DETECTION OF ANEURYSMS BY GAMMA-CAMERA IMAGING AFTER INJECTION OF AUTOLOGOUS LABELLED PLATELETS

DETECTION OF ANEURYSMS BY GAMMA-CAMERA IMAGING AFTER INJECTION OF AUTOLOGOUS LABELLED PLATELETS

352 DETECTION OF ANEURYSMS BY GAMMA-CAMERA IMAGING AFTER INJECTION OF AUTOLOGOUS LABELLED PLATELETS Fig 2-Effect of nicardipine aggregation. and as...

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352 DETECTION OF ANEURYSMS BY GAMMA-CAMERA IMAGING AFTER INJECTION OF AUTOLOGOUS LABELLED PLATELETS

Fig 2-Effect of nicardipine aggregation.

and

aspirin

on

whole blood

platelet

Mean±SEM of 5 experiments. a=control; b=5 pg/ml aspirin; c=10 gg/ml nicardipme; d = 5 fig/ml aspirin and 10 fig/ml nicardipine. *p<0’05 compared with control and with aspirin and nicardipine alone.

SiR,-Dr Sinzinger and colleagues (Dec 15, p 1365) recommend that abdominal gamma-camera imaging with background subtraction should be done in all patients investigated by indium-111 platelet labelling to detect aortic aneurysms. Autologous lllIn-labelled platelets have been used extensively to image aneurysmsl,2 without the need for background subtraction. Although in Sinzinger’s series angiography was used to confirm the diagnosis, this investigation is unreliable since the aneurysm lumen may be compromised by thrombus and appear no wider than that of adjacent artery. No reference is made to the false negative rate in their 860 patients. We have investigated 111In-platelet uptake in 11 aneurysms (8 atherosclerotic, 3 false) in an attempt to select those likely to produce peripheral emboli. Background subtraction was not used. Mean counts over the aneurysm were 9910±2924 (SEM) compared with 5193:t 1164 over the same area of normal artery (p<0 05, Wilcoxon). The platelet uptake ratio was 1-74-tO-14 and was higher for atherosclerotic (mean 1-81) than for false aneurysms (mean 1-55).

v/v). Samples were then incubated with labetalol, nicardipine, or their vehicles (controls) for 25 mm at 37°C. Aspirin or its vehicle was then added and incubation continued for a further 5 mm. The concentrations of all three drugs were known from prior assessment to have little effect on aggregation when lI used alone in all subjects studied. Whole blood aggregation was carried out with the Clay Adams ’Ultra Flo 100’ whole blood platelet counter, platelet counts bemg measured 1, 2, 3, and 5 min after addmon of the aggregating agent (0-55 pglml collagen) and expressed as a percentage of the count at time zero. At concentrations of labetalol and aspirin which on their own had little effect on platelet aggregation, a combination of both drugs resulted in a significantly greater inhibition of platelet aggregation (fig 1). Similar findings were seen with nicardipine plus aspirin (fig 2). This synergism may be due to sequential inhibition of the enzymes involved in thromboxane A2 production; adrenergic and calcium-channel-blocking agents can inhibit phospholipase A2 while aspirin irreversibly inhibits cyclo-oxygenase. The concentrations of labetalol and nicardipine were low but it is difficult to correlate these with in-vivo concentrations since such drugs accumulate within platelets in vivo.7 These findings suggest that a combination of low-dose aspirin and an adrenergic or calcium-channel-blocking agent may be of value in the prophylaxis of vascular problems where platelet aggregation is involved in the pathogenesis, and this may represent a major advance in the treatment of vascular disease. I. A. GREER J. J. WALKER A. A. CALDER C. D. FORBES

University Departments of Medicine and

Obstetrics,

Royal Infirmary, Glasgow G31 2ER

G, Cerletti C, Bertel V Pharmacology of antiplatelet drugs and clinical trials on thrombosis prevention: a difficult link. Lancet 1982, ii: 974-77. 2. The Persantine-Aspirin Reinfarction Study Research Group. Persantine and aspirin in coronary heart disease. Circulation 1980, 62: 449-61 3 Canadian Co-operative Study Group. A randomised trial of aspirin and 1978, 299: 53-59 J sulphinpyrazone in threatened stroke. N Engl Med 4 Norwegian Multicentre Study Group. Timolol induced reduction in mortality and 1 DeGaetano

reinfarction

in

patients surviving

acute

Hjalmarson A, Elmfeldt D, Herlitz J, et al. Effect on mortality of metoprolol myocardial infarction Lancet 1981, ii 823-27.

in acute

6. Braunwald E. Mechanism of action 7

of calcium-channel-blocking agents. N EnglJ Med 1982; 307: 1618-27. Weksler BB, Gillick M, Pink J. Effect ofpropranolol on platelet function Blood 1977, 49: 185-96

8. Dale 9.

10 11

J, Landmark KH, Myhre E. The effects of nifedipine, a calcium antagonist, on platelet function Am Heart J 1983, 105: 103-05 Saniabadi AR, Lowe GDO, Barbenel JC, Forbes CD A comparison of spontaneous platelet aggregation in whole blood with platelet rich plasma: additional evidence for the role of ADP. Thromb Haemostas 1984, 51: 115-18. Blackwell GJ, Flower RJ, Russell-Smith N, Salmon JA, Thorogood PB, Vane JR Prostacyclin is produced in whole blood. Br J Pharmacol 1978; 64: 436 Saniabadi AR, Lowe GDO, Forbes CD, Prentice CRM, Barbenel JC. Platelet aggregation studies

in

luIn-labelled platelets will locate thrombus within aneurysms background subtraction (figure) but are not suitable as a diagnostic investigation. Clinical examination and B-mode ultrasound are more reliable, especially when used for population screening. without

Department of Surgery, Charing Cross Hospital Medical School, London W6 8RF

I. F. LANE K. R. POSKITT M. SINCLAIR C. N. MCCOLLUM

A, Hussey JK, Smith FW, Dendy PP, Bennett B, Douglas AS. Diagnosis of aneurysm using autologous platelets labelled with indium-111 oxine Br Med J 1981; 282: 1122 Ritchie JL, Stratton JR, Thiele B, et al Indium-111 platelet imaging for detection of platelet deposition in abdominal aneurysms and prosthetic arterial grafts Am J Cardiol 1981; 47: 882-89.

1 Feneck

aortic

2.

myocardial infarction. N Engl J Med 1981,

304: 801-07 5

image with increased platelet uptake in right groin demonstrating thrombus within false femoral aneurysm.

Gamma-camera

whole human blood Thromb Res

1983, 30: 625-32.

PREOPERATIVE ANTIBIOTIC PROPHYLAXIS IN ACUTE APPENDICECTOMY

SIR,-Metronidazole prophylaxis against wound infection after has been widely used since the 1976 report of Willis et al.1 Arnbjornsson and Mikaelsson2 have again emphasised its importance and we were impressed that the data provided were based on a relevant definition of a wound infection. Bates et al3 cast doubt on the value of metronidazole prophylaxis in appendicectomy because he found that 60% of wound mfecnons developed after patients had left hospital, and the overall infection rate was similar to that in untreated controls. Ljungquist and Lund’ define a wound infection after a "clean operation" as the presence of

appendicectomy