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T-Wave Inversions: Sorting Through the Causes

Article

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. Here: a discussion of conditions that can cause T-wave inversions in leads V1 through V4.

In addition to ischemia, what conditions can cause T-wave inversions in leads V1 through V4?
- William Morris, MD
   Athens, Tenn


The T wave is the ECG manifestation of ventricular repolarization of the cardiac electrical cycle. 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. Thus, T-wave inversions in leads V1 and V2 may be fully normal. 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.

Primary and secondary T-wave inversions

The causes of T-wave inversions have commonly been grouped into 2 categories: primary T-wave changes and secondary T-wave changes. 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. Secondary T-wave changes result from aberrant ventricular activation in the context of normal action potential characteristics. Examples include bundle branch blocks, preexcitation states, and ventricular ectopic or paced beats.

Coronary artery disease

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. In addition, an important subgroup of patients with unstable angina present with significantly abnormal T-wave inversions-either symmetric, deeply inverted T waves or biphasic T waves in the precordial leads (V2 and V3 in particular). Patients with this history and these ECG findings have Wellen syndrome, which is frequently associated with proximal left anterior descending coronary artery critical stenosis.

Neurogenic causes

There are a number of neurogenic causes of primary T-wave inversions, each of which has characteristic features. For example, T waves in patients who have sustained a cerebrovascular accident (CVA) have a distinctly deep, widely splayed appearance with an outward bulge of the ascending limb that results in a striking asymmetry. This has been termed the “CVA T-wave pattern.” CNS hemorrhage and status epilepticus are also associated with T-wave abnormalities.

Pulmonary causes

Patients with pulmonary embolism (PE) may also display T-wave abnormalities, including T-wave inversions. The T-wave findings in these patients are typically shallow inversions in the inferior leads. Deeper T-wave inversions- attributed to acute right ventricular strain and occasionally seen in patients with massive PE-are generally observed in the right to mid precordial leads.

Arrhythmias

Right bundle branch block, with its associated depolarization- repolarization changes, may produce marked ST-segment–T-wave changes. The QRS complex in leads V1 to V3 may assume any of the following morphologies:

  • Monophasic R waves.
  • Biphasic RSR complex.
  • qR formations.

The expected ST-segment–T-wave configurations are discordant, directed opposite from the terminal portion of the QRS complex; this pattern is called QRS-complex–T-wave axis. Leads with largely positive QRS complexes will demonstrate depressed ST segments and/or inverted T waves. The right precordial leads, which have predominantly positive forces, are usually associated with ST-segment depression and T-wave inversion. Patients with Wolff-Parkinson-White syndrome present at times with ST-segment and T-wave changes as well as abnormalities of the QRS complex- the so-called pseudo-infarction findings. For example, Q waves may be seen in leads II, III, and aVF that mimic past inferior MI. There may also be tall R waves in the right precordial leads, suggestive of a posterior wall acute MI; T-wave inversions are sometimes seen in these leads with prominent R waves.

Benign causes

These include the digitalis effect and the persistent juvenile T-wave pattern. Digitalis compounds have been implicated as a cause of T-wave inversions in otherwise healthy persons. The “digitalis effect” refers to ECG findings that are observed with therapeutic levels of the drug. These include T-wave inversions, flattened T waves, an increased U wave, a prolonged PR interval, ST-segment depression with a distinct “scooped” appearance, and a shortened QTc interval (secondary to abbreviated ventricular action potential). Juvenile T-wave inversions may appear in the precordial leads (eg, V1, V2, and V3) with an accompanying early repolarization pattern. These findings may continue into adulthood, and some patients demonstrate persistent T-wave inversions in the precordial leads.

- William J. Brady, Jr, MD
   Associate Professor and Vice Chair
   Department of Emergency Medicine
   University of Virginia School of Medicine
   Charlottesville

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