Author + information
- Received April 28, 1995
- Revision received April 26, 1996
- Accepted May 7, 1996
- Published online October 1, 1996.
- JOHN B. NEWELL and
- IGOR F. PALACIOS
- MICHAEL H. PICARD* ()
- ↵*Address for correspondence: Dr. Michael H. Picard, Cardiac Ultrasound Laboratory, VBK 508, Massachusetts General Hospital, Boston, Massachusetts 02114.
Objectives. This study aimed to evaluate the prevalence and time course of wall motion abnormalities associated with rotational coronary atherectomy.
Background. Although initial clinical studies found evidence of transient wall motion abnormalities after rotational coronary atherectomy, the prevalence and duration of these wall motion abnormalities are unknown.
Methods. Using simultaneous echocardiography, we prospectively evaluated 22 patients undergoing rotational atherectomy and compared their wall motion abnormalities with those of 10 patients undergoing coronary angioplasty alone. The extent of wall motion abnormality was quantified and plotted against time to produce curves of abnormal wall motion development and recovery for the two groups.
Results. The cumulative ischemic time was similar for the two groups ([mean ± SD] 10.3 ± 6 min for rotational atherectomy vs. 9.6 ± 4.2 min for coronary angioplasty, p = 0.73). The rate of return to baseline function was significantly lower in the rotational atherectomy group than in the coronary angioplasty group (rotational atherectomy rate constant 0.069 ± 0.079/min vs. coronary angioplasty rate constant 1.250 ± 0.47/min, p = 0.0001). The mean time to recovery of baseline wall motion in the rotational atherectomy group (153 min, 95% confidence interval [CI] 6.5 to 3,600) was significantly longer than in the coronary angioplasty group (2.6 min, 95% CI 1.3 to 5.5, p = 0.0001). Rotational atherectomy burr time was longer in the patients who developed myocardial infarction than in those without myocardial infarction (4.7 ± 2.4 vs. 3 ± 1.4 min, p = 0.045).
Conclusions. Transient wall motion abnormalities are common after rotational coronary atherectomy and have a longer duration than those observed after coronary angioplasty. This disparity may be a consequence of differences in the mechanisms by which rotational coronary atherectomy and coronary angioplasty produce their effect.
Rotational coronary atherectomy is being used with increasing frequency, especially for calcified and complex coronary lesions. Although this technique produces small particles of atheromatous debris [1, 2], initial studies in normal canine arteries demonstrated that the majority of the particles could be expected to pass harmlessly through the coronary microcirculation without distal embolization . Later studies, however, have documented histologic evidence of isolated myocardial microinfarcts after intracoronary infusion of atherectomized debris, suggesting that not all debris passes through the coronary microcirculation .
Transient impairment of left ventricular function was noted during the early application of rotational coronary atherectomy, using left ventriculography to assess regional function, in a subset of patients with diffuse coronary artery disease . Because these angiograms were not performed simultaneously with the atherectomy and because single-plane ventriculography does not visualize all left ventricular segments, this approach might represent a conservative estimate of the prevalence of wall motion abnormalities. In addition, the time course of resolution of wall motion abnormalities related to rotational atherectomy is not known. Echocardiography overcomes the limitations of ventriculography by enabling real-time, continuous assessment of regional wall motion.
The objective of this study was to examine, using serial echocardiography, the prevalence and time course of wall motion abnormalities associated with rotational coronary atherectomy and adjunct coronary angioplasty.
Study group. Patients undergoing rotational atherectomy at the Massachusetts General Hospital from May 1994 through October 1994 were assessed for inclusion in the study. The patient group included those with adequate echocardiographic imaging of the left ventricle who had normal or minimal impairment of wall motion in the territory where rotational atherectomy was to be performed. Patients with extensive akinetic wall motion abnormalities or coronary artery bypass grafts were excluded. The study protocol was approved by the Human Studies Committee of the Massachusetts General Hospital and written informed consent was obtained from all patients before the procedure.
Thirty-one patients were screened for inclusion, 26 of whom were enrolled. Of the excluded patients, three had inadequate echocardiographic imaging of the left ventricle, two of whom did not proceed to atherectomy (one patient experienced dissection of the target artery during passage of the guide wire, and in the remaining patient the lesion could not be crossed with the guide wire). Four of the 26 patients who had rotational atherectomy were found to have technically inadequate serial echocardiographic studies; thus, 22 patients formed the final study group.
Study protocol. Echocardiograms were performed on either a Hewlett-Packard 77020A phased-array sector scanner or an Interspec Apogee CX 200 mechanical sector scanner, and images were recorded on 0.5-in. VHS videotape. All studies were performed by the same echocardiographer (M.J.A.W.). A baseline echocardiogram was performed with the patient lying supine on the catheterization table before commencing the procedure. Four standard views were evaluated to assess which best demonstrated the territory supplied by the artery having rotational atherectomy—parasternal long and short axes and apical four- and two-chamber views. Two orthogonal views were then recorded for later analysis.
Procedural medications included intravenous heparin (adjusted to maintain an activated clotting time >300 s) and intracoronary nitroglycerin. A pacing catheter was placed in the right ventricle; a 9F guiding catheter was positioned at the ostium of the stenotic artery; and a 0.009-in. (0.02-cm) C guide wire was used to cross the lesion. A Rotablator burr (Heart Technology) was then advanced through the lesion at 160,000 to 180,000 rpm. The burr sizes ranged from 1.5 to 2.25 mm, with rotational atherectomy periods ranging from 11 to 65 s. Rotational atherectomy was repeated two to seven times per lesion. A second larger Rotablator burr was used in 45% of patients in whom further upsizing of the lesion was indicated to reach a target burr/artery ratio of 0.80. The mean cumulative burr duration was 3.38 ± 1.75 min.
Adjunct coronary angioplasty was performed in all patients at a mean 20 ± 8.3 min after commencing the first pass of the rotational atherectomy burr. The balloon catheters used ranged in size from 2.5 to 3.5 mm, with inflation durations of 1 to 6 min at pressures ranging from 4 to 8 atm. The mean number of inflations was 2.3 ± 1.0 and the mean cumulative balloon inflation time was 6.9 ± 6 min.
Serial echocardiograms using the same two views as at the baseline study were performed starting immediately or within <15 s after cessation of the first rotational atherectomy period. Typically, the subsequent echocardiograms were performed between each period of rotational atherectomy or coronary angioplasty and then at 1, 8, 24 and 48 h after the procedure or until wall motion returned to baseline. The number of echocardiographic studies per patient ranged from 4 to 13 (mean 6.4 ± 1.8).
During the procedure, the limb and MCL1 leads were monitored for ST segment changes, and the duration of ST segment elevation ≥2 mm was recorded. A 12-lead electrocardiogram (ECG) was obtained before the procedure and 1 h and 24 h after the procedure. The ECGs were assessed for the presence of new Q waves or T wave inversion, either of which was classified as ECG changes.
Serum creatine kinase (CK) activity levels and creatine kinase, MB fraction (CK-MB) mass levels were obtained before and up until 24 h after the procedure at 8-h intervals.
The occurrence of complications related to the procedure were recorded. Major complications were defined as death, emergency bypass surgery or Q wave myocardial infarction during or after the procedure. Other recorded complications included non-Q wave myocardial infarction, coronary dissection and the use of stents or adjunct directional coronary atherectomy.
Angiographic analysis. Quantitative coronary angiography was performed with a Cardiovascular Measurement System (Medis, Nuenen, The Netherlands) in two views according to the standard method described by Reiber et al. . A reference diameter proximal to the stenosis was measured, and the diameter of the stenosis was expressed as a percentage of this reference diameter. Minimal lumen diameter and length of the lesion were calculated using the guiding catheter diameter as a standard reference. A burr/artery ratio was defined as the ratio of the largest burr size used to the reference diameter. The minimal lumen diameter and residual percent stenosis were calculated on the final postprocedure angiogram. The degree of calcification of each lesion was graded as follows: none = 0; mild = 1; moderate = 2; severe = 3. The lesions were also graded for lesion type according to the modified American College of Cardiology/American Heart Association (ACC/AHA) lesion score . The presence of no-reflow was defined as delayed anterograde flow (Thrombolysis in Myocardial Infarction trial flow grade <2) in the absence of dissection, thrombus or spasm at or adjacent to the original lesion .
Procedural success was defined as a reduction in the severity of the stenosis of at least 20%, with a residual lesion <50% in the absence of major complications . A Q wave myocardial infarction was defined as the presence of new Q waves with elevation of CK >200 U/liter and CK-MB >7.5 ng/liter. Non-Q wave myocardial infarction was defined as an increase in CK to >200 U/liter and CK-MB to >7.5 ng/liter, with new T wave changes in the absence of new Q waves .
Echocardiographic analysis. The videotapes of the echocardiograms were subsequently reviewed to quantitate both the extent and severity of the induced wall motion abnormalities. The echocardiographic view that demonstrated the maximal wall motion abnormality was used to calculate an index of the extent of abnormal wall motion . An experienced observer (M.H.P.) who had no knowledge of the patients' treatment group and time of echocardiogram assessed the presence and extent of abnormal wall motion. The total endocardial segment length of the left ventricle and the length of endocardium with abnormal wall motion were measured at end-diastole (Sony Cardiologic Analysis System, Sony Medical Electronics). The length of endocardium with abnormal wall motion was expressed as a percentage of the total endocardial segment length ([%AWM] Fig. 1). Three consecutive diastolic frames were measured at each point in time and mean values for the results were obtained. Where present, small regions of hypokinesia on the baseline study were quantitated and subtracted from subsequent stages so that the index reflected only new wall motion abnormalities. The %AWM for each patient was then plotted as a function of time to produce a graphic display of the extent and duration of abnormal wall motion (Fig. 2, squares). The mathematical function f(x) = A exp(−λ1x)[1 −exp(−λ2x)] was then fitted to this data (RS-1, BBN software) to produce a continuous curve of %AWM (Fig. 2, line) . The variables of the mean fitted functions of the two groups were compared using the Student t test to assess differences between the groups. In this model, λ1 represents the rate constant of the descending limb of the curve (i.e., a rate constant of recovery of abnormal wall motion). The other variable, λ2, represents the rate constant of the upstroke of the curve or a rate constant of onset of abnormal wall motion, and A is a scaling factor that determines the peak %AWM.
In addition, the severity of segmental dysfunction was assessed by calculating a wall motion score from the same echocardiographic views that %AWM was quantitated from according to the recommendations of the American Society of Echocardiography (1 = normal or hyperkinesia; 2 = hypokinesia; 3 = akinesia; 4 = dyskinesia; 5 = aneurysm) . The wall motion score index was derived by dividing the sum of the segment scores by the number of segments assessed .
Control group. A control group of patients that had percutaneous transluminal coronary angioplasty alone was studied with serial echocardiography using the same method as outlined for the rotational atherectomy group. During the last month of the study, these patients were selected at random from those patients referred to the catheterization laboratory for an elective coronary angioplasty. Of 13 patients studied, 10 had echocardiograms suitable for quantitative analysis. Echocardiography was performed before and during each balloon inflation using the previously described approach. Coronary angioplasty was performed with balloon catheters ranging in size from 2.5 to 3.5 mm at pressures of 6 to 12 atm from a range of 1 to 11.5 min for a mean of 2.9 ± 0.7 inflations (range 2 to 4). Quantitative coronary angiography was performed on the angiograms of the control group subjects using the same methods as described earlier.
Echocardiograms between balloon inflations demonstrated that wall motion returned to baseline after each inflation. Quantitation of the %AWM and its time course was performed on the final balloon inflation for each patient. The extent and duration of new abnormal wall motion during the coronary angioplasty and in the recovery period were then plotted and fitted to the same exponential function as described earlier. Clinical and laboratory data identical to that collected for the rotational atherectomy group were recorded.
Statistical analysis. Normally distributed continuous variables are expressed as mean value ± 1 SD. Comparisons were made using the unpaired Student's t test for normally distributed continuous variables, and the Fisher exact probability test for categoric variables (RS-1, BBN software). The times to recovery of baseline wall motion were logarithmically transformed (to render the distribution normal) before t test comparison between the patient groups . Student t tests comparing variables of the fitted model between patient groups were weighted to correct for unequal variances estimated for λ1. Stepwise (forward stepping) multiple linear regression analysis was used to assess correlates of rate of recovery of abnormal wall motion. The variables examined included age, gender, lesion characteristics, burr size, burr/artery ratio, burr duration, coronary angioplasty duration, CK level, cumulative duration of interventions and ECG changes. At each step of the analysis, the F values of the variables were tested, and the independent variable with maximal F value corresponding to p < 0.05 was included in the model. This was continued until no more independent variables had an F value with p < 0.05.
Baseline characteristics. The atherectomy and control groups were similar with respect to mean age and proportion of men in each group (Table 1). No patient had ECG evidence of a previous Q wave infarction. The left anterior descending coronary artery was the most common artery undergoing intervention, and both groups had similar baseline ejection fractions. Stenoses in the rotational atherectomy group had a significantly higher median calcium score than those in the control group (2 vs. 1, p = 0.004). The lesion length and modified ACC/AHA score were not significantly different between the groups. There were no significant differences between the groups in the proportion of patients presenting with acute ischemic syndromes and restenosis.
Procedural results. The cumulative ischemic time in patients undergoing rotational atherectomy was not significantly different from that in the coronary angioplasty control group (Table 2). The total burr plus angioplasty time for the rotational atherectomy group was 10.3 min, and the total balloon inflation time in the angioplasty control group was 9.6 min. There were no significant differences in the mean preprocedure and postprocedure minimal lumen diameter or severity of preprocedure and postprocedure stenoses between the groups.
Rotational atherectomy was successful in 21 patients (95%). The mean maximal burr size/artery ratio was 0.83 ± 0.22. Complications (rescue stenting and a non-Q wave myocardial infarction) were observed in one patient who had an extensive dissection. Two other patients had a dissection and an inadequate initial result, and they were treated with a stent and directional atherectomy, respectively, without other sequelae. Four patients (18%) had non-Q wave infarctions, with a mean CK value of 331 U/liter (range 234 to 515). Four other patients had an elevated CK-MB >7.5 ng/liter without 24-h ECG changes. Three patients had no-reflow after rotational atherectomy, and one of them had a non-Q wave myocardial infarction. Prolonged coronary artery spasm was seen in three patients and was not associated with elevation of CK-MB >7.5 ng/liter.
Burr time was longer in the myocardial infarction group than in those without myocardial infarction (4.7 ± 2.4 min vs. 3.0 ± 1.4 min, p = 0.045). There was a trend for the mean burr/artery ratio to be higher in the group with myocardial infarction (1.00 ± 0.35 vs. 0.78 ± 0.19, p = 0.07) than in those without myocardial infarction.
Coronary angioplasty was successful in all patients. Complications were observed in three patients; one patient had an extensive dissection, rescue stenting and a non-Q wave myocardial infarction. Two other patients had a dissection, one treated with a stent and the other with directional atherectomy without other sequelae.
Echocardiography. All patients in both the rotational atherectomy and the control group developed wall motion abnormalities while the vessel was occluded (Table 3). On the preprocedure echocardiogram, the majority of patients had normal wall motion in the territory supplied by the artery undergoing intervention (mean wall motion score index 1.06 ± 0.20 for rotational atherectomy, vs. 1.01 ± 0.05 for coronary angioplasty, p = 0.49). The mean peak %AWM was similar between the groups, indicating similar risk areas in the two groups (28.9 ± 14% for rotational atherectomy, vs. 33.9 ± 7% for coronary angioplasty, p = 0.22). The wall motion score index at this peak was also not different between the groups (1.51 ± 0.29 for rotational atherectomy, vs. 1.48 ± 0.27 for coronary angioplasty, p = 0.81). Fig. 3 displays the mean fitted functions for the time course of development and resolution of wall motion abnormalities for the two groups. From this fitted function, the rotational atherectomy group had a 50% decrease from the peak wall motion abnormality at 17 min from the onset of the procedure. In contrast, for the coronary angioplasty control group, the induced wall motion abnormality decreased to 50% of its peak at 2.26 min from the onset of the final inflation.
All patients in the control group and 21 of 22 rotational atherectomy patients had complete resolution of the procedure-induced wall motion abnormalities. The one inferior wall motion abnormality, persistent at 48 h after rotational atherectomy, occurred in the patient who suffered a Q wave myocardial infarction. The patients in the rotational atherectomy group, excluding the patient with a Q wave myocardial infarction, returned to their baseline wall motion at 153 min (geometric mean, 95% confidence interval [CI] 6.5 to 3600 min) from the onset of the procedure. This contrasts with the control group subjects, whose wall motion returned to baseline at 2.7 min (geometric mean, 95% CI 1.3 to 5.5 min, p = 0.0001) after the onset of the final inflation. The rate of recovery of baseline wall motion for the rotational atherectomy group was significantly less than that for the control group (0.069 ± 0.079/min for atherectomy rate constant vs. 1.250 ± 0.47/min for angioplasty rate constant, p = 0.0001).
In the rotational atherectomy group, stepwise linear regression analysis showed no relation between the rate of recovery of baseline wall motion and gender, age, lesion site, lesion length, burr size, burr time, burr/artery ratio, coronary angioplasty inflation time, CK level, prolonged procedural ST segment elevation and 24-h ECG changes.
In the coronary angioplasty group a return to baseline wall motion was observed between each of the serial balloon inflations. The mean time to recovery of baseline wall motion taken from the time of the final balloon deflation was 38 ± 3.4 s. There was no relation between the duration of the final inflation and time to recovery of baseline wall motion after balloon deflation.
Electrocardiography. Despite the fact that all patients had wall motion abnormalities 10 min after rotational atherectomy, only five patients (23%) had ≥2 mm ST segment elevation at that point. There was no correlation between prolonged ST segment elevation and no-reflow, nor time to baseline wall motion. Although ST segment elevation was observed in the control group during balloon inflation, there was prompt resolution of ST segment changes on balloon deflation in all subjects. Nine patients in the rotational atherectomy group had isolated T wave inversion at 24 h after the procedure, but all had normal segmental wall motion at this point.
This study demonstrates that significant wall motion abnormalities in association with coronary rotational atherectomy occur with a much higher frequency than previously appreciated. These alterations in regional ventricular function persisted for at least 45 min in 77% of cases, but in the absence of Q wave myocardial infarction resolved by 30 h. Although the wall motion abnormalities developed in predictable territories related to the artery undergoing the intervention, neither the presence nor the duration was predicted by traditional markers such as ECG changes or CK fluctuations. This study also shows that isolated ST segment changes commonly seen after rotational atherectomy do not reflect significant myocardial dysfunction.
Prevalence of abnormal wall motion. Transient wall motion abnormalities after rotational atherectomy were first described in the early clinical report by Teirstein et al. . These wall motion abnormalities were detected by single-plane left ventricular angiography in 10% of patients and had all resolved by the time of follow-up angiography performed from 4 days to 6 months later. Our study demonstrates a higher prevalence of regional wall motion abnormality and defines the time course of these changes. The higher prevalence in this study may be explained by differences in the extent of disease in the patients, the procedural technique or the imaging methods used to evaluate wall motion. This point is further highlighted when comparing our study to that of Zotz et al. , who found no wall motion abnormalities by echocardiography. In that report, the burr times were much shorter (by an average of 55 s) and were interrupted by 1 to 2 min for recovery.
Two-dimensional echocardiography, as employed in the present study, enabled simultaneous, real-time evaluation of multiple left ventricular myocardial segments at repeated intervals before, during and after the intervention. This allowed detection of abnormalities in multiple territories, which is not always possible with single-plane ventriculography. For example, in our study, during interventions involving the left anterior descending coronary artery, the distal septal segments were most frequently affected; wall motion abnormalities at this site would not have been as well delineated by right anterior oblique ventriculography. In addition, a proportion of the wall motion abnormalities might have resolved before ventriculography performed at the end of the catheterization procedure. Assessment of wall motion by echocardiography also has the advantage of combining an examination of regional wall thickening and wall motion, which is a more sensitive approach to the detection of abnormalities than using wall motion alone, especially for small regions of dysfunction .
Duration of abnormal wall motion. Wall motion abnormalities after rotational atherectomy persisted longer than after coronary angioplasty alone, despite similar cumulative periods of obstruction to coronary flow and similar sized territories of risk. The control coronary angioplasty group consistently demonstrated rapid resolution of abnormal wall motion after balloon deflation, similar to the 17- to 43-s recovery times previously reported [15, 16]. Up until the time of the adjunct coronary angioplasty at 20 ± 8 min, only one patient in the rotational atherectomy group had regained baseline function, again suggesting that at least up until this time it was the atherectomy procedure alone that was responsible for prolongation of abnormal wall motion.
Mechanism of prolonged abnormal wall motion. The more prolonged duration of wall motion abnormalities observed in the rotational atherectomy group compared with the coronary angioplasty group suggests a difference in the mechanism responsible for the regional dysfunction. Although this study was not designed to identify the mechanism, the possibilities include the effects of distal embolization, coronary spasm, microvascular flow disturbances or platelet activation.
Embolization of atheromatous debris has been proposed as an explanation for flow impairment or obstruction after coronary atherectomy and is supported by the appearance of no-reflow or slow reflow in a proportion of patients immediately after the procedure [8, 17]. In experimental settings, direct coronary arterial injection of debris collected during rotational atherectomy has yielded variable effects on myocardial function [4, 18]. In our series, no-reflow was qualitatively present only in a minority of patients, suggesting that a persistent reduction in epicardial coronary flow secondary to obstruction from atherosclerotic debris was not the sole or dominant mechanism for the wall motion abnormalities observed in all patients having rotational atherectomy. We found there were no independent correlations between estimates of plaque burden, such as lesion length, burr time, burr size or burr/artery ratio, and the duration of abnormal wall motion. This suggests that the volume of atherosclerotic debris alone is not directly related to the transient wall motion abnormalities seen in this study.
In in vitro settings, high speed rotational atherectomy has been demonstrated to produce microcavitation with creation of microbubbles with a mean 90 ± 33 μm diameter and a calculated collapse time of 10 s . However, the brief duration of possible flow obstruction by microbubbles after cessation of rotational atherectomy would seem an unlikely explanation for the persistent wall motion abnormalities observed in this study.
Reversible periods of impaired flow are induced by coronary artery spasm, and spasm has been described as a complication of rotational atherectomy [5, 19]. Although epicardial spasm was only visualized in three patients in this study, this does not exclude the possibility that changes in microvascular tone and flow, independent of mechanical obstruction, could also lead to regional dysfunction. Recent preliminary studies have shown that although angiographic estimation of flow after rotational atherectomy may appear to normalize, coronary flow reserve remains abnormal, suggesting that a persistent or new defect exists in the coronary microcirculation . Such alterations could contribute to the delay in recovery of wall motion abnormalities.
Lastly, another potential mechanism is that rotational atherectomy could lead to platelet activation, aggregation and embolization, resulting in an immediate transient decrease in the coronary flow , leading to wall motion abnormalities, which subsequently resolve as the platelet emboli undergo lysis and flow recovers. Thromboxane B2, an inactive metabolite of thromboxane A2, is present at elevated levels after rotational atherectomy , which is consistent with increased production of thromboxane A2, a promoter of platelet aggregation. Support for such a role for platelets in distal embolization or vasoconstriction, or both, during new device interventional procedures is found from the Evaluation of IIb/IIIa Platelet Receptor Antagonist 7E3 in Preventing Ischemic Complications (EPIC) trial, in which the incidence of non-Q wave myocardial infarction after directional coronary atherectomy was significantly reduced in the group treated with IIa/IIIb platelet inhibitor .
Myocardial infarction. In this study, non-Q wave infarction was identified in 18% of patients, which is similar to that noted in a previous study using a similar definition for non-Q wave myocardial infarction . A recent report of a multi-center registry described a 5.2% prevalence of non-Q myocardial infarction and a significant association with female gender and a history of previous myocardial infarction . The higher rate of non-Q wave infarction seen in our study group appears to be related to the lower CK threshold used for this diagnosis, as the rate of non-Q wave infarction was reduced to 4.5% when using the criteria of a CK elevation 1.5 times the upper limit of normal, which was used by the registry . We found rotational atherectomy burr time to be a significant predictor of the risk of non-Q wave or Q wave infarction (p = 0.045). There was also a trend toward increased maximal burr/artery ratio in the infarct group. One possible explanation is that these factors are associated with a greater volume of atherectomized debris, which results in myocardial infarction. Further studies with larger sample sizes will be required to identify other predictors and the mechanism of postprocedural infarction.
Creatine kinase. Transient mild elevation in CK and CK-MB without ECG changes have been noted after rotational atherectomy in up to 11% of patients , and in our study were present in four patients (18%); however, the significance of this biochemical abnormality is unclear. In one previous study, CK elevations were found to be associated with abrupt vessel closure, spasm and in-hospital morbidity . In our study there was no evidence of persistent wall motion abnormalities in the group with elevated CK-MB in the absence of new Q waves on the ECG. In addition, there was no relation between isolated elevation in CK and the duration of abnormal wall motion. These findings suggest that minor elevations in CK and CK-MB may be overly sensitive markers of infarction in this setting where small areas of microinfarction may occur in the absence of permanent alterations in regional myocardial function.
Clinical implications. Although we did not observe any acute hemodynamic effects of the transient regional wall motion abnormalities, all subjects in this study had preserved baseline global systolic function. Further studies will be required to determine if transient regional dysfunction after rotational atherectomy will have an adverse impact on patients with preexisting moderate to severe impairment of left ventricular function.
If echocardiography is performed early after rotational atherectomy to evaluate persistent ECG abnormalities, clinicians should be aware that regional dysfunction present at this time is likely to be transient in the absence of Q waves. Echocardiograms performed late (>24 h) after rotational atherectomy will provide a more accurate assessment of left ventricular regional function.
Study limitations. Although the wall motion abnormalities observed in this study appear to be related to rotational atherectomy, all patients received adjunct balloon angioplasty, and this may have contributed to the persistence of the abnormalities. We attempted to control for this factor by comparing the duration of abnormal wall motion to a group of patients having coronary angioplasty with similar total occlusion times. In the atherectomy group, the wall motion abnormalities developed before the adjunct coronary angioplasty and persisted much longer than in the control group. The wall motion abnormalities observed in this study are likely to be typical of many rotational atherectomy procedures, because adjunct coronary angioplasty is commonly used to achieve a maximal final lumen diameter .
Another limitation is that the small number of events occurring in the study group precludes statistical evaluation of predictors of these events. However, the sample size is sufficient to study the stated purpose—namely, to identify the prevalence and duration of postprocedural wall motion abnormalities.
Finally, there was no precise measurement of flow, but only qualitative assessment of epicardial flow with contrast angiography. Thus, one is unable to determine the degree or duration of decreased epicardial or microvascular flow associated with rotational atherectomy in this study group or to determine the association between abnormal flow and the time course of the observed wall motion abnormalities. This relation is critical to our understanding of the etiology of these transient wall motion abnormalities.
Conclusions. Transient wall motion abnormalities are common after rotational coronary atherectomy. These wall motion abnormalities have a longer duration than observed after coronary angioplasty alone and were not predicted by ECG or enzymatic changes. These observations may have implications for the development of optimal treatment strategies using rotational atherectomy, especially in the presence of preexisting ventricular dysfunction.
We thank the staff of the Knight Cardiac Catheterization Laboratory for their assistance in the recruitment of patients.
A.1 Abbreviations and Acronyms
ACC/AHA = American College of Cardiology/American Heart Association
%AWM = percent abnormal wall motion
CI = confidence interval
CK = creatine kinase
CK-MB = creatine kinase, MB fraction
ECG = electrocardiogram, electrocardiographic
- Received April 28, 1995.
- Revision received April 26, 1996.
- Accepted May 7, 1996.
- THE AMERICAN COLLEGE OF CARDIOLOGY
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