(Stroke. 2005;36:1109.)
© 2005 American Heart Association, Inc.
Letters to the Editor |
Contrast Ultrasound Techniques in the Detection and Quantification of Patent Foramen Ovale: Myth Versus Reality—A Clarification
The John Rankin Laboratory of Pulmonary Medicine, Department of Population Health Sciences, University of Wisconsin—Madison, Wisconsin
The John Rankin Laboratory of Pulmonary Medicine, Department of Population Health Sciences, University of Wisconsin—Madison, and, University of Wisconsin School of Medicine, Department of Pediatrics and Critical Care Medicine, Madison, Wisconsin
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
Acknowledgments
Funding by the National Heart, Lung, and Blood Institute (NHLBI) Grant HL-15469 and the Department of Pediatrics, University of Wisconsin–Madison. A.T.L. was supported by a NHLBI Training Grant–T32 HL07654–16 and M.K.S. was supported by the Natural Sciences and Engineering Research Council of Canada.
References
1. Schuchlenz HW. Contrast ultrasound techniques in the detection and quantification of patent foramen ovale: myth versus reality. Stroke. 2004; 35: 2755–2756.
2. Anzola GP, Morandi E, Casilli F, Onorato E. Response. Stroke. 2004; 35: 2755–2756.
3. Eldridge MW, Dempsey JA, Haverkamp HC, Lovering AT, Hokanson JS. Exercise-induced intrapulmonary arteriovenous shunting in healthy humans. J Appl Physiol. 2004; 97: 797–805.
4. Stickland MK, Welsh RC, Haykowsky MJ, Petersen SR, Anderson WD, Taylor DA, Bouffard M, Jones RL. Intra-pulmonary shunt and pulmonary gas exchange during exercise in humans. J Physiol. 2004; 561: 321–329.
5. Lovering AT, Stickland MK, Eldridge MW. Intrapulmonary shunt during normoxic and hypoxic exercise in healthy humans. In: Roach RC, Wagner PD, Hackett PH, eds. Hypoxia: Exercise and Hypoxia. New York: Kluwer Academic/Plenum Publishers; 2005. (In press).
6. Bogousslavsky J, Pierre P. Ischemic stroke in patients under age 45. Neurol Clin. 1992; 10: 113–124.[Medline] [Order article via Infotrieve]
7. Foulkes MA, Wolf PA, Price TR, Mohr JP, Hier DB. The Stroke Data Bank: design, methods, and baseline characteristics. Stroke. 1988; 19: 547–554.
8. Stern BJ, Kittner S, Sloan M, Meyd C, Buchholz D, Rigamonti D, Woody R, Meyerhoff J, Bell W, Price T. Stroke in the young. (Part I). Md Med J. 1991; 40: 453–462.[Medline] [Order article via Infotrieve]
9. Stern BJ, Kittner S, Sloan M, Meyd C, Buchholz D, Rigamonti D, Woody R, Meyerhoff J, Bell W, Price T. Stroke in the young. Part II. Md Med J. 1991; 40: 565–571.[Medline] [Order article via Infotrieve]
10. Lamy C, Giannesini C, Zuber M, Arquizan C, Meder JF, Trystram D, Coste J, Mas JL. Clinical and imaging findings in cryptogenic stroke patients with and without patent foramen ovale: the PFO-ASA Study. Atrial Septal Aneurysm. Stroke. 2002; 33: 706–711.
11. Ranoux D, Cohen A, Cabanes L, Amarenco P, Bousser MG, Mas JL. Patent foramen ovale: is stroke due to paradoxical embolism? Stroke. 1993; 24: 31–34.
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