T-wave inversions associated with coronary artery disease may result from myocardial ischemia, non–ST-segment elevation acute myocardial infarction (MI) (Figure), or previous MI. Examples include bundle branch blocks, preexcitation states, and ventricular ectopic or paced beats. Secondary T-wave changes result from aberrant ventricular activation in the context of normal action potential characteristics. Alterations in the duration or morphology of the action potential, without concurrent changes in the orderly sequence of activation, are termed “primary changes.” Primary T-wave inversions are associated with benign syndromes, such as the persistent juvenile T-wave pattern and the digitalis effect, as well as morbid conditions, including acute coronary ischemic events and CNS catastrophe.
The causes of T-wave inversions have commonly been grouped into 2 categories: primary T-wave changes and secondary T-wave changes.
A variety of clinical syndromes can cause T-wave inversions these range from life-threatening events, such as acute coronary ischemia, pulmonary embolism, and CNS injury, to entirely benign conditions. Thus, T-wave inversions in leads V1 and V2 may be fully normal. The T wave is normally upright in leads I, II, and V3 to V6 inverted in lead aVR and variable in leads III, aVL, aVF, V1, and V2. The T wave is the ECG manifestation of ventricular repolarization of the cardiac electrical cycle. In addition to ischemia, what conditions can cause T-wave inversions in leads V1 through V4? - William Morris, MD Athens, Tenn