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Year: 2014 Volume: 2 Issue: 1

Year: 2013 Volume: 1

Left ventricular amyloid deposition in patients with heart failure and preserved ejection fraction.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Mohammed, Selma F. Mirzoyev, Sultan A. Edwards, William D. Dogan, Ahmet Grogan, Donna R. Dunlay, Shannon M. Roger, Veronique L. Gertz, Morie A. Dispenzieri, Angela Zeldenrust, Steven R. Redfield, Margaret M.
Description	Author Affiliation: Mohammed SF ( Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota); Mirzoyev SA ( Mayo Medical School, Mayo Clinic, Rochester, Minnesota.); Edwards WD ( Division of Anatomic Pathology, Mayo Clinic, Rochester, Minnesota.); Dogan A ( Division of Hematology, Mayo Clinic, Rochester, Minnesota.); Grogan DR ( Clementia Pharmaceuticals, Montreal, Canada.); Dunlay SM ( Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota.); Roger VL ( Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota); Gertz MA ( Division of Hematology, Mayo Clinic, Rochester, Minnesota.); Dispenzieri A ( Division of Hematology, Mayo Clinic, Rochester, Minnesota.); Zeldenrust SR ( Division of Hematology, Mayo Clinic, Rochester, Minnesota.); Redfield MM ( Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota. Electronic address: redfield.margaret@mayo.edu.)
Abstract	OBJECTIVES: This study sought to determine the frequency of left ventricular amyloid in heart failure with preserved ejection fraction (HFpEF). BACKGROUND: Left ventricular amyloid deposition can cause diastolic dysfunction and HFpEF. METHODS: Autopsy of left ventricular specimens from patients with antemortem diagnosis of HFpEF without clinically apparent amyloid (n = 109) and from control subjects (n = 131) were screened with sulfated Alcian blue and subsequent Congo red staining with microdissection for mass spectrometry-based proteomics to determine amyloid type. Fibrosis was assessed with quantitative whole-field digital microscopy. RESULTS: The presence of wild-type transthyretin (wtTTR) amyloid was associated with age at death and male sex, but the age- and sex-adjusted prevalence of wtTTR amyloid was higher in HFpEF patients than in control subjects (odds ratio: 3.8, 95% confidence interval: 1.5 to 11.3; p = 0.03). Among HFpEF patients, moderate or severe interstitial wtTTR deposition, consistent with senile systemic amyloidosis as the primary etiology of HFpEF, was present in 5 (5%) patients (80% men), with mild interstitial and/or variable severity of intramural coronary vascular deposition in 13 (12%) patients. While, wtTTR deposition was often mild, adjusting for age and presence of HFpEF, wtTTR amyloid was associated with more fibrosis (p = 0.005) and lower age, sex, and body size-adjusted heart weight (p = 0.04). CONCLUSIONS: Given the age- and sex-independent association of HFpEF and wtTTR deposition and an emerging understanding of the pathophysiology of the amyloidoses, the current findings support further investigation of the role of wtTTR in the pathophysiology of HFpEF.
File Format	HTM / HTML
ISSN	22131779
e-ISSN	22131787
DOI	10.1016/j.jchf.2013.11.004
Journal	JACC: Heart Failure
Issue Number	2
Volume Number	2
Language	English
Publisher	Elsevier
Publisher Date	2014-04-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cardiology Amyloidosis Pathology Cardiomyopathies Heart Failure Amyloid Metabolism Physiopathology Autopsy Biological Markers Case-control Studies Heart Ventricles Mass Spectrometry Prealbumin Stroke Volume Physiology Comparative Study Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cardiology and Cardiovascular Medicine

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