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Immunoscintigraphy for Detecting Acute Myocardial Infarction Without Electrocardiographic Changes

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Immunoscintigraphy for Detecting Acute Myocardial Infarction Without Electrocardiographic Changes PAPERS BMJ: first published as 10.1136/bmj.300.6718.151 on 20 January 1990. Downloaded from Immunoscintigraphy for detecting acute myocardial infarction without electrocardiographic changes Diwakar Jain, Avijit Lahiri, Edward B Raftery Abstract tions2; this technique has a high sensitivity and Objective-To establish whether immunoscinti- specificity. graphy with antibody to myosin may detect acute We describe the use of myosin antibody labelled myocardial infarction without electrocardiographic with indium-111 as a diagnostic tool in patients changes. with suspected acute myocardial infarction without Design-Prospective study of patients with sus- electrocardiographic changes. pected acute myocardial infarction or unstable angina with cardiac imaging with "'indium myosin antibody, estimation of cardiac enzyme concentra- Patients and methods tions, electrocardiography, 20Ithallium imaging, and One hundred and nineteen consecutive patients radionuclide ventriculography. admitted to the coronary care unit of this hospital with Setting-Coronary care unit in a district general chest pain <48 hours duration suspected to be due to hospital. acute myocardial infarction or unstable angina had Patients-119 Consecutive patients with suspec- immunoscintigraphy with "'In myosin antibody. ted acute myocardial infarction or unstable angina. Patients with cardiomyopathy, myocarditis, valvular Patients with cardiomyopathy, myocarditis, valvular heart disease, myocardial infarction, or cardiac surgery heart disease, myocardial infarction or cardiac in the preceding two weeks or those in whom the surgery in the previous two weeks or with left electrocardiogram showed left bundle branch block bundle branch block and women of childbearing age were excluded, as were women of childbearing age. were excluded. Twelve lead electrocardiograms were performed at the Results-Of 75 patients with suspected acute time of admission, during episodes of chest pain, and myocardial infarction, seven had no diagnostic daily during the period of hospital stay. Blood samples electrocardiographic changes despite normal con- were collected six to eight hourly for 48-72 hours for duction patterns. Immunoscintigraphy with myosin estimating total serum creatine kinase concentration antibody disclosed necrosis in all seven patients, and its MB isoenzyme concentration. The Fab fraction which was localised in regions supplied by diseased of murine monoclonal myosin antibody (0-5 mg) http://www.bmj.com/ coronary arteries in all but one. Six patients had (Myoscint, Centocor, United States) was labelled with abnormal images on 20'thallium imaging, and all 74-83 MBq of "'In and was injected intravenously soon seven had abnormal wall motion at the site of after admission. Planar gammacamera imaging was antibody uptake. One patient with minimal left main performed in three standard views (anterior, left stem and right coronary artery atheroma had uptake anterior oblique, and left lateral) at 24 and 48 hours of antibody at two discrete sites. after the injection of tracer. Conclusions-Immunoscintigraphy with antibody The scans were compared with conventional non- to myosin confirms myocardial infarction in the invasive radionuclide techniques: scanning with on 1 October 2021 by guest. Protected copyright. absence of electrocardiographic changes and dis- thallium-201 for assessing regional blood flow of the closes the site of infarction. myocardium and 99Tc blood pool scanning for assess- ing abnormalities of the left ventricular chamber (abnormal wall motion and ejection fraction). The 20'Tl Introduction scans were performed during the second (48 hour) The diagnosis ofacute myocardial infarction is based imaging with labelled myosin antibody with identical on typical chest pain, evolving electrocardiographic views and 740 MBq of 20'T1. Blood pool scans were changes, and increased concentrations ofserum cardiac obtained two to six weeks later with the in vivo enzymes. Patients commonly present, with Department of Cardiology however, labelling method for red cells and 740 MBq 99Tc. The and Division of Clinical chest pain and a small increase in cardiac enzyme "gated" images were acquired in the same three views, Sciences, Northwick Park concentrations but with no electrocardiographic from which abnormal wall motion was defined and Hospital and Clinical changes of acute myocardial infarction. Several non- ejection fraction was calculated. Selective coronary Research Centre, Harrow cardiac conditions may also produce a small increase arteriography was also performed at two to six weeks. HAI 3UJ in cardiac enzyme concentrations, even in the MB The diagnosis of acute myocardial infarction was Diwakar Jain, MRCP, isoenzyme of creatine kinase.' This observation based on the presence of at least two of the three honorary registrar has lent impetus to the development of a new imaging standard criteria: chest pain, increased cardiac enzyme Avijit Lahiri, FACC, honorarv technique that may be used to detect and localise concentration, and evolving electrocardiographic consultant necrotic myocardium. studies Edward B Raftery, FRCP, Experimental have changes. The patients were classified into three diag- consultant cardiologist shown that antibody against the cardiac contractile nostic categories: acute myocardial infarction, unstable protein myosin binds specifically to the myocardial angina, and no evidence of acute myocardial infarction Correspondence to: Dr cells if there is irreversible injury to the cell mem- or resting ischaemia. Raftery. brane. When the antibody is labelled with a radioactive The images obtained with labelled myosin antibody isotope a standard gammacamera can be used to were interpreted independently for evidence of BrMedJ 1990;300:151-3 localise experimental' and human myocardial infarc- abnormal uptake of tracer and its localisation in the BMJ VOLUME 300 20 JANUARY 1990 151 Characteristics ofand scintigraphicfindings in patients with acute myocardial infarction but without diagnostic electrocardiograms Previous Peak creatine "'Ti Wall Left ventricular Case myocardial kinase Location of uptake of "'In labelled perfusion motion ejection No Age Sex infarction Coronary artery affected (%) (IU/1) antibody to myosin defect abnormality fraction 1 41 M _ Left circumflex (100) 1205 Apex + 76 2 50 M - Left main (<25) 844 Two discrete sites + + 69 3 48 M - Left anterior descending (50) 429 Anterior wall + + 47 BMJ: first published as 10.1136/bmj.300.6718.151 on 20 January 1990. Downloaded from 4 62 M - Left anterior descending (99) 559 Apex + + 58 5 65 M - Left circumflex (95) 382 Apex, lateral wall + + 57 6 46 M Inferior wall Left circumflex (100) 945 Lateral wall + + 52 7 79 F Anterior and Left anterior descending, right coronary inferior wall artery (100) 823 Lateral wall, interventricular septum + + 26 + = Present, - absent. myocardium. The images obtained with 2'°thallium diseased coronary arteries (figs 1 and 2). One patient were interpreted for any evidence of abnormalities of had uptake ofthe labelled antibody at two discrete sites myocardial perfusion.6 The blood pool ventriculo- (fig 2), and the rest all had a single region of uptake grams were analysed for abnormalities in wall motion, involving one or more contiguous walls of the left and the left ventricular ejection'fraction was determined ventricle. The myocardial infarction in these seven using standard techniques.7 All images were interpre- patients was further confirmed by the presence of a ted blind by a panel of three expert investigators with localised perfusion abnormality in six and regional wall standard computer enhanced images. motion abnormalities in all. The study was approved by the hospital ethical No adverse effects were observed in any patient after committee, and informed consent was obtained from administration of labelled myosin antibody, and the each patient. blood samples obtained two weeks and six weeks after its injection showed no antibody response. Results Of the 119 patients who had imaging, 75 had acute Discussion myocardial infarction, 17 unstable angina, and 27 no An appreciable proportion of patients with acute evidence ofinfarction or resting ischaemia. The images myocardial infarction show no changes on serial obtained with labelled myosin antibody were of good electrocardiography. We observed this phenomenon in quality and easy to interpret, and differentiating 9% of our patients with acute myocardial infarction. negative from positive images was not difficult. Furthermore, it is well known that acute infarction is Seventy four of the 75 patients with acute myocardial difficult to diagnose with left bundle branch block, infarction had positive images with labelled myosin pre-excitation syndromes, and old infarction scars. An antibody, seven of whom had typical chest pain and alternative method of diagnosing infarction is needed increase in cardiac enzyme concentration but did not in these patients but in this study we excluded patients have any electrocardiographic evidence of acute myo- with uninterpretable electrocardiograms and concen- cardial infarction. The table outlines the clinical trated on those with no electrocardiographic changes. characteristics and the scintigraphic findings in these The twelve lead electrocardiogram has a low sensitivity patients. Only two out of the seven patients had had a for diagnosing small apical, lateral wall, and non- previous myocardial infarction; all but one had signi- transmural infarctions,"9 but serial estimation of the ficant
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