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Cardiovascular Research 1999 42(1):193-200; doi:10.1016/S0008-6363(98)00270-3
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Downstream resistance effects of intracoronary thrombosis in the stenosed canine coronary artery1

M Mansaraya,*, P.R Belcherb, I Vergroesenc, Z.M Wrighta, J.W Hynda, A.J Drake-Hollanda and M.I.M Noblea

aNational Heart and Lung Institute, Imperial College School of Medicine, Charing Cross Hospital, London W6 8RF, UK
bCardiothoracic Surgery, University of Glasgow, Royal Infirmary, Glasgow, UK
cMedical Physics, Academic Medical Centre, Amsterdam, Netherlands

* Corresponding author. Room 5L16, National Heart and Lung Institute, ICSM, Charing Cross Hospital, Fulham Palace Road, London W6 8RF, UK. Tel.: +44-181-846-1033; fax: +44-181-846-7678. E-mail address: m.mansaray@cxwms.ac.uk (M. Mansaray)

Objective: The presence is well established in unstable angina of intracoronary thrombosis in a stenosed epicardial coronary artery. The effects of the thrombus formation on the distal microcirculation are however still unclear. Methods: We adapted the Folts canine model of left circumflex coronary arterial stenosis and intracoronary thrombosis by the insertion of a pressure catheter distal to the stenosis and by the use of 15 µm radioactive microspheres for measurement of regional myocardial blood flow. This permitted measurement during circumflex artery occlusion of collateral flow, downstream vascular resistance and collateral resistance. Results: Distal circumflex resistance, obtained by dividing the distal circumflex coronary pressure gradient by the collateral flow, significantly increased with thrombosis (94.47±35.72 to 120.06±34.47; p=0.0018) mmHg/ml/min/g. Changes in collateral flow and resistance in the presence of thrombosis, during maximum ischaemic vasodilatation, were inconsistent. Conclusion: Thrombosis causes increased vascular resistance in the microcirculation distal to the site of injury. This may be of clinical relevance in unstable angina, characterised by episodes of thrombus growth and embolization, in which ischaemic episodes may be worsened by generalised downstream vascular changes.

KEYWORDS Regional blood flow; Platelets; Thrombosis


1 See pages 6–8.


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