Premium
Myocardial perfusion imaging with thallium‐201 to assess left ventricular hypertrophy and regional ischaemia in hypertensive patients
Author(s) -
FOLMER S. C. C. REINDERS,
WIELING W.,
DUNNING A. J.
Publication year - 1981
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1981.tb02119.x
Subject(s) - medicine , cardiology , left ventricular hypertrophy , ventricle , perfusion , coronary artery disease , scintigraphy , muscle hypertrophy , thallium , ischemia , blood pressure , inorganic chemistry , chemistry
. The increase in mortality from cardiovascular disease in the presence of electrocardiographic signs of left ventricular hypertrophy (LVH) has been ascribed to ischaemic changes in the hypertrophied left ventricle even in the absence of overt coronary artery disease. To test this hypothesis and to investigate the usefulness in the detection of LVH myocardial perfusion scintigraphy with thallium‐201 and echocardiography was performed in thirty‐three hypertensive patients. Sixteen had had electrocardiographic signs of left ventricular hypertrophy. Twelve patients had symptoms of cardiovascular disease. In twenty‐six subjects the scintigraphic procedure consisted of a combined restexercise study, in the other seven only resting images were obtained. Measurement of septa1 wall thickness on the scintiscans correlated fairly well with echographic dimensions and allowed separation of a group of patients with LVH from a group without. In individual patients, however, the perfusion scan was not a reliable tool to affirm the presence of LVH. A total of eight patients, six with LVH on the echocardiogram, had an abnormal rest‐exercise perfusion scan, either with a new perfusion defect after exercise and/or with a resting defect alone. In nine other patients with echocardiographic LVH, on the other hand, no abnormal perfusion was found. Thus, perfusion abnormalities did not correlate with the presence of LVH. The presence of such abnormalities in relation to increasing age and symptomatic cardiovascular disease could well be the expression of anatomic coronary artery disease and cannot be differentiated from the possible ischaemia of the hypertrophied left ventricle.