Author + information
- Karthik Murugiah, MD,
- Nihar N. Desai, MD, MPH and
- Harlan M. Krumholz, MD, SM∗ ()
- ↵∗Section of Cardiovascular Medicine, Department of Internal Medicine, Yale School of Medicine, 1 Church Street, Suite 200, New Haven, Connecticut 06510
We thank Dr. Madias for his interest in our paper and for his comments. With regard to the first comment concerning the cohort with a principal diagnosis of Takotsubo cardiomyopathy (TTC), we would like to clarify that by “coronary presentations of TTC,” we mean patients presenting with symptoms suggestive of an acute coronary syndrome, as opposed to those being admitted with infective symptoms (e.g., sepsis) or neurological symptoms, as in a stroke, etc. We are not suggesting that the causal mechanism for TTC among principal TTC patients involves a pathological or functional alteration of the coronaries.
With his second comment, Dr. Madias makes an important observation about differences in cardiac risk factor burden. There is likely to be important heterogeneity between U.S. and international studies of TTC in terms of risk factor and coronary artery disease (CAD) burden, and we are not surprised by this finding. We know this to be true in terms of the prevalence of comorbidities, health care delivery, and socioeconomics and other contextual factors between different global populations in general (1), factors that are likely also relevant in TTC.
With regard to CAD and TTC, CAD is frequently encountered in patients with TTC, and we don’t think it must be regarded as a “contamination” of a true phenotype of TTC. A recently published report from the International Takotsubo Registry showed that patients with TTC had a 15.3% prevalence of coexistent CAD (2). Other studies reporting angiographic findings in patients with TTC have reported a 40% to 80% prevalence of CAD (3,4). The Mayo criteria for establishing a diagnosis of TTC require the absence of “obstructive” CAD or evidence of acute plaque disruption (5). If CAD is found but the wall motion abnormalities are not in the distribution of the stenosis, the diagnosis of TTC can still be made. However, the role of CAD or coronary artery dysfunction in the pathogenesis of TTC, as Dr. Madias points out, is unclear.
Please note: Dr. Krumholz is the recipient of research agreements from Medtronic and from Johnson & Johnson (Janssen), through Yale University, to develop methods of clinical trial data sharing and is chair of a cardiac scientific advisory board for UnitedHealth. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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