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J Am Coll Cardiol, 1999; 34:1985-1994
© 1999 by the American College of Cardiology Foundation
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CLINICAL STUDIES

Simultaneous intracoronary velocity- and pressure-derived assessment of adenosine-induced collateral hemodynamics in patients with one- to two-vessel coronary artery disease

Christian Seiler, MD, FACCa, Martin Fleisch, MDa, Michael Billinger, MDa and Bernhard Meier, MD, FACCa

a Division of Cardiology, University Hospital, Swiss Cardiovascular Center Bern, Bern, Switzerland

Manuscript received September 10, 1998; revised manuscript received August 16, 1999, accepted September 1, 1999.

Reprint requests and correspondence: Dr. Christian Seiler, Division of Cardiology, Swiss Cardiovascular Center Bern, Inselspital, CH-3010 Bern, Switzerland.
christian.seiler.cardio{at}insel.ch

OBJECTIVES

The purpose of this investigation in patients with poorly and well developed coronary collaterals was to assess the influence of collateral and collateral adjacent vascular resistances and, in part, a stenotic lesion of the collateral supplying vessel on the hemodynamic collateral responses to adenosine.

BACKGROUND

In humans, little is known about the functional behavior of the coronary collateral circulation.

METHODS

In 50 patients with one- and two-vessel coronary artery disease (CAD) undergoing percutaneous transluminal coronary angioplasty (PTCA), collateral flow index (CFI, no unit) changes and vascular resistance index (R, cm/mm Hg) changes of the collateral (Rcoll) and the distal collateral receiving (R4) vessel in response to adenosine (140 µg/min/kg IV) were measured by intracoronary (i.c.) Doppler and pressure guidewires. The variables were determined at baseline and during adenosine in patients with poor (angiographic collateral degree before PTCA <2 of 0 to 3) and good coronary collaterals.

RESULTS

Pressure-derived CFI (CFIp) decreased under adenosine in patients with poor collaterals, and it increased in the group with good collaterals. There were inverse correlations between the adenosine-induced change in CFIp and the change in Rcoll (r = 0.61, p = 0.0001). In the group with good, but not with poor collaterals, there was also a significant correlation between CFIp increase and the decrease in R4, between the severity of the contralateral stenosis and CFIp augmentation and among the left versus right coronary artery as ipsilateral vessel and CFIp change.

CONCLUSIONS

Overall, patients with well, versus poorly developed coronary collaterals do better regarding the capacity to increase collateral flow in response to adenosine. In patients with good, but not poor, collaterals, an adenosine-induced collateral flow increase depends on the ipsilateral distal vascular resistance decrease, but is also directly influenced by the severity of a contralateral stenosis and probably by the size of the collateralized vascular bed.

Abbreviations and Acronyms
  ANOVA = analysis of variance
  CAD = coronary artery disease
  CFI = collateral flow index
  CFIp = pressure-derived collateral flow index
  CFIv = velocity-derived collateral flow index
  CFVR = coronary flow velocity reserve
  CVP = central venous pressure
  ECG = electrocardiogram
  FFR = fractional flow reserve
  i.c. = intracoronary
  LAD = left anterior descending artery
  LCX = left circumflex artery
  Pao = mean aortic pressure
  Poccl = distal coronary occlusive (wedge) pressure
  PTCA = percutaneous transluminal coronary angioplasty
  RCA = right coronary artery
  Rcoll = collateral resistance index
  R1 = epicardial vascular resistance
  R3 = contralateral resistance index
  R4 = ipsilateral resistance index
  Vioccl = distal velocity time integral during vessel occlusion
  Viø-occl = distal velocity time integral during vessel patency




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