Published online before print January 29, 2007, doi: 10.1161/CIRCULATIONAHA.106.660779
(Circulation. 2007;115:600-608.)
© 2007 American Heart Association, Inc.
Interventional Cardiology |
Detection of Coronary Microembolization by Doppler Ultrasound in Patients With Stable Angina Pectoris Undergoing Elective Percutaneous Coronary Interventions
From Clinic of Internal Medicine I, Friedrich Schiller University, Jena (P.B., M.F., T.C.P., H.R.F.), Clinic of Internal Medicine I, Clinical Centre, Darmstadt (G.S.W.), Institute of Pathophysiology, University School of Medicine, Essen (G.H.), and Department of Medical Engineering, University of Applied Sciences, Jena (A.V.), Germany.
Correspondence to Philipp Bahrmann, MD, Clinic of Internal Medicine I, Friedrich Schiller University, Erlanger Allee 101, 07740 Jena, Germany. E-mail philipp.bahrmann{at}med.uni-jena.de
Received August 25, 2006; accepted November 12, 2006.
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Abstract |
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Background— Intracoronary Doppler guidewires can be used for real-time detection and quantification of microembolism during percutaneous coronary interventions (PCIs). We investigated whether the frequency of Doppler-detected microembolism is related to the incidence of myonecrosis during elective PCI.
Methods and Results— The study population included 52 consecutive patients (aged 64±10 years; 36 men, 16 women) with coronary artery disease who underwent elective PCI of a single-vessel stenosis. Using intracoronary Doppler ultrasound, we compared the frequency of microembolism during PCI in 22 patients with periprocedural non–ST-segment elevation myocardial infarctions (pNSTEMI) and 30 patients without pNSTEMI. The 2 groups were comparable with regard to their clinical and procedural characteristics. In the group with pNSTEMI, the total number of coronary microemboli after PCI (27±10 versus 16±8, P<0.001) was higher than in the group without pNSTEMI. Although high-sensitivity C-reactive protein plasma levels were similar before PCI (2.9±2.2 versus 3.4±1.7 mg/L, P=NS), they were higher in the group with pNSTEMI after PCI (12.6±10.4 versus 6.1±5.1 mg/L, P<0.05). Microembolic count independently correlated to postprocedural cardiac troponin I elevation (r=0.565, P<0.001), coronary flow velocity reserve (r=–0.506, P<0.001), and baseline average peak velocity (r=0.499, P<0.001).
Conclusions— Patients with pNSTEMI had a significantly higher frequency of coronary microembolization during PCI, and their systemic inflammatory response and microvascular impairment after PCI were more pronounced. Intracoronary Doppler ultrasound provides evidence that pNSTEMI in patients undergoing elective PCI is caused by microembolization during the procedure.
Key Words: coronary disease • embolism • myocardial infarction • stents • ultrasonics
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Introduction |
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Embolization of atherosclerotic and thrombotic debris can induce myocardial necrosis during percutaneous coronary interventions (PCIs).1 The occurrence of coronary microembolism can be assumed when coronary flow velocity reserve (CFVR) remains impaired and periprocedural cardiac markers are elevated.2 Patients who experience no normalization of postprocedural CFVR after coronary microembolization also typically have an increase in basal average peak velocity.3,4 Experimentally, a progressive contractile dysfunction developed in response to coronary microembolization over a period of hours; it was not associated with reduced regional myocardial blood flow (perfusion-contraction mismatch) but rather with a local inflammatory reaction.5,6 Reminiscent of these experimental studies, elevated levels of high-sensitivity C-reactive protein (hsCRP) as a marker of systemic inflammation provide prognostic information for patients undergoing PCI.7 The source of C-reactive protein (CRP) was traditionally assumed to be the atherosclerotic plaque, but it equally well may be derived from the microcirculatory inflammation in response to microembolization and associated microinfarcts.8
Clinical Perspective p 608
In a previous study,9 we reported that an intracoronary Doppler guidewire is a feasible device for real-time detection and quantification of microembolism during PCI. Coronary microembolism often occurred immediately after balloon deflation, especially after stent deployment. However, we did not observe any correlation between the incidence of coronary microemboli and CFVR after balloon dilatation or stent deployment. Recently, Okamura et al10 confirmed our findings that an intracoronary Doppler guidewire can be used to visualize and count microemboli. They evaluated the effectiveness of distal protection devices in patients with acute myocardial infarction during PCI.
To test the hypothesis that coronary microembolization is related to periprocedural myocardial injury, we determined the frequency of Doppler-detected microembolism during elective PCI in the present study. We quantified coronary microemboli with respect to the frequency of periprocedural non–ST-segment elevation myocardial infarctions (pNSTEMI), which was defined according to the 2003 definition.11 We also investigated the systemic inflammatory response to microembolization and the extent of microvascular impairment after PCI in patients with pNSTEMI compared with patients without pNSTEMI.
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Methods |
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Study Population
The prospective study included 52 consecutive patients with coronary artery disease (aged 64±10 years; 36 men, 16 women), who were treated successfully with balloon dilatation followed by stent deployment in all but 6 patients for a single-vessel stenosis and who underwent periprocedural Doppler analysis. The Institutional Ethics Committee of the University Hospital of Jena approved the study protocol. All patients gave written informed consent before study inclusion. The study conformed with the principles outlined in the Declaration of Helsinki.
Inclusion criteria were (1) age between 18 and 80 years, and (2) written informed consent. Exclusion criteria were (1) elevation of cardiac troponin I (cTnI) and CRP before PCI; (2) myocardial infarction during the last 4 weeks before PCI; (3) terminal renal insufficiency, hypothyroidism, or skeletal muscle injury; (4) chronic occlusion, bifurcation lesion, or in-stent restenosis; (5) multivessel intervention; (6) side-branch occlusion or prolonged vasospasm; (7) contraindication for antiplatelet medications; and (8) administration of glycoprotein IIb/IIIa receptor antagonists.
Procedural Protocol
PCI was performed via femoral approach with 6F guiding catheters. A Doppler guidewire (FloWire System, Volcano Therapeutics, Rancho Cordova, Calif) was placed with its tip in the coronary artery 1 to 2 cm distal to the single-vessel stenosis before the first balloon inflation. Careful attention was paid to the positioning to obtain an optimal flow velocity signal. At this position, the average peak velocity (APV) was recorded. Before and after each interventional step, the CFVR was measured. After stabilization of the baseline APV, maximum hyperemia was induced by intracoronary injection of 30 to 40 µg of adenosine. CFVR was calculated as the ratio of maximum APV to baseline APV. The validity of these Doppler wire measurements has been demonstrated in prior in vitro experiments.12,13
The balloon or stent catheter was advanced over the Doppler guidewire at the site of the coronary narrowing. Consecutive balloon inflations of 1-minute duration were performed, and coronary stents were implanted in 46 patients. Balloon inflations without stent deployment were performed in 6 patients. Biplane angiography was performed after successful stent deployment in the same projection as before balloon angioplasty. Angiographic success was defined as a final angiographic residual stenosis of <20% diameter by visual estimation. All patients were prospectively observed regarding periprocedural complications (cTnI, ECG findings, clinical symptoms, death, or need for urgent revascularization) during hospitalization.
All patients received 100 mg of acetylsalicylic acid once daily before the procedure and thereafter. A heparin bolus of 10 000 U was given after insertion of the arterial sheath. Those patients not already taking clopidogrel medication received 300 mg immediately after PCI. All patients received 75 mg of clopidogrel once daily for 4 weeks. All other medication was given at the discretion of the attending physician.
Intracoronary Doppler Measurements
The measurement of microemboli was divided into the following phases: (1) balloon and/or stent advancement over the Doppler guidewire, (2) predilation, (3) stent deployment, and (4) postdilation (Figure 1). The principles of detection of microemboli with multifrequency Doppler have been described previously.9 A 0.014-inch Doppler guidewire with a 12-MHz pulsed Doppler transducer was connected to a console (FloMap System, Volcano Therapeutics). The system insonated at a depth of 5.2 mm and used a 128-point fast Fourier transform for signal-intensity measurement. The pulse-repetition frequency was set at 100 Hz. The detection threshold for Doppler signals was adjusted to a low-intensity level. A fast sweep speed (display duration 1.6 seconds) was chosen for all patients in the present study. We adjusted the Doppler velocity range spectrum to the expected maximum velocity.
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The microembolic signals were defined by the following characteristics: (1): high-intensity signal, (2) short duration, (3) unidirectional within the Doppler velocity spectrum, and (4) accompanied by a "snap," "chirp," or "moan" on the audible output.14,15 The signals were recorded on Super VHS tape and analyzed offline for microemboli. Two observers had to agree that the signal met the identification criteria of Doppler microembolic signals. The intensity increase of microemboli was unidirectional within the Doppler velocity spectrum and maximal over a narrow frequency range. The intensity increase of artifact signals was bidirectional and maximal at low frequencies. The observed intraobserver (R=0.99, P<0.001) and interobserver (R=0.84, P<0.001) agreement in a prior study suggested a good reproducibility for intracoronary Doppler–derived quantification of microemboli.9
By convention, 1 second of microembolic shower signals was considered 10 microemboli.16 All microemboli recorded during contrast injections were excluded from the analysis because they may indicate microbubbles, which may be less hazardous than solid particles in the coronary circulation.17 All Doppler measurements were made without any knowledge of the biochemical results.
Quantitative Coronary Angiography
The final result of stent implantation (reference diameter, minimum lumen diameter, residual stenosis, and lesion length) was assessed by quantitative angiography with the smallest diameter from 2 orthogonal planes (QCA 4.0, PieMedical Imaging, Maastricht, Netherlands). Angiographic lesion characteristics were classified according to the modified American Heart Association/American College of Cardiology classification.18
Biochemistry
Venous blood samples were taken immediately before the beginning of PCI (baseline) and again at 8 to 12 and 18 to 24 hours after PCI, respectively. Creatine kinase (CK), CK-MB, cTnI, and hsCRP were analyzed in these samples. CK (upper limit of normal 2.78 µmol/L/s for women and 3.17 µmol/L/s for men) and CK-MB (upper limit of normal 0.2 µmol/L/s) were determined enzymatically at 37°C (synchronic LX-system, Beckman Coulter, Fullerton, Calif). cTnI (threshold 0.08 ng/mL) was measured by a 2-site immunoenzymatic (sandwich) immunoassay (Access AccuTnI Troponin I Assay, Beckman Coulter). The 99th percentile of the cTnI level in a reference population was below the lower limit of detection of 0.04 ng/mL. The variation coefficient as a measure of the precision within the lower concentration range was below 10%.19 The measurement of hsCRP was based on near-infrared particle immunoassay rate methodology (Immage CRPH Immunochemistry System, Beckman Coulter). The minimal detectable range of the assay was 0.4 mg/L, and the upper limit was 84 mg/L. The variation coefficient as a measure of the precision within the lower concentration range was below 6%.
Diagnostic classification of myocardial infarction according to the 2003 definition was performed with cTnI as the biomarker of myocardial injury.11 The cTnI threshold of at least 1 value exceeding the 99th percentile of the cTnI level in a reference population was used to determine periprocedural myocardial infarction. This cutoff value had a sensitivity of 97% and a specificity of 90%. All biochemical measurements were made without any knowledge of the procedural results.
Statistical Analysis
Data are expressed as mean±SD and categorical data as percent. To analyze differences between groups, we used the Pearson 
2 test for data in categories. Differences of parameters within a group were evaluated by the paired-samples t test. The independent-samples t test was used to compare means of parameters between 2 groups. Pearson’s coefficient was used for correlations. Stepwise multiple regression analysis was performed to determine predictors of coronary microembolization. We included postprocedural CK, CK-MB, cTnI, and hsCRP as parameters. Receiver operating characteristics analysis was presented with area under the curve, 95% CI, and corresponding probability value. All probability values were 2-sided, and a probability level of P<0.05 was considered significant. All calculations were done with SPSS for Windows (version 13.0.1, SPSS, Chicago, Ill).
The authors had full access to and take full responsibility for the integrity of the data. All authors have read and agree to the manuscript as written.
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Results |
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Study Population
Twenty-two (42%) of 52 patients fulfilled the criteria of pNSTEMI according to the 2003 definition.11 These 22 patients had at least 1 elevated cTnI measurement among the 2 measurements made after PCI. Additionally, 2 of these 22 patients had cardiac symptoms, and 3 developed minor ST-T depressions/inversions in postprocedural ECGs. Thus, 22 of 52 patients had definite pNSTEMI. The group without pNSTEMI included the remaining 30 patients.
Baseline Characteristics
All of the procedures were angiographically successful. In-hospital major complications (death or need for urgent revascularization) did not occur within 24 hours after PCI.
Table 1 summarizes the baseline clinical characteristics. There were no significant differences in age, sex, clinical comorbidities, symptoms, medications, and hemodynamics between the 2 groups at baseline. However, multivessel coronary disease was significantly more frequent in the group with pNSTEMI. Target vessels, lesion characteristics, and complication rates during PCI were similar in both groups (Table 2). We did not find side-branch occlusions, thrombus formations at the lesion site, or intermittent occlusions due to spasm, dissection, or intramural hematoma during PCI. Table 3 summarizes the angiographic and procedural data. There were no significant differences in angiographic lesion or procedural characteristics between the 2 groups. The maximum balloon diameter and stent length tended to be higher in the group with pNSTEMI than in the group without pNSTEMI. In patients with pNSTEMI and a high incidence of microembolism (>20 microemboli), the maximum inflation pressure during PCI was significantly higher than in patients with pNSTEMI and without a high incidence of microembolism (10.3±1.3 versus 13.2±2.2 bar, P<0.05).
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Frequency of Microembolization
In all but 1 patient, coronary microemboli were detected in each of the procedural phases. In the group with pNSTEMI, the total number of coronary microemboli was significantly higher than in the group without pNSTEMI (27±10 versus 16±8, P<0.001). Although baseline concentrations were similar in both groups (2.9±2.2 versus 3.4±1.7 mg/L, P=NS), hsCRP was significantly higher in the group with pNSTEMI (12.6±10.4 versus 6.1±5.1 mg/L, P<0.05). The mean numbers of coronary microemboli were highest after stent deployment and during balloon or stent advancement over the Doppler guidewire in both groups (Figure 2). Predilation and postdilation accounted for smaller mean numbers of coronary microemboli in both groups. All phases in the group with pNSTEMI were characterized by significantly higher numbers of coronary microemboli (Figure 2).
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, NSTEMI). Vertical lines indicate mean microembolic counts±SD. The dashed horizontal line indicates the lower threshold limit for microembolic count and a value of cTnI <0.04 ng/mL. *P<0.05 vs No NSTEMI.In the bivariate analysis (r=0.565, P<0.001), coronary microemboli were significantly correlated to the postprocedural cTnI elevation (Figure 3). In the multiple regression analysis to determine predictors of coronary microembolization, we included postprocedural CK, CK-MB, cTnI, and hsCRP as parameters. Microembolic count was the only independent predictor of postprocedural cTnI elevation (r=0.695, P=0.022). By receiver operating characteristics curve analysis (area under the curve 0.802 [0.680 to 0.925], P<0.001), 20 microemboli was identified as the best discriminating value between positive and negative postprocedural cTnI status (Figure 4). Thus, for a number >20 microemboli, the sensitivity, specificity, positive predictive value, and negative predictive value for a positive cTnI test result after PCI were 77%, 63%, 60%, and 79%, respectively.
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Microembolization and Postprocedural CFVR
Intracoronary Doppler measurements are presented in Table 4. Postprocedural CFVR was significantly lower in the group with pNSTEMI (1.96±0.53 versus 2.76±0.77, P<0.001). A postprocedural CFVR <2.0 was observed in 12 (55%) of 22 patients. Baseline APV after PCI in the group with pNSTEMI was significantly higher than in the group without pNSTEMI (30.9±11.9 versus 23.2±12.6 cm/s, P=0.038). However, hyperemic APV after PCI was not significantly different between groups. Figure 5 shows 2 bivariate analyses: Coronary microemboli were significantly correlated to the postprocedural CFVR (r=–0.506, P<0.001) and to the postprocedural baseline APV (r=0.499, P<0.001).
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Discussion |
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We demonstrate with this study for the first time that the frequency of Doppler-detected microembolism is related to the incidence of pNSTEMI. If a number >20 microemboli was used as a predictor for pNSTEMI, the sensitivity was 77%, and the specificity was 63%. The microvascular impairment after PCI and the systemic inflammatory response to microembolization in patients with pNSTEMI were more pronounced than in patients without pNSTEMI.
Frequency of Microembolization
In a previous study, we investigated the frequency of coronary microemboli, counted solely after predilation and stent deployment, in relation to CFVR.9 In the present study, the frequency of coronary microemboli was higher because we included 2 more procedural phases. We also counted microemboli during balloon or stent advancement over the guidewire and after dilation.
The frequency of microemboli during the phase of balloon or stent advancement over the Doppler guidewire was the second highest, after the phase of stent deployment. During all phases, we observed significantly more microemboli in those patients with pNSTEMI than in those without pNSTEMI. Not only PCI but also the passage of the stenosis with the balloon or stent over the guidewire appeared to be a critical phase that was responsible for increased coronary microemboli during PCI in patients with pNSTEMI. Stygall et al20 also found high numbers of microemboli in the cerebrovascular circulation during cardiac catheterization with a guidewire.
What might induce microembolization during PCI in addition to wire passage of the stenosis? It is known that generalized atherosclerosis, reflected by multivessel coronary artery disease, is more frequent in patients with pNSTEMI. Procedure-related risk factors are balloon and stent size. Although balloon inflation involves plaque redistribution alone, stent deployment involves an additional decrease in plaque volume due to plaque embolization, compression, or fragmentation.21 In the present study, these risk factors were more frequently seen in the pNSTEMI group, in which we more often found microembolization. In particular, the maximum inflation pressure during PCI was a risk factor for a higher incidence of microembolism in the pNSTEMI group. Thus, microembolization appears to be the leading pathophysiological cause of pNSTEMI.
Microembolization and Cardiac Biomarker Elevations
Recently, clinical studies showed that the extent of myocardial necrosis measured by delayed-enhancement cardiac MRI directly correlated to cardiac biomarker elevations.22,23 The extent of myocardial necrosis in patients with pNSTEMI represented roughly 5% of left ventricular myocardial mass.23,24 Two different patterns of myocardial necrosis were observed: first, immediately adjacent to the stent, consistent with side-branch occlusion, and second, downstream from the target vessel, consistent with embolization or temporary vessel closure. The majority of patients showed new myocardial necrosis in a previously normal area distal from the inserted stent. Coronary microembolism was the most likely explanation for myocardial necrosis in these studies. Using the real-time technique of monitoring coronary embolism, we were able to confirm that microembolism during PCI led to periprocedural cTnI elevations. In the present study, these were defined as an increase of periprocedural cTnI >2 times the upper limit of normal in accordance with the 2003 definition.11
Malyar et al25 showed that the embolized, nonperfused myocardial volume increases linearly with increasing size and dose of injected microspheres. One recent clinical study demonstrated that the volume of embolized material relates directly to the volume of new necrosis detected by delayed-enhancement MRI.24 Thus, the extent of myocyte damage is not only related to the number but also to the size of the emboli. It is also conceivable that many patients experience microembolization but do not develop myonecrosis either because the embolic burden is small or because there are adaptive responses to accommodate the process.26
We could not derive the size of an individual embolus from its signal intensity in the Doppler spectrum. However, the size of a single embolus might determine its clinical consequences.27 This fact may explain why the results of the receiver operating characteristics analysis showed only a relatively modest sensitivity and specificity for the prediction of a positive cTnI status in the present study. The emboli that were collected by distal protection devices during PCI differed widely in size, ranging from 47 to 2504 µm.28 As evidenced by experimental studies, microembolization from a fissuring/rupturing atherosclerotic plaque in an epicardial coronary artery caused not only physical obstruction of the downstream microcirculation but also a marked inflammatory response in the affected myocardium.5,6,8 Elevated levels of hsCRP as a marker of inflammation strongly predicted early complications (30-day risk of death or MI) after stent deployment in patients with coronary artery disease, and the risk associated with elevated CRP was independent of but additive to the American College of Cardiology/American Heart Association lesion score.7,29
In the present study, 30 patients did not show a postprocedural cTnI elevation, although 8 of these 30 had >20 microemboli during PCI. These patients might not have experienced a cTnI elevation because the emboli were smaller and only temporarily obstructed the microcirculation. Significantly, the systemic inflammatory response of these 30 patients to microembolization was smaller than that of patients with pNSTEMI, which indicates a lesser extent of affected myocardium.
Microembolization and CFVR
In the group with pNSTEMI, we observed a postprocedural CFVR <2.0 in 55% of patients. The high incidence of an impaired CFVR was due to an elevated baseline APV after PCI. Hori et al30,31 showed that coronary microembolization increased baseline APV by release of adenosine in anesthetized dogs. Herrmann et al2 reported an association of a periprocedural enzyme elevation with increased baseline APV and a reduced CFVR after stenting in patients with stable angina pectoris. The number of coronary microemboli correlated to the postprocedural CFVR and to the postprocedural baseline APV in the present study. These observations support the contention that Doppler-detected coronary microembolism caused microvascular impairment in patients with pNSTEMI.
A reduction of CFVR by sustained postprocedural baseline APV increase might also be caused by repeated brief periods of ischemia32; however, maximum and cumulative inflation times were similar in both groups. Frequent injection of contrast agent can reduce CFVR by increasing postprocedural baseline APV33,34; however, the amount of contrast medium did not differ significantly between groups.
Clinical Implications
The present findings suggest that coronary microembolization is a common event in each of the procedural phases during PCI. In particular, patients with multivessel coronary disease, >20 microemboli, and a high inflation pressure during PCI are at risk for pNSTEMI. An increased systemic inflammatory state after PCI, as indicated by increased hsCRP, reflects the embolic burden of the distal microcirculation. Despite the same antiplatelet and anticoagulant therapy, which consisted of aspirin, clopidogrel, and heparin in both groups, we were able to detect coronary microemboli during PCI in all but 1 patient. Interestingly, a recent study by Porto et al24 showed that periprocedural myonecrosis occurred in almost one fourth of patients undergoing complex procedures despite a pharmacological intervention that included aspirin, clopidogrel, heparin, and glycoprotein IIb/IIIa inhibitors. Therefore, microembolization is more likely to consist of plaque debris rather than thrombotic material, and distal protection devices may be required during implantation of extensive coronary stents in patients with generalized atherosclerosis. Intracoronary administration of propranolol before PCI may also protect the myocardium and reduce the incidence of myonecrosis during elective PCI, as shown in 2 recent studies.35,36
Study Limitations
We were unable to detect all cardiac microemboli during PCI because phases such as ventriculography, catheter flushings, selective catheterization of the coronary ostia, advancement of the Doppler guidewire to the vessel stenosis, and withdrawal of the catheter were not monitored continuously. However, phases that are known to have high numbers of microemboli, such as ventriculography and catheter flushings, may be more hazardous to the brain than to the coronary circulation.37
Our method of detecting microemboli also does not differentiate between air microbubbles and solid materials. In the present experimental setting for simulation of PCI, we did not find air microbubbles after repeated balloon deflations that might be generated by excavations.9 However, contrast injections generate air microbubbles. Therefore, we excluded the phase of contrast injections in the present analysis, which may occlude the coronary microcirculation only for a short time.17 Thus, air embolism did not account for the microemboli detected in the present study.
Because the size of the present study is small, results must be interpreted with caution. Given a study size of 52 patients, with a total of 27 coronary microemboli in patients with pNSTEMI versus 16 in those without pNSTEMI, the power of the present study can be retrospectively calculated to be 0.98.
We must acknowledge the apparent discrepancy of the present findings from those of the very recently published PROTECT-TIMI 30 trial (randomized trial to evaluate the relative PROTECTion against post-PCI microvascular dysfunction and post-PCI ischemia among antiplatelet and antithrombotic agents–Thrombolysis In Myocardial Infarction 30), in which there was no correlation between the postprocedural rise in biomarkers and postprocedural coronary reserve, as assessed from the corrected TIMI frame count before and after adenosine.38 Because Doppler flow velocity measurements reflect only a single point in the coronary vascular tree, whereas the corrected TIMI frame count integrates blood flow through the entire coronary vasculature, baseline flow measurements based on these 2 techniques may differ. Nevertheless, coronary reserve measurements based on both techniques are expected to correlate.39 Therefore, the apparent discrepancy between the present study and the PROTECT-TIMI 30 trial is probably not technical in nature but rather relates to the different patient cohort studied. Whereas we have focused on patients with chronic stable angina undergoing elective PCI, patients in the PROTECT-TIMI 30 trial had acute coronary syndromes with prior microembolization and subsequent release of adenosine, as well as thrombogenic and vasoconstrictor substances that may have confounded the assessment of coronary reserve.30,31,40
Conclusions
The present study demonstrated for the first time that downstream microembolization during PCI is involved in pNSTEMI. Intracoronary Doppler ultrasound is a valid and useful tool to detect microembolization in the coronary circulation. Further studies should develop a system that will automatically detect different microembolic sizes and discriminate between solid and gaseous microemboli. In addition, different therapeutic options for reducing the incidence of coronary microembolism in high-risk patients can be evaluated in future studies with this approach.
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Acknowledgments |
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Disclosures
Dr Heusch has received a research grant from the German Research Foundation. Dr Ferrari has served on speakers bureaus for Pfizer and Novartis. Dr Figulla has received research grants from IZKF and BMBF and served on speakers bureaus for Novartis, Pfizer, and Berlin Chemie. The other authors report no conflicts.
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[Abstract/Free Full Text]
CLINICAL PERSPECTIVE
Despite procedural success rates exceeding 90%, cardiac biomarker elevation indicating periprocedural myocardial injury is observed in up to 30% of otherwise successful percutaneous coronary interventions. Earlier studies demonstrated that a reduced improvement of coronary flow velocity reserve due to an increase of baseline average peak velocity was linked to cardiac biomarker elevation. These findings indirectly support the concept of coronary microembolization as a cause of cardiac biomarker elevation. In a previous study, we demonstrated that high-intensity transient signals as indicators of embolic particles can be feasibly detected by intracoronary Doppler ultrasound. In the present study, we used this new intracoronary approach of monitoring microembolism in real time together with measurements of coronary flow velocity reserve and cardiac biomarker elevation to provide further evidence that coronary microembolization is related to periprocedural myocardial injury. We now show that patients with periprocedural non–ST-elevation myocardial infarction had a significantly higher frequency of coronary microembolization during all phases of percutaneous coronary intervention, especially after stent implantation. Our data suggest that patients with generalized atherosclerosis and high inflation pressures during percutaneous coronary intervention are especially at risk for periprocedural non–ST-elevation myocardial infarction. These patients may benefit from distal protection devices during implantation of extensive coronary stents.
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