Learning Objectives: After reading this article, the physician should be able to:
- Discuss the EKG manifestations of Wellens' syndrome.
- Describe the clinical significance of the findings of an EKG for Wellens' syndrome.
- Summarize the prudent ED approach to intervention for Wellens' syndrome.
Release Date: August 2009
Some EKG findings foreshadow significant morbidity and even mortality, and some subtle yet serious results escape even seasoned cardiologists. Like QTC prolongation and Brugada syndrome, which I discussed in previous columns, Wellens' syndrome is a medical zebra that is a disaster waiting to happen, but one that is not familiar or apparent to most ED clinicians.
This syndrome is a wolf in sheep's clothing ready to ruin your day — and the day of the unfortunate owner of this EKG pattern. Most disturbing, the classic EKG findings of Wellens' syndrome can be obscure during the symptomatic phase of acute ischemia, and appear after chest pain has subsided when everyone breathes a sigh of relief and proceeds at a more relaxed pace.
Electrocardiographic Manifestations of Wellens' Syndrome
Rhinehardt J, et al
Am J Emerg Med
2002;20(7):638
This is one of only a few articles in the emergency medicine literature describing an uncommon but important and potentially catastrophic cardiac condition manifesting rather subtle EKG findings. The details of Wellens' syndrome are not omnipresent in the extant emergency medicine literature; likely this syndrome would not be something that most emergency physicians would readily appreciate.
Wellens' syndrome is defined as a preinfarction stage of coronary artery disease or the left anterior descending coronary T wave syndrome. The relatively subtle characteristics are clandestine and befuddling to the unwary clinician, consisting of T wave abnormalities in the anterior chest leads. The importance of these EKG findings is an associated significant occlusion of the proximal left anterior descending (LAD) coronary artery. This vessel is known as the coronary artery of sudden death, described in the lay literature and in the courtroom as the “widow maker.” This dead-spouse moniker has been embraced by malpractice attorneys, and is a very powerful eponym when describing an unfortunate outcome. Individuals with Wellens' syndrome frequently develop an acute MI of the anterior wall, and it may be fatal or precipitate significant cardiac morbidity.
;)
Figure: Wellens' syndrome is easily mistaken as nonspecific EKG findings or a plethora of other conditions. Type I Wellens' syndrome demonstrates deeply inverted T waves in V2-V3, occasionally in V4–V6.
The key is recognizing the EKG findings and instituting appropriate intervention, usually coronary angiography. Just as key is eschewing the otherwise business-as-usual approach to chest pain, the most concerning symptom that has, for the moment, evaporated. Importantly, patients with this syndrome should not undergo any form of exercise stress testing. Exercise stress testing is a common reflex in someone with mildly abnormal EKG findings after acute MI has been ruled out in the ED, but the clinician has the desire to embark upon a proactive, seemingly laudable, cardiac workup prior to discharge. So much for going the extra mile for your patient. And so much for trying to thwart an admission that won't be paid by the ever-stingy CMS and other parties eager to save money at the patient's and hospital's expense.
This illustrative report, written by some erudite emergency physicians with enviable cardiology expertise, describes three cases of relatively young individuals presenting to the ED with chest pain. I urge all EPs to carefully study the EKG examples in this paper. The first case is quite characteristic. A 49-year-old man presented with chest pain and diaphoresis. He had an unremarkable examination and negative serum markers for acute MI, and an admission was orchestrated for an inpatient workup following standard treatment for unstable angina/ACS. In retrospect, Wellens' syndrome appeared on the EKG during a pain-free hiatus. A cardiac catheterization revealed 95% proximal LAD occlusion, and a stent was placed, fortunately prior to an acute event.
The second case chronicles a 54-year-old woman who presented with symptoms suggestive of acute ischemia and the characteristic EKG findings of Wellens' syndrome. In the ED, she remained pain-free, and serum markers were initially normal. She did not undergo immediate angiography, and developed an acute MI approximately six hours later. A subsequent catheterization demonstrated a near-complete proximal LAD occlusion.
In the third case, a 54-year-old man presented with symptoms concerning for acute MI and an EKG not indicative of acute MI but with Wellens' criteria. He was treated with nitrates and morphine. The pain resolved. Serum markers were normal. An exercise stress test was ordered by the primary physician while the patient was still in the ED, and within one minute of stress testing, the patient developed severe chest pain and an EKG consistent with acute anterior MI. A cardiac catheterization revealed proximal LAD occlusion treated with angioplasty.
This case series describes three seemingly routine, garden-variety ED patients with cardiac-sounding histories and an appropriate concern for ischemia. Obviously, they are rather scary cases, but these are scenarios we see every shift but without such dramatic outcomes. Under most circumstances, a moderately abnormal EKG in the presence of so-called nonspecific findings, normal enzymes, and a pain-free state would prompt further investigation, either expeditiously as an outpatient or more leisurely as an inpatient. One might even opt for the chest pain center or observation alternative. Inpatient treatment usually consists of an acute MI rule-out for the first 24 hours, perhaps angiography, or merely stress testing and discharge. It is paramount to realize that exercise stress testing, an otherwise very reasonable next step albeit not overly diagnostic, administered to a patient with Wellens' syndrome can be disastrous. Such an intervention can precipitate an acute MI.
The characteristic EKG findings indicating critical stenosis of the proximal LAD were first described in 1982. (Am Heart J 1982;103[4]:730.) The original description was a profile of unstable angina with specific precordial T wave changes and the subsequent development of a large anterior wall MI. It has received little attention in the emergency medicine literature. (Ann Emerg Med 1999; 33[3];347.) This article has only eight references. The characteristic EKG findings are exemplified by the figures.
Comment: There are two EKG patterns of Wellens' syndrome, neither of which exhibits the obvious habitus of an acute MI waiting to happen. The deep T wave inversions or biphasic T wave in leads V1 to V4 are characteristic. The T wave is symmetric, unlike the asymmetric T wave of LVH. The online reference source, emedicine.com, states that the EKG pattern of Wellens' Syndrome is present in 14 percent to 18 percent of patients with unstable angina. This is puzzling because acute anterior MI is not that prevalent with ACS. The T wave changes should get one's attention for sure. The morphology is abnormal, but could seemingly appear benign or only suggestive of ischemia. Wellens' syndrome, like Brugada syndrome, is likely to be interpreted by the EKG computer as nonspecific changes. If only the computer were intuitive enough to alert one to a pattern that could be a harbinger of sudden death.
Patients with very marginal coronary circulation often become pain-free in the supportive ED milieu with little or no intervention. In Wellens' syndrome, the EKG taken while the patient experiences pain may be deceptively normal. Without Q waves or ST segment elevation, this EKG is quickly perused and read as possibly concerning yet not really that worrisome. If the pain does not return, a repeat EKG is often not considered standard.
Prior to understanding this syndrome and likely still today, such patients do not receive emergency catheterization or revascularization, and can proceed to extensive anterior wall infarction within a few days or weeks after the onset of chest pain. The mean time from first presentation to acute MI is said to be just eight days!
Curiously, the EKG findings appear to be present more often when the patient is pain-free, and they actually may normalize with acute chest pain. This is concerning indeed, and it doesn't seem fair. In the initial report by Wellen, only 21 of 180 patients (12%) with EKG changes had elevated cardiac enzymes. I don't think troponins were available at that time. The bottom line is that EKG manifestations may be the only indication of impending extensive anterior wall infarction. Although most clinicians would view these markedly abnormal T waves with concern, the requisite concern for impending infarction would likely escape all but the most astute clinician. It may be standard to admit such patients for further evaluation, but it's likely not standard for the EP to recognize and act on this condition immediately. The importance of Wellens' syndrome has likely escaped the attention of even the most astute internist.
Of course, almost any squirrelly EKG can be associated with a number of conditions, ranging from relatively benign to life-threatening. Many T wave configurations have nothing to do with coronary circulation. The very subtle changes in Brugada syndrome, discussed here last month, are classic examples. Who would think that seemingly non-concerning syncope in an otherwise healthy young person who only demonstrates an incomplete right bundle branch block, is at risk for sudden death. The EKG findings of Wellens' criteria also can be seen in pulmonary embolism, CNS injury, and perhaps a persistent juvenile pattern, and can occur from a plethora of drug effects. Myocarditis, bundle branch block, preexcitation syndrome, electrolyte perturbations, and pericarditis also can cause similar patterns, enigmatic enough to lead you astray and into the pleasant ennui of a leisurely ED approach. Alternatively, one is lulled into yet another admission for monitoring, serial enzymes/EKGs, and low-level observation with a routine cardiology consultation in the morning.
Figure: Type II Wellens' syndrome is less common, and consists of biphasic T waves. It also can demonstrate minimal ST segment elevation. This pattern will likely be read by the EKG computer as a variety of nonspecific descriptions, such as LVH. Do not order a stress test if an acute MI is ruled out in the ED; it may precipitate an acute MI. The clinical approach is variable, but in acute chest pain or possible ACS, a prudent intervention is consultation with a cardiologist, with a consideration for emergent cardiac catheterization and possible revascularization.
The accompanying table and EKG tracings should be etched in the cortex of the EP faced with a patient with myocardial ischemia by history. I think it is quite instructive to note that the patients in this particular report were relatively young. Prior risk factors, vagaries of the history, and vicissitudes of the chest pain were not listed. We have recently come to know that there is probably no such thing as classic chest pain or concerning risk factors with regard to coronary artery disease. All you need is coronary arteries and some symptoms that could be related to these vessels. Although the clinical scenario of ACS is likely secondary to ischemia caused by Wellens' syndrome and the standard anti-ischemia drug regimens are reasonably instituted, the clinician's anxiety should not be allayed. We all like to see an EKG during pain, but the importance of serial EKGs is obvious, especially the tracing taken after pain has disappeared.
Finally, exercise stress tests (treadmill and stress echo) are strongly discouraged if this syndrome is considered. I have had a stress echo, and can testify to the exertion required to get a good look at cardiac function.
Wellens' Syndrome
Tandy T, et al
Ann Emerg Med
1999;33(3):347
This was likely one of the first articles in the emergency medicine literature describing Wellens' syndrome. I totally missed it or quickly forgot it. This disease was not around until 1982 so many experienced clinicians did not learn about it in medical school or on their cardiology rotations. This particular report describes a 39-year-old man who presented to an ED with sharp substernal chest pain of several weeks duration. That's just another cocaine chest pain in my ED; I see it daily and am very nonchalant, if not complacent, about sending these pain-free patients home with stern advice about the evils of drugs.
Although this patient had a history of hypertension, diabetes, and smoking, his rather atypical symptoms for two weeks would cause many to diagnose a noncardiac origin for chest pain. As with all the other soon-to-be problematic cases, the exam was normal and the patient became pain-free. Classic Wellens' T wave changes were clearly present on the EKG. As noted by this author, the computerized interpretation likewise failed to recognize this potentially lethal syndrome. (Someone needs to make a program for identifying Brugada and Wellens'.)
This patient underwent the standard reflex action that is routine throughout the country for any denizen of the ED with chest pain who is low risk and becomes asymptomatic. Plans were made to do an exercise stress echo test, a test that is often ordered right from the ED by many well intentioned EPs. Within three minutes on the treadmill, the patient developed ventricular tachycardia and an acute MI, and he died shortly thereafter. Autopsy revealed occlusion of the proximal LAD.
These authors offer several caveats about Wellens' syndrome:
- ▪ Patients have a prior history of angina-like chest pain.
- ▪ They have little or no cardiac enzyme elevation.
- ▪ There are no pathologic precordial Q waves.
- ▪ There is little or no ST segment elevation.
- ▪ There is no loss of precordial R waves.
- ▪ The T waves can be biphasic or asymmetrically deeply inverted.
These are the classic criteria, but these findings don't classically call for immediate action, such as marshalling the interventionist to the cath lab. The criteria are quite specific for LAD disease, and critical LAD disease, at that. Myocardial ischemia is likely responsible for the T waves abnormalities, but there may be concomitant hypoxia, cocaine effects, vasospasm, or increased cardiac demand.
Comment: A recurrent theme is that the EKG abnormalities of Wellens' syndrome typically occur during a pain-free interval. These findings may be somewhat transient, and taking a single EKG in a patient with an atypical history can lead one astray. There are reports that T waves actually can normalize in the presence of acute ischemia. Figure out that one.
You can now add Brugada and Wellens' syndromes to the list of specific EKG findings to look for, document, and rule out on your EKG readings in the ED. A covert harbinger of a potential cardiac disaster, these seemingly nonspecific findings are very specific indeed. I will start to diagnose this syndrome more than necessary, but that's probably a good idea. When you start mentioning the legacy of Drs. Brugada and Wellen to the sleepy cardiologist on the other end of the phone, hopefully you will garner interest if not accolades for your clinical prowess. An equally important caveat is to eschew the reflexive action of trying to be patient-proactive by providing a stress test in the ED for a patient who has been ruled out by enzymes, who lacks specific infarction-like EKG abnormalities, and who is pain-free. The role-model clinician would opt for expeditious angiography rather than a casual admission for rule-out MI. Such a course would be prudent but not likely chosen unless one specifically knows this syndrome. The whole world seems to have chest pain and a voracious appetite for an ED visit to get checked out. Cherry-picking those with Wellens' syndrome from the rest of the pack is a daunting task.
Criteria for Wellens' Syndrome
These EKG findings are subtle, can mimic nonspecific changes or other conditions, and do not portray an acute AMI picture. Findings may be transient.
- ▪ Prior history of chest pain.
- ▪ EKG pattern observed in pain-free state; it may change or appear more normal in presence of pain.
- ▪ Little or no cardiac enzyme elevation.
- ▪ No pathologic precordial Q waves.
- ▪ Little or no ST-segment elevation.
- ▪ No loss of precordial R waves.
- ▪ Symmetric deeply inverted T waves in leads V2 and V3 (the more common Type 1). Biphasic T waves in leads V2 and V3 (the less common type 2). Changes also may include leads V4-V6.
Wellens' criteria are quite specific for left anterior descending artery disease of 50% narrowing of the left anterior descending artery (mean=85% narrowing) with complete or near-complete occlusion in 59%.
Source: Am J Emerg Med 2002;20(7):638.
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Dear Dr. Roberts:
I have enjoyed your series about the use of methadone. I was wondering if you would comment on the treatment of methadone overdoses, both in the patient who received naloxone and the patient who might just be lethargic. — Derek Isenberg, MD, New Haven, CT
Dr. Roberts responds: The treatment of a significant methadone overdose is straightforward: Naloxone by any route possible (even ET, SL, PR). Even an IM injection works well. If it's a first or sporadic exposure, I will usually try 2 mg naloxone, and that's enough for most methadone overdoses, and it lasts about one hour. Re-sedation is a possibility. There is no maximum naloxone dose, and 10 mg to 20 mg should be allotted before considering another etiology. If the patient is addicted, a nasty withdrawal will surely be precipitated, so some use small naloxone IV bolus doses if time permits (0.1–0.2 mg), and titrate to response.
That's a bit tricky, and you might have to accept withdrawal if respiratory depression is severe. I would opt for withdrawal over intubation any day. Adding 5 mg to 10 mg of naloxone to 500 ml to 1000 ml of saline, and titrating the infusion to keep the patient awake yet not in withdrawal can be mastered quickly. Doses range from 0.5 mg to 2 mg per hour.
A few other caveats: Methadone will not be identified by a routine, unenhanced urine immunoassay drug screen, even though it's an opiate. Neither will oxycodone (news to most), fentanyl, propoxyphene, or meperidine. In my mind, any symptomatic oral opiate overdose, especially methadone, requires 12 to 24 hours of observation in the hospital unless other circumstances are pristine. Methadone has a long and unpredictable half-life. It is flummoxing when the history suggests oral opioid overdose and the individual is totally asymptomatic, but I still prefer observation for a good eight to 10 hours without prior naloxone. Keeping the recalcitrant and eager-to-leave methadone user in the hospital, especially if he is in withdrawal, is always a royal pain. I would eschew the good-riddance-sign-him-out-AMA reflex. The prescient clinician can more easily defend a charge of violating a patient's rights than a death after discharge. An involuntary psych commitment works nicely, and by the time the red tape is finished, so is the methadone effect. Heroin has a very short half-life and re-sedation is not usually a problem after the naloxone wears off.
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