The relationship between the EA of the QRS complex and the T wave was referred to by Wilson as the ventricular gradient.17 In contrast to what occurs in an epicardial-to-endocardial muscle strip (as mentioned previously), in the isolated muscle strip, the sequence of ventricular depolarization occurs in the same direction as that of repolarization.12 Although the QRS and T deflections have opposite polarity, the algebraic sum of QRS and T areas is zero. In the human heart, however, not only is the sequence different, but the pathways of ventricular depolarization and repolarization are not exactly the same.12 Thus the algebraic sum of QRS and T areas is no longer zero. Therefore, a gradient is said to exist. The ventricular gradient can be calculated by determining the electrical axis of the QRS and T (using areas) and then obtaining the resultant by the parallelogram method. Wilson considered that the ventricular gradient could be of help in differentiating between T-wave inversion of various causes (primary changes) and the obligatory secondary T-wave changes resulting from abnormalities in depolarization, such as bundle branch block, ventricular hypertrophy, ventricular pacing, and preexcitation syndromes.12,13,17 In practice, calculation of the ventricular gradient is difficult and time consuming because it has to be determined by areas and not maximal amplitude.

Apparent Challenges to the Concept of the Ventricular Gradient

Rosenbaum et al.18 studied the prolonged depolarization occurring during long periods of ventricular stimulation and found two types of altered ventricular repolarization. One, corresponding to Wilson's classic theory, was transient and proportional in magnitude to the QRS complex but of opposite polarity. The other, concealed by (and during) the former, required a longer time (even days) to reach maximal effect as well as to disappear, becoming apparent only when normal activation recurred (BhB; Fig. 11-1). The latter type was attributed to modulated electrotonic interactions occurring during cardiac activation in such a way that repolarization was accelerated at ventricular sites where depolarization begins and delayed in areas where depolarization terminates. T-wave changes appearing after prolonged depolarization was no longer present showed accumulation and (fading) long-term memory for variable time (see "Secondary ST-T-Wave Changes," below).18 Recently, Goyal et al.19 reported the occurrence of short-term memory after periods of altered ventricular repolarization as short as 1 min in duration. In addition, according to Surawicz,20 the term memory also has been applied to gradual adjustments of action potential duration (corresponding to QT intervals) after abrupt changes in cycle lengths (events influenced by past history) without necessarily requiring abnormal ventricular repolarization (Fig. 11-2). The cellular mechanism responsible for any form of cardiac memory is beyond the scope of this chapter.

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