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Myocardial steal produced by coronary vasodilation in chronic coronary artery occlusion

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Summary

Chronic occlusion of the circumflex branch of the left coronary artery was produced in dogs. All animals developed a collateral circulation fast and efficient enough to prevent myocardial infarction. Tracer microsphere experiments together with 133-Xenon studies showed a homogeneous distribution of flow over the entire left ventricle. Drug-induced coronary vasodilation caused a grossly non-homogenous distribution of coronary blood flow. The collateral dependent areas of the heart received much less blood than the areas which are supplied by normal arterial channels. Within the collateral-dependent area the endocardial myocardium received less blood than the epicardial layers. Previously well perfused areas can become underperfused during overperfusion of normal myocardium. Similar changes were not observed in hearts with normal coronary arteries.

Nitroclycerine did not produce changes in blood flow in hearts with coronary artery occlusion. Consequently changes in the distribution of myocardial flow were not observed with this drug. A computer model is presented for the explanation of the experimental findings which facilitated the analysis of contributing factors.

Zusammenfassung

Bei Hunden wurde ein chronischer Verschluß des ramus circumflexes der linken Koronararterie erzeugt. Bei allen Tieren entwickelte sich ein Kollateralkreislauf, der das Auftreten von Infarkten verhinderte. Die Durchblutung des linken Ventrikels bei chronischem Koronarverschluß war normal und die Durchblutungsverteilung war homogen, wie aus der 133-Xenon clearance zusammen mit der Gewebekonzentration von Tracer Microspheren hervorging. Pharmakologisch induzierte Koronardilation verursachte eine ungleichmäßige Durchblutungsverteilung. Das von Kollateralen abhängige Perfusionsgebiet erhielt bedeutend weniger Blut als der Teil des Myokards, der über normale Koronararterien versorgt wird. Innerhalb des kollateralabhängigen Myokards erhielt das subendokardiale Gebiet bedeutend weniger Blut pro Zeiteinheit als das subepikardiale Gebiet. Zonen, die vor der Dilation normal und homogen durchblutet waren, erhielten während der Dilatation weniger Blut. Derartige Verteilungsänderungen wurden nicht beobachtet bei Herzen mit normalen Koronararterien.

Nitroglycerin verursachte keine Umverteilung der Durchblutung bei Herzen mit chronischem Koronarverschluß. Nitroglycerin verursachte allerdings auch keine nennenswerte Koronardilatation. Ein Komputermodell wird beschrieben zum besseren Verständnis der haemodynamischen Zusammenhänge bei Koronardilatation.

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Author notes

  1. W. Schaper

    Present address: Abteilung für Experimentelle Kardiologie am W. G. Kerckhoff-Institut der Max-Planck-Gesellschaft, Sprudelhof 11, 635, Bad Nauheim

Authors and Affiliations

  1. Departments of Cardiovascular Research and Physiological Data-Systems, Research Laboratoria Janssen Pharmaceutica, Beerse, (Belgium)

    W. Schaper, P. Lewi, W. Flameng & L. Gijpen

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  1. W. Schaper
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  2. P. Lewi
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  3. W. Flameng
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  4. L. Gijpen
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With 5 figures and 7 tables

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Schaper, W., Lewi, P., Flameng, W. et al. Myocardial steal produced by coronary vasodilation in chronic coronary artery occlusion. Basic Res Cardiol 68, 3–20 (1973). https://doi.org/10.1007/BF01907653

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