Clinical applications of the Doppler coronary flow velocity guidewire for interventional procedures.
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Biomedical subjects
Publications and source records attributed to R G Bach.
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BACKGROUND: Coronary artery bypass conduits derived from internal mammary arteries show relative resistance to atherosclerosis and significantly improved long-term patency compared with saphenous vein grafts. Atherothrombotic occlusion of venous conduits has previously been correlated with lower flow rates measured intraoperatively. To quantitate coronary bypass conduit flow velocity, we examined the phasic blood flow velocity patterns by intravascular Doppler spectral analysis in patients during cardiac catheterization to test the hypothesis that resting systolic and diastolic phasic blood flow velocity patterns differ significantly between arterial and venous bypass conduits. METHODS AND RESULTS: Spectral phasic blood flow velocity was measured using an intravascular Doppler-tipped angioplasty guidewire in the proximal, mid, and distal segments of 18 internal mammary artery conduits and 11 saphenous vein grafts in 27 patients at a mean of 4 years (range, 1 to 11) postoperatively. In situ internal mammary artery conduits demonstrated a gradual longitudinal transition in the phasic flow pattern from predominantly systolic velocity proximally (diastolic/systolic peak velocity ratio, 0.6 +/- 0.2) to predominantly diastolic velocity distally (diastolic/systolic peak velocity ratio, 1.4 +/- 0.3; P < .001). Saphenous vein graft flow velocity pattern, however, showed a consistently diastolic predominance, both proximally and distally (diastolic/systolic peak ratios, 1.4 +/- 0.6 and 1.5 +/- 0.7, respectively; P = NS). Mean flow velocities, total velocity integral, and calculated maximal shear rates were significantly higher in all segments of internal mammary arteries compared with values in saphenous vein grafts. CONCLUSIONS: Patterns of resting phasic blood flow, as well as mean velocity and total velocity integral, differ significantly between internal mammary artery and saphenous vein bypass conduits. These differences may have implications regarding blood-vessel wall interactions, the development of degenerative graft disease, and long-term conduit patency.
This is a description of the first two reported cases of double-balloon valvuloplasty in the treatment of porcine bioprosthetic valve stenosis in the tricuspid position. In both cases, the double-balloon technique resulted in a better hemodynamic improvement than single-balloon valvuloplasty and was well tolerated. Double-balloon valvuloplasty is a reasonable alternative to surgical replacement of a stenotic bioprosthesis in the tricuspid position.
The p15(E)-related polypeptides of radiation leukemia virus (RadLV)-derived viruses and of cells infected with prototype MuLV were analyzed by immunoprecipitation, SDS-PAGE, and immunofluorescence analyses. It was found that the p15(E)-related molecules of ecotropic and xenotropic viruses derived from RadLV lymphoma cell lines were distinguishable by reactivity with monoclonal anti-p15(E) antibodies and by SDS-PAGE profile. Ecotropic MuLV of RadLV origin encoded the p15(E)a antigen and produced a Pr15(E) of 20K MW. In contrast, xenotropic virus derived from RadLV did not express the p15(E)a antigen and by SDS-PAGE its Pr15(E) migrated at 21K. A previously undescribed, p15(E)-related molecule of 18.5K MW was associated with xenotropic RadLV. These differences were also reproduced by the prototype ecotropic, xenotropic, and dualtropic viruses.
Radiation leukemia virus (RadLV) causes thymic lymphoma in 90% of susceptible mice after a latent period of several months. The virally encoded polypeptides produced by RadLV-induced lymphoma cells were analyzed by immunoprecipitation and NaDodSO4/polyacrylamide gel electrophoresis. Along with the expected precursor and mature forms of gag and env gene products, a polypeptide of 36,000 molecular weight (p36) was precipitated by anti-gag antisera. It was not precipitable by normal sera or anti-env antibodies. Like the gag-associated fusion proteins of some acute leukemia viruses, p36 was found to be phosphorylated in vivo, although it lacked detectable ATP-specific protein kinase activity in vitro. By kinetics during pulse-chase labeling experiments and by comparison of two-dimensional tryptic peptide maps, this protein is not an intermediate in gag precursor processing. One lymphoma cell line is described that resembles a nonproducer RadLV-transformant, synthesizing relatively large amounts of p36 in the absence of Pr66gag or p30 production. Several RadLV-induced lymphoma cell lines also produce p36, while it was not detectable in the radiation-induced lines tested. In addition, p36 was not produced by mouse or mink fibroblasts or cultured thymocyte cell lines infected with virus passaged from the RadLV-induced lymphomas. We conclude that p36 may represent a previously unrecognized transformation-related protein induced directly or indirectly by infection with RadLV.
BACKGROUND: Absolute coronary flow velocity reserve (CVR) after stenting may remain abnormal as a result of several different mechanisms. Relative CVR (rCVR=CVR(target)/CVR(reference)) theoretically normalizes for global microcirculatory disturbances and facilitates interpretation of abnormal CVR. METHODS AND RESULTS: To characterize potential mechanisms of poststent physiology, CVR was measured using a Doppler-tipped angioplasty guidewire in 55 patients before and after angioplasty, after stenting, and in an angiographically normal reference vessel. For the group, the percent diameter stenosis decreased from 75+/-13% to 40+/-18% after angioplasty and to 10+/-9% (all P<0.05) after stent placement. After angioplasty, CVR increased from 1.63+/-0.71 to 1.89+/-0.55 (P<0.05) and after stent placement, to 2.48+/-0.75 (P<0.05 versus pre- and postangioplasty). After angioplasty, rCVR increased from 0.64+/-0.26 to 0.75+/-0.23 and after stent placement to 1.00+/-0.34. In 17 patients with CVR(stent) < or = 2.0, increased basal coronary flow, rather than attenuated hyperemia, was responsible in large part for the lower CVR(stent) compared with patients having CVR(stent) >2.0. In 8 patients with CVR(stent) <2.0, a normal rCVR supported global microvascular disease. The subgroup of 9 patients with CVR(stent) <2.0 and abnormal rCVR (16% of the studied patients) may require a pressure-derived fractional flow reserve to differentiate persistent obstruction from diffuse atherosclerotic disease or microvascular stunning. CONCLUSIONS: Although a majority of patients after stenting normalize CVR for the individual circulation (ie, normal CVR or normal rCVR), in those with impaired CVR(stent), the analysis of coronary flow dynamics suggests several different physiological mechanisms. Additional assessment may be required to fully characterize the physiological result for such patients to exclude remediable luminal abnormalities.