US Case of the Month - Watchers of the Walls

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The Case…

The patient is a woman in her 50s with type 2 diabetes mellitus, hyperlipidemia, hypertension and morbid obesity who presents to the emergency department with chest pain. She reports the onset of pressure-like chest pain starting four days ago that radiates to both shoulders and is rated 10/10 in severity. The pain has been intermittent since onset, lasting for about 15 minutes at a time, exacerbated with exertion and alleviated with rest. She reports associated shortness of breath, but denies nausea, vomiting or diaphoresis. She denies any previous history of myocardial infarction, deep vein thrombosis or pulmonary embolism. She has limited mobility due to chronic back pain that has rendered her wheelchair-dependent.

The vital signs are T 36.6 C, HR 84 bpm, BP 113/67 mmHg, RR 18 bpm, SpO2 99% on ambient air. Physical exam reveals a morbidly obese female in mild respiratory distress with normal rate and rhythm, no appreciable cardiac murmurs or notable peripheral edema. There are symmetric breath sounds in bilateral lung fields without crackles.

An electrocardiogram demonstrates ST segment depressions in leads V4-V6 with associated with T-wave inversions, along with T-wave inversions in leads 1 and aVL. These changes are new from previous electrocardiogram from several months prior. Labs are notable for troponin of 6.08 and BNP 557. A transthoracic echocardiogram is obtained.

And now for the ultrasound images…

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What do you see on ultrasound?

Four views are provided - parasternal long and short, as well as apical 2 and 4 chamber views. Collectively they demonstrate a mild to moderately depressed left ventricular systolic function with regional wall motion abnormality as depicted by apical hypokinesis of the left ventricle.

ACS evaluation

Chest pain continues to be one of the most common chief concerns in patients presenting to emergency departments (ED) across the United States, accounting for more than 7 million ED visits annually1. Acute coronary syndrome, a critical and time-dependent spectrum of diagnoses, only contributes to an estimated 12-13% of these visits 2. Of this total, approximately 70% will be secondary to non-ST-segment elevation acute coronary syndromes (NSTE-ACS)3. Although the mismatch of oxygen supply to oxygen demand in NSTE-ACS can be due to a variety of etiologies, it is difficult to predict which of these patients have occult, but significant, coronary artery insults that can progress to myocardial infarction and necrosis if treatment is delayed. Thus, emergency physicians continue to face difficulties in determining which thresholds of conventional diagnostic modalities render a more morbid and mortal outcome, leading many of these patients to go underdiagnosed.

In order to understand the utility of echocardiography in the diagnosis of NSTE-ACS, we must first identify the limitations of current conventional diagnostic approach.

Electrocardiogram

While the electrocardiogram (ECG) is considered standard of care, it continues to be an imperfect diagnostic tool. Studies have demonstrated that only 40-65% of initial ECGs are indicative of ischemia in patients later diagnosed with acute myocardial infarction, with upwards of 20% of initial ECGs found to be completely normal3-7. ECGs are even less sensitive and specific in diagnosing NSTE-ACS, where findings can be subtle and difficult to interpret, especially in the setting of previous infarctions and conduction abnormalities. Several studies have demonstrated serial 12-lead ECG monitoring to have increased diagnostic utility, and national recommendations encourage providers to order serial ECGs every 15-30 minutes if clinical suspicion for ACS remains high, however sensitivity still falls shy of 70%6,7. Therefore, ECGs continue to be a suboptimal test in diagnosing this highly morbid disease spectrum.

Troponin

Troponin is a myocardium-specific serum marker that rises a few hours after myocardial injury, ischemia or infarct3. Sensitivity and specificity are high, however trends in troponin are generally valued over an absolute value in NSTE-ACS. Studies have demonstrated that upwards of 80% of patients who present with myocardial injury in the form of STEMI or NSTE-ACS will have troponin elevations within 2-3 hours3,8-10. However, this can be difficult to interpret if time of symptom onset is unclear. Therefore, the American Heart Association (AHA) currently recommends trending troponins out to at least six hours from initial symptom onset, and if clinical suspicion remains high and the patient is at intermediate- to high-risk for a coronary event, may require trending out to 24 hours in order to optimize ability to detect true ACS pathology3. A significant amount of time can elapse waiting for resulting of this test which may compromise outcome if intervention for true cardiac ischemia is being delayed. Furthermore, troponin is often elevated in clinical situations other than primary coronary pathology; any stress on the myocardium can lead to myocardial leak of troponin as seen in hypotension, sepsis, tachydysrhythmias, heart failure, myocarditis, renal failure, to name just a few. Thus, there may be diagnostic uncertainty, especially in the setting of co-morbid illnesses. The implementation of high-sensitivity troponins may alleviate some of this delay and diagnostic uncertainty, however further evaluation will be required after widespread use of these newer assays.

Two-Dimensional Transthoracic Echocardiography

Two to three percent of highly morbid and mortal ACS pathologies continue to be discharged from the ED11. Echocardiography can be used to increase sensitivity and specificity for significant acute cardiac disease, primarily NSTE-ACS, in the setting of non-diagnostic ECGs and lab work. In fact, the AHA and several other national agencies have recommended the use of two-dimensional transthoracic echocardiography (2DTTE) as a class I recommendation when encountered with possible ACS12. Regional wall motion abnormalities (RWMA) diagnosed with 2DTTE have long been demonstrated to provide value in detecting myocardial ischemia that will benefit from invasive intervention or inpatient monitoring. Robust literature published in the 1980s-1990s demonstrated sensitivities ranging 83-91% and specificities ranging 71-100% that outperform ECG, and rival myocardial perfusion imaging13-19.

Timing

Experimental and clinical studies have demonstrated that the earliest clinical manifestation of myocardial ischemia is RWMA, followed by ECG changes and onset of anginal symptoms (Figure 1)20-22. RWMA develop within seconds of coronary artery occlusion during animal and human coronary angioplasties21,22 therefore proving that 2DTTE can be utilized immediately upon patient presentation if NSTE-ACS is suspected. Even if the patient’s symptoms resolve spontaneously in the ED or shortly after administration of analgesics, RWMA have been shown to last anywhere from one to 24 hours after resolution of anginal symptoms22-27. Moreover, as little as five minutes of coronary disruption can lead to myocardial dysfunction for up to six hours after reperfusion, indicating some degree of myocardial stunning that occurs with even transient ischemic injury 22-24. The delay in return of myocardial function may correlate with the length of anginal symptoms, degree of coronary occlusion, area of affected myocardium and presence of collateral blood flow. Thus, the highest yield of using 2DTTE to detect RWMA will be during acute symptoms, and while a negative study during active symptoms likely indicates another disease process, a negative study obtained after resolution of symptoms cannot definitively rule out NSTE-ACS 28.

Figure 1. Pathophysiologic and clinical progression of coronary ischemia. Vascular dysfunction precedes regional wall motion abnormalities, which can be apparent prior to ECG changes (Adapted from Beller, 1988)

Figure 1. Pathophysiologic and clinical progression of coronary ischemia. Vascular dysfunction precedes regional wall motion abnormalities, which can be apparent prior to ECG changes (Adapted from Beller, 1988)

Ultrasound Pearls

Echocardiographically, the myocardium thickens during systole, followed by symmetric excursion. During active ischemia, there will be abnormal thinning of the myocardium during systole and asymmetry in myocardial excursion. RWMA can be identified as akinesia, hypokinesia or dyskinesia of the affected myocardium. The evaluation of wall thickening is preferred to wall motion abnormality in assessing for acute myocardial dysfunction, however, these changes can be more subtle in the setting of previously damaged myocardium, as scarred tissue will also appear thin during contraction29. Thus, findings on 2DTTE are more helpful when applied in the appropriate clinical setting - if ECG abnormalities are present, whether acute with ST segment and T wave changes, or chronic with Q waves, correlating RWMA with the expected lesion on ECG is helpful to discern acute from chronic pathology.

The American Heart Association and several other national committees sought to standardize a method to identify location and degree of wall motion abnormalities found on 2DTTE, and developed a 17-segment, quantitative evaluation schema30. While studies completed in the 1980s-1990s were primarily performed by radiologists or cardiologists, this is a cumbersome and impractical method to employ in the emergency department. Thus, in the setting of emergency physician performed echo, evaluation is condensed to a 3-segment assessment, with each analyzed segment anatomically correlating with a coronary artery perfusion territory: anterior left ventricular (LV) wall correlates with the left anterior descending artery; inferior LV with the right coronary artery; lateral with the left circumflex artery27,31-34 (See Figure 2). Each wall is assessed in two orthogonal views at minimum, collected via a parasternal long, parasternal short and apical four view. The degree of RWMA is assessed qualitatively and dichotomously, either demonstrating wall motion abnormality or not. This methodology has been shown to be efficient without sacrificing quality in identifying large RWMA for the purposes of ED evaluation of significant ischemic pathology14.

The degree of RWMA detected has been shown to correlate with the degree of ischemia or infarction, meaning multivessel disease will correlate with a larger and more severe myocardial dysfunction as detected on 2DTTE19,27,35. This indicates a larger swathe of at risk of myocardium that may benefit from early invasive therapy. Furthermore, when comparing global LV systolic dysfunction assessment with focal wall motion abnormalities, more focal abnormalities have been determined to be a greater predictor of morbidity and mortality in ACS, especially in the NSTE-ACS cohort26. The finding of any RWMA at rest is associated with an eightfold increase in adverse cardiac events in the first 48 hours, and fourfold in the next two years5,36. Thus, despite equivocal ECG and troponin levels, 2DTTE may more readily identify patients that are at high risk of progressing to myocardial infarction and require early invasive intervention.

Although identifying RWMA can be difficult, several recent studies demonstrate emergency physician are be able to utilize 2DTTE with short periods of training. A case series completed with emergency physician-performed point-of-care ultrasounds for three patients presenting with anginal equivalents with initially non-diagnostic conventional work up identified significant RWMA that correlated with severe single vessel coronary artery stenosis27. These studies were completed by ultrasound-fellowship trained ED physicians, with no formal echocardiography training, after a brief 10-minute didactic training video. Another study demonstrated statistically significant improvement in post-test performance in identifying RWMA after a 30-minute module depicting qualitative changes in normal and abnormal echocardiograms37. Standardized approach to echocardiogram, including assessment of RWMA, also improves the detection of other mimickers of NSTE-ACS, including aortic dissection, pericardial effusion, valvular pathology, acute heart failure, pulmonary embolus, and others, when utilized routinely by residents38,39. Thus, it is feasible for emergency physicians to perform this in real-time with brief didactic and clinical application, and can provide diagnostic clarity with relative ease and widespread availability.

Figure 2. Vascular territories on electrocardiogram matched to the corresponding Myocardial regions as seen on transthoracic echocardiogram. Views include (FroM Left to right) parasternal short, parasternal long, and apical four chamber.

Figure 2. Vascular territories on electrocardiogram matched to the corresponding Myocardial regions as seen on transthoracic echocardiogram. Views include (FroM Left to right) parasternal short, parasternal long, and apical four chamber.

Technical difficulties

Pitfalls in assessing for RWMA are twofold: during image acquisition and during image interpretation. Images are best analyzed when sufficient quality is obtained to assess for abnormalities, and that those abnormalities can be compared in multiple views. Oftentimes image acquisition can be difficult due to body habitus, underlying pulmonary disease or inability to reposition the patient. Suboptimal images run the risk of leading to a false positive or false negative. Additionally, image interpretation can be difficult, specifically when delineating between acute versus chronic changes. Furthermore, significant valvular pathology, previous cardiomyopathy, acute myocarditis and bundle branch blocks will all make it difficult to assess which changes are new or old, ischemic or non-ischemic. Thus, it can be helpful to compare previous echocardiography imaging with current imaging to assess for acute change.

Furthermore, experimental data has shown that a certain degree of myocardial thickness (>20%) and ventricular mass (>5%) needs to be affected in order to be detected as RWMA on 2DTTE40. On the other hand, a non-transmural injury only including subendocardial regions or a transmural infarct affecting only a small portion of the ventricular wall are unlikely to cause significant morbidity or mortality compared to the occult lesions causing obvious RWMA.

Case resolution

With apical hypokinesis matching new T wave changes, the patient is taken by interventional cardiology for a left heart catheterization. She is found to have severe 3-vessel obstructive coronary artery disease including a 95% de novo stensosis of the mid left anterior descending artery, left circumflex artery with 80% stenosis and right coronary artery with 100% total occlusion. Cardiothoracic surgery was consulted, but given her limited functional capacity, she is deemed a poor candidate for surgical intervention. The following day she underwent high risk percutaneous coronary intervention with drug-eluting stent x2 to the LAD, has an uncomplicated hospital course and is discharged. Cardiology starts the patient on guideline directed medical therapy, and she continues to follow up in clinic with no repeat ischemic episodes.

Take home points

  • 2DTTE can be beneficial in identifying patients that may benefit from early invasive intervention if suspicion for NSTE-ACS is high and conventional work up is non-diagnostic
  • Three cardiac views are required at minimum: parasternal long, parasternal short, apical four
  • RMWA can be evident by myocardial thinning during contraction or asymmetric myocardial excursion as witnessed on two orthogonal views
  • Correlations with ECG abnormalities and previous echocardiograms can be crucial in identifying acute versus chronic changes

Authored by Sim Mand, MD

Dr. Mand is a PGY3 at the University of Cincinnati Emergency Medicine residency, and will be pursuing an ultrasound fellowship.

Faculty Edits by Jessica Baez, MD

Dr. Baez is a current second year fellow and faculty at the University of Cincinnati Emergency Medicine residency.

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