Julien Ternacle1, Diane Bodez1, Aziz Guellich1, Etienne Audureau2, Stephane Rappeneau1, Pascal Lim3, Costin Radu4, Soulef Guendouz1, Jean-Paul Couetil5, Nicole Benhaiem6, Luc Hittinger1, Jean-Luc Dubois-Randé1, Violaine Plante-Bordeneuve7, Dania Mohty8, Jean-François Deux9, Thibaud Damy10. 1. UPEC, Créteil, France; Mondor Amyloidosis Network, Créteil, France; Department of Cardiology, AP-HP, Henri-Mondor Teaching Hospital, Créteil, France; INSERM U955, GRC Amyloid Research Institute, Créteil, France; DHU ATVB, Créteil, France; INSERM Clinical Investigation Center 006, Créteil, France. 2. Mondor Amyloidosis Network, Créteil, France; Department of Cardiology, AP-HP, Henri-Mondor Teaching Hospital, Créteil, France; Department of Public Health, AP-HP, Henri-Mondor Teaching Hospital and Clinical Epidemiology and Aging EA 4393, Créteil, France. 3. UPEC, Créteil, France; Mondor Amyloidosis Network, Créteil, France; Department of Cardiology, AP-HP, Henri-Mondor Teaching Hospital, Créteil, France; DHU ATVB, Créteil, France; INSERM Clinical Investigation Center 006, Créteil, France. 4. UPEC, Créteil, France; Mondor Amyloidosis Network, Créteil, France; DHU ATVB, Créteil, France; INSERM Clinical Investigation Center 006, Créteil, France; Department of Public Health, AP-HP, Henri-Mondor Teaching Hospital and Clinical Epidemiology and Aging EA 4393, Créteil, France. 5. Mondor Amyloidosis Network, Créteil, France; DHU ATVB, Créteil, France; Department of Cardiovascular Surgery, AP-HP, Henri-Mondor Teaching Hospital, Créteil, France. 6. Department of Pathology, AP-HP, Henri-Mondor Teaching Hospital, Créteil, France. 7. UPEC, Créteil, France; Mondor Amyloidosis Network, Créteil, France; INSERM Clinical Investigation Center 006, Créteil, France; Department of Neurology, AP-HP, Henri-Mondor Teaching Hospital, Créteil, France. 8. Department of Cardiology, Dupuytren Hospital, CHU Limoges, Pôle Cœur-Poumon-Rein, Limoges, France. 9. UPEC, Créteil, France; Mondor Amyloidosis Network, Créteil, France; Department of Cardiology, AP-HP, Henri-Mondor Teaching Hospital, Créteil, France; INSERM Clinical Investigation Center 006, Créteil, France; Department of Radiology, AP-HP, Henri-Mondor Teaching Hospital, Créteil, France. 10. UPEC, Créteil, France; Mondor Amyloidosis Network, Créteil, France; Department of Cardiology, AP-HP, Henri-Mondor Teaching Hospital, Créteil, France; INSERM U955, GRC Amyloid Research Institute, Créteil, France; DHU ATVB, Créteil, France; INSERM Clinical Investigation Center 006, Créteil, France. Electronic address: thibaud.damy@hmn.aphp.fr.
Abstract
OBJECTIVES: The aim of this study was to compare left ventricular longitudinal strain (LS) evaluated by 2-dimensional echocardiography with cardiac magnetic resonance (CMR) in cardiac amyloidosis (CA), establish correlations between histological and imaging findings, and assess the prognostic usefulness of LS measurement and CMR. BACKGROUND: CA is a condition with a poor prognosis due chiefly to 3 forms of amyloidosis: light-chain amyloidosis (AL), hereditary transthyretin (M-TTR), and wild-type transthyretin (WT-TTR). Two-dimensional echocardiography measurement of LS has been reported to detect early left ventricular systolic dysfunction. The pathophysiological underpinnings, regional distribution, and prognostic significance of LS in CA are unclear. METHODS: All patients underwent echocardiography, and 53 underwent CMR. The native hearts of the 3 patients who received heart transplants were subjected to histological examination. For each of the 17 left ventricular segments in the American Heart Association model, we evaluated LS, late gadolinium enhancement (LGE) by CMR, and cardiac amyloid deposition. Univariate and multivariate analyses were performed at 6 months to identify variables associated with major adverse cardiac events (MACE). RESULTS: We studied 79 patients with CA; 26 had AL, 36 M-TTR, and 17 WT-TTR. Mean LS was -10 ± 4%. Both LS and amyloid deposits showed a basal-to-apical gradient. The mean LS and number of segments with LGE were similar across the 3 CA types. LS correlated with LGE and amyloid burden (r = 0.72). LGE was seen in the 6 basal segments in all WT-TTR patients. During the median follow-up of 11 months (range 4 to 17 months), 36 (46%) patients experienced MACE. Independent predictors of MACE were apical LS (cutoff, -14.5%), N-terminal pro-B-type natriuretic peptide (cutoff, 4,000 ng/l), and New York Heart Association functional class III to IV heart failure. CONCLUSIONS: Basal-to-apical LS abnormalities are similar across CA types and reflect the amyloid burden. Apical LS independently predicts MACE.
OBJECTIVES: The aim of this study was to compare left ventricular longitudinal strain (LS) evaluated by 2-dimensional echocardiography with cardiac magnetic resonance (CMR) in cardiac amyloidosis (CA), establish correlations between histological and imaging findings, and assess the prognostic usefulness of LS measurement and CMR. BACKGROUND: CA is a condition with a poor prognosis due chiefly to 3 forms of amyloidosis: light-chain amyloidosis (AL), hereditary transthyretin (M-TTR), and wild-type transthyretin (WT-TTR). Two-dimensional echocardiography measurement of LS has been reported to detect early left ventricular systolic dysfunction. The pathophysiological underpinnings, regional distribution, and prognostic significance of LS in CA are unclear. METHODS: All patients underwent echocardiography, and 53 underwent CMR. The native hearts of the 3 patients who received heart transplants were subjected to histological examination. For each of the 17 left ventricular segments in the American Heart Association model, we evaluated LS, late gadolinium enhancement (LGE) by CMR, and cardiac amyloid deposition. Univariate and multivariate analyses were performed at 6 months to identify variables associated with major adverse cardiac events (MACE). RESULTS: We studied 79 patients with CA; 26 had AL, 36 M-TTR, and 17 WT-TTR. Mean LS was -10 ± 4%. Both LS and amyloid deposits showed a basal-to-apical gradient. The mean LS and number of segments with LGE were similar across the 3 CA types. LS correlated with LGE and amyloid burden (r = 0.72). LGE was seen in the 6 basal segments in all WT-TTRpatients. During the median follow-up of 11 months (range 4 to 17 months), 36 (46%) patients experienced MACE. Independent predictors of MACE were apical LS (cutoff, -14.5%), N-terminal pro-B-type natriuretic peptide (cutoff, 4,000 ng/l), and New York Heart Association functional class III to IV heart failure. CONCLUSIONS: Basal-to-apical LS abnormalities are similar across CA types and reflect the amyloid burden. Apical LS independently predicts MACE.
Authors: F Aus dem Siepen; R Bauer; A Voss; S Hein; M Aurich; J Riffel; D Mereles; C Röcken; S J Buss; H A Katus; Arnt V Kristen Journal: Clin Res Cardiol Date: 2017-09-27 Impact factor: 5.460
Authors: David Kassop; Jason J Nam; Brennan R Cebula; Palak Shah; Ron Blankstein; Rodney H Falk; Edward A Hulten Journal: J Nucl Cardiol Date: 2016-11-08 Impact factor: 5.952
Authors: Priya Mehta; David B Chapel; Neha Goyal; Dong Bo Yu; Victor Mor-Avi; Akhil Narang; Karima Addetia; Nitasha Sarswat; Roberto M Lang; Aliya N Husain; Amit R Patel Journal: Echocardiography Date: 2018-12-28 Impact factor: 1.724
Authors: Mirela Tuzovic; Eric H Yang; Arnold S Baas; Eugene C Depasquale; Mario C Deng; Daniel Cruz; Gabriel Vorobiof Journal: Curr Oncol Rep Date: 2017-07 Impact factor: 5.075
Authors: Shawn C Pun; Heather J Landau; Elyn R Riedel; Jonathan Jordan; Anthony F Yu; Hani Hassoun; Carol L Chen; Richard M Steingart; Jennifer E Liu Journal: J Am Soc Echocardiogr Date: 2017-10-27 Impact factor: 5.251