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J Am Coll Cardiol, 2000; 36:2198-2203 © 2000 by the American College of Cardiology Foundation |




* Servei de Cardiologia, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain
Servei de Medicina Nuclear, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain
Unitat dHipertensió del Servei de Medicina Interna, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain
Institut Municipal dInvestigació Mèdica, Barcelona, Spain
|| Division of Cardiology, Allegheny University Hospitals, Philadelphia, Pennsylvania, USA
Manuscript received October 14, 1999; revised manuscript received June 5, 2000, accepted July 14, 2000.
Reprint requests and correspondence: Dr. G. Pons-Lladó, Secció de Imatge Cardiaca, Servei de Cardiologia, Hospital de la Santa Creu i Sant Pau, Sant Antoni M. Claret 167, 08025-Barcelona, Spain
gponsl{at}meditex.es
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.
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