Key result
Intracoronary collagen injection decreased retrograde coronary collateral blood flow by 53% (from 32.7 to 16.8 ml/min, p<0.05), a vasoconstrictor effect attenuated by TxA2-receptor blockade.
Why the study?
Does intracoronary collagen decrease coronary collateral blood flow, and is this effect mediated by thromboxane A2?
Does intracoronary collagen decrease coronary collateral blood flow, and is this effect mediated by thromboxane A2?
Effect estimate: decreased by 53 +/- 6%
Absolute Event Rate: 16.8% vs 32.7%
p-value: p=< 0.05
Intravascular collagen exerts a potent vasoconstrictor effect on coronary collateral vessels, primarily mediated by thromboxane released by activated platelets.
TxA2 may mediate collagen-induced collateral vasoconstriction in animals; hypothesis-generating for human CAD relevance, no practice change.
This study investigated the effects of intravascular collagen on coronary collateral blood flow. Collateral vessel growth was stimulated in 11 dogs by embolizing the left anterior descending (LAD) coronary artery with a hollow stainless steel plug. Experiments were performed 41 +/- 7 days after coronary embolization when collateral vessels were moderately well developed. Under alpha-chloralose anesthesia, the LAD was cannulated, and retrograde blood flow was used as a measure of collateral flow. Collagen (10-100 microg/kg) injected into the left main coronary artery caused a decrease of coronary collateral blood flow that became maximal at 3 min after injection and subsided within 9 min. At peak effect intracoronary collagen decreased retrograde flow by 53 +/- 6% from 32.7 +/- 8.2 to 16.8 +/- 3.7 ml/min (p < 0.05) with no change in systemic hemodynamics. Selective thromboxane A2 (TxA2)-receptor blockade with SQ30,741 had no effect on collateral blood flow during basal conditions but attenuated the collateral constriction in response to collagen. Thus, after SQ30,741, collagen caused only a nonsignificant decrease retrograde flow from 35.9 +/- 9.0 to 31.7 +/- 9.62 ml/min. The findings indicate that intravascular collagen exerts a potent vasoconstrictor effect on coronary collateral vessels. Attenuation of this response by TxA2-receptor blockade suggests that thromboxane released by activated platelets is the principal mediator of this response.
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Klassen et al. (2000) studied Coronary collateral blood flow (n=11). Intracoronary collagen vs. Basal conditions / Selective TxA2-receptor blockade (SQ30,741) was evaluated on Retrograde blood flow (measure of collateral flow) (decreased by 53 +/- 6%, p=< 0.05). Intracoronary collagen injection decreased retrograde coronary collateral blood flow by 53% (from 32.7 to 16.8 ml/min, p<0.05), a vasoconstrictor effect attenuated by TxA2-receptor blockade.
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