Contrast ultrasound techniques in the detection and quantification of patent foramen ovale: myth versus reality--a clarification.

Contrast Ultrasound Techniques in the Detection and Quantification of Patent Foramen Ovale: Myth Versus Reality—A Clarification To the Editor: We were pleased to see that our research was cited in a Letter to the Editor in Stroke, particularly in the context of paradoxical embolization and cryptogenic stroke.1 However, in both the Letter to the Editor and the Response to the Letter to the Editor, the results of our study were cited inaccurately.1,2 As such, we feel obliged to clarify some very important results from our study, so that misconceptions can be prevented. Specifically, in the Letter to the Editor, Dr. Schuchlenz stated that: “. . . there is evidence that physiological arteriovenous intrapulmonary shunts do exist in most healthy humans.”3 While these arteriovenous intrapulmonary shunts appear to exist in most humans, it is important to point out they are not open when the subjects are resting quietly in the seated position, and were only recruited with exercise.3 Stickland et al report similar findings and also found that some (2 of 8) subjects recruit arteriovenous intrapulmonary shunts in the supine position.4 Thus, it appears that these intrapulmonary shunts are not recruited in the normal resting upright human, but are primarily inducible during hyperdynamic conditions, such as exercise. In the Response to the Letter to the Editor by Anzola et al, the authors wrote that: “Physiological intrapulmonary shunts are activated after prolonged strenuous exercise. . . ”3 First, a graded exercise protocol was used to examine intrapulmonary shunting, and shunting occurred at submaximal exercise intensities in 90% of subjects tested to date.3,4,5 As well, we found that some subjects demonstrated exercise-induced intrapulmonary shunting after only 3 minutes of exercise at workloads less than 100 watts. Finally, arteriovenous intrapulmonary shunts were not present in any subject 3 minutes following exercise. Accordingly, our results do not support the statement that prolonged strenuous exercise is required to induce intrapulmonary shunting in normal healthy human subjects, nor that these shunts remain open following exercise. Without question, the opening of these arteriovenous intrapulmonary shunts has the potential to contribute to the gas exchange dysfunction during exercise.4 Furthermore, and possibly more importantly, these dynamic anatomic shunts may provide inducible conduits for the passage of embolic particles that may play a role in paradoxical embolization and thus, cryptogenic stroke and embolic heart disease. This is highlighted by the fact that cryptogenic stroke is more common among young people6–9 and is associated with exertion.10,11