Author + information
- Carl J. Pepine, MD∗ (, )
- C. Noel Bairey Merz, MD and
- B. Delia Johnson, PhD
- ↵∗Division of Cardiovascular Medicine, University of Florida, 1600 SW Archer Road, PO Box 100277, Gainesville, Florida 32610-0277
We appreciate the interest in our State-of-the-Art Review on nonobstructive coronary artery disease (CAD) (1) and the interesting data about migraine, and are pleased to add our comments.
In a previous report from the original Women’s Ischemia Syndrome Evaluation (WISE) cohort, among 905 women, mean age 58 years, 220 reported a migraine history (2). They had lower angiographic CAD severity scores and less severe (≥70% stenosis) angiographic CAD versus women without migraine history (n = 685). These differences remained significant after adjustment for important cardiac risk factors. We prospectively followed 873 of the WISE cohort and found that migraine was not associated with a significant increase in adverse outcomes after 4.4 years. In addition, a preliminary analysis of that cohort concluded migraine was not linked to alterations in endothelial function (unpublished observations).
We have since reported WISE 10-year outcomes that now included a National Death Registry search (3). In response to this letter we updated our prior analyses, and now note that of a total cohort of 902 women included in extended follow-up 177 women died. Among those reporting migraine headaches, 32 of 220 (14%) died (all-cause) versus 145 of 682 (21%) in those without migraine (hazard ratio: 0.66; 95% confidence interval: 0.45 to 0.96; p = 0.031 [unadjusted]). However, when adjusted for age, diabetes, body mass index, smoking, family history of CAD, race, aspirin use, dyslipidemia, and CAD severity score, absence of migraine is no longer a significant predictor for either all-cause death (hazard ratio: 1.12; 95% confidence interval: 0.73 to 1.72; p = 0.60) or cardiovascular death.
We also use this opportunity to reemphasize that it is no longer possible to support use of the term “cardiac syndrome X” for the rationale described in our recent article (1). A comprehensive review confirmed that there were no standard definitions for this terminology among published data (4). Furthermore, at least 1 pathophysiological mechanism present in many of these patients is attributable to coronary microvascular dysfunction, and therefore no longer “unknown” as implied by this term.
Please note: This work was supported by contracts N01-HV-68161, N01-HV-68162, N01-HV-68163, N01-HV-68164 from the National Heart, Lung, and Blood Institutes; grants U0164829, U01 HL649141, U01 HL649241, K23HL105787, T32HL69751, R01 HL090957, 1R03AG032631 from the National Institute on Aging; GCRC grant MO1-RR00425 from the National Center for Research Resources; the National Center for Advancing Translational Sciences Grants UL1TR000124 and UL1TR001427; and grants from the Gustavus and Louis Pfeiffer Research Foundation, Danville, New Jersey; The Women’s Guild of Cedars-Sinai Medical Center, Los Angeles, California; The Ladies Hospital Aid Society of Western Pennsylvania, Pittsburgh, Pennsylvania; QMED, Inc., Laurence Harbor, New Jersey; the Edythe L. Broad and the Constance Austin Women’s Heart Research Fellowships; Cedars-Sinai Medical Center, Los Angeles, California; the Barbra Streisand Women’s Cardiovascular Research and Education Program, Cedars-Sinai Medical Center, Los Angeles, California; The Society for Women’s Health Research (SWHR), Washington, D.C.; The Linda Joy Pollin Women’s Heart Health Program; and the Erika Glazer Women’s Heart Health Project, Cedars-Sinai Medical Center, Los Angeles, California. All authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation
- Pepine C.J.,
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- Shaw L.J.,
- et al.
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