Correlation between ST-segment elevation and negative T waves in the precordial leads in acute pulmonary embolism: insights into serial electrocardiogram changes

Abstract

Background: Acute pulmonary embolism (APE) is often misdiagnosed as acute coronary syndrome because of the similarity of the presenting symptoms and of the electrocardiogram (ECG) manifestations. In APE, ST-segment elevation (STE) in leads V1 to V3 /V4 , mimicking anteroseptal myocardial infarction, is not a rare phenomenon. Negative T waves (NTW) in the precordial leads mimicking the "Wellens' syndrome" is an important ECG manifestation of APE. The evolution of these ECG changes-STE and NTW-in APE has not been thoroughly studied.

Methods: We present two patient cases with APE and their evolving serial ECGs to analyze the correlation between STE and NTW.

Results: NTW developed later than STE in these two patient cases.

Conclusions: NTW might represent a "postischemic" ECG pattern indicating a previous stage with transmural myocardial ischemia.

Keywords: acute pulmonary embolism; electrocardiogram; myocardial ischemia; right ventricular dysfunction.

Figure 1

(A) The ECG on admission showed sinus tachycardia, SI–SII–SIII pattern, qs pattern in V₃R, V₄R, V₅R and V₁, transitional zone in precordial leads is dislocated to left, minor STE in leads aVR, V₁–V₃, and V₃R–V₅R, and NTW waves in leads III, V₃R–V₅R, V₁–V₄. (B) The ECG during cardiogenic shock showed sinus tachycardia, obvious STE in leads III, aVR, V₁–V₃, and V₃R–V₅R, newly emerging ST‐segment depression in leads I, II, aVL and V₅–V₆, and pseudo‐normalization of NTW in leads V₃R–V₅R, V₁–V₄. (C) The ECG after thrombolytic therapy showed reappearance of NTW in leads V₁–V₅, deeper than that at admission, without ST deviation in any lead. (D) The ECG 4 days later showed NTW in leads II, III, aVF, V₁–V₅, and V₃R–V₅R. (E) The ECG 1 month later showed disappearance of NTW in leads II, III, aVF, V₂–V₅.

Figure 2

(A) and (B) Color Doppler examination showed severe tricuspid regurgitation and 83 mmHg of the regurgitation pressure gradient. (C) The apical 4‐chamber view at the apex of the heart revealed enlarged right ventricle, which was greater than the left ventricle. (D) Parasternal short‐axis view at end diastole showed interventricular septal flattening and thus formed the D‐shaped left ventricle. (E) The apical 4‐chamber view at the apex of the heart after treatment revealed normal right ventricle and left ventricle morphology. (F) Parasternal short‐axis view at end diastole after treatment showed disappearance of the D‐shaped left ventricle.

Figure 3

(A) A previous ECG showed left‐axis deviation of the frontal plane QRS axis, but was otherwise normal. (B) The ECG on admission showed SI–QIII pattern, minor STD in leads I, II, aVF, V₄–V₆ and minor STE in leads aVR and V₁. (C) The ECG during cardiogenic shock showed deeper STD in leads I, II, aVF, V₄–V₆ and higher STE in the leads aVR, V₁ and V₂. (D) The ECG after successful thrombolytic therapy showed NTW in leads V₁–V₄ without ST‐segment deviation. (E) The ECG 8 days later showed disappearance of SI–QIII and NTW in lead V₄.

Figure 4

(A) The apical 4‐chamber view at the apex of the heart revealed enlarged right ventricle, which was greater than the left ventricle. (B) Color Doppler examination showed severe tricuspid regurgitation and 35 mmHg of the regurgitation pressure gradient. (C) The apical 4‐chamber view at the apex of the heart after treatment revealed normal right ventricle and left ventricle morphology. (D) Color Doppler examination showed mild tricuspid regurgitation and 25 mmHg of the regurgitation pressure gradient.