Pharmacological modulation of the human collateral vascular resistance in acute and chronic coronary occlusion assessed by intracoronary blood flow velocity analysis in an angioplasty model

Background The pharmacological responsiveness of the coronary collateral circulation in humans has been studied only by indirect means. Methods and Results Patients with one-vessel disease and recruitable (n=14) or spontaneously visible (n=24) collateral vessels were studied during coronary angioplasty. Collateral Bow in the recipient coronary artery was determined with a 0.014-in Doppler guide wire during balloon coronary occlusion and expressed as the diastolic blood flow velocity integral (dVi). Collateral blood flow velocity, mean aortic pressure (Pao) and coronary wedge pressure (Pw) were used to calculate the collateral vascular resistance index: Rcoll = (Pao - Pw)/dVi (mm Hg/cm) and the peripheral vascular resistance index of the recipient coronary artery: R4=Pw/dVi (mm Hg/cm). Adenosine (12 to 18 mu g) and nitroglycerin (0.2 mg) were injected as a bolus in the donor coronary artery during subsequent balloon inflations to assess their effect on these hemodynamic variables. The administration of adenosine or nitroglycerin in patients with recruitable collateral vessels did not induce a change in dVi and Pw/Pao ratio. In patients with spontaneously visible collateral vessels, dVi increased from 8.0+/-4.5 to 10.8+/-8.0 cm (P=.01) after adenosine and from 7.4+/-4.5 to 10.3+/-6.9 cm (P=.003) after nitroglycerin. The Pw/Pao ratio remained unchanged after adenosine and nitroglycerin. Rcoll decreased from 10.3+/-9.5 to 8.6+/-8.5 mm Hg/cm (P=.01) after adenosine and from 11.6+/-10.4 to 8.3+/-8.9 mmHg/cm (P<.001) after nitroglycerin. R4 decreased from 7.7+/-5.5 to 5.9+/-5.1 mm Hg/cm (P<.001) after adenosine and from 8.4+/-6.6 to 7.1+/-7.2 mm Hg/cm (P=.01) after nitroglycerin. Conclusions Coronary collateral blood Bow can be increased with adenosine and nitroglycerin in patients with one-vessel disease and spontaneously visible collateral vessels, which is in contrast to patients with recruitable collateral vessels. This effect is the result of a reduction in the collateral vascular resistance and peripheral vascular resistance of the recipient coronary artery.