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Relation Between Temperature Extremes and Symptom Exacerbation in Patients With Hypertrophic Cardiomyopathy - 26/02/16

Doi : 10.1016/j.amjcard.2015.12.046 
John P. Bois, MD, Jonathon C. Adams, MD, Gautam Kumar, MD, Steve R. Ommen, MD, Rick A. Nishimura, MD, Kyle W. Klarich, MD
 Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota 

Corresponding author: Tel: (507) 284-1226; fax: (507) 284-3968.

Abstract

Warm temperatures induce peripheral vasodilation, decrease afterload, and may concurrently increase the left ventricular outflow tract (LVOT) gradient. We aimed to assess the impact of subjective ambient temperature on hypertrophic cardiomyopathy (HC) symptoms and determine whether they were associated with LVOT gradient, patient quality of life (QOL), and risk of sudden cardiac death (SCD). We identified consecutive patients with HC presenting to a tertiary referral center. Of the 173 patients in the study, 143 (83%) had HC symptoms, with ambient temperature change worsening symptoms for 72 patients (50%). Symptom exacerbation occurred only with heat for 57 (79%), whereas symptoms were exacerbated with cold only or with cold and heat equally for 15 (21%). Patients affected by any temperature exacerbation more commonly were women (p = 0.009), had a lower QOL (p = 0.04), had a family history of HC (p = 0.007), or underwent myectomy (p = 0.01). A greater proportion of patients with heat-only exacerbation had a family history of HC (p = 0.005) and SCD (p = 0.05). The presence of an LVOT gradient either at rest or with provocation was similar in all groups. In conclusion, although no appreciable difference in LVOT gradients were observed between patient groups, approximately half of the patients with HC reporting symptoms at baseline noted worsening of symptoms with temperature changes, with >75% describing heat-induced symptom exacerbation. Furthermore, affected patients more frequently were women, underwent surgical intervention and device implantation, and had an overall lower QOL.

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 This publication was made possible by CTSA grant number UL1 TR000135 from the National Center for Advancing Translational Sciences, a component of the National Institutes of Health (NIH), Bethesda, Maryland. Its contents are solely the responsibility of the authors and do not necessarily represent the official view of NIH. The funding source had no role in study design; in the collection, analysis, and interpretation of data; in writing the report; and in the decision to submit the article for publication.
 See page 964 for disclosure information.


© 2016  Elsevier Inc. Tutti i diritti riservati.
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