title: Diagnosis of cardiac amyloidosis based on the myocardial velocity profile in the hypertrophied left ventricular wall.
abstract: The myocardial velocity profile (MVP), derived from color-coded tissue Doppler imaging (TDI), can identify transmural heterogeneity based on the physiology and pathology of the myocardium. This study sought to clarify whether the MVP can differentiate cardiac amyloidosis from other causes of left ventricular hypertrophy. We recorded the MVP and determined its myocardial velocity gradient (MVG) in the ventricular septum and left ventricular posterior wall using color-coded TDI in 10 patients with cardiac amyloidosis, in 25 patients with hypertensive hypertrophied left ventricular wall, in 25 patients with asymmetric septal hypertrophy of hypertrophic cardiomyopathy, and in 20 clinically normal controls. End-diastolic ventricular septal thickness was similar among the cardiac amyloidosis, hypertension, and hypertrophic cardiomyopathy groups. Percent systolic thickening of the ventricular septum and left ventricular posterior wall calculated from M-mode left ventricular echocardiograms was lower in the cardiac amyloidosis group than in the hypertension, hypertrophic cardiomyopathy, or control group. Peak MVGs during systole and early diastole were lowest in the cardiac amyloidosis group, followed, in order, by the control, hypertension, and hypertrophic cardiomyopathy groups. The systolic and early diastolic MVPs in the ventricular septum and left ventricular posterior wall showed a characteristic serrated pattern in all patients with cardiac amyloidosis, but not in any other patient groups. In conclusion, MVPs in the ventricular septum and left ventricular posterior wall show a distinctive serrated pattern that may be related to amyloid deposition in the myocardium. Myocardial tissue characterization using color-coded TDI provides diagnostic information in patients with cardiac amyloidosis.
authors.affiliation: Cardiovascular Section, National Higashi Tokushima Hospital, Itano, Japan. oki@higasitokusima.hosp.go.jp
authors.forename: Takashi
authors.initials: T
authors.lastname: Oki
authors.forename: Hideji
authors.initials: H
authors.lastname: Tanaka
authors.forename: Hirotsugu
authors.initials: H
authors.lastname: Yamada
authors.forename: Tomotsugu
authors.initials: T
authors.lastname: Tabata
authors.forename: Yoshifumi
authors.initials: Y
authors.lastname: Oishi
authors.forename: Takeo
authors.initials: T
authors.lastname: Ishimoto
authors.forename: Norio
authors.initials: N
authors.lastname: Nagase
authors.forename: Hisanori
authors.initials: H
authors.lastname: Shinohara
authors.forename: Koichi
authors.initials: K
authors.lastname: Sakabe
authors.forename: Nobuo
authors.initials: N
authors.lastname: Fukuda
mesh_terms: D000328:Adult; D000686:Amyloidosis / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D002312:Cardiomyopathy, Hypertrophic / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology; D003937:Diagnosis, Differential; D018618:Echocardiography, Doppler, Color; D018619:Echocardiography, Doppler, Pulsed; D005260:Female; D006331:Heart Diseases / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology*