This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Herrmann, J. Articles by Erbel, R. Search for Related Content PubMed PubMed Citation Articles by Herrmann, J. Articles by Erbel, R. Related Collections Other arteriosclerosis Catheter-based coronary and valvular interventions: other Catheter-based coronary interventions: stents Coronary imaging: angiography/ultrasound/Doppler/CC Acute coronary syndromes Chronic ischemic heart disease Platelets Other Vascular biology

(Circulation. 2001;103:2339.)
© 2001 American Heart Association, Inc.

Clinical Investigation and Reports

Abnormal Coronary Flow Velocity Reserve After Coronary Intervention Is Associated With Cardiac Marker Elevation

Joerg Herrmann, MD; Michael Haude, MD; Amir Lerman, MD; Rainer Schulz, MD; Lothar Volbracht, MD; Junbo Ge, MD; Axel Schmermund, MD; Heinrich Wieneke, MD; Clemens von Birgelen, MD, PhD; Holger Eggebrecht, MD; Dietrich Baumgart, MD; Gerd Heusch, MD; Raimund Erbel, MD

From the Department of Cardiology (J.H., M.H., A.S., H.W., C.v.B., H.E., D.B., R.E.), the Department of Clinical Chemistry (L.V.), and the Department of Pathophysiology (R.S., G.H.), University Clinic Essen, Essen, Germany; the Department of Cardiology (J.G.), Zhongshan Hospital, Shanghai, China; and the Division of Cardiovascular Diseases (A.L.), Mayo Clinic, Rochester, Minn.

Correspondence to Prof R. Erbel, MD, FESC, FACC, Department of Cardiology, University of Essen, Hufelandstraße 55, 45122 Essen, Germany. E-mail erbel{at}uni-essen.de

	Abstract

Top Abstract Introduction Methods Results Discussion References

 
Background—Residual reduction of relative coronary flow velocity reserve (rCVR) after successful coronary intervention has been related to microvascular impairment. However, the incidence of cardiac enzyme elevation as a surrogate marker of an underlying embolic myocardial injury in these cases has not been studied.

Methods and Results—A series of 55 consecutive patients with successful coronary stenting, periprocedural intracoronary Doppler analysis, and determination of creatine kinase (CK; upper limit of normal [ULN] for women 70 IU/L, for men 80 IU/L) and cardiac troponin T (cTnT; bedside test, threshold 0.1 ng/mL) before and 6, 12, and 24 hours after intervention were studied. Postprocedural rCVR was the only intracoronary Doppler parameter that independently correlated with cTnT (r=-0.498, P<0.001) and CK outcome (r=-0.406, P=0.002). Receiver operating characteristic analysis identified a postprocedural rCVR of 0.78 as the best discriminating value, with a sensitivity of 83.3% and 69.2% and a specificity of 79.1% and 76.2% for detection of cTnT and CK elevation, respectively. Stratified according to this cutoff value, the incidence of cTnT elevation was 52.6% in patients with (n=19) and 5.6% in patients without (n=36) a postprocedural rCVR <0.78 (P<0.001), associated with a CK elevation >1 times the ULN in 36.8% and 5.6% (P=0.005) of patients, respectively.

Conclusions—Cardiac marker elevation can frequently be found after coronary procedures that are associated with a persistent reduction of rCVR, indicating procedural embolization of atherothrombotic debris with microvascular impairment and myocardial injury as a potential underlying mechanism.

Key Words: blood flow • creatine kinase • myocardial infarction • stents

	Introduction

Top Abstract Introduction Methods Results Discussion References

 
Embolization of atherosclerotic debris during coronary procedures has been considered a rare event until recent trials with new protection devices demonstrated retrieval of particulate matter in percutaneous interventions of both saphenous vein grafts and native coronary arteries.^{1 2} Before this era, various clinical studies only indirectly outlined the incidence and significance of microvascular obstruction due to percutaneous coronary intervention (PCI), using cardiac enzymes as surrogate markers of myocardial injury.^{1 2 3 4}

On a functional level, procedural embolization has been suggested as one of the potential explanations for abnormal coronary Doppler flow parameters after PCI, which have been well documented in a number of clinical trials.^{5 6 7 8 9} Moreover, in an experimental model, it has been shown that acute embolic myocardial injury is associated with an early increase in coronary blood flow due to adenosine release from the ischemic myocardium.^{10 11} Notably, this functional effect was recorded at the electromagnetic flow probe attached to the bypass tube that was used to inject microspheres into the left anterior descending coronary artery.^{10 11} Whether or not these alterations in Doppler parameters also occur during coronary intervention, with the coronary artery being both the site of Doppler recording and the origin of release of particulate debris, is unknown and is the aim of the present study.

	Methods

Top Abstract Introduction Methods Results Discussion References

 
Patient Population
This study examined a consecutive series of 55 patients with successful coronary stenting for routine clinical indication¹² and periprocedural Doppler analysis at the University Clinic Essen. Procedural success was defined as a reduction of lumen diameter stenosis to <30% without incidence of death, CABG, or Q-wave acute myocardial infarction (AMI). Exclusion criteria were (1) elevation of cardiac markers before intervention; (2) AMI during the last 4 weeks before the procedure; (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; and (7) contraindication for antiplatelet medication. The study was approved by the local ethics committee, and all patients gave written informed consent.

Interventional Procedure
Implantation of tubular slotted stents was performed in a routine manner using the femoral route for vascular access and 6F or 8F guiding catheters for intubation of the target vessel.^{13 14} Intravenous heparin medication was started before intervention (10 000 IU bolus and 1000 IU/h infusion). After coronary stenting was performed, ticlopidine (500 mg/d) or clopidogrel (75 mg/d) was given for 4 weeks in addition to lifelong aspirin medication (100 mg/d).

Intracoronary Doppler Analysis
Intracoronary Doppler Analysis (ICD) parameters were analyzed with a 0.014-inch Doppler-tipped guidewire (FloWire, Endosonics, Inc) 3 to 5 minutes after intracoronary application of 200 µg of nitroglycerin. A stable signal was secured before baseline parameters were recorded. Peak hyperemic flow conditions were determined by intracoronary bolus injection of adenosine (12 µg for the right coronary artery and 18 µg for the left circumflex artery and the left anterior descending coronary artery). Coronary flow velocity reserve (CVR) was computed as the ratio of hyperemic average peak velocity (hAPV) to baseline average peak velocity (bAPV). All measurements were made in duplicate with calculation of the mean value from 2 consecutive measurements. ICD parameters were measured in a nonstenosed reference vessel and at least 2 cm distal to the stenosis before and after PCI in the target vessel. Relative coronary flow velocity reserve (rCVR) was defined as the ratio of CVR in the target vessel to CVR in the reference vessel.¹⁴

Intravascular Ultrasound Analysis
Intravascular ultrasound (IVUS) analysis was performed with either the Endosonics Cardiovascular Imaging System, with a 20-MHz transducer, or the Boston Scientific Corporation Cardiovascular Imaging System, with a 30-MHz transducer, to control the postprocedural result wherever possible and only after injection of 200 µg of nitroglycerin.¹⁵ All IVUS images were recorded in a digital format for offline analysis of lesion sites and distal and proximal reference sites. Cross-sectional narrowing (CSN), also called plaque burden, was calculated as (EEM CSA-lumen CSA)/EEM CSA, where EEM is external elastic membrane and CSA is cross-sectional area.^{15 16}

Quantitative Coronary Analysis
Quantitative coronary angiographic analysis was performed with a computer-based system (CMS, Medis), which provided automated vessel-edge detection and the following standard parameters before and after intervention: reference diameter (mm), minimal lumen diameter (mm), diameter stenosis (%), and lesion length (mm).¹⁷ Angiographic lesion characteristics were classified according to the modified American Heart Association/American College of Cardiology classification.¹⁸ All procedural complications were noted based on commonly used definitions.¹⁹

Determination of Cardiac Markers
Venous blood samples were taken before and 6, 12, and 24 hours after PCI. Immediate serum marker analysis was done by an enzymatic assay (Bayer Diagnostics; activator N-acetylcysteine) for determination of total creatine kinase (CK) activity (upper limit of normal [ULN] 70 IU/L for women, 80 IU/L for men). For cardiac troponin T (cTnT), a point-of-care test was used with a threshold value of 0.1 ng/mL (Roche Diagnostics) as described previously.²⁰

Statistical Analysis
Data were analyzed by SPSS software package 9.0. Continuous variables were reported as mean±SD, categorical variables as percentages. Either a Student’s t test or a Mann-Whitney U test (continuous variables) or a Fisher’s exact test (categorical variables) was used for group comparison. Univariate analysis followed by multivariate logistic regression analysis was used to identify predictors of cardiac marker elevation that included all available study data. Independent predictors were presented as odds ratio (95% CI) and corresponding P value. Receiver operating characteristic analysis was presented with area under the curve (AUC), 95% CI, and corresponding P value. For all analyses, a P value <0.05 was considered statistically significant.

	Results

Top Abstract Introduction Methods Results Discussion References

 
Study Population
Clinical and procedural variables for the entire study population are presented in Tables 1 through 4. Stratification is based on the results of cardiac marker outcome and Doppler flow parameters.

View this table: [in this window] [in a new window]   Table 1. Demographics

View this table: [in this window] [in a new window]   Table 2. Interventional Results

View this table: [in this window] [in a new window]   Table 3. Angiographic and Procedural Results

View this table: [in this window] [in a new window]   Table 4. ICD Measurements

Cardiac Marker Outcome
The overall incidence of cTnT elevation was 21.8%, associated with a CK elevation 1 to 2 times the ULN and >2 times the ULN in 12.7% and 5.6% (P=NS) of patients, respectively. Postprocedural/preprocedural bAPV ratio (r=0.280, P=0.04), postprocedural/preprocedural lesion length ratio (r=-0.353, P=0.01), postprocedural CVR (r=-0.385, P=0.004), and postprocedural rCVR (r=-0.498, P<0.001) correlated with postprocedural cTnT elevation in the univariate analysis. Parameters that were associated with postprocedural CK elevation in the univariate analysis included postprocedural/preprocedural bAPV ratio (r=0.278, P=0.04), postprocedural CVR (r=-0.294, P=0.03), and postprocedural rCVR (r=-0.406, P=0.002) (Figure 1). Postprocedural rCVR was identified as the only independent predictor of cTnT and CK elevation (0.001 [0.000 to 0.084], P=0.002 and 0.011 [0.000 to 0.321], P=0.009).

View larger version (21K): [in this window] [in a new window]   Figure 1. Relationship between postprocedural peak CK value (IU/L) and postprocedural/preprocedural bAPV ratio (A), postprocedural absolute CVR (B), and postprocedural rCVR (C).

By receiver operating characteristic curve analysis, a postprocedural rCVR of 0.78 was identified as the best discriminating value between positive and negative cTnT outcome (Figure 2). Thus, for a postprocedural rCVR<0.78, the sensitivity, specificity, positive predictive value, and negative predictive value for a positive cTnT test result were 83.3%, 79.1%, 52.6%, and 94.4%, respectively, and 69.2%, 76.2%, 47.4%, and 88.9%, respectively, for a CK elevation >1 times the ULN. The likelihood ratio was 3.99 for rCVR <0.78 and cTnT elevation and 2.91 for rCVR<0.78 and CK elevation.

View larger version (21K): [in this window] [in a new window]   Figure 2. Receiver operating characteristic curves for postprocedural/preprocedural bAPV ratio (A), postprocedural absolute CVR (B), and postprocedural rCVR (C) to detect postprocedural cTnT elevation. Note inverse relationship with latter 2 parameters. For all 3 parameters, arrows mark cutoff values discriminating best between positive and negative postprocedural cTnT status.

Stratification of cardiac marker outcome revealed a higher incidence of cTnT elevation for patients with postprocedural rCVR <0.78 (52.6% versus 5.6%, P<0.001; Figure 3). This was associated with CK elevation 1 to 2 times the ULN in 26.3% versus 5.6% (P=0.03) and CK elevation 2 to 3 times the ULN in 10.5% versus 0.0% of the cases (P=0.05). No patient had CK elevation >3 times the ULN.

View larger version (20K): [in this window] [in a new window]   Figure 3. Bar graphs demonstrating higher incidence of positive (pos.) point-of-care test for cTnT (pos. cTnT, solid column; 52.6% vs 5.6%, P<0.001) and higher peak total CK levels (peak total CK, open column; 81±54 IU/L vs 49±32 IU/L, P<0.05) in patients with postprocedural rCVR <0.78 vs patients (pts) without this rCVR impairment.

Stratified Baseline Parameters
Demographic and angiographic data are presented in Tables 1 and 2. Patients with rCVR <0.78 tended more frequently to have a positive history of AMI (42% versus 17%, P=0.06). However, there was no substantial difference concerning history of AMI in the region of the target vessel (21% versus 14%, P=0.5).

Stratified Procedural Parameters
Procedural parameters are presented in Table 3. IVUS analysis was available in 64% of the patients. There was no difference between patients with rCVR <0.78 and patients with rCVR 0.78 concerning CSN at the reference site (45.0±11.0% versus 42.6±10.5%, P=NS) and CSN at the lesion site after PCI (48.1±6.5% versus 48.3±6.0%, P=NS). However, plaque burden at the lesion site before PCI was higher in the patient group with rCVR <0.78 (76.4±11.4% versus 68.9±8.1%, P=0.03).

Stratified Doppler Parameters
Before intervention, absolute and relative CVR values were lower in patients with postprocedural impairment of CVR because of a slightly lower hAPV. After intervention, this difference was even more pronounced, because bAPV increased in these patients (19.9±7.6 versus 28.8±9.8, P=0.002) while it remained nearly unchanged in patients without residual impairment of CVR. In both groups, there was a significant increase in hAPV after PCI (P0.001; Table 4).

	Discussion

Top Abstract Introduction Methods Results Discussion References

 
In this prospective study, we found that postprocedural rCVR <0.78 was independently predictive of postprocedural elevation of a cardiac marker. The incidence of cTnT and CK elevation was 9 and 6 times higher in patients with such residual rCVR impairment.

Postprocedural Impairment of CVR
Various clinical trials reported on abnormal Doppler flow parameters in a large percentage of successful PCI, ranging from 33% after balloon angioplasty to 86% after rotablation.^{5 6} In the most recent study, Kern et al⁷ reported on residual impairment of CVR (<2.0) in 30% of the patients undergoing coronary stenting, with 53% of these patients having a reduction of both absolute and relative CVR.

In the present study, we found nearly the same rate of residual reduction of absolute CVR (32.7%), with a concomitant reduction of rCVR <0.78 in 77.7%. This overall high incidence of microvascular impairment confined to the region of the target vessel (25.5%) was associated with a high incidence of both cTnT and CK elevation, supporting the idea of procedural embolization, resulting in myocardial injury.^{5 6 7}

Procedural Embolization
In analogy to the model of Hori et al,^{10 11} procedural embolization of atherothrombotic debris could cause (1) an increase in postprocedural bAPV and (2) an impairment of both absolute and relative CVR, which were observed in the present study. Moreover, the overall better correlation between cardiac marker outcome and CVR is explained by the experimental finding that an increase in bAPV preferably characterizes minor forms of embolic myocardial injury.^{10 11} However, further trials with distal protection devices would be required to define procedural embolism as the common denominator of both cardiac marker elevation and abnormal Doppler flow parameters.

Alternative Mechanisms of CVR Reduction
Repeated brief periods of ischemia might cause CVR reduction by sustained postprocedural bAPV increase.²¹ However, inflation periods were similar in both study groups, and no correlation between the number or duration of inflations and postprocedural cardiac marker and Doppler status was noted.

Frequent injection of contrast material is another mechanism that can reduce CVR by increasing postprocedural bAPV.^{22 23} Nevertheless, there was neither a difference in the amount of contrast dye nor a correlation between the volume of contrast material used and postprocedural Doppler parameters.

Alteration in the regulation of vasomotor tone on the level of both the microcirculation and the epicardial conduit vessel and differences in pharmacological therapy are additional factors to be considered.^{24 25} However, prolonged vasospasm was a predefined exclusion criteria, and patient groups did not differ in drug therapy.

The overall higher rate of prior AMI in patients with residual rCVR impairment is of particular interest. Subanalysis according to the region of the target vessel, however, did not demonstrate a substantial difference between the 2 study groups. Furthermore, exclusion of all patients with prior AMI did not change the study outcome (data not shown).

Extent of epicardial disease and extent of residual stenosis might have differed considerably between the 2 study groups despite the favorable angiographic result.²⁶ However, IVUS analysis did not reveal a substantial difference in CSN either at the reference site or at the lesion site after the coronary procedure. Nevertheless, the higher initial plaque burden in patients with rCVR impairment must be taken into consideration for the outcome of both Doppler parameters and cardiac markers.

Alternative Mechanisms of Cardiac Marker Elevation
Various predictors of postprocedural elevation of cardiac markers have been identified.^{2 4} Among these, aggressiveness of the coronary procedure and atherosclerotic burden are considered most important.¹⁶ However, catheter-based interventions other than coronary stenting and procedural complications such as side-branch occlusion were excluded from the present study to limit the extent of interfering variables. As far as coronary dissection is concerned, this complication was equally distributed among the study groups and was not associated with cardiac marker elevation in the present study.

Procedural embolization as an underlying mechanism of cardiac marker elevation and rCVR impairment is further supported by the finding that extent of lesion length reduction correlated with cTnT elevation in univariate analysis. Moreover, atherosclerotic plaque burden and number of stents were higher in patients with a postprocedural rCVR <0.78, resembling the findings by Mehran et al¹⁶ on the complex interplay between extent of atherosclerotic disease, extent of coronary intervention, and myocardial injury.

Study Limitations
The technical limitations of ICD analysis are well known, including the dose of adenosine used in this and other trials before.^{6 7 14} However, the systematic nature of this error is very unlikely to cause a substantial difference between the study groups. Likewise, the diagnostic window used in the present study must be considered as a potential source of systematic error, and the limitations of cTnT point-of-care analysis must be acknowledged. The most important limitation of this study remains its small size. Therefore, prospective trials with distal protection devices and/or glycoprotein IIb/IIIa receptor inhibitors are warranted to provide further insight into a causal relationship between procedural embolism and cardiac marker and ICD outcome.

Conclusions
Cardiac marker elevation can frequently be found after coronary procedures that are associated with a persistent reduction of rCVR, suggesting procedural embolization of atherothrombotic debris with microvascular impairment and myocardial injury as a potential underlying mechanism.

	Acknowledgments

 
This study was supported by a grant from the Deutsche Forschungsgemeinschaft (DFG 155/4-2).

Received December 12, 2000; revision received February 27, 2001; accepted February 28, 2001.

	References

Top Abstract Introduction Methods Results Discussion References

 
1. Erbel R, Heusch G. Coronary microembolization. J Am Coll Cardiol. 2000;36:22–24.[Free Full Text]

2. Topol EJ, Yadav JS. Recognition of the importance of embolization in atherosclerotic vascular disease. Circulation. 2000;101:570–580.[Free Full Text]

3. Abdelmeguid AE, Topol EJ, Whitlow PL, et al. Significance of mild transient release of creatine kinase-MB fraction after percutaneous coronary intervention. Circulation. 1996;94:1528–1536.[Abstract/Free Full Text]

4. Califf RM, Abdelmeguid AE, Kuntz RE, et al. Myonecrosis after revascularization procedures. J Am Coll Cardiol. 1998;31:241–251.[Abstract/Free Full Text]

5. Bowers TR, Stewart RE, O’Neill WW, et al. Effect of rotablator atherectomy and adjunctive balloon angioplasty on coronary blood flow. Circulation. 1997;95:1157–1164.[Abstract/Free Full Text]

6. Van Liebergen RAM, Piek JJ, Koch KT, et al. Immediate and long-term effect of balloon angioplasty or stent implantation on the absolute and relative coronary blood flow velocity reserve. Circulation. 1998;98:2133–2140.[Abstract/Free Full Text]

7. Kern MJ, Puri S, Bach RG, et al. Abnormal coronary flow velocity reserve after coronary artery stenting in patients: role of relative coronary reserve to assess potential mechanisms. Circulation. 1999;100:2491–2498.[Abstract/Free Full Text]

8. Nato S, Kodama K, Hori M, et al. Temporal increase in resting coronary blood flow causes an impairment of coronary flow reserve after coronary angioplasty. Am Heart J. 1992;124:28–36.

9. Serruys PW, di Mario C, Piek J, et al. Prognostic value of intracoronary flow velocity and diameter stenosis in assessing the short- and long-term outcomes of coronary balloon angioplasty: the DEBATE study (Doppler Endpoints Balloon Angioplasty Trial Europe). Circulation. 1997;96:3369–3377.[Abstract/Free Full Text]

10. Hori M, Inoue M, Kitakaze M, et al. Role of adenosine in hyperemic response of coronary blood flow in microembolization. Am J Physiol. 1986;250:H509–H518.[Abstract/Free Full Text]

11. Hori M, Tamai J, Kitakaze M, et al. Adenosine-induced hyperemia attenuates myocardial ischemia in coronary microembolization in dogs. Am J Cardiol. 1989;257:H244–H251.

12. Ryan TJ, Bauman WB, Kennedy JW, et al. Guidelines for percutaneous transluminal coronary angioplasty: a report of the American College of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Subcommittee on Percutaneous Transluminal Coronary Angioplasty). Circulation. 1988;78:486–502.[Free Full Text]

13. Haude M, Caspari G, Baumgart D, et al. Comparison of myocardial perfusion reserve before and after coronary balloon predilatation and after stent implantation in patients with postangioplasty restenosis. Circulation. 1996;94:286–297.[Abstract/Free Full Text]

14. Baumgart D, Haude M, Goerge G, et al. Improved assessment of coronary stenosis severity using the relative flow velocity reserve. Circulation. 1998;98:40–46.[Abstract/Free Full Text]

15. Jeremias A, Görge G, Konorza T, et al. Stepwise intravascular ultrasound (IVUS) guidance of high-pressure coronary stenting does not result in an improved acute or long-term outcome: a randomized comparison to "final look" IVUS assessment. Cathet Cardiovasc Intervent. 1999;45:135–141.

16. Mehran R, Dangas G, Mintz GS, et al. Atherosclerotic plaque burden and CK-MB enzyme elevation after coronary interventions: intravascular ultrasound study of 2256 patients. Circulation. 2000;101:604–610.[Abstract/Free Full Text]

17. Von Birgelen C, Haude M, Herrmann J, et al. Early clinical experience with the implantation of a novel synthetic coronary stent graft. Cathet Cardiovasc Interv. 1999;47:496–503.[Medline] [Order article via Infotrieve]

18. Ellis SG, Vandormael MG, Cowley MJ, et al. Coronary morphologic and clinical determinants of procedural outcome with angioplasty for multivessel coronary disease. Circulation. 1990;82:1193–1202.[Abstract/Free Full Text]

19. Klein LW, Kramer BL, Howard E, et al. Incidence and clinical significance of transient creatine kinase elevations and the diagnosis of non-Q wave myocardial infarction associated with coronary angioplasty. J Am Coll Cardiol. 1991;17:612–616.

20. Hirschl MM, Herkner H, Laggner AN, et al. Analytical and clinical performance of an improved qualitative troponin T rapid test in laboratories and critical care units. Arch Pathol Lab Med. 2000;124:583–587.[Medline] [Order article via Infotrieve]

21. Eikens E, Wilcken DEL. Myocardial reactive hyperemia and coronary vascular reactivity in the dog. Circ Res. 1973;33:267–274.[Abstract/Free Full Text]

22. Bassan M, Ganz W, Marcus HS, et al. The effect of intracoronary injection of contrast medium upon coronary blood flow. Circulation. 1975;51:442–445.[Abstract/Free Full Text]

23. Holman BL, Cohn PF, Adams DF, et al. Regional myocardial blood flow during hyperemia induced by contrast agent in patients with coronary artery disease. Am J Cardiol. 1976;38:416–421.[Medline] [Order article via Infotrieve]

24. Gregorini L, Fajadet J, Robert G, et al. Coronary vasoconstriction after percutaneous transluminal coronary angioplasty is attenuated by antiadrenergic agents. Circulation. 1994;90:895–907.[Abstract/Free Full Text]

25. Fischell TA, Bausback MJ, McDonald TV. Evidence for altered epicardial coronary artery autoregulation as a cause of distal coronary vasoconstriction after successful percutaneous transluminal coronary angioplasty. J Clin Invest. 1990;86:575–584.

26. Kern MJ, Dupouy P, Drury JH, et al. Role of coronary artery lumen enlargement in improving coronary blood flow after balloon angioplasty and stenting: a combined intravascular ultrasound Doppler flow and imaging study. J Am Coll Cardiol. 1997;29:1520–1527. [Abstract]

This article has been cited by other articles:

				G. Heusch, P. Kleinbongard, D. Bose, B. Levkau, M. Haude, R. Schulz, and R. Erbel Coronary Microembolization: From Bedside to Bench and Back to Bedside Circulation, November 3, 2009; 120(18): 1822 - 1836. [Abstract] [Full Text] [PDF]

				G. Heusch and R. Schulz Neglect of the coronary circulation: some critical remarks on problems in the translation of cardioprotection Cardiovasc Res, October 1, 2009; 84(1): 11 - 14. [Full Text] [PDF]

				M. Carlsson, M. Wilson, A. J. Martin, and M. Saeed Myocardial Microinfarction after Coronary Microembolization in Swine: MR Imaging Characterization Radiology, March 1, 2009; 250(3): 703 - 713. [Abstract] [Full Text] [PDF]

				K. Nassenstein, F. Breuckmann, C. Bucher, G. Kaiser, T. Konorza, L. Schafer, I. Konietzka, A. de Greiff, G. Heusch, R. Erbel, et al. How Much Myocardial Damage Is Necessary to Enable Detection of Focal Late Gadolinium Enhancement at Cardiac MR Imaging? Radiology, December 1, 2008; 249(3): 829 - 835. [Abstract] [Full Text] [PDF]

				T. Kawamoto, H. Okura, Y. Koyama, I. Toda, H. Taguchi, K. Tamita, A. Yamamuro, Y. Yoshimura, Y. Neishi, E. Toyota, et al. The Relationship Between Coronary Plaque Characteristics and Small Embolic Particles During Coronary Stent Implantation J. Am. Coll. Cardiol., October 23, 2007; 50(17): 1635 - 1640. [Abstract] [Full Text] [PDF]

				J. B. Selvanayagam, A. S.H. Cheng, M. Jerosch-Herold, K. Rahimi, I. Porto, W. van Gaal, K. M. Channon, S. Neubauer, and A. P. Banning Effect of Distal Embolization on Myocardial Perfusion Reserve After Percutaneous Coronary Intervention: A Quantitative Magnetic Resonance Perfusion Study Circulation, September 25, 2007; 116(13): 1458 - 1464. [Abstract] [Full Text] [PDF]

				A. Lerman, D. R. Holmes, J. Herrmann, and B. J. Gersh Microcirculatory dysfunction in ST-elevation myocardial infarction: cause, consequence, or both? Eur. Heart J., April 1, 2007; 28(7): 788 - 797. [Abstract] [Full Text] [PDF]

				P. Bahrmann, G. S. Werner, G. Heusch, M. Ferrari, T. C. Poerner, A. Voss, and H. R. Figulla Detection of Coronary Microembolization by Doppler Ultrasound in Patients With Stable Angina Pectoris Undergoing Elective Percutaneous Coronary Interventions Circulation, February 6, 2007; 115(5): 600 - 608. [Abstract] [Full Text] [PDF]

				I. Porto, J. B. Selvanayagam, W. J. Van Gaal, F. Prati, A. Cheng, K. Channon, S. Neubauer, and A. P. Banning Plaque Volume and Occurrence and Location of Periprocedural Myocardial Necrosis After Percutaneous Coronary Intervention: Insights From Delayed-Enhancement Magnetic Resonance Imaging, Thrombolysis in Myocardial Infarction Myocardial Perfusion Grade Analysis, and Intravascular Ultrasound Circulation, August 15, 2006; 114(7): 662 - 669. [Abstract] [Full Text] [PDF]

				M. Thielmann, P. Massoudy, M. Neuhauser, K. Tsagakis, G. Marggraf, M. Kamler, K. Mann, R. Erbel, and H. Jakob Prognostic Value of Preoperative Cardiac Troponin I in Patients Undergoing Emergency Coronary Artery Bypass Surgery With Non-ST-Elevation or ST-Elevation Acute Coronary Syndromes Circulation, July 4, 2006; 114(1_suppl): I-448 - I-453. [Abstract] [Full Text] [PDF]

				J. Herrmann Peri-procedural myocardial injury: 2005 update Eur. Heart J., December 1, 2005; 26(23): 2493 - 2519. [Abstract] [Full Text] [PDF]

				L. Babuin and A. S. Jaffe Troponin: the biomarker of choice for the detection of cardiac injury Can. Med. Assoc. J., November 8, 2005; 173(10): 1191 - 1202. [Abstract] [Full Text] [PDF]

				M. Thielmann, P. Massoudy, A. Schmermund, M. Neuhauser, G. Marggraf, M. Kamler, U. Herold, I. Aleksic, K. Mann, M. Haude, et al. Diagnostic discrimination between graft-related and non-graft-related perioperative myocardial infarction with cardiac troponin I after coronary artery bypass surgery Eur. Heart J., November 2, 2005; 26(22): 2440 - 2447. [Abstract] [Full Text] [PDF]

				M. Thielmann, P. Massoudy, M. Neuhauser, S. Knipp, M. Kamler, J. Piotrowski, K. Mann, and H. Jakob Prognostic Value of Preoperative Cardiac Troponin I in Patients With Non-ST-Segment Elevation Acute Coronary Syndromes Undergoing Coronary Artery Bypass Surgery Chest, November 1, 2005; 128(5): 3526 - 3536. [Abstract] [Full Text] [PDF]

				P Bahrmann, H R Figulla, M Wagner, M Ferrari, A Voss, and G S Werner Detection of coronary microembolisation by Doppler ultrasound during percutaneous coronary interventions Heart, September 1, 2005; 91(9): 1186 - 1192. [Abstract] [Full Text] [PDF]

				M. Thielmann, P. Massoudy, M. Neuhauser, S. Knipp, M. Kamler, G. Marggraf, J. Piotrowski, and H. Jakob Risk stratification with cardiac troponin I in patients undergoing elective coronary artery bypass surgery Eur. J. Cardiothorac. Surg., May 1, 2005; 27(5): 861 - 869. [Abstract] [Full Text] [PDF]

				B.-J. Verhoeff, M. Siebes, M. Meuwissen, B. Atasever, M. Voskuil, R. J. de Winter, K. T. Koch, J. G.P. Tijssen, J. A.E. Spaan, and J. J. Piek Influence of Percutaneous Coronary Intervention on Coronary Microvascular Resistance Index Circulation, January 4, 2005; 111(1): 76 - 82. [Abstract] [Full Text] [PDF]

				G S Werner, U Emig, P Bahrmann, M Ferrari, and H R Figulla Recovery of impaired microvascular function in collateral dependent myocardium after recanalisation of a chronic total coronary occlusion Heart, November 1, 2004; 90(11): 1303 - 1309. [Abstract] [Full Text] [PDF]

				A. Skyschally, M. Haude, H. Dorge, M. Thielmann, A. Duschin, A. van de Sand, I. Konietzka, A. Buchert, S. Aker, P. Massoudy, et al. Glucocorticoid Treatment Prevents Progressive Myocardial Dysfunction Resulting From Experimental Coronary Microembolization Circulation, May 18, 2004; 109(19): 2337 - 2342. [Abstract] [Full Text] [PDF]

				D. O. Williams A twist in our understanding of enzyme elevation after coronary intervention J. Am. Coll. Cardiol., December 3, 2003; 42(11): 1906 - 1908. [Full Text] [PDF]

				G Heusch and R Schulz Pathophysiology of coronary microembolisation Heart, September 1, 2003; 89(9): 981 - 982. [Full Text] [PDF]

				R Erbel Spontaneous and interventional coronary microembolisation Heart, September 1, 2003; 89(9): 986 - 989. [Full Text] [PDF]

				G. S. Werner, P. Bahrmann, O. Mutschke, U. Emig, S. Betge, M. Ferrari, and H. R. Figulla Determinants of target vessel failure in chronic total coronary occlusions after stent implantation: The influence of collateral function and coronary hemodynamics J. Am. Coll. Cardiol., July 16, 2003; 42(2): 219 - 225. [Abstract] [Full Text] [PDF]

				G. K. Lund, N. Watzinger, M. Saeed, G. P. Reddy, M. Yang, P. A. Araoz, D. Curatola, M. Bedigian, and C. B. Higgins Chronic Heart Failure: Global Left Ventricular Perfusion and Coronary Flow Reserve with Velocity-encoded Cine MR Imaging: Initial Results Radiology, April 1, 2003; 227(1): 209 - 215. [Abstract] [Full Text] [PDF]

				S. Mohlenkamp, P. E Beighley, E. A Pfeifer, T. R Behrenbeck, P. F Sheedy II, and E. L Ritman Intramyocardial blood volume, perfusion and transit time in response to embolization of different sized microvessels Cardiovasc Res, March 1, 2003; 57(3): 843 - 852. [Abstract] [Full Text] [PDF]

				L. Gregorini, J. Marco, B. Farah, M. Bernies, C. Palombo, M. Kozakova, I. M. Bossi, B. Cassagneau, J. Fajadet, C. Di Mario, et al. Effects of Selective {alpha}1- and {alpha}2-Adrenergic Blockade on Coronary Flow Reserve After Coronary Stenting Circulation, December 3, 2002; 106(23): 2901 - 2907. [Abstract] [Full Text] [PDF]

				J. Herrmann, A. Lerman, D. Baumgart, L. Volbracht, R. Schulz, C. von Birgelen, M. Haude, G. Heusch, and R. Erbel Preprocedural Statin Medication Reduces the Extent of Periprocedural Non-Q-Wave Myocardial Infarction Circulation, October 22, 2002; 106(17): 2180 - 2183. [Abstract] [Full Text] [PDF]

				A. W. Bonz, B. Lengenfelder, J.o. Strotmann, S. Held, O. Turschner, K. Harre, C. Wacker, C. Waller, N. Kochsiek, M. Meesmann, et al. effect of additional temporary glycoprotein IIb/IIIa receptor inhibition on troponin release in elective percutaneous coronary interventions after pretreatment with aspirin and clopidogrel (TOPSTAR trial) J. Am. Coll. Cardiol., August 21, 2002; 40(4): 662 - 668. [Abstract] [Full Text] [PDF]

				G. C. Wong, D. A. Morrow, S. Murphy, N. Kraimer, R. Pai, D. James, D. H. Robertson, L. A. Demopoulos, P. DiBattiste, C. P. Cannon, et al. Elevations in Troponin T and I Are Associated With Abnormal Tissue Level Perfusion: A TACTICS-TIMI 18 Substudy Circulation, July 9, 2002; 106(2): 202 - 207. [Abstract] [Full Text] [PDF]

				M. Thielmann, H. Dorge, C. Martin, S. Belosjorow, U. Schwanke, A. van de Sand, I. Konietzka, A. Buchert, A. Kruger, R. Schulz, et al. Myocardial Dysfunction With Coronary Microembolization: Signal Transduction Through a Sequence of Nitric Oxide, Tumor Necrosis Factor-{alpha}, and Sphingosine Circ. Res., April 19, 2002; 90(7): 807 - 813. [Abstract] [Full Text] [PDF]

				S.J. Brener and E.J. Topol Epicardial versus microcirculatory dissociation Eur. Heart J., February 2, 2002; 23(4): 274 - 276. [Full Text] [PDF]

				A. Skyschally, R. Schulz, R. Erbel, and G. Heusch Reduced coronary and inotropic reserves with coronary microembolization Am J Physiol Heart Circ Physiol, February 1, 2002; 282(2): H611 - H614. [Abstract] [Full Text] [PDF]

				M. Thielmann, H. Dorge, C. Martin, S. Belosjorow, U. Schwanke, A. van de Sand, I. Konietzka, A. Buchert, A. Kruger, R. Schulz, et al. Myocardial Dysfunction With Coronary Microembolization: Signal Transduction Through a Sequence of Nitric Oxide, Tumor Necrosis Factor-{alpha}, and Sphingosine Circ. Res., April 19, 2002; 90(7): 807 - 813. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Herrmann, J. Articles by Erbel, R. Search for Related Content PubMed PubMed Citation Articles by Herrmann, J. Articles by Erbel, R. Related Collections Other arteriosclerosis Catheter-based coronary and valvular interventions: other Catheter-based coronary interventions: stents Coronary imaging: angiography/ultrasound/Doppler/CC Acute coronary syndromes Chronic ischemic heart disease Platelets Other Vascular biology