Nuklearmedizin 2003; 42(03): 99-103
DOI: 10.1055/s-0038-1625305
Editorial
Schattauer GmbH

Myocardial indium-111-antimyosin uptake in essential hypertension

Myokardialer 111 In-Antimyosin-Uptake bei essenzieller Hypertonie
M. Ünlü
1   Departments of Nuclear Medicine
,
N. H. Temiz
1   Departments of Nuclear Medicine
,
A. Hengel
2   Cardiology, Gazi University School of Medicine, Department of Nuclear Medicine, Ankara, Turkey
› Author Affiliations
Further Information

Publication History

Received: 10 July 2002

10 October 2002

Publication Date:
11 January 2018 (online)

Summary

Aim: Evaluation of myocardial uptake of 111In-anti-myosin antibodies in patients with essential hypertension for the verification of our hypothesis that it may increase in stage 1 in the left ventricle as a result of myocardial damage. Patients, methods: Twelve men (mean age: 59 ± 2.4 years) suffering from angina like symptoms and essential hypertension in clinical stage 1 according to the JNC-VI criteria were included into the study. These patients showed normal perfusion as revealed by thallium-201 myocardial study and coronary angiography. Left ventricular mass index was determined in echocardiography. Planar antimyosin images were obtained 48 h after the intravenous injection of the tracer. Heart to lung ratios were calculated as a parameter of myocardial tracer uptake using appropriate region of interests; values >1.52 were considered as abnormal. Results: We observed increased anti-myosin uptake (mean: 1.71 ± 0.12) consistent with myocardial damage in 11 of 12 patients. Nine of 12 patients had a left ventricular hypertrophy with left ventricular mass index values (mean: 131 g/m2 ± 9.48) above 115 g/m2. Heart to lung ratio was correlated significantly to left ventricular mass index (r = 0.902, p <0.001) and duration of hypertension (r = 0.948, p <0.001). Conclusion: Our results suggest that 111In-antimyosin imaging may indicate myocyte damage in early phases of hypertensive heart disease.

Zusammenfassung

Ziel: Auswertung des myokardialen Uptake der 111InAntimyosin-Antikörper bei Hypertonie-Patienten zur Überprüfung unserer Hypothese nach der im Stadium 1 ein erhöhter Uptake im linken Ventrikel aus der myokardialen Schädigung resultiert. Patienten, Methoden: Zwölf Männer (Alter: 59 ± 2,4 Jahre), die unter Angina-ähn-lichen Symptomen und essenzieller Hypertonie im klinischen Studium 1 (nach JNC-VI-Kriterien) litten, wurden in die Studie einbezogen. Sie zeigten normale Perfusion in der Myokardstudie mit Thallium-201- und in der Koronarangiographie. Der linke ventrikulare Massenindex wurde mittels Echokardiographie bestimmt. Planare Antimyosin-Aufnahmen wurden 48 Stunden nach der intravenösen Tracer-Applikation erhalten. Die Herz/ Lungenflügelverhältnisse wurden als Parameter des myokardialen Uptake mit passenden ROIs (regions of interest) berechnet. Werte >1,52 galten als anormal. Ergebnisse: Wir beobachteten erhöhten AntimyosinUptake (Mittel: 1,71 ± 0,12) in Übereinstimmung mit der Myokardschädigung bei 11 der 12 Patienten. Neun von 12 Patienten hatten eine Linksherzhypertrophie mit Massenindexwerten (Mittel: 131 ± 9,48 g/m2) über 115 g/m2. Das Herz/Lungenflügelverhältnis war signifikant mit dem linken ventrikularen Massen-index korreliert (r = 0,902; p <0,001). Schlussfolgerung: Unsere Resultate deuten darauf hin, dass die Bildgebung mit 111In-Antimyosin eine Myozytenschädigung in den frühen Phasen der hypertonen Herzkrankheit anzeigen kann.

 
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