Measurement of coronary collateral flow and resistance in the presence of an open critical stenosis, and the response to intra-arterial thrombosis

Mansaray, M; Hynd, J.; Vergroesen, Isabelle; Belcher, Philip R.; Drake-Holland, Angela J.; Noble, Mark I. M.

doi:10.1016/s0008-6363(00)00109-7

Cited by 7 publications

(3 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Because at the onset of our study protocol, intracoronary nitroglycerin was given, nitric oxide-dependent collateral vasodilatation during exercise was probably not part of the mechanism by which it effected collateral function. Coronary collateral vasoconstriction has been recently documented to be the result of platelet activation via the production of serotonin and thromboxane A 2 [30, 31]. Statistically, the 15 patients in our study not on acetylsalicylic acid at the time of the protocol did not reveal exercise-induced collateral flow decrease more often than the patients on this drug.…”

Section: Discussioncontrasting

confidence: 39%

Exercise-Induced Human Coronary Collateral Function: Quantitative Assessment during Acute Coronary Occlusions

Pohl

Wustmann²,

Zbinden³

et al. 2003

Cardiology

View full text Add to dashboard Cite

In 50 patients undergoing percutaneous transluminal coronary angioplasty because of chronic angina pectoris, a collateral flow index (CFI) was determined at the start and the end of two 1-min coronary occlusions, randomly accompanied by a resting state or a 3-min dynamic handgrip exercise (DHE). CFI expressing collateral flow relative to normal antegrade flow was determined by simultaneous coronary occlusive pressure, mean aortic pressure and central venous pressure measurements. When comparing CFI without and with DHE at the start as well as at the end of balloon occlusions, a significant increase was observed with DHE (overall p < 0.0001); start: 0.18 ± 0.12 vs. 0.22 ± 0.13, respectively (p = 0.01); end of occlusion: 0.21 ± 0.14 vs. 0.25 ± 0.14, respectively (p = 0.007).

show abstract

Section: Discussioncontrasting

confidence: 39%

Exercise-Induced Human Coronary Collateral Function: Quantitative Assessment during Acute Coronary Occlusions

Pohl

Wustmann²,

Zbinden³

et al. 2003

Cardiology

View full text Add to dashboard Cite

show abstract

“…It would be of interest if our observations of collateral vessel constriction with thrombosis [4] are applicable to humans, since restricted collateral flow would have a deleterious effect if it occurred in unstable angina. The collaterals are proximal vessels that do not directly feed the terminal coronary microcirculation.…”

Section: Discussionmentioning

confidence: 99%

“…This could be attributed to the accumulation of emboli shed from the thrombosis site, although we did not observe a progressive increase in the phenomenon as predicted by this hypothesis. However, in a subsequent study without occlusion [4] but with tight stenosis of the LCx, we observed that thrombosis caused an increase in resistance of the collateral vessels supplying the distal LCx vascular bed from the left anterior descending coronary artery (LAD) and right coronary artery. These vessels are not in the stream of blood flowing from the thrombus site, and cannot therefore be the conduit for emboli.…”

Section: Introductionmentioning

confidence: 87%

Thrombosis in one coronary artery causes generalized coronary vasoconstriction in a dog model of unstable angina

MANSARAY¹,

HYND²,

VERGROESEN³

et al. 2001

Clinical Science

View full text Add to dashboard Cite

We investigated the effect of thrombosis in one coronary artery upon the vascular resistance of another coronary artery. In previous investigations, using an animal model of unstable angina, we have observed increased resistance downstream from thrombus within a left circumflex coronary artery (LCx) stenosis and vasoconstriction of collateral vessels from the left anterior descending artery (LAD) supplying the distal LCx vascular bed. In the present paper, we induced thrombosis within a stenosis of the LCx of 16 beagle dogs, and observed the changes in blood flow to the myocardium supplied by the LAD using the radioactive microsphere technique. This blood flow decreased with thrombosis (P = 0.005) in these animals, whereas it did not do so in three time-control experiments. The pressures across the coronary vascular bed, i.e. arterial pressure to coronary venous pressure (coronary sinus catheter), did not change. Thus the vascular resistance of the LAD bed increased significantly from 147 +/- ll.5 mmHg/ml/sec/g of tissue to 172 +/- 13.4 mmHg/ml/sec/g of tissue (P = 0.02). As the LAD territory is not perfused with blood from the artery containing thrombus, we conclude that the effect observed is caused either by release of vasoconstrictors from the thrombus into the general circulation, or by activation of a neural reflex vasoconstriction. The study suggests that unstable angina involving thrombosis in one coronary artery is a global coronary vascular disease.

show abstract

Integrated Coronary Physiology and Pathophysiology

Bassenge¹,

Schwemmer²

2002

Pan Vascular Medicine

View full text Add to dashboard Cite

Measurement of coronary collateral flow and resistance in the presence of an open critical stenosis, and the response to intra-arterial thrombosis

Abstract: Coronary collateral flow around an open stenosis can be measured by reference back to control conditions. The coronary collaterals vasoconstrict in the presence of thrombosis even though they are in the stream of blood coming from normal coronary arteries.

Cited by 7 publications

References 28 publications

Exercise-Induced Human Coronary Collateral Function: Quantitative Assessment during Acute Coronary Occlusions

Exercise-Induced Human Coronary Collateral Function: Quantitative Assessment during Acute Coronary Occlusions

Thrombosis in one coronary artery causes generalized coronary vasoconstriction in a dog model of unstable angina

Integrated Coronary Physiology and Pathophysiology

Contact Info

Product

Resources

About