doi: 10.1161/01.STR.0000147969.77538.c2
(Stroke. 2004;35:2755.)
© 2004 American Heart Association, Inc.
Letters to the Editor |
Contrast Ultrasound Techniques in the Detection and Quantification of Patent Foramen Ovale: Myth Versus Reality
Graz-West Hospital, Graz, Austria
To the Editor:
I read with great interest the study of Anzola et al. The authors declared contrast-enhanced transcranial Doppler (ce-TCD) as the ideal tool to follow up patients after interventional device closure.1
Data show a high correlation between ce-TCD and contrast enhanced transesophageal echocardiograpgy (cTTE) which is the current "gold standard" for detection of a right-to-left shunt through a patent foramen ovale (PFO), although there is a highly reported interobserver and intraobserver variability of the latter.2 Furthermore, there are major methodological limitations of these techniques that need to be addressed.
The numbers of microbubbles reaching the brain can be quantified by ce-TCD, however the therapeutic impact of this information is unknown. There is no prospective study (neither by ce-TCD nor by cTEE) demonstrating that the amount of contrast shunting has any relevance for the outcome of these patients.2,3 We have previously shown that the amount of contrast shunting does not correlate with the size of the PFO measured by 2-dimensional TEE or invasively by balloon sizing.4
Devuyst and colleagues reported that the amount of right-to-left contrast shunting through a PFO measured my ce-TCD mainly depends on strain rate and duration of the Valsalva maneuver.5 As Anzola et al did not perform the ce-TCD follow up under these controlled conditions, 2 contrast studies may lead to different results in the same patient even if the PFO would not have been closed.
It has been shown previously that ce-TCD with saline contrast can remain positive, even without difference in the intensity, after complete occlusion of anatomical arteriovenous malformations.6
According to recent findings one must accept that there is no rigid diagnostic time window for differentiation between interatrial and intrapulmonary shunts.7–10 And there is evidence that physiological arteriovenous intrapulmonary shunts do exist in most healthy humans.11 As we know so far, shunting through this dynamic vascular network is influenced on a variety of patient dependent and methodological reasons like cardiac output, blood pressure, or drugs.11–13
Before and after PFO-closure we recommend, irrespective of the results of a ce-TCD, to perform a TEE examination, as it provides direct anatomic information regarding the site and nature of the shunt and regarding the device to exclude a thrombus formation.14
References
1. Anzola GP, Morandi E, Casilli F, Onorato E. Does transcatheter closure of patent foramen ovale really "shut the door?". A prospective study with transcranial Doppler. Stroke. 2004; 35: 2140–2144.
2. Mas JL, Arquizan C, Lamy C, Zuber C, Cabanas L, Derumeaux G, Coste J. Recurrent cerebrovascular events associated with patent foramen ovale, atrial septal aneurysm, or both. N Engl J Med. 2001; 345: 1740–1746.
3. Homma S, Sacco RL, Di Tullio M, Sciacca, Mohr JP. Effect of medical treatment in stroke patients with patent foramen ovale. Circulation. 2002; 105: 2625–2631.
4. Schuchlenz HW, Weihs W, Beitzke A, Stein JI, Gamillscheg A, Rehak P. Transesophageal echocardiography for quantifying size of patent foramen ovale in patients with cryptogenic cerebrovascular events. Stroke. 2002; 33: 293–296.
5. Devuyst G, Piechowski-Jozwiak B, Karapanayiotides T, Fitting JW, Kemeny V, Hirt L, Urbano LA, Arnold P, van Melle G, Despland PA, Bogouslavsky J. Controlled contrast transcranial Doppler and arterial blood gas analysis to quantify shunt through patent foramen ovale. Stroke. 2004; 35: 859–863.
6. Yeung M, Khan KA, Antecol DH, Walker DR, Shuaib A. Transcranial Doppler ultrasonography and transesophageal echocardiography in the investigation of pulmonary arteriovenous malformation in a patient with hereditary hemorrhagic teleangiectasia presenting with stroke. Stroke. 1995; 26: 1941–1944.
7. Jauss M, Zanette E for the consensus conference. Detection of right–to-left shunts with ultrasound contrast agent and transcranial Doppler sonography. Cerebrovascular Dis. 2000; 10: 490–496.[CrossRef][Medline] [Order article via Infotrieve]
8. Nanthakumar K, Graham AT, Robinson TI, Grande P, Pugash RA, Clarke JA, Hutchinson SJ, Mandzia JL, Hyland RH, Faughnan ME. Contrast echocardiography for detection of pulmonary arteriovenous malformations. Am Heart J. 2001; 141: 243–246.[CrossRef][Medline] [Order article via Infotrieve]
9. Naqvi TZ, Nagai T, Atar S, Siegel RJ. Early appearance of echo-contrast simulating an intracardiac shunt in a patient with liver cirrhosis and intrapulmonary shunting. J Am Soc Echocardiogr. 2002; 15: 379–381.[CrossRef][Medline] [Order article via Infotrieve]
10. Droste DW, Kriete JU, Stypman J, Castrucci M, Wichter T, Tietje R, Weltermann B, Young P, Ringelstein EB. Contrast transcranial Doppler ultrasound in the detection of right-to-left shunts. Comparison of different procedures and different contrast agents. Stroke. 1999; 30: 1827–1832.
11. Eldridge MW, Dempsey JA, Haverkamp HC, Lovering AT, Hokanson JS. Exercise-induced intrapulmonary arteriovenous shunting in healthy humans. J Appl Physiol. 2004Sep; 97: 797–805.
12. Sokoll MD, Gergis SD, Kassell NF. Comparativ effects of barbiturate or enflurane anesthesia with induced hypotension on intrapulmonary shunting. J Neurosurg. 1984; 60: 248–251.[Medline] [Order article via Infotrieve]
13. Nomoto S, Berk JL, Hagen JF, Koo R. Pulmonary anatomic arteriovenous shunting caused by epinephrine. Arch Surg. 1974 Feb; 108: 201–204.
14. Krumsdorf U, Ostermayer S, Billinger K, Treples T, Zadan E, Horvath K, Sivert H. Indcidence and clinical course of thrombus formation on atrial septal defect and patent foramen ovale closure devices in 1000 consecutive patients. J Am Coll Cardiol. 2004; 43: 302–309.
Response:
Service of Neurology, S. Orsola Hospital FBF, Brescia, Italy
Department of Cardiology, Humanitas Gavazzeni Clinic, Bergamo, Italy
Dr Schuchlenz’s letter seems to put a special emphasis on the lack of specificity of contrast-enhanced transcranial Doppler (ce-TCD) in differentiating the source of a right-to-left shunt (RLS), namely patent foramen ovale (PFO) versus pulmonary fistulas. In our opinion, however, instead of showing limitation, this is an argument in favor of transcranial Doppler (TCD) as an ideal tool for screening and follow-up purposes inasmuch as paradoxical embolism is suspected responsible for otherwise cryptogenic strokes. It is commonly recognized that TCD detects more RLSs than transesophageal echocardiography (TEE), not only because TEE may miss pulmonary fistulas but also because even in cases of PFO, the patient may be unable to perform a Valsalva strain valid enough to divert bubbles from the right to the left atrium across the PFO.1 This raises some doubt on the concept of TEE as the gold standard for PFO detection.
There are at least 2 studies that have shown a relationship between the amount of RLS as assessed with TCD and stroke occurrence or relapse.2,3
The ce-TCD test was always performed in controlled conditions following the recommendations of the Consensus of Venice4 and the strength of Valsalva was regulated so as to obtain a reduction of at least 20% of the spectral amplitude. For these reasons we believe that the bubble load assessed in the middle cerebral arteries at follow-up testing truly reflected the degree of residual shunt.5
The fact that TCD (and TEE) remain positive after apparently successful embolization of a pulmonary arteriovenous malformation (AVM) in a patient with Rendu-Osler disease, as is reported in Yeung et al6 is not surprising for at least 2 reasons. First, the embolization of a macroscopic pulmonary AVM may not abolish the local RLS. Second, Rendu-Osler disease entails the presence of multiple microscopic AVMs that can escape angiography but nonetheless bring about a cumulatively significant RLS.
Physiological intrapulmonary shunts are activated after prolonged strenuous exercise7 whereas ce-TCD requires a simple Valsalva strain for a few seconds.
None of the patients in our series was under the effect of drugs likely to affect intrapulmonary shunts.8,9
Our policy is to perform TEE after TCD demonstrates RLS to confirm the intracardiac site before PFO closure and to repeat it postprocedurally only in those patients in whom TCD has shown a significant residual shunt or in those who relapse after successful closure. Routine use of TEE to detect thrombus formation in the left atrium does not seem justified in asymptomatic patients given the very low absolute incidence of thrombus formation with the more recent devices.10
References
1. Droste DW, Lakemeier S, Wichter T Stypmann J, Dittrich R, Ritter M, Moeller M, Freund M, Ringelstein EB MD. Optimizing the technique of contrast transcranial Doppler ultrasound in the detection of right-to-left shunts. Stroke. 2002; 33: 2211–2216.
2. Anzola GP, Zavarise P, Morandi E, Rozzini L, Parrinello G. Transcranial Doppler and the risk of recurrence in patients with stroke and patent foramen ovale. European JNeurology. 2003; 10: 1–7.
3. Serena J, Segura T, Perez-Ayuso MJ, Bassaganyas J, Molins A, Davalos A. The need to quantify right-to-left shunt in acute ischemic stroke: a case-control study. Stroke. 1998; 29: 1322–1328.
4. Jauss M, Zanette E. Detection of right-to-left shunt with ultrasound contrast agent and transcranial Doppler sonography. Cerebrovasc Dis. 2000; 10: 490–496.[CrossRef][Medline] [Order article via Infotrieve]
5. Zanette EM, Mancini G, De Castro S, Solaro M, Cartoni D, Chiarotti F. Patent foramen ovale and transcranial Doppler. Comparison of different procedures. Stroke. 1996; 27: 2251–2255.
6. Yeung M, Khan KA, Antecol DH, Walker DR, Shuaib A. Transcranial Doppler ultrasonography and transesophageal echocardiography in the investigation of pulmonary arteriovenous malformation in a patient with hereditary hemorrhagic teleangiectasia presenting with stroke. Stroke. 1995; 26: 1941–1944.
7. 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.
8. Sokoll MD, Gergis SD, Kassell NF. Comparative effects of barbiturate or enflurane anesthesia with induced hypotension on intrapulmonary shunting. J Neurosurg. 1984; 60: 248–251.[Medline] [Order article via Infotrieve]
9. Nomoto S, Berk JL, Hagen JF, Koo R. Pulmonary anatomic arteriovenous shunting caused by epinephrine. Arch Surg. 1974Feb; 108: 201–204.
10. Krumsdorf U, Ostermayer S, Billinger K, Treples T, Zadan E, Horvath K, Sivert H. Indcidence and clinical course of thrombus formation on atrial septal defect and patent foramen ovale closure devices in 1000 consecutive patients. J Am Coll Cardiol. 2004; 43: 302–309.
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