A 20 year old male with end stage renal disease (ESRD) and hypertension presented with 1 hour of chest pain ("cramps").
He was hypertensive at 170/100. Here is his initial ECG:
He had been admitted 24 hours prior with fluid overload. Here was his ECG from that visit:
During that visit, his BP had been as high as 220/110. He had been dialyzed and discharged.
Back to this visit
Is this Wellens' syndrome?
NO. Wellens' syndrome is a PAIN-FREE syndrome. It is also not associated with LVH or hypertension, which may result in Wellens' mimics. It depends to a high degree on pretest probability, which is very low (but not zero!) in a 20 year old.
He underwent a bedside cardiac echo (there was no previous echo for comparison). Here is the parasternal short axis view:
This shows concentric LVH and no anterior wall motion abnormality.
If this were Wellens' syndrome, and the patient were pain free, then it would be common to have no wall motion abnormality, as Wellens' syndrome represents a state of reperfusion, when there is no persistent transmural ischemia and the wall motion may have recovered. Normal wall motion after reperfusion (after resolution of chest pain) should not be reassuring, but normal wall motion during pain should be reassuring.
An immediate formal echo was also normal:
Enlarged left ventricular size, marked concentric left ventricular hypertrophy and lower limits of normal systolic function. The estimated left ventricular ejection fraction is 55% There is no left ventricular wall motion abnormality identified.
He ruled out for MI by serial contemporary (not high sensitivity) troponins (troponin I, all undetectable). He was supposed to get a stress echo to evaluate for coronary disease but he signed out against medical advice.
Case continued
7 weeks later he presented to the ED with dyspnea again and had this ECG. BP was 170/100.:
He was discharged.
He returned one week later with chest pain and pulmonary edema. His BP was 193/120. Here is his ECG:
I saw him at this time and treated with Noninvasive ventilation and high dose IV nitroglycerine (250 mcg/min). Pulmonary edema resolved and he was admitted. I did not think he was having ACS.
And 8 hours later, this was his ECG:
His troponin I was elevated, and rose slowly to 0.394 ng/mL, and then slowly dropped. This is diagnostic of MI, but troponin does not differentiate between supply/demand ischemia (Type II MI) and ACS (type I MI).
These EKG and troponin findings are not at all unusual for a patient with LVH and severe hypertension and pulmonary edema with hypoxia.
The patient underwent an angiogram. It was normal.
Learning Points
1. Wellens' syndrome is a syndrome, not merely an ECG finding.
2. The syndrome does not include LVH, elevated BP, or pulmonary edema, and these findings will cause false positive ECGs.
3. "Anterior" T-wave inversions that look like Wellens' waves have many mimics; they are only fairly specific in the appropriate clinical syndrome.
4. The diagnosis here is type II MI due to demand ischemia from hypertension and hypoxia.
He was hypertensive at 170/100. Here is his initial ECG:
There is high voltage of LVH and biphasic T-waves, reminiscent of Wellens' waves. The clinicians were concerned for Wellens' syndrome. |
There were no T-wave inversions at this time. Voltage is somewhat high, but not diagnostic of LVH. |
Back to this visit
Is this Wellens' syndrome?
NO. Wellens' syndrome is a PAIN-FREE syndrome. It is also not associated with LVH or hypertension, which may result in Wellens' mimics. It depends to a high degree on pretest probability, which is very low (but not zero!) in a 20 year old.
He underwent a bedside cardiac echo (there was no previous echo for comparison). Here is the parasternal short axis view:
This shows concentric LVH and no anterior wall motion abnormality.
If this were Wellens' syndrome, and the patient were pain free, then it would be common to have no wall motion abnormality, as Wellens' syndrome represents a state of reperfusion, when there is no persistent transmural ischemia and the wall motion may have recovered. Normal wall motion after reperfusion (after resolution of chest pain) should not be reassuring, but normal wall motion during pain should be reassuring.
An immediate formal echo was also normal:
Enlarged left ventricular size, marked concentric left ventricular hypertrophy and lower limits of normal systolic function. The estimated left ventricular ejection fraction is 55% There is no left ventricular wall motion abnormality identified.
He ruled out for MI by serial contemporary (not high sensitivity) troponins (troponin I, all undetectable). He was supposed to get a stress echo to evaluate for coronary disease but he signed out against medical advice.
Case continued
7 weeks later he presented to the ED with dyspnea again and had this ECG. BP was 170/100.:
T-wave inversion is less deep, still biphasic. |
He returned one week later with chest pain and pulmonary edema. His BP was 193/120. Here is his ECG:
Shallow terminal T-wave inversion |
I saw him at this time and treated with Noninvasive ventilation and high dose IV nitroglycerine (250 mcg/min). Pulmonary edema resolved and he was admitted. I did not think he was having ACS.
And 8 hours later, this was his ECG:
These are typical of Wellens' Pattern B (deep symmetric) T-waves and are diagnostic of ischemia. They are NOT diagnostic of ACS or Wellens' syndrome. |
His troponin I was elevated, and rose slowly to 0.394 ng/mL, and then slowly dropped. This is diagnostic of MI, but troponin does not differentiate between supply/demand ischemia (Type II MI) and ACS (type I MI).
These EKG and troponin findings are not at all unusual for a patient with LVH and severe hypertension and pulmonary edema with hypoxia.
The patient underwent an angiogram. It was normal.
Learning Points
1. Wellens' syndrome is a syndrome, not merely an ECG finding.
2. The syndrome does not include LVH, elevated BP, or pulmonary edema, and these findings will cause false positive ECGs.
3. "Anterior" T-wave inversions that look like Wellens' waves have many mimics; they are only fairly specific in the appropriate clinical syndrome.
4. The diagnosis here is type II MI due to demand ischemia from hypertension and hypoxia.
thank you for every good case I think
ReplyDeletethe first and last case mimick Wellens'
most----these ecg's QT IS VERY PROLONGED and the mimicking is caused by electrolyte abnomality ex)
HypoCa or u wave ?
There was no electrolyte abnormality.
DeleteGREAT case! - Thank you - :)
ReplyDeleteThanks, Ken!
Delete