Why we need continuous 12-lead ST segment monitoring in Wellens' syndrome

Also see this incredible case of the use of 12-lead ST Segment monitoring.

This was a male in his 50's with a history of hypertension and possible diabetes mellitus who presented to the emergency department with a history of squeezing chest pain, lasting 5 minutes at a time, with several episodes over the past couple of months.  It was worse on the evening prior to presentation while lying in bed, then recurred and resolved while at rest just prior to arriving in the ED.

Here is the first ED ECG, with no pain:

Sinus rhythm.  Computerized QTc = 419.  There is very subtle Wellens' waves in V2, less subtle in V3, still  less in V4.  This is nearly diagnostic of Wellens' syndrome: pain that resolves, biphasic T-waves with preservation of R-waves.  It extends all the way out to V6, and there is some T flattening in I and aVL, so this is probably a proximal LAD lesion.

The ECG in the chart was read as "no obvious ST changes," (even though no previous ECG was available) and the formal read by the emergency physicians was: "ST deviation and moderated T-wave abnormality, consider lateral ischemia."

Comment: most T-wave inversion is nonspecific, but not these ones!  This T-wave inversion morphology is very specific for Wellens' waves.  You've read in my previous posts that I have a lot of evidence that Wellens' represents spontaneously reperfused STEMI in which the STEMI went unrecorded.  The T-wave inversions are of two types: Pattern A and Pattern B. They occur in the distribution of the LAD and should be in consecutive leads.  (They do also occur with inferior and lateral MI, but are somewhat different and these were not described by Wellens).

Pattern A are biphasic, but with a slightly elevated ST segment and a slight ST upslope.  The  T-wave then drops quickly, as in V2 and V3 here.  This morphology is worth memorizing!  If there is only one wave showing it, it is usually lead V2.

As hours go by, these T inversions always evolve, [unless 1) there is re-occlusion, in which case they go upright and become hyperacute, with or without additional ST elevation, ("pseudonormalize") or 2) no infarction at all (negative troponin, true unstable angina with dynamic T-waves, in which they may normalize).  The evolution is to deeper and more symmetric waves (Wellens pattern B).

Also, as you get further out towards lateral precordial leads, the T-waves are usually more symmetric and more deeply inverted.

The above principles are all well illustrated with this figure from my book, The ECG in Acute MI (2002).  See the Caption:

This figure illustrates the evolution of Wellens' waves from Type A to Type B:

Case Continued:

The physicians considered this ECG nondiagnostic.  Plan was for admission for chest pain workup.  Troponin I level was of course sent.  The first returned at 0.042, which is above the 99% reference of 0.025 ng/mL.  The patient remained asymptomatic, but because of the positive troponin, another ECG was recorded:

Sinus. Computerized QTc = 417.  New ST elevation diagnostic of STEMI [equation value = 25.3 (anterior STEMI) in case you are wondering]

This patient with acute anterior STEMI is without symptoms, even when questioned again!!

It is well documented with continuous 12-lead monitoring that acute re-occlusion is frequently asymptomatic.  Here is the classic article on continuous 12-lead monitoring (in full text) showing that the ECG is a much more reliable indicator of re-occlusion than are symptoms.

Here is another classic article.  It shows that on a 7 day angiogram, only 58% of re-occlusions were symptomatic: Ohman EM, Califf RM, Topol EJ et al.  Consequences of reocclusion after successful reperfusion therapy in acute myocardial infarction.  Circulation 1991;84:1454-1455.

It is important to recognize that coronary thrombosis is dynamic, with spontaneous opening and lysing of the thrombus in the infarct-related artery (we all have endogenous tPA and plasmin to lyse thrombi). The classic article by de Wood (see below) shows that even in completely untreated (not even aspirin) coronary thrombosis, the later the angiogram is done in coronary occlusion, the more likely the artery is to be open. 

Case Continued:

The cath lab was activated.  Before the patient went upstairs (15 minutes later), he remained asymptomatic and another ECG was recorded:

Spontaneous reperfusion again

At cath, there was an 80% mid-LAD active lesion (not proximal, interestingly).  It was stented.  Here is the post PCI ECG:

Minimal change

--Initial and 3 hours troponin I's were (ng/mL):  0.042, 0.054, 0.056, 0.040, 0.039, 0.037

--20 hour echocardiogram showed no wall motion abnormality.  There are those who think that an echo that is done after resolution of ischemia is sensitive for that previous ischemia.  It is not.  When the ischemia is resolved, the wall motion may completely recover, or there may be persistent stunning.

References 

1.  Akkerhuis KM, et al. Recurrent ischaemia during continuous multilead ST-segment monitoring identifies patients with acute coronary syndromes at high risk of adverse cardiac events; meta-analysis of three studies involving 995 patients. Eur Heart J 2001;22:1997–2006.

2.  Gottlieb SO, et al. Silent ischemia as a marker for early unfavorable outcomes in patients with unstable angina. N Engl J Med 1986;314:1214–1219.

3. Jernberg T, et al. The combination of a continuous 12-lead ECG and troponin T; a valuable tool for risk stratification during the first 6 h in patients with chest pain and a non-diagnostic ECG. Eur Heart J 2000;21:1464–1472.

4. Patel DJ, et al. Early continuous ST segment monitoring in unstable angina: prognostic value additional to the clinical characteristics and the admission electrocardiogram. Heart 1996;75:222–228.

5. Alsaab A.  American Journal of Cardiology (Online First, In Press).  Here is the most recent documentation that T-wave inversion does indicate reperfusion: http://www.ajconline.org/article/S0002-9149%2813%2901937-1/abstract

6.  de Wood et al.  Prevalence of Total Coronary Occlusion during the Early Hours of Transmural Myocardial Infarction.  NEJM 1980;303(16):897-902.

Abstract To define the prevalence of total coronary occlusion in the hours after transmural myocardial infarction, we used coronary arteriography to study the degree of coronary obstruction in 322 patients admitted within 24 hours of infarction. Total coronary occlusion was observed in 110 of 126 patients (87 per cent) who were evaluated within four hours of the onset of symptoms; this proportion decreased significantly, to 37 of 57 (65 per cent), when patients were studied 12 to 24 hours after the onset of symptoms. Among 59 patients with angiographic features of coronary thrombosis, the thrombus was retrieved by Fogarty catheter in 52 (88 per cent) but was absent in seven (12 per cent false positive). Among an additional 20 patients without angiographic features of thrombosis, a thrombus was discovered in five (25 per cent false negative). Thus, total coronary occlusion is frequent during the early hours of transmural infarction and decreases in frequency during the initial 24 hours, suggesting that coronary spasm or thrombus formation with subsequent recanalization or both may be important in the evolution of infarction. (N Engl J Med. 1980; 303:897–902.)