Wellens' syndrome is characterized by a high-grade LAD stenosis and denotes a high likelihood of progression to OMI in the near future (next several days). These patients will present in the reperfusion stage. This means that they had vasospasm to cause OMI (they have chest pain at this stage), but the spasm resolved and they no longer have a OMI on their EKG. Given their reperfusion state, they do not have chest pain. In other words, a patient with active chest pain CANNOT have Wellens' syndrome. It is important to understand the progression of OMI to reperfusion as Wellens' syndrome exhibits this in a specific location (leads V2 and V3). The reperfusion in this area is noted as it consists of the highest amount of myocardium at risk compared to other territories.
There are 2 patterns depending on the timeframe of resolution of their occlusion to acquisition of the EKG. Type A has biphasic T waves; this T wave as noted above initially is upright but has terminal inversion. Type B has deep, symmetric T wave inversion. Most patients will fall into the latter type. However, there is no practical difference between the two as management is the same. Note also that these patients will not have pathologic Q waves unless the Q waves are old. Some consider this to be a OMI equivalent; whether or not the cath lab is emergently activated will be institution dependent. Note also that the biphasic T waves are the up-down type; down-up biphasic T waves are not found in Wellens' syndrome (usually hypokalemia).
Patients with T wave inversion or biphasic T waves in leads other than V2 or V3 cannot have Wellens' syndrome by definition. Sometimes, these are indicative of reperfusion (commonly seen otherwise in the inferior leads). However, these do not always represent Wellens' syndrome.
Pseudo-Wellens' syndrome
This EKG demonstrates left ventricular hypertrophy with repolarization changes ('strain'). The biphasic T waves in V4-V6 cannot be Wellens' syndrome as that is only found in leads V2 and V3.
Examples:
Type A
Type B