Effect of Rotablator Atherectomy and Adjunctive Balloon Angioplasty on Coronary Blood Flow
Background The purpose of this study was to assess serial changes in coronary blood flow velocity before and after Rotablator atherectomy and after adjunctive percutaneous transluminal coronary angioplasty (PTCA). Since Rotablator atherectomy results in luminal enlargement by plaque pulverization and distal embolization, improvement in coronary blood flow could be attenuated despite luminal enlargement.
Methods and Results Intracoronary Doppler blood flow velocity measurements were obtained with a Doppler Flowire. Basal average peak velocity (bAPV), hyperemic APV (hAPV), diastolic/systolic velocity ratio (DSVR), and coronary flow reserve (CFR) were assessed before intervention, after Rotablator, and after adjunctive PTCA. Complete clinical, angiographic, and Doppler data were obtained in 22 patients. There was a small but significant difference (P=.02) in resting heart rate and mean arterial pressure before and after Rotablator and after adjunctive PTCA. Minimum lumen diameter increased from 0.8±0.1 to 1.5±0.2 to 2.0±0.1 mm (P<.001), corresponding to decreases in diameter stenosis from 72±3% to 41±4% to 36±3% (P<.001). Although bAPV, hAPV, and DSVR increased significantly (P<.001), CFR remained abnormally low in 19 of 22 patients (despite an increase from baseline to post-PTCA). hAPV >30 cm/s was the best Doppler correlate of angiographic success.
Conclusions Rotablator atherectomy and adjunctive PTCA significantly improve distal coronary blood flow velocity and DSVR but not CFR. Failure to normalize CFR could be secondary to parallel increases in bAPV and hAPV, “acquired” microvascular disease due to distal microembolization or spasm, and/or angiographically inapparent dissection or residual stenosis. Adjunctive PTCA contributes significantly to the overall physiological benefit of a combined procedure.
Successful percutaneous coronary revascularization with directional atherectomy, excimer laser, and balloon angioplasty is associated with objective improvement in coronary artery flow dynamics by Doppler flow techniques.1 2 3 High-speed MRA (Rotablator) is also an effective device for percutaneous coronary revascularization. Although Rotablator-mediated luminal enlargement would be expected to improve coronary blood flow dynamics by improving vessel geometry, the mechanism of luminal enlargement is plaque pulverization and distal embolization, which could theoretically attenuate improvements in blood flow.4 5 6 7 8 9 Accordingly, the purpose of this study was to assess serial changes in coronary blood flow velocity before and after Rotablator atherectomy and after adjunctive PTCA.
Between June 15, 1994, and January 12, 1995, 22 consecutive patients underwent Rotablator atherectomy, adjunctive PTCA, and intracoronary Doppler assessment. Clinical exclusions included old or recent myocardial infarction, diabetes mellitus, congestive heart failure, renal failure, valvular heart disease, left ventricular hypertrophy, or left ventricular ejection fraction <50%. Angiographic exclusions included visible thrombus, lesion length >25 mm, chronic total occlusion, diffuse distal disease, left main coronary artery narrowing >50%, or angiographically apparent collaterals to the target vessel. Anti-ischemic medications and antiplatelet agents were prescribed as clinically indicated. Informed consent was obtained from each patient according to a protocol approved by the Human Investigations Committee of William Beaumont Hospital.
After baseline coronary angiography, a 0.014- or 0.018-in Doppler Flowire (Cardiometrics) was placed in the target vessel at least 2 cm distal to the target lesion. Special care was taken to avoid placement into a side branch or poststenotic velocity jet. Baseline flow velocity was recorded once a stable, maximal Doppler signal was obtained and the instantaneous peak velocity tracking correlated with a crisp gray-scale Doppler envelope, as previously described.1 10 11 Once basal flow velocity stabilized for >60 seconds, maximal hyperemic velocity was induced with intracoronary adenosine (10 to 15 μg in the RCA, 20 to 30 μg in the LCA), as previously reported.12 13 Flow velocity spectra were tracked for at least 60 seconds after each adenosine bolus and were analyzed for bAPV, hAPV, continuous DSVR, and CFR, as previously defined.1 After intervention, the basal and hyperemic velocity spectra were monitored until stable, consistent signals were obtained, and APV was recorded after the velocity equilibrated and remained constant for >60 seconds. Doppler flow velocities were obtained ≥10 minutes after the administration of 200 μg intracoronary nitroglycerin. Measurements were obtained in all patients before intervention, after Rotablator, and after adjunctive PTCA with the Flowire in the same position.
Rotablator Atherectomy and Adjunctive PTCA
All Rotablator atherectomy procedures were performed with a Rotablator C guidewire (Heart Technologies) and a stepped-burr approach, as previously described.14 15 After Rotablator, the C-wire was exchanged for the Doppler Flowire, and Doppler assessment and coronary angiography were repeated. Adjunctive PTCA was performed in all cases to achieve final luminal enlargement, and final Doppler assessment and angiography were repeated as described above.
The single view that identified the most severe stenosis was selected for quantitative analysis, and measurements of MLD, reference diameter, lesion length, and DS were obtained by computerized edge detection, as previously described.16 Measurements were performed at baseline, immediately after Rotablator, and after adjunctive PTCA. Antegrade flow was graded by standard TIMI criteria.17 Procedural success was defined as final DS <50% in the absence of a major complication (death, Q-wave myocardial infarction, coronary bypass surgery).
Continuous data are reported as mean±SEM unless stated otherwise. ANOVA was used to compare baseline, post-Rotablator, and post-PTCA Doppler, hemodynamic, and angiographic variables. A two-tailed paired Student's t test with Bonferroni's correction was used to compare mean values if significant by ANOVA. Conventional Student's t test was used to compare mean values of unpaired data for DS, MLD, and DSVR. Linear regression was used to evaluate the relationship between Doppler, clinical, hemodynamic, and angiographic data. Differences were considered significant if P<.05.
Complete clinical, angiographic, and Doppler data were obtained in 22 patients (22 vessels) 63.2±12.2 years old (mean±SD). Baseline clinical and angiographic characteristics are presented in Table 1⇓. Prior percutaneous intervention had been performed on 9 lesions.
All patients were hemodynamically stable and asymptomatic at rest at the time of intervention. There were small but statistically significant differences in resting heart rate (P=.02) and mean arterial pressure (P=.02) from baseline to after Rotablator to after adjunctive PTCA (Fig 1⇓).
Procedural success was achieved in all 22 patients. Fig 2⇓ shows representative angiographic and spectral displays at various stages of the procedure. Quantitative angiography revealed an increase in MLD from 0.8±0.1 mm at baseline to 1.5±0.2 mm after Rotablator to 2.0±0.1 mm after adjunctive PTCA (P<.001), corresponding to decreases in DS from 72±3% to 41±4% and to 26±3%, respectively (P<.001). Two patients had transient TIMI 2 flow (Table 2⇓, patients 2 and 7) after Rotablator, which improved to TIMI 3 flow after intracoronary nitroglycerin and before assessment of distal flow velocity; TIMI 3 flow was present at baseline, after Rotablator, and after adjunctive PTCA at all other times of assessment. Single burrs were used in 15 patients and multiple burrs in 7; final burr-to-artery ratio was 0.7±0.3 (mean±SD). The mean lesion length was 9.4±5.1 mm (mean±SD) (range, 3.0 to 20.4 mm). Moderate to severe calcification was evident fluoroscopically in 6 of 22 patients (27%) in the target vessel. No patient had sustained “no reflow,” flow-limiting dissection, coronary perforation, or persistent spasm after Rotablator or adjunctive PTCA.
Assessment of Distal Coronary Flow Velocity
Stable velocity signals were obtained 10±7 minutes after each intervention; there was no difference after Rotablator or adjunctive PTCA with regard to the time to achieving a stable signal. bAPV increased from 17.8±1.9 to 28.8±3.6 cm/s after Rotablator to 39.5±3.7 cm/s after adjunctive PTCA (P<.001) (Fig 3⇓). bAPV increased in 18 patients (82%) after Rotablator, with further increases in 19 patients (86%) after PTCA. hAPV increased from 21.1±2.5 cm/s at baseline to 37.0±4.7 cm/s after Rotablator to 53.4±5.0 cm/s after PTCA (P<.001) (Fig 3⇓). hAPV increased in 19 patients (86%) after Rotablator, with further increases in 18 patients (81%) after adjunctive PTCA. hAPV increased in all patients from baseline to after PTCA; the 4 patients with no sequential increase after Rotablator (2 patients, no change; 2 patients, trivial decrease) (Table 2⇑) had a threefold increase, on average, in hAPV from baseline to after Rotablator. There was no difference in distal reference vessel diameter at the site of Doppler assessment from baseline (2.3±0.2 mm) to after Rotablator (2.1±0.2 mm) to after PTCA (2.3±0.3) (P=NS), suggesting that changes in basal and hyperemic blood flow velocity were due to increases in volumetric flow. hAPV >30 cm/s was observed in 4 patients (18%) before intervention, 12 patients (55%) after Rotablator, and 21 patients (95%) after adjunctive PTCA (Fig 4⇓). Patients with hAPV >30 cm/s after Rotablator had a significantly lower DS (33.8±4.7 versus 55.5±5.0%, P<.01) and larger MLD (1.3±0.1 versus 1.0±0.1 mm, P<.01) than patients with hAPV <30 cm/s.
Coronary Flow Reserve
Baseline CFR was 1.2±0.1 (range, 0.9 to 1.6); CFR was <2.0 in all patients, consistent with the physiological significance of the target lesion. Although CFR increased to 1.3±0.1 after Rotablator and to 1.5±0.1 after adjunctive PTCA (P<.01) (Fig 5⇓), CFR >2.0 was achieved in only 3 patients (14%) after adjunctive PTCA. The final DS for the 3 patients with final CFR >2.0 was 37±3%, which was similar to the final DS of 28±3% for the 19 patients with final CFR <2.0. The failure to further increase CFR to “normal” levels was associated with parallel increases in bAPV and hAPV; compared with baseline, bAPV increased 157% and hAPV increased 209% after adjunctive PTCA.
Phasic Coronary Flow Parameters
DSVR increased from 1.3±0.1 before intervention to 1.5±0.1 after Rotablator to 1.8±0.1 after PTCA (P<.01). Normal DSVR (>1.7 in the LCA, >1.4 in the RCA) was observed in 5 patients (23%) before intervention, in 11 patients (50%) after Rotablator, and in 12 patients (55%) immediately after adjunctive PTCA. When changes in DSVR were stratified for the RCA and LCA, there was a significant increase in DSVR only in the LCA (P<.001) (Fig 6⇓): Whereas 10 of 17 patients (59%) achieved DSVR >1.7 in the LCA, only 1 of 5 patients (20%) achieved DSVR >1.4 in the RCA (See Table 2⇑ and Fig 6⇓).
Effect of Baseline Characteristics and Angiographic and Hemodynamic Variables on Measured Doppler Variables After Adjunctive Angioplasty
There was no relationship between age, sex, history of hypertension, presence of multivessel disease, or smoking status and hAPV or CFR after adjunctive PTCA. Final hAPV and CFR after PTCA did not correlate with percent DS, MLD, or lesion length. Interestingly, although bAPV and hAPV were not associated with heart rate or mean arterial pressure, postprocedure CFR weakly correlated with mean arterial pressure (r=.55, P=.007) after adjunctive PTCA.
Rotablator and Microparticle Embolization
Rotablator atherectomy has a unique mechanism of action that relies on plaque pulverization and microparticle embolization to achieve luminal enlargement.18 19 Experimental studies suggest that these particles are usually small enough to pass through the capillary circulation and are subsequently removed by the reticuloendothelial system.6 8 20 21 22 Other experimental6 and clinical7 19 23 studies reported no significant impact on resting wall motion, myocardial perfusion, or other clinical markers of myocardial ischemia after uncomplicated Rotablator atherectomy. In contrast, the physiological effects of Rotablator-induced microembolization are unclear. Detailed angiographic analyses after rotational atherectomy reported slow or no reflow in 7% to 8% of patients with associated myocardial infarction in 25%4 14 and ECG evidence of ischemia in 43% of patients.5 In the absence of gross disturbances in flow by angiography, the effects of microparticulate embolization5 and burr-induced microcavitation7 on physiological measures of coronary flow have not been reported previously. This study demonstrates that angiographically successful Rotablator atherectomy is associated with increases in basal and hyperemic coronary blood flow velocity and normalization of the diastolic predominance of coronary blood flow (only in the left coronary artery) but persistent impairment in CFR despite increases in hyperemic blood flow.
Coronary Flow Velocity After Rotablator
In the absence of changes in vessel diameter, APV is a surrogate for volumetric coronary flow.2 The increase in APV in this study is similar to those reported after successful PTCA,1 24 laser angioplasty,3 and directional atherectomy25 and probably represents increased distal flow. Distal APV improves almost immediately after the procedure and correlates with successful luminal enlargement after angioplasty.1 2 The increase in flow after Rotablator may be secondary to relief of stenosis severity and/or endogenous release of adenosine secondary to endothelial activation leading to arteriolar vasodilation.26 Interestingly, transient “slow reflow” (TIMI flow grade 2) was seen immediately after Rotablator in 2 patients (Table 2⇑, patients 2 and 7). These 2 patients had residual stenoses of 61% and 52% after Rotablator, respectively, compared with 40% for the remaining 20 patients. Angiographically, the lesions for these 2 patients were complex (B2, C) and long (18.5 mm, 20.4 mm), possibly representing a greater atheroma burden in these patients.4 bAPV and hAPV decreased in both patients 8 to 10 minutes after Rotablator, yet by the time of Doppler assessment, TIMI 3 flow had been restored by intracoronary nitroglycerin and the time window necessary to reposition the Doppler guidewire. Furthermore, after PTCA there was a substantial increase in bAPV (15 to 24 cm/s, 16 to 29 cm/s) and hAPV (15 to 39 cm/s, 17 to 36 cm/s) along with unchanged TIMI 3 flow. The cause of “no reflow” after Rotablator remains speculative but could be secondary to severe spasm,18 21 unrecognized dissection,14 microcavitation,7 or microparticulate embolization.5 14 21 Because of the transient nature of the slow reflow in both patients and substantial improvement in basal and hyperemic flow after adjunctive PTCA, it appears that microembolization did not have a sustained adverse effect on distal flow. On the basis of this observation, transient burr-induced microcavitations or spasm are likely explanations for transient slow flow after Rotablator.
DSVR After Rotablator
The normal diastolic predominance of coronary flow is lost in the presence of a severe epicardial stenosis,27 but successful PTCA results in immediate normalization of DSVR.1 2 The increase in DSVR in this study is consistent with reports after other techniques.1 2 24 25 Although an experimental study in dogs reported a significant decrease in DSVR after microembolization without changes in mean flow,28 DSVR increased in our study, suggesting that microparticulate debris did not have a profound adverse effect on coronary flow dynamics. This change was noted, however, only in the LCA, in which the diastolic predominance of coronary flow is most pronounced. DSVR normalized2 in the LCA in 11 of 17 patients (65%).
Improvement in the diastolic predominance of coronary flow velocity is heterogeneous. In addition to epicardial factors, hemodynamic, microcirculatory, and myocardial influences most likely play a role in changes of the DSVR. An increase in myocardial contractility, in particular, would lead to a decrease in the systolic component of coronary flow and a resultant increase in the DSVR if the diastolic flow velocity remained unchanged. Small amounts of microparticulate debris may incite vasomotor changes leading to such an increase, whereas a large amount of embolization would be expected to cause significant ischemia, resulting in impaired contractility (and an increase in systolic flow) in the myocardial beds studied. The systolic velocity integral was not assessed to isolate the systolic flow velocity changes that occurred. Nevertheless, the observed improvement in DSVR is most likely the result of both an increase in the diastolic velocity due to a decrease in the epicardial stenosis and a decrease in the systolic velocity due to an improvement in myocardial contractility immediately after the procedure.
CFR After Rotablator
CFR, unlike bAPV, hAPV, and DSVR, remained abnormally low after Rotablator and adjunctive PTCA in this study, although there was a small but statistically significant increase in CFR from baseline to post-PTCA levels. These results are similar to those reported after PTCA29 and other atherectomy devices.1 3 Failure to normalize CFR may be due to an increase in basal coronary blood flow velocity, decreased capacity of the arteriolar bed to vasodilate (microvascular disease), resistance to hyperemic flow due to angiographically inapparent persistent stenosis or dissection,29 and/or diffuse residual atherosclerosis.30 In this study, “acquired microvascular disease” due to microparticle embolization and/or microvascular spasm cannot be totally excluded. However, the unexplained substantial increase in basal flow velocity to >150% above baseline levels undoubtedly contributed to impaired CFR ratios after Rotablator. As with other interventions, CFR immediately after Rotablator and adjunctive PTCA does not correlate with angiographic or other Doppler parameters. Post-PTCA hAPV >25 to 30 cm/s, seen in angiographically normal vessels,31 correlated more closely with procedural success than CFR, and substantial increases in hAPV support the elimination of hemodynamically significant stenoses in these patients. Nevertheless, recent preliminary studies suggest that impaired CFR after successful PTCA can be improved by stenting32 33 ; these data suggest that persistent abnormal CFR after Rotablator may be due, at least in part, to angiographically inapparent significant residual stenosis.
Effects of Adjunctive PTCA on Doppler Variables After Rotablator
APV, DSVR, DS, and MLD significantly improve after adjunctive angioplasty, findings similar to those reported after laser angioplasty.3 Most of the gain in lumen area after Rotablator and adjunctive PTCA is secondary to PTCA.14 34 The sequential improvement after balloon angioplasty may be explained by lumen enlargement, treatment of a dissection, transient effects of microcavitations, relief of vasospasm induced by Rotablator, or platelet adhesion after exposure of the media leading to local vasoactive factors that may transiently limit the flow response. The physiological improvement after combined Rotablator and adjunctive PTCA raises the question as to whether PTCA alone would lead to similar physiological improvement.
Lack of Correlation of Doppler and Angiographic Variables After Rotablator
In this study, there was no correlation between hyperemic blood flow velocity or CFR and quantitative assessment of stenosis severity before or after intervention, which is consistent with prior studies.35 36 37 CFR immediately after PTCA or Rotablator and adjunctive PTCA does not reflect the success of the procedure in removing the physiological obstruction to blood flow. A better measure of success (not stenosis severity) appears to be hAPV: A “normal” hAPV (>30 cm/s) was achieved in 95% of patients with “angiographic success.” Impaired distal hyperemic response after Rotablator may identify a persistent suboptimal physiological result after the procedure; this is supported by a significantly higher residual stenosis after Rotablator in the group with hAPV <30 cm/s (Fig 4⇑). It will be important to assess whether clinical outcome correlates with these postprocedure blood flow velocities.
There are several potential limitations of this study. First, proper use of the Doppler guidewire requires careful positioning of the transducer parallel to blood flow, and technical problems may influence accuracy.10 13 35 To minimize these problems, meticulous attention was given to careful positioning of the tip of the guidewire to maximize the Doppler signal, as previously reported.10 11 Second, alterations in arterial blood pressure may have a modest parallel effect on basal and hyperemic flow velocities,38 but the decrease in arterial pressure in this study would be expected to decrease flow velocity. However, bAPV and hAPV increased in this study, which must have occurred despite the decrease in blood pressure. It is possible, however, that hAPV did not increase to maximum levels because of an overriding effect of lower MAP, which would potentially lead to a relative decrease in hyperemic flow.38 Nevertheless, CFR should not change, because bAPV and hAPV would be altered to a parallel and similar degree. Fractional flow reserve was not assessed because of the inaccuracies of obtaining distal coronary pressures through a 2.2F catheter; the 0.018-in end-hole wire remains experimental. Third, coronary flow velocity may increase with increases in preload. Although filling pressures were not measured, it is unlikely that they changed significantly during the procedure. Furthermore, although changes in preload could confound bAPV and CFR, they would not affect hyperemic flow velocity.38 Fourth, the assessment of CFR may be confounded by unrecognized microvascular disease; however, patients with predisposing factors for abnormal vasodilator reserve were excluded. Furthermore, reasonable vasodilatory reserve is inferred from the 2.2-fold increase in hAPV after adjunctive PTCA compared with pre-Rotablator levels (Fig 3⇑). Although the increased flow may be due to removal of the epicardial obstruction alone, it is manifested by decreases in arteriolar resistance and represents vasodilation of the microvasculature. Finally, translesional velocity gradients and “normal” reference vessel measurements were not obtained; therefore, compensatory flow velocity changes in adjacent territories remain undefined.
Rotablator atherectomy and adjunctive PTCA significantly improve basal and hyperemic blood flow velocity and restore the diastolic predominance of coronary blood flow. Although CFR increases, it is still impaired despite excellent luminal enlargement by quantitative angiography. Further studies are needed to differentiate angiographically inapparent, significant residual stenosis or impaired microcirculation from transient increases in basal flow velocity as a cause of abnormal CFR.
Selected Abbreviations and Acronyms
|APV||=||average peak velocity|
|bAPV||=||basal average peak velocity|
|CFR||=||coronary flow reserve|
|DSVR||=||diastolic to systolic flow velocity ratio|
|hAPV||=||hyperemic average peak velocity|
|LCA||=||left coronary artery|
|MLD||=||minimal lumen diameter|
|MRA||=||mechanical rotational (Rotablator) atherectomy|
|PTCA||=||percutaneous transluminal coronary angioplasty|
|RCA||=||right coronary artery|
This study was supported in part by a research grant from Cardiometrics, Inc, Mountain View, Calif. We thank Dianna Frye and Diane Parsons for their thoughtful preparation of the manuscript, Carl Dmuchowski for his statistical analysis, and the staff of the Cardiac Catheterization Laboratory for their assistance in performing the Doppler studies.
- Received April 23, 1996.
- Revision received October 7, 1996.
- Accepted October 23, 1996.
- Copyright © 1997 by American Heart Association
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