic blood pressure) increases with increased treadmill time, regional myocardial dysfunction occurs before ST depression or angina. [6]
What else can cause regional wall motion abnormalities besides acute coronary occlusion?
The biggest limitation with any ultrasound is that it is patient and operator-dependent. If you cannot obtain adequate views due to patient characteristics (obesity, artifact, unable to lie still) or the physician lacks adequate training or skill, the test will be obviously limited and therefore indeterminate. Additionally, if you do not have a prior TTE, it will be impossible to distinguish new from old wall motion abnormalities, hence limiting the specificity. There are other conditions besides acute coronary occlusion that may result in “false positive” regional wall motion abnormalities, including prior myocardial infarction, focal myocarditis, Takotsubo’s cardiomyopathy, prior cardiac surgery, left bundle branch block, paced rhythm, and ventricular aneurysm.[2]
What is the reliability of regional wall motion abnormalities in the ED?
With that being said, how well do EPs do when evaluating for RWMA?
Early studies have shown that the use of TTE to detect RWMA in the ED has reasonably good sensitivity and may add value when used with history and ECG to predict cardiac events and in hospital complications.[7,8] Before we drop the ECG in our hands and run for the nearest ultrasound, we should understand these older studies have significant limitations. In the Kontos study, ultrasounds were performed by sonographers or cardiac fellows, thus limiting generalizability to EPs. More concerning, abnormal TTE was defined as RWMA or ejection fraction < 40%, therefore this study was not specifically studying RWMA. Additionally, the endpoint of “Cardiac events” included revascularization or MI. We know that “MI”, defined in the study as ischemic symptoms with elevated enzymes is not specific for occlusion MI. In fact, of the 4 patients with normal TTE who had cardiac events, 3 underwent revascularization, however all 3 were considered “high risk” by EP evaluation. Therefore, we should understand that we should not use RWMA in isolation but should use it in the context of ECG and EP gestalt.
For more on how to critically appraise evidence: https://www.thesgem.com/2014/03/make-it-so-beem-appraisal-tools/
The expanded use of bedside of ultrasound in the ED makes it likely that EP can learn how to detect RWMA. Studies have shown EP can be trained to detect RWMA in a short as 30 minutes.[9]
My takeaway:
Existing studies analyzing the role of RWMA are limited by multiple biases including: imperfect gold-standard bias, selection bias, spectrum bias, lack of generalizability. A future study aimed at measuring the likelihood ratio of RWMA for predicting OMI is needed. However, existing study suggests that the presence or absence of RWMA may be helpful for ruling in or out OMI. RWMA should not be used in isolation but should be applied appropriately, in patients with moderate to high likelihood of OMI, especially when ECG is non-diagnostic. For example, a patient with a moderate to high pre-test probability of OMI with evidence of new RWMA would make OMI likely, and necessitate emergent catheterization or reperfusion therapy whereas a patient without RWMA and without ECG suggestive of OMI should be further evaluated for other diagnoses.
Case Resolution:
The patient did not have definitive RWMA. Further history elucidated recent cocaine use. Chest pain resolved with benzodiazepine therapy. Even so, given the patient’s history of a prior stent, cardiology offered the patient non-emergent cardiac catheterization which did not show OMI but did show reducible vasospasm, confirming the diagnosis of cocaine-induced vasospasm.
Take home:
1. Regional wall motion abnormalities occur early, before ECG changes or pain
2. Consider TTE if ECG is non-diagnostic for OMI
3. Look at a prior TTE, if available
4. Know the “false-positive” cause of regional wall motion abnormalities
5. Learn the coronary anatomy to correlate with regional wall motion abnormalities
References:
[1] American College of Cardiology Foundation Appropriate Use Criteria Task Force; American Society of Echocardiography; American Heart Association; ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography. A Report of the American College of Cardiology Foundation Appropriate Use Criteria Task Force, American Society of Echocardiography, American Heart Association, American Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, Society of Critical Care Medicine, Society of Cardiovascular Computed Tomography, and Society for Cardiovascular Magnetic Resonance Endorsed by the American College of Chest Physicians. J Am Coll Cardiol. 2011;57(9):1126-1166. doi:10.1016/j.jacc.2010.11.002
[2] Johnson B, Lovallo E, Fenkel O, Nagdev A. Detect Cardiac Regional Wall Motion Abnormalities by Point-of-Care Echocardiography. ACEPNow. Accessed Sepetember 7, 2021. https://www.acepnow.com/article/detect-cardiac-regional-wall-motion-abnormalities-point-care-echocardiography/
[3] Cerqueira MD, Weissman NJ, Dilsizian V, et al. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart. A statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association. Circulation. 2002;105(4):539-542. doi:10.1161/hc0402.102975
[4] Avila J, Smith B. 5 Minute Sono – Regional Wall Motion Abnormalities. Core Ultrasound. Accessed September 7, 2021. https://www.coreultrasound.com/5ms_rwma/
[5] Wohlgelernter D, Cleman M, Highman HA, et al. Regional myocardial dysfunction during coronary angioplasty: evaluation by two-dimensional echocardiography and 12 lead electrocardiography. J Am Coll Cardiol. 1986;7(6):1245-1254. doi:10.1016/s0735-1097(86)80143-7
[6] Beller GA. Myocardial perfusion imaging for detection of silent myocardial ischemia. Am J Cardiol. 1988;61(12):22F-28F. doi:10.1016/0002-9149(88)90051-3
[7] Sabia P, Afrookteh A, Touchstone DA, Keller MW, Esquivel L, Kaul S. Value of regional wall motion abnormality in the emergency room diagnosis of acute myocardial infarction. A prospective study using two-dimensional echocardiography. Circulation. 1991;84(3 Suppl):I85-I92.
[8] Kontos MC, Arrowood JA, Paulsen WH, Nixon JV. Early echocardiography can predict cardiac events in emergency department patients with chest pain. Ann Emerg Med. 1998;31(5):550-557. doi:10.1016/s0196-0644(98)70200-8
[9] Kerwin C, Tommaso L, Kulstad E. A brief training module improves recognition of echocardiographic wall-motion abnormalities by emergency medicine physicians. Emerg Med Int. 2011;2011:483242. doi:10.1155/2011/483242
Robby
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