ST-segment depression and T-wave inversion: Classification, differential diagnosis, and caveats

Acute pulmonary embolism

An anterior ischemic pattern of symmetric T-wave inversion in the precordial leads V₁ through V₄ may also be a sign of acute or chronic right ventricular strain, particularly acute pulmonary embolism. Sinus tachycardia is usually present, but other signs of pulmonary embolism, such as right ventricular hypertrophy and right bundle branch block, may be absent. In fact, T-wave inversion in leads V₁ through V₄ is noted in 19% of patients with nonmassive pulmonary embolism and in 85% of patients with massive pulmonary embolism, and is the most sensitive and specific electrocardiographic finding in massive pulmonary embolism.²³

In addition, acute pulmonary embolism may be associated with T-wave inversion in leads III and aVF,²⁴ and changes of concomitant anterior and inferior ischemia should always raise the question of this diagnosis.

In one retrospective study of patients with acute pulmonary embolism, nonspecific ST-segment or T-wave changes were the most common finding on electrocardiography, noted in 49%.²⁵ Rapid regression of these changes on serial tracings favors pulmonary embolism rather than myocardial infarction.

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ST-segment depression reciprocal to a subtle ST-segment elevation

When ST-segment elevation occurs in two contiguous standard leads while ST-segment depression occurs in other leads, and when the ST-segment and T-wave abnormalities are ischemic rather than secondary to depolarization abnormalities, ST-segment elevation is considered the primary ischemic abnormality whereas ST-segment depression is often considered a reciprocal “mirror image” change. This “reciprocal” change may also represent remote ischemia in a distant territory in patients with multivessel coronary disease.^26,27

Reciprocal ST-segment depression is present in all patients with inferior myocardial infarction and in 70% of patients with anterior myocardial infarction.²⁸

However, it is important to recognize that the magnitude of ST-segment elevation and reciprocal ST-segment depression is affected by the distance of the leads recording these changes from the ischemic region and their angle of deviation from the ischemic region.²⁹ This explains why occasionally—and particularly when the overall amplitude of the QRS complex is low—the magnitude of ST-segment elevation is small, whereas the reciprocal ST-segment depression is more prominent. In fact, in the absence of left ventricular hypertrophy or left bundle branch block, the reciprocal ST-segment depression should be sought. It is of great utility in patients with acute cardiac symptoms and mild elevation of ST segments of 1 to 1.5 mm in two contiguous leads, as it strongly suggests the diagnosis of STEMI rather than other causes of mild ST-segment elevation (1–1.5 mm) (Figure 6).³⁰ The less-pronounced ST-segment elevation is often overlooked, and the patient is erroneously diagnosed with non–ST-segment elevation acute coronary syndrome rather than STEMI. This has a marked impact on patient management, as STEMI requires emergency revascularization, while non–ST-segment elevation ischemia requires early (but not emergency) coronary angiography.

Hypokalemia and digitalis effect

ST-segment depression, T-wave flattening, and prominent U waves are the hallmarks of hypokalemia and can be mistaken for ischemic changes, including ischemic lengthening of the QT interval (Figure 7).^31–34 Digitalis also produces ST-segment depression, low or inverted T waves, and prominent U waves, but the U waves rarely are of the giant variety seen with severe hypokalemia, and the ST-segment depression has a sagging shape. In addition, digitalis shortens the QT interval.

DIFFUSE (GLOBAL) T-WAVE INVERSION

Reproduced with permission from Glancy DL, et al. Global T-wave inversion in a 77-year-old woman. Proc (Bayl Univ Med Cent) 2009; 22:81–82.

This term is applied when the T wave is inverted in most of the standard leads except aVR, which shows a reciprocal upright T wave. The QT interval is often prolonged, and T-wave inversion is often symmetric and “giant” (> 10 mm) (Figure 8).^1,35

Walder and Spodick³⁶ have found this pattern to be caused most often by myocardial ischemia or neurologic events, particularly intracranial hemorrhage, and it seems more prevalent in women. Other causes include hypertrophic cardiomyopathy, stress-induced cardiomyopathy (takotsubo cardiomyopathy), cocaine abuse, pericarditis, pulmonary embolism, and advanced or complete atrioventricular block.^36,37

The prognosis in patients with global T-wave inversion is determined by the underlying disease, and the striking T-wave changes per se do not imply a poor prognosis.³⁸

Of note, takotsubo cardiomyopathy is characterized by electrocardiographic changes that mimic ischemia, especially STEMI, and is often impossible to differentiate from myocardial ischemia related to a coronary event without performing coronary arteriography. The most common abnormality on the admission electrocardiogram is ST-segment elevation (present in 46%–100% of patients), typically seen in the precordial leads. Within 48 hours of presentation, almost all patients also develop postischemic diffuse T-wave inversion and prolongation of the QT interval. New Q waves may be seen in 6% to 31% of patients and are usually transient.^39,40

OTHER CAUSES OF T-WAVE INVERSION OR ST-SEGMENT DEPRESSION

Various other entities may cause T-wave inversion, notably acute pericarditis or myocarditis, ^41,42 memory T-wave phenomenon,^43,44 and normal variants of repolarization (Table 1, Figure 9).⁴⁵ Additionally, a nonpathologic junctional ST-segment depression may be seen in tachycardia (Figure 10).