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(Stroke. 2009;40:e531.)
© 2009 American Heart Association, Inc.

Letters to the Editor

Response to Letter by Altieri et al

Thomas J. Kiernan, MD; Bryan P. Yan, MD Pablo Rengifo-Moreno, MD

Department of Interventional Cardiology and Vascular Medicine, Massachusetts General Hospital, Boston, Mass

MingMing Ning, MD

Cardio-Neurology Clinic, Stroke Service, Department of Neurology, Massachusetts General Hospital, Boston, Mass, and Clinical Proteomics Research Center, Department of Neurology, Massachusetts General Hospital, Boston, Mass

Zareh N. Demirjian, MD

Hematology Unit, Department of Medicine, Massachusetts General Hospital, Boston, Mass

Michael R. Jaff, DO

Section of Vascular Medicine, Department of Cardiology, Massachusetts General Hospital, Boston, Mass

Ferdinando S. Buonanno, MD

Cardio-Neurology Clinic, Stroke Service, Department of Neurology, Massachusetts General Hospital, Boston, Mass, and Clinical Proteomics Research Center, Department of Neurology, Massachusetts General Hospital, Boston, Mass

Robert M. Schainfeld, DO Igor F. Palacios, MD

Department of Interventional Cardiology and Vascular Medicine, Massachusetts General Hospital, Boston, Mass

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Response:

We thank Altieri and colleagues for their response letter and for their insightful comments regarding our novel article.

The core message that pervades our manuscript is that May-Thurner syndrome potentially represents a novel risk factor for embolic stroke. The diagnosis of May-Thurner syndrome in a patient who had sustained a stroke of cryptogenic etiology, as a sole entity, likely does not increase the risk of embolic stroke. However, in association with other concomitant risk factors such as a thrombophilic disorder, birth control pills and a patent foramen ovale (PFO), then May-Thurner syndrome can potentially lead to a higher risk of embolic stroke. It must be also pointed out that in the context of embolic stroke, not all thrombophilic conditions warrant lifelong anticoagulation and some patients may be genetically resistant to antiplatelet therapy.¹ The benefits of PFO closure in these patients outweigh the associated risks of the procedure, which are low, approximately 2.2% when performed in centers of excellence.² Because the risk of stroke in the general population is estimated to be 1% per year, and PFO is an independent risk factor for stroke,³ a therapeutic intervention to lower this risk appears justified, particularly given that the current best alternative strategy of initiating permanent oral anticoagulation is not only cumbersome but carries a substantial risk for bleeding.

We agree with the authors that the current definition of "cryptogenic stroke" can indeed be "cryptic" and often times reflects the lack of an exhaustive, comprehensive work-up to determine etiology. Mohr and colleagues . . . [Full Text of this Article]