Myocardial indium-111-antimyosin uptake in essential hypertension

M. Ünlü; N. H. Temiz; A. Hengel

doi:10.1055/s-0038-1625305

Nuklearmedizin - NuclearMedicine, Table of Contents

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

¹Departments of Nuclear Medicine

,

N. H. Temiz

¹Departments of Nuclear Medicine

,

A. Hengel

²Cardiology, Gazi University School of Medicine, Department of Nuclear Medicine, Ankara, Turkey

› Author Affiliations

Abstract

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.

Keywords

Antimyosin - scintigraphy - hypertension - hypertrophy - echocardiography

Schlüsselwörter

Antimyosin - Szintigraphie - Hypertonie - Hypertrophie - Echokardiographie

Full Text

References

References
1 Ballester M, Carrio I, Abdal ML. et al. Patterns of evolution of myocyte damage after human heart transplantation detected by 111indium monoclonal antimyosin. Am J Cardiol 1988; 62: 623-7.
2 Brilla CG, Weber KT. Reactive and reparative myocardial fibrosis in arterial hypertension in the rat. Cardiovasc Res 1992; 26: 671-7.
3 Brush JE, Cannon III RO, Schenke WH. et al. Angina due to coronary microvascular disease in hypertensive patients without left ventricular hypertrophy. N Engl J Med 1988; 319: 1302-7.
4 Cannon III RO, Watson RM, Rosing DR. et al. Angina caused by reduced vasodilator reserve of the small coronary arteries. J Am Coll Cardiol 1989; 1: 1359-73.
5 Carrio I, Berna L, Ballester M. et al. Indium-111 antimyosin scintigraphy to assess myocardial damage in patients with suspected myocarditis and cardiac rejection. J Nucl Med 1988; 29: 1893-900.
6 Dec SW, Palacios I, Yasuda T. et al. Antimyosin antibody cardiac imaging: its role in the diagnosis of myocarditis. J Am Coll Cardiol 1990; 16: 97-104.
7 Diez J, Fortuno MA, Ravassa S. Apoptosis in hypertensive heart disease. Curr Opin Cardiol 1998; 13: 317-25.
8 Edwalds GM, Said JW, Block MI. Myocytolysis (vacuolar degeneration) of myocardium: immunohistochemical evidence of viability. Human Pathol 1984; 15: 753-6.
9 Flameng W, Suy R, Schwarz F. Ultrastructural correlates of left ventricular contraction abnormalities in patients with chronic ischaemic heart disease: determinants of reversible segmental asnergy post-revascularization surgery. Am Heart J 1981; 102: 846-57.
10 Geer JC, Crago CA, Gardner LL. et al. Subendocardial ischaemic myocardial lesions associated with coronary atherosclerosis. Am J Pathol 1980; 8: 663-80.
11 Gonzalez A, Lopez B, Ravassa S. et al. Stimulation of cardiac apoptosis in essential hypertension: potential role of angiotensin II. Hypertension 2002; 39: 75-80.
12 Khaw BA, Gold HK, Yasuda T. Acute myocar-dial infarct imaging with indium-111 labelled monoclonal antimyosin Fab. J Nucl Med 1987; 28: 1671-8.
13 Khaw BA, Gold HK, Yasuda T. Scintigraphic quantitation of myocardial necrosis in patients after intravenous injection of myosin-specific antibody. Circulation 1986; 74: 501-8.
14 Koren MJ, Devereux RB, Casale PN. et al. Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med 1991; 114: 345-52.
15 Laine GA. Microvascular changes in the heart during chronic arterial hypertension. Circ Res 1988; 62: 953-60.
16 Levy D, Anderson KM, Savage DD. et al. Risk of ventricular arrhytmias in left ventricular hypertrophy: the Framingham Heart Study. Am J Cardiol 1987; 60: 560-5.
17 Levy D, Garrison RJ, Savage DD. Left ventricular mass and incidence of coronary heart disease in an elderly cohort: the Framingham Heart Study. Ann Intern Med 1989; 110: 101-7.
18 Lüscher TH, Seo B, Bühler FR. Potential role of endothelin in hypertension. Hypertension 1993; 21: 747-51.
19 Motz W, Vogt M, Rabenau O. Evidence of endothelial dysfunction in coronary resistance vessels in patients with angina pectoris and normal coronary angiograms. Am J Cardiol 1991; 68: 996-1003.
20 Narula J, Kharbanda S, Khaw B. Apoptosis and the heart. Chest 1997; 112: 1358-62.
21 Narula J, Khaw BA, Dec GW. Recognition of myocarditis masquerading as acute myocardial infarction. N Engl J Med 1993; 328: 100-4.
22 Narula J, Sauthern JF, Dec GW. et al. Anti-myosin uptake and myofibrillarlysis in dilated cardiomyopathy. J Nucl Cardiol 1995; 2: 470-7.
23 Narula J, Strauss HW, Khaw BA. Antimyosin positivity in doxorubicin toxicity: earlier than the conventional evidence. J Nucl Med 1993; 34: 1507-9.
24 Obrador D, Ballester M, Carrio I. et al. High prevalence of monoclonal antimyosin antibody uptake in patients with chronic idiopathic dilated cardiomyopathy. J Am Coll Cardiol 1989; 13: 1289-93.
25 Puig M, Ballester M, Matias-Guiu X. et al. Burden of myocardial damage in cardiac allograft rejection: scintigraphic evidence of myocardial injury and histological evidence of myocyte necrosis and apoptosis. J Nucl Cardiol 2000; 7: 132-9.
26 Schiffrin EL, Devy LY, Larochelle P. Morphology of resistance arteries and comparison of effects of vasoconstrictors in mild essential hypertensive patients. Clin Invest Med 1993; 16: 177-86.
27 Schiffrin EL. Endothelin potential role in hypertension and vascular hypertrophy. Brief review. Hypertension 1995; 25: 1135-43.
28 Schlesinger MJ, Reiner L. Focal myocytolysis of the heart. Am J Pathol 1955; 31: 443-59.
29 Shane DJ, Demur A, Chisels J. et al. The Committee on M-mode standardization of the American Society of Echocardiography. Recommendations regarding quantification in M-mode echocardiography. Circulation. 1978; 58: 1072-83.
30 Strauer BE. Significance of coronary circulation in hypertensive heart disease for development and prevention of heart failure. Am J Cardiol 1990; 65: 34G-41G.
31 The sixt report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med 1997; 157: 2413-46.
32 Vanhoutte PM. Is endothelin involved in the pathogenesis of hypertension?. Hypertension 1993; 21: 747-51.
33 Weber KT, Anversa P, Armstrong PW. et al. Remodelling and reparation of the cardiovascular system: an international perspective. J Am Coll Cardiol 1992; 20: 3-16.
34 Weber KT, Brilla CG. Pathological hyper-trophy and the cardiac interstitium: fibrosis and the renin-angiotensin-aldosteron system. Circulation 1990; 83: 1849-65.
35 Wikstrand J. Calculation of the left ventricular mass in man-a comment. J Hypertens 1997; 15: 811-3.