TY - JOUR
T1 - Myocardial cell damage in human hypertension
AU - Pons-Lladó, Guillem
AU - Ballester, Manel
AU - Borrás, Xavier
AU - Carreras, Francesc
AU - Carrió, Ignasi
AU - López-Contreras, Joaquin
AU - Roca-Cusachs, Alex
AU - Marrugat, Jaume
AU - Narula, Jagat
N1 - Funding Information:
Supported by a grant from the Fondo de Investigación Sanitaria (92/0706), Ministerio de Sanidad y Consumo, Spain.
PY - 2000
Y1 - 2000
N2 - OBJECTIVES: The goal of this study was to investigate the presence of myocardial cell damage in patients with systemic hypertension and its relationship with left ventricular hypertrophy (LVH). BACKGROUND: Although initially compensatory, LVH adversely affects myocellular integrity and contributes to congestive heart failure in hypertensive patients. Noninvasive detection of myocardial damage can be of value. METHODS: We performed imaging studies with 111In-labeled monoclonal antimyosin antibodies to identify myocardial damage in 39 patients with systemic hypertension and variable degrees of LVH. Three groups were considered: 16 asymptomatic patients with normal echocardiographic left ventricular mass (LVM) (group I); 14 asymptomatic patients with LVH (group II) and 9 patients with symptomatic hypertensive heart disease and advanced LVH (group III). The severity of myocardial damage was represented as heart-to-lung (target-to-background) antibody uptake ratio (normal: <1.55). RESULTS: Mean LVM index was 105 ± 14 g/m2 in group I, 124 ± 24 in group II and 174 ± 29 in group III. Heart-to-lung ratios of antimyosin uptake were: 1.45 ± 0.14 in group I, 4 of the 16 (25%) patients showing an abnormal scan; 1.50 ± 0.07 in group II with abnormal scans in 2 of the 14 (16%) patients and 1.77 ± 0.16 (p < 0.001) in group III, all 9 patients presenting with abnormal antimyosin scans. On multivariate regression analysis LVM index was the main variable that independently correlated with the degree of myocardial uptake of antimyosin (r = 0.815; p = 0.001). CONCLUSIONS: This study provides the first in vivo evidence of myocyte damage in patients with hypertension. The severity of myocardial damage can be related to the magnitude of LVH. (C) 2000 by the American College of Cardiology.
AB - OBJECTIVES: The goal of this study was to investigate the presence of myocardial cell damage in patients with systemic hypertension and its relationship with left ventricular hypertrophy (LVH). BACKGROUND: Although initially compensatory, LVH adversely affects myocellular integrity and contributes to congestive heart failure in hypertensive patients. Noninvasive detection of myocardial damage can be of value. METHODS: We performed imaging studies with 111In-labeled monoclonal antimyosin antibodies to identify myocardial damage in 39 patients with systemic hypertension and variable degrees of LVH. Three groups were considered: 16 asymptomatic patients with normal echocardiographic left ventricular mass (LVM) (group I); 14 asymptomatic patients with LVH (group II) and 9 patients with symptomatic hypertensive heart disease and advanced LVH (group III). The severity of myocardial damage was represented as heart-to-lung (target-to-background) antibody uptake ratio (normal: <1.55). RESULTS: Mean LVM index was 105 ± 14 g/m2 in group I, 124 ± 24 in group II and 174 ± 29 in group III. Heart-to-lung ratios of antimyosin uptake were: 1.45 ± 0.14 in group I, 4 of the 16 (25%) patients showing an abnormal scan; 1.50 ± 0.07 in group II with abnormal scans in 2 of the 14 (16%) patients and 1.77 ± 0.16 (p < 0.001) in group III, all 9 patients presenting with abnormal antimyosin scans. On multivariate regression analysis LVM index was the main variable that independently correlated with the degree of myocardial uptake of antimyosin (r = 0.815; p = 0.001). CONCLUSIONS: This study provides the first in vivo evidence of myocyte damage in patients with hypertension. The severity of myocardial damage can be related to the magnitude of LVH. (C) 2000 by the American College of Cardiology.
UR - http://www.scopus.com/inward/record.url?scp=0033666289&partnerID=8YFLogxK
U2 - 10.1016/S0735-1097(00)00983-9
DO - 10.1016/S0735-1097(00)00983-9
M3 - Article
C2 - 11127461
AN - SCOPUS:0033666289
SN - 0735-1097
VL - 36
SP - 2198
EP - 2203
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 7
ER -