T-wave inversions on ECG may be indicative of ischemia. Alteration in ventricular activation or depolarization, as seen with intermittent LBBB, ventricular pacing, or preexcitation can also cause these T-wave changes. Cardiac memory describes the development and cessation of T-wave changes with intermittent or transient ventricular activation.
1,5 The study by Chatterjee et al
2 was one of the earliest to demonstrate that artificial pacing was the cause of T-wave inversions without QRS changes in a nonpaced beat. He also found that the duration of pacing influenced the duration of T-wave changes. In normal conduction, ventricular repolarization is in the opposite direction of ventricular depolarization, resulting in the polarity of the T wave and QRS being the same. The T-wave inversions that occur in cardiac memory with normal QRS duration are in the direction of the previous altered QRS complex, resulting in opposite polarity of the QRS and T wave.
7
Although no clear definition exists, there are certain criteria, such as those by Rosenbaum et al,
3 who noted 3 elements: (1) T wave with vector during sinus rhythm approaching that of the paced or widened QRS; (2) accumulation of the size of the T wave with abnormal activation of the ventricle; and (3) persistence of T-wave changes for a variable period even after restoration of sinus rhythm.
1,8 Rosenbaum
3 referred to the T-wave changes as pseudoprimary. Initially, the T-wave changes were thought to be secondary because they were initiated by a change in the QRS complex. Yet the T-wave changes persisted after the QRS had normalized, mimicking a primary change.
The exact underlying mechanisms that lead to cardiac memory are unclear. Some consider it a reversible form of electrical remodeling.
9 There are data suggesting that modification of specific potassium channels,
4,10 modification of calcium channels,
11,12 angiotensin II production,
13,14 myocardial stretch,
15,16 transient outward current It0,
3,10 transcription factors,
17 and alterations in the phosphorylation of the cyclic adenosine monophosphate–responsive element binding protein are all involved in cardiac memory.
4,17-19
It is unknown how long an intermittent LBBB or ventricular pacing needs to be present for cardiac memory to develop. In the canine heart, cardiac memory was induced after 20 minutes of right ventricular pacing.
10 In humans, T-wave changes developed within 1 week.
5 Studies on patients with intermittent LBBB demonstrate the incidence of T-wave inversions during sinus rhythm range from 72% to 83%.
20,21 The cardiac memory pattern on ECG can last for minutes to hours, or as long as weeks to months. Although the exact mechanism is still unknown, the duration of cardiac memory is somewhat proportionally related to the length of abnormal ventricular activation.
1,9,18 The morphology of the QRS/T ratio with LBBB determines the magnitude of the T-wave vector change with cardiac memory.
18
There are still unanswered questions regarding cardiac memory and the mechanisms involved. If intermittent LBBB is unknown or not observed, is it possible to differentiate ischemic T-wave changes from cardiac memory T-wave changes? Shvilkin et al
22 developed 3 criteria to differentiate cardiac memory from ischemia:
(1) positive T wave in aVL; (2) positive or isoelectric T wave in lead I; and (3) maximal precordial T-wave inversion is greater than the T-wave inversion in lead III. These criteria were 92% sensitive and 100% specific for detecting cardiac memory as the cause of T-wave changes
22 (
Figure 3 and
Figure 4). Fifteen of the 16 patients in our medical record review met the above criteria for cardiac memory. Therefore, it appears the criteria developed by Shvilkin et al
22 can be accurately used to differentiate between ischemia and cardiac memory.