Mechanism of ST-elevation in precordial leads V 1–V 4 in acute pulmonary embolism

Abstract

In a recent case report [1] of massive pulmonary embolism (PE) with ST-elevations in precordial leads V1–V4, the authors offered several possible explanations for this paradoxical pattern but failed to mention paradoxical coronary embolism as the most likely mechanism. In contrast to the usual ST depression in precordial leads V1–V4 from right heart strain, [2,3] patients with PE have occasionally shown ST elevations in the right to mid precordial leads on ECG [4–9]. The most likely explanation is paradoxical coronary embolism secondary to PE [10–21]. Paradoxical embolism usually occurs in the setting of a sudden rise of right heart pressure, e.g., acute PE, or Valsalva maneuver during straining at defecation or cough, which causes a rightto-left shunt through a pre-existing patent foramen ovale or small atrial septal defect or atrial septal aneurysm [10–21]. Patent foramen ovale is a frequent finding, occurring in approximately one quarter of the population, both at autopsy (27.3% [22]) and by echocardiography in a large populationbased Stroke Prevention: Assessment of Risk in a Community (SPARC) study (25% [23]) and in divers (27.6% [24]). The prevalence is even higher in patients with PE (35% [25]) and unexplained stroke (54% [26]–75% [27]). Formerly considered merely an innocent incidental postmortem finding, patent foramen ovale began to attract increasing attention in the clinical arena in recent years for its role in causing paradoxical embolism and with the recent introduction of several percutaneous devices for its successful closure.