Author + information
- Received December 16, 2011
- Accepted January 20, 2012
- Published online April 1, 2012.
- Tobias M. Freilinger, MD⁎,†,⁎ (, )
- Andreas Schindler, BSc§,
- Caroline Schmidt, MD⁎,
- Jochen Grimm, MD§,
- Clemens Cyran, MD§,
- Florian Schwarz, MD§,
- Fabian Bamberg, MD§,
- Jennifer Linn, MD∥,
- Maximilian Reiser, MD§,
- Chun Yuan, PhD‡,
- Konstantin Nikolaou, MD§,
- Martin Dichgans, MD† and
- Tobias Saam, MD§
- ↵⁎Reprint requests and correspondence:
Dr. Tobias M. Freilinger, Neurologische Klinik und Poliklinik und Institut für Schlaganfall- und Demenzforschung, Klinikum Großhadern der Ludwig-Maximilians-Universität München, Marchioninistrasse 15, 81377 München, Germany
Objectives Our goal was to assess the prevalence of complicated American Heart Association (AHA) lesion type VI plaques in the carotid arteries of patients with cryptogenic stroke.
Background In up to 40% of ischemic stroke patients, no definite cause can be established despite extensive workup (i.e., cryptogenic stroke). To test the hypothesis if nonstenosing complicated carotid plaques may be the underlying etiology in some of these patients, we used high-resolution black-blood carotid magnetic resonance imaging (MRI), which can quantitatively assess plaque composition and morphology with good correlation to histopathology. Specifically, we focused on AHA type VI plaques, which are characterized by hemorrhage, thrombus, or fibrous cap rupture.
Methods Thirty-two consecutive patients (22 male; mean age 71.7 ± 11.9 years) with cryptogenic stroke and nonstenosing (<50%) eccentric carotid plaques were recruited from a single stroke unit. All patients underwent extensive clinical workup (brain MRI, duplex sonography, electrocardiography and Holter monitoring, transthoracic and transesophageal echocardiography, and laboratory investigations) to exclude other causes of stroke. All patients received a black-blood carotid MRI at 3-T with fat-saturated pre- and post-contrast T-1–, proton density–, and T-2–weighted and time-of-flight images using surface coils and parallel imaging techniques. Prevalence of AHA type VI plaque was determined in both carotid arteries on the basis of previously published MRI criteria.
Results AHA type VI plaques were found in 12 of 32 arteries (37.5%) ipsilateral to the stroke, whereas there were no AHA type VI plaques contralateral to the stroke (p = 0.001). The most common diagnostic feature of AHA type VI plaques was intraplaque hemorrhage (75%), followed by fibrous plaque rupture (50%) and luminal thrombus (33%).
Conclusions This pilot study suggests that arterio-arterial embolism from complicated, nonstenosing carotid atherosclerotic plaques may play a role in a subgroup of patients previously diagnosed with cryptogenic stroke. To further evaluate the significance of AHA type VI plaques in cryptogenic stroke, future studies will have to analyze both clinical and imaging follow-up data, including event rates for secondary strokes.
Dr. Bamberg has received a speakers fee from Siemens Healthcare, Forchheim, Germany. Dr. Reiser serves on the editorial board of Der Radiologe (Zeitschrift für diagnostische und interventionelle Radiologie, Radioonkologie, Nuklearmedizin). Dr. Yuan has been a consultant to Pfizer, Merck, Bristol Myers Squibb, and ImagePace, and has received grant support from Philips and VP Diagnostics. Dr. Nikolaou has served on a scientific advisory board for Bayer Schering Pharma; serves as Cardiac Section Editor for European Radiology; receives royalties from the publication of Multislice CT, Third Edition (Springer, 2005); and serves on the Speaker's Bureaus for and has received speaker honoraria from Bayer Schering Pharma, Bracco S.p.A., and Siemens Medical Solutions. Dr. Dichgans served as Genetics Section Editor for Stroke and receives research support from BMB, NGFN-Plus, Wellcome Trust, and the Foundation for Vascular Dementia Research; he has been a consultant to Bayer Vital GmbH, Boehringer Ingelheim Pharma GmbH & Co. KG, and Trommsdorff GmbH & Co. KG; and has received honoraria from Bayer Vital GmbH, Boehringer Ingelheim Pharma GmbH & Co. KG, Lundbeck GmbH, Sanofi-Aventis Deutschland GmbH, Shire Deutschland GmbH, DZNE, Georg Thieme Verlag KG, UpToDate, and W. Kohlhammer GmbH. Dr. Saam receives research support from Bayer Schering Pharma and Diamed Medizintechnik. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. A. Schindler and Dr. Schmidt contributed equally to the paper.
- Received December 16, 2011.
- Accepted January 20, 2012.
- American College of Cardiology Foundation