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Vasodilator myocardial perfusion imaging: demonstration of local electrophysiological changes of ischaemia
  1. Roy M John,
  2. Peter I Taggart,
  3. Peter M Sutton,
  4. Durval C Costa,
  5. Peter J Ell,
  6. Howard Swanton
  1. Department of Cardiology, The Middlesex Hospital, London
  2. Department of Physiology, University College and Middlesex School of Medicine, London
  3. Institute of Nuclear Medicine, University College and Middlesex School of Medicine, London

    Abstract

    Objective—To examine the incidence and severity of myocardial ischaemia provoked in the course of perfusion scintigraphy by coronary vasodilators using endocardial recordings of steady state monophasic action potentials as an independent marker of early localised myocardial ischaemia.

    Patients—31 men undergoing routine cardiac catheterisation for investigation of chest pain were studied.

    Setting—A tertiary cardiac referral centre.

    Design—Single site monophasic action potentials were recorded from the left or right ventricle or both (50 recording sites) during intravenous infusion of dipyridamole (0·015 mg/kg/min) for four minutes. Heart rate was held constant with atrial pacing at 20% above the patient's resting rate. Technetium-99m hexakis-2-methoxy-2-methylpropyl-isonitrile (MIBI) was administered four minutes after dipyridamole, and single photon emission tomographic imaging was performed an hour later. Rest images were obtained the next day (two day, two dose protocol). Recordings were divided into three groups based on the scintigraphic perfusion characteristics and coronary anatomical data for the action potential recording site: group 1—recordings from areas with a normal perfusion pattern (n = 30), group 2—recordings from areas with a perfusion defect and subtended by significantly narrowed coronary arteries without obvious angiographic collateral supply (n = 10), and group 3—recordings from areas with a perfusion defect and subtended by occluded arteries with angiographically evident collaterals from adjacent vessels (n = 10).

    Results—There were changes in the duration of the monophasic action potential indicative of ischaemia—that is, shortening of duration of steady state action potential—in 18 of the 20 recordings from areas of abnormal perfusion. Peak changes were apparent eight minutes from the start of the dipyridamole infusion. Mean (SEM) values for duration of the action potential between control and peak effect at eight minutes were 276·5 (5·3) ms ν 276·6 (5·4) for group 1 (NS), 289·6 (4·7) ms ν 278·4 (4·9) ms for group 2 (p < 0·001), and 269·6 (5·7) ms ν 242·0 (4·4) for group 3 (p < 0·0001). These changes were significantly different between the three groups (p < 0·01). ST segment changes on the surface electrocardiogram were seen in only eight patients, all with areas of viable myocardium supplied by collateral vessels.

    Conclusions—These data provide strong evidence for the presence of myocardial ischaemia in regions of reversible perfusion defects induced by dipyridamole. This study also shows that such ischaemia is more intense and more likely to be seen when myocardial viability is dependent on collateral circulation.

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