European Heart Journal Advance Access originally published online on February 1, 2006
European Heart Journal 2006 27(10):1139-1145; doi:10.1093/eurheartj/ehi755
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
EMERALD, AIMI, and PROMISE: is there still a potential for embolic protection in primary PCI?
1 Cardiology Unit, Cardiovascular Department, ASL 6, Livorno, Italy
2 Department of Cardiology, Center of Excellence on Aging, ‘G. d'Annunzio’ University of Chieti, C/o Ospedale S. Camillo de Lellis Via Forlanini, 50 66100 Chieti, Italy
3 CNR Institute of Clinical Physiology, Pisa, Italy
Received 20 October 2005; revised 11 December 2005; accepted 13 January 2006; online publish-ahead-of-print 1 February 2006.
* Corresponding author. Tel: +39 0871 41512; fax: +39 0871 402817. E-mail address: rdecater{at}unich.it
 |
Abstract |
|---|
Top
Abstract
Embolic protection devices in...The recent trials of routine use of embolic protection devices for primary percutaneous coronary interventions (PCI) (the EMERALD, PROMISE, and AIMI trials) have demonstrated neutral or even negative effects of these devices on myocardial reperfusion and final infarct size. Despite these results, there is still ground to believe that PCI-induced embolization may be clinically relevant in specific subsets of patients with acute myocardial infarction (AMI). Significant clinical consequences may be expected when embolization is quantitatively relevant and/or is qualitatively characterized by lipid-rich athero-embolism (as is the case of lipid core embolization through the ruptured cap of a fibro-atheroma). Future trials on embolic protection devices in primary PCI should adopt a selective, rather than a routine strategy, through the identification, by angiographic or intravascular imaging parameters, of patients at highest risk of clinically relevant embolization. Such trials should also adopt specific endpoints able to evaluate the effect of micro-embolization, which is currently far from optimally assessed by the standard markers of myocardial reperfusion.
Key Words: Myocardial infarction • Percutaneous coronary interventions • Angioplasty • Embolization • Reperfusion
|
Embolic protection devices in primary PCI: a short chronicle |
|---|
After the positive results of large trials on distal protection during percutaneous coronary intervention (PCI) on diseased saphenous vein grafts, embolic protection has also been proposed as a strategy to improve myocardial reperfusion during primary PCI in patients with acute myocardial infarction (AMI). To test this logical and attractive hypothesis, several single-centre studies have been performed over the past 5 years to evaluate safety, feasibility, and efficacy of various devices in this clinical setting, overall demonstrating that embolic protection can be safely performed during primary PCI with promising positive effects on myocardial reperfusion markers.1–6 More recently, the results of three large randomized AMI trials on the routine use of embolic protection devices during primary PCI—the EMERALD, AIMI, and PROMISE trials—have become available.7–9 These trials, evaluating three different devices (Guardwire, Medtronic; AngioJet, Possis; and FilterWire, Boston Scientific) (Figure 1A–C), with different structure and operational mechanisms, failed to demonstrate any positive effect of routine embolic protection on myocardial reperfusion or clinical outcome. A fourth trial, the X-AMINE ST trial evaluating the X-sizer (eV3) thrombectomy device, showed a slight improvement in ST-segment early resolution without any effect on TIMI flow grade, myocardial blush grade, or clinical outcome.10 Taken as a whole, these data provide enough evidence against the routine use of embolic protection during primary PCI (Table 1).
|
|
But, is it the end of the story? Probably not. We believe that at least two fundamental questions still need to be answered before the file can be considered closed:
- does embolization during primary PCI play any role on myocardial reperfusion?
- if distal embolization does play a role but the routine use of embolic protection devices is not effective, what about the selective use of embolic protection?
|
Pathophysiology of PCI-induced embolization in AMI |
|---|
In an experimental study on mongrel dogs, Sakuma et al.11 evaluated myocardial reperfusion and infarct size after primary PCI performed in the presence or absence of an intracoronary thrombus. The actual occurrence of thrombus embolization during PCI was documented by platelet autoradiography. In the group with intracoronary thrombus and distal embolization, the perfusion defect at myocardial contrast echo and the final infarct size were increased by 139 and 70%, respectively, when compared with the control group. In patients undergoing PCI on degenerated saphenous vein grafts, distal embolization has been demonstrated to play a role in the no-reflow phenomenon, as well as to significantly impact on clinical outcome.12,13 The above mentioned pathophysiological link is much less clear in the clinical setting of AMI. It has been argued that PCI-induced embolic burden is about one order of magnitude smaller in AMI compared with vein grafts (1.2 vs. 16 mm3 on average).14 However, such estimates were based on data derived from different methods of morphometric analysis (histological 3D reconstruction vs. Coulter RapidView digital visual system).15,16 Quan et al.,17 using the same method of morphometric analysis (RapidView) and the same protection device (FilterWire) in native coronaries and venous grafts, reported no statistically significant differences in median volumes (9 vs. 13 mm3) of retrieved debris. Although the average amount of embolic load is possibly too low to play a relevant pathophysiological role in all patients undergoing primary PCI, based on our data on histological 3D reconstruction of the retrieved emboli, the embolic load in AMI was found to be >2 mm3 in 15% and >6 mm3 in 5% of cases, a volume compatible with an angiographically detectable embolization.15,18 In an observational study, a distal embolization large enough to be angiographically visible was demonstrated to occur in up to 15% of primary PCI and to be adversely related to myocardial reperfusion and prognosis, with a five-fold increase in 5-year mortality compared with patients without angiographic signs of embolization.19 The hypothesis that, in a subset of AMI patients, embolization may be quantitatively relevant enough to impair myocardial reperfusion is also supported by Yip et al.,20 reporting on 794 consecutive patients with AMI. These authors observed that the incidence of no-reflow after PCI was significantly higher in patients with baseline angiographic signs of a high thrombus burden at the level of the culprit lesion vs. those without such signs.
However, as it often occurs when dealing with biological phenomena, quantity may not be the only or the most important determinant of the pathophysiological consequences of coronary embolization. To this regard, intravascular imaging studies provide additional insight to the relationship between the qualitative characteristics of distal embolization and the no-reflow phenomenon. At intravascular ultrasound (IVUS), plaque volume reduction after stenting, evaluated by a volumetric analysis of the proximal and distal edges, provided that the occurrence of plaque shift can be excluded or taken into account, can be interpreted as an indirect sign of distal embolization. After PCI for acute coronary syndromes, plaque volume reduction was reported to average 1036 mm3 in two different reports21,22 and, most importantly, to be about nine times greater in patients with final TIMI 0–2 myocardial perfusion grade compared with patients with perfusion grade 3.21 Plaque volume reduction after stenting was also the only significant predictor of creatinine kinase-MB post-procedural release in a multiple regression model performed on 110 consecutive patients with stable or unstable angina (P<0.047).22
The lipid core of a fibro-atheroma is typically imaged at IVUS as a lipid ‘pool-like’ image that often disappears after stenting. Tanaka et al.23 reported that the pre-procedural evidence of a lipid pool-like image at IVUS is a strong predictor of the no-reflow phenomenon after primary PCI, with an odds ratio for subsequent suboptimal (<3) TIMI flow grade of 118. In 110 consecutive patients with AMI undergoing primary PCI, Mizote et al.24 reported that the pre-procedural angioscopic evidence of a ruptured plaque implied a significantly higher risk of no-reflow after PCI (19.4 vs. 6.3%, P<0.0001) compared with the absence of such finding. A role for the embolization of lipid plaque components was also hypothesized by Kotani et al.,25 who performed intracoronary blood suction after primary PCI and reported a significantly higher prevalence of both plaque-derived debris and cholesterol crystals in the blood aspirated from patients with the no-reflow phenomenon compared with patients with good reflow (42 vs. 6%, P<0.01 and 67 vs. 13%, P<0.01 for both parameters, respectively). Taken as a whole, these data support a causal link between PCI-induced athero-embolism, most likely involving the lipid core of a ruptured fibro-atheroma and the no-reflow phenomenon. In 46 consecutive patients undergoing primary PCI with the adjunctive use of a distal protection device, the direct histopathological analysis of the embolic debris showed that plaque-derived, lipid-rich, emboli were the prevalent histopathological pattern in 24% of cases15 (Figure 1E). There was an increasing trend for such prevalence from patients with small embolic volumes to patients with large embolic volumes (from 0 to 40% in patients from the lowest to the highest quartile), suggesting that athero-embolism may be particularly frequent in patients with higher embolic burden.
Finally, substantial evidence exists about the biological consequences of coronary micro-embolization, that is, embolization of debris <60 µm. In mongrel dogs, coronary micro-embolization with 42 µm microspheres induces a contractile impairment, mainly mediated by myocardial infiltration with inflammatory cells and subsequent cytokine release.26 The contractile impairment is characteristically unparalleled by an equivalent decrease in basal coronary blood flow or myocardial perfusion, which are actually even increased after micro-embolization (perfusion/contraction mismatch).27 Because of this mismatch, the clinical consequences of micro-embolization can be evaluated by the analysis of regional left ventricular function or coronary flow reserve, but not by commonly used markers of myocardial reperfusion such as the TIMI flow grade or the corrected TIMI frame count; the effect of micro-embolization on more accurate markers of myocardial reperfusion such as blush grade or ST-segment analysis is presently unknown.
Micro-embolization is a frequent spontaneous event in patients with acute coronary syndromes, inducing malignant arrhythmias, patchy micro-infarctions, and contractile dysfunction.26,28 Besides its spontaneous occurrence, is micro-embolization also a PCI-induced phenomenon? Rogers et al.16 reported on the size distribution of particulates retrieved from 64 venous grafts PCI with distal protection: over 65% of PCI-induced emboli were smaller than 56 µm in their longest diameter. In a report from Quan et al.,17 the size distribution of PCI-induced emboli retrieved from native coronary arteries showed a percentage of micro-emboli in a range from 40 to 65% according to the protection device used. These data suggest that iatrogenic micro-embolization does occur during PCI, possibly affecting regional myocardial function in the absence of changes in epicardial blood flow velocity.
|
Embolic protection strategies: the failure of routine use |
|---|
Three recent AMI trials on the routine use of distal protection devices (EMERALD and PROMISE) or thrombus suction (AIMI) have demonstrated neutral or even negative effects on myocardial reperfusion and final infarct size7–9 (Table 1). In the wake of these unexpected results, several possible explanations have been proposed.14,29
- Distal embolization does occur during PCI for AMI (visible debris were aspirated in 73% of patients in the EMERALD trial) and it may induce a significant, although limited, additional myocardial necrosis. However, such limited increase in myocardial necrosis plays a minor role against the large background of necrosis due to ischaemia/reperfusion. These circumstances greatly differ from the clinical setting of PCI on degenerated vein grafts in which the myocardial area distal to the graft is viable by definition and its relative weight on global left ventricular function might have been amplified by previous infarctions in other territories.
- The infarct-size-to-risk-area ratio, rather than the final infarct size, may be the best endpoint to evaluate myocardial salvage in medium-sized trials.
- There is an operator-dependent randomization bias in trials requiring randomization after coronary angiography.
- In most cases, the above mentioned trials tested just ‘first generation’ devices and improvements in efficacy may be hypothesized for newer devices. First generation devices have a limited protective efficacy on native coronary arteries. The FilterWire device has a significant crossing profile that can itself induce embolization during the act of crossing the lesion. When compared with previous trials on saphenous vein grafts, this problem might have been amplified by the significantly smaller diameter of native coronary arteries. In the case of AngioJet, it may be hypothesized that not all the athero-thrombotic material prone to embolization during stenting is effectively aspirated. The GuardWire device and, to a lesser extent, the FilterWire device provide effective protection of the main branch only, whereas parent side branches located proximal to the device are still exposed to the risk of embolization. In the case of the GuardWire device, total occlusion of the main vessel may even favour a shunting of the liberated debris towards the side branches that provide circulatory supply to peripheral regions of the ongoing infarct. Unfortunately, these regions are those with a more prolonged viability after coronary occlusion and therefore are those for which PCI-induced myocardial salvage is more likely. Ineffective side branch protection by distal protection devices, when used on native arteries, might partially account for the differences from previous trials testing the same devices on saphenous vein grafts, which are free of branches.12,13
- Finally, filter-based distal protection devices might have pores too large (typically >100 µm) to effectively protect against micro-embolization and they cannot prevent release of soluble mediators into the bloodstream from captured embolic particles, with consequent potential detrimental effect on myocardial reperfusion.
All these considerations are plausible. The fact remains that recent randomized trials provide enough evidence against the routine use of embolic protection in primary PCI.
|
Embolic protection strategies: rationale for a selective use |
|---|
PCI is a very efficient reperfusion therapy for the majority of patients with AMI, with only a fraction of them experiencing a no-reflow phenomenon after PCI. A suboptimal final TIMI flow grade (>3) has been observed in a range from 3 to 12% of cases.7,9,19,30,31 When other surrogate markers of myocardial reperfusion are considered, such as the ST-segment early resolution or myocardial blush grade, the 50th lowest percentiles of these markers (<50% ST-segment resolution, blush grade 0 or 1) still include <30% of patients.7,9,30 Whichever relevant pathophysiological role might be played by distal embolization in AMI, this cannot apply to all patients, but only to the fraction, or part of that fraction, experiencing unsatisfactory myocardial reperfusion. Consequently, a beneficial effect of embolic protection can only be expected to apply to that fraction of patients. This has, in any case, to be balanced against the problems connected with the use of such devices, which are not trivial in terms of procedural safety and feasibility. In the EMERALD trial, the use of the GuardWire device increased procedural time by 14 min on average and, due to the occlusive nature of the device, such an increase almost completely translated into a reperfusion delay with likely consequent additive muscle loss. Furthermore, the use of embolic protection devices restricts the feasibility and optimal performance of PCI: (i) the support offered by the device guidewire is often suboptimal; (ii) in the case of insufficient distance between the landing zone of the device and the culprit lesion, the choice of stent length may be limited; and (iii) last but not least, serious complications have been sporadically reported, including the occurrence of filter entrapment into the stent struts or the development of coronary aneurysms secondary to the occlusive balloon inflation.32,33 Such considerations all contribute to explaining the failure of the routine use of embolic protection, because the potential benefits for few are at the cost of significant procedural limitations for all. Conversely, a strategy aimed at selective protection of patients at high risk for clinically relevant embolization might be optimal in AMI. The problem is how to select candidate patients.
|
Clues for a selective strategy of embolic protection and pathways for future research |
|---|
In the EMERALD trial, a subgroup analysis for the primary study endpoints did not identify any subset of patients in whom an advantage of distal protection was occurring.7 The infarct size was actually increased by GuardWire in patients with a putative high thrombus burden (i.e. those with totally occluded vessels or angiographic signs of intracoronary thrombus). Although this finding fuels perplexities on device-related detrimental effects deriving from emboli shunted through side branches into peripheral, most viable areas of the ongoing infarction, it also provides support to the hypothesis that the embolic load contributes, in this case iatrogenically, to infarct size. Besides the thrombus burden, however, none of the EMERALD subsets analysed was specifically related to culprit lesion morphology. At present, an IVUS analysis of the EMERALD study is ongoing to this regard. This is important because, when planning a selective approach for embolic protection, both markers of quantitatively relevant embolization (i.e. large embolic load) and markers of qualitatively relevant embolization (i.e. lipid-rich athero-embolism) are likely to be related to outcome. As previously discussed, specific plaque morphologies and the extent of athero-embolism, as evaluated by plaque volume reduction after stenting, have been shown to be related to the no-reflow phenomenon.21–25 Therefore, a lipid pool-like image at IVUS, or a ruptured plaque image at angioscopy might both be useful markers to identify lesions at high risk of clinically relevant athero-embolism. Mizote et al.24 reported that distal protection with the GuardWire device led to a significant improvement in markers of myocardial reperfusion and left ventricular function in patients with an angioscopically defined plaque rupture compared with historical controls, whereas the same device was ineffective in patients without signs of rupture. The rate of retrieval of plaque-derived debris in the aspirated samples was significantly higher in the former study group compared with the latter (95 vs. 31%, P<0.05), supporting the hypothesis that specific plaque morphologies are more prone to athero-embolism. In the near future, given the low technical feasibility of angioscopy in the clinical setting of AMI, a satisfactory visualization of cap integrity might be obtained by optical coherence tomography, whereas IVUS virtual histology might be of help in identifying a large lipid core in a plaque before stenting.34,35
With regard to quantitative criteria for a large embolic load, a variety of angiographic or IVUS markers may be used. We have previously shown that a complete vessel occlusion with a cut-off pattern (as opposed to a tapered pattern) or an angiographic thrombus with the greatest linear dimension more than three times the reference luminal diameter is an independent predictor of a higher total embolic volume at multivariate analysis (OR 15.8, P<0.005).15 These angiographic markers were also reported to be independent predictors of the no-reflow (rate of no-reflow in the presence vs. absence of cut-off or angiographic thrombus signs: 52 vs. 10%, P<0.001 and 52 vs. 4%, P<0.0001 for the two markers, respectively).20 In the same study, a persistent stasis of contrast medium distal to the obstruction, or a reference luminal diameter 
4.0 mm, was an additional angiographic sign predictive of no-reflow.20 In 140 consecutive patients with AMI, the IVUS evidence of a floating thrombus before PCI was, among several clinical, angiographic, and IVUS parameters, the only significant predictor of subsequent angiographically evident distal embolization at multivariate analysis (OR 53, confidence interval 2.7–1040, P<0.01).36
According to the above mentioned markers, the population of AMI patients candidate for selective protection might be not trivial, but certainly far from the totality of AMI patients submitted to primary PCI. The prevalence of angiographic signs of a high thrombus burden has been reported to range from 32 to 63%,15,20 the angioscopic evidence of ruptured plaque was found in 55% of AMI patients,24 and a floating thrombus or a lipid pool-like image at IVUS was observed in 21 and 34% of patients, respectively.23,36
|
The missing trial |
|---|
Any selective strategy proposed for the use of embolic protection devices should be prospectively tested in clinical trials which should have the following features.
- Selection of AMI patients should be done according to the markers of clinically relevant distal embolization. The adopted markers should be predictive of ‘quantitatively’ relevant embolization (angiographic signs of large thrombus burden, IVUS evidence of a floating thrombus) or predictive of a ‘qualitatively’ relevant embolization (intravascular imaging signs of a plaque prone to generate lipid-rich athero-embolism after stenting: a large lipid pool-like image, a ruptured thin-cap fibro-atheroma). At present, a major limitation in patient selection might derive from the lack of sufficiently reliable and feasible intravascular imaging techniques. However further developments in IVUS virtual histology, palpography, and optical coherence tomography are expected to render intravascular imaging markers of plaques at high risk of embolization soon available for routine clinical use.
- Embolic protection should be performed with a latest generation device, characterized by (a) the lowest possible crossing profile in the case of distal protection or, alternatively, a proximal protection mechanism of action in order to minimize or avoid device-induced embolization; (b) being minimally time-consuming, translating in negligible reperfusion delay, especially in the case of proximal or distal occlusive systems; (c) yielding effective protection against micro-embolization (current filter-based devices have pores size >100 µm). Embolic shunting through side branches might be prevented by proximal protection devices or be minimized by allowing simultaneous selective distal protection of two branches through the use of stents pre-mounted on a ‘bi-rail’ delivery system.
- Assessment should be done of final infarct-size-to-risk area ratio rather than just infarct size, in order to avoid potential biases in baseline infarct estimates (possibly occurring in small trials).
- Regional left ventricular function recovery should be evaluated in order to assess the prevention of micro-embolization. In fact, basal epicardial flow velocity may be unchanged, or even increased, after micro-embolization, whereas its effect on myocardial reperfusion markers such as ST-segment shift and blush grade is totally unknown.
- A clinical endpoint, such as major adverse cardiac events, should also be evaluated; the study population size should be large enough to at least rule out any detrimental effect of the device on the short-term clinical outcome.
|
Conclusions |
|---|
PCI-induced embolization in AMI is likely to be clinically important in specific subsets of patients. Significant clinical consequences may be expected when embolization is quantitatively and/or qualitatively relevant, this latter consisting of lipid-rich athero-embolism, as is the case of lipid core embolization through the ruptured cap of a fibro-atheroma. A routine strategy for embolic protection in the clinical setting of AMI is substantially ineffective because distal embolization seems to play a pathophysiological role only in specific conditions, and the use of first-generation embolic protection devices entails an increase in myocardial ischaemia, procedural times, and complications. Future primary PCI trials on embolic protection should adopt a strategy aimed at identifying, through the use of angiographic or intravascular imaging markers, patients at highest risk of clinically relevant embolization. Such trials should also adopt specific endpoints to evaluate the effect of micro-embolization, now poorly assessed by the standard markers of myocardial reperfusion.
Conflict of interest: no conflict of interest is declared by the authors as to the content of this manuscript.
|
References |
|---|
- Napodano M, Pasquetto G, Sacca S, Cernetti C, Scarabeo V, Pascotto P, Reimers B. Intracoronary thrombectomy improves myocardial reperfusion in patients undergoing direct angioplasty for acute myocardial infarction. J Am Coll Cardiol 2003; 42: 1395–1402.
[Abstract/Free Full Text] - Yip HK, Wu CJ, Chang HW, Fang CY, Yang CH, Chen SM, Hung WC, Chen CJ, Cheng CI, Hsieh YK. Effect of the PercuSurge GuardWire device on the integrity of microvasculature and clinical outcomes during primary transradial coronary intervention in acute myocardial infarction. Am J Cardiol 2003; 92: 1331–1335.[CrossRef][ISI][Medline]
- Beran G, Lang I, Schreiber W, Denk S, Stefenelli T, Syeda B, Maurer G, Glogar D, Siostrzonek P. Intracoronary thrombectomy with the X-sizer catheter system improves epicardial flow and accelerates ST-segment resolution in patients with acute coronary syndrome: a prospective, randomized, controlled study. Circulation 2002; 105: 2355–2360.
[Abstract/Free Full Text] - Limbruno U, Micheli A, De Carlo M, Amoroso G, Rossini R, Palagi C, Di Bello V, Petronio AS, Fontanini G, Mariani M. Mechanical prevention of distal embolization during primary angioplasty: safety, feasibility, and impact on myocardial reperfusion. Circulation 2003; 108: 171–176.
[Abstract/Free Full Text] - Belli G, Pezzano A, De Biase AM, Bonacina E, Silva P, Salvade P, Piccalo G, Klugmann S. Adjunctive thrombus aspiration and mechanical protection from distal embolization in primary percutaneous intervention for acute myocardial infarction. Catheter Cardiovasc Interv 2000; 50: 362–370.[CrossRef][ISI][Medline]
- Antoniucci D, Valenti R, Migliorini A, Parodi G, Memisha G, Santoro GM, Sciagra R. Comparison of rheolytic thrombectomy before direct infarct artery stenting versus direct stenting alone in patients undergoing percutaneous coronary intervention for acute myocardial infarction. Am J Cardiol 2004; 93: 1033–1035.[CrossRef][ISI][Medline]
- Stone GW, Webb J, Cox DA, Brodie BR, Qureshi M, Kalynych A, Turco M, Schultheiss HP, Dulas D, Rutherford BD, Antoniucci D, Krucoff MW, Gibbons RJ, Jones D, Lansky AJ, Mehran R; Enhanced Myocardial Efficacy and Recovery by Aspiration of Liberated Debris (EMERALD) Investigators. Distal microcirculatory protection during percutaneous coronary intervention in acute ST-segment elevation myocardial infarction. A randomized controlled trial. JAMA 2005; 293: 1063–1072.
[Abstract/Free Full Text] - Gick M, Jander N, Bestehorn HP, Kienzle RP, Ferenc M, Werner K, Comberg T, Peitz K, Zohlnhofer D, Bassignana V, Buettner HJ, Neumann FJ. Randomized evaluation of the effects of filter-based distal protection on myocardial perfusion and infarct size after primary percutaneous catheter intervention in myocardial infarction with and without ST-segment elevation. Circulation 2005; 112: 1462–1469.
[Abstract/Free Full Text] - Ali A. AngioJet rheolytic thrombectomy in patients undergoing primary angioplasty for acute myocardial infarction. (TCT abstract presentation), 2004. Information available through http://www.tctmd.com.
- Lefevre T, Garcia E, Reimers B, Lang I, di Mario C, Colombo A, Neumann FJ, Chavarri MV, Brunel P, Grube E, Thomas M, Glatt B, Ludwig J; X AMINE ST Investigators. X-sizer for thrombectomy in acute myocardial infarction improves ST-segment resolution: results of the X-sizer in AMI for negligible embolization and optimal ST resolution (X AMINE ST) trial. J Am Coll Cardiol 2005; 46: 246–252.
[Abstract/Free Full Text] - Sakuma T, Leong-Poi H, Fisher NG, Goodman NC, Kaul S. Further insights into the no-reflow phenomenon after primary angioplasty in acute myocardial infarction: the role of microthromboemboli. J Am Soc Echocardiogr 2003; 16: 15–21.[CrossRef][ISI][Medline]
- Baim DS, Wahr D, George B, Leon MB, Greenberg J, Cutlip DE, Kaya U, Popma JJ, Ho KK, Kuntz RE; Saphenous vein graft Angioplasty Free of Emboli Randomized (SAFER) Trial Investigators. Randomized trial of a distal embolic protection device during percutaneous intervention of saphenous vein aortocoronary bypass grafts. Circulation 2002; 105: 1285–1290.
[Abstract/Free Full Text] - Stone GW, Rogers C, Hermiller J, Feldman R, Hall P, Haber R, Masud A, Cambier P, Caputo RP, Turco M, Kovach R, Brodie B, Herrmann HC, Kuntz RE, Popma JJ, Ramee S, Cox DA; FilterWire EX Randomized Evaluation Investigators. Randomized comparison of distal protection with a filter-based catheter and a balloon occlusion and aspiration system during percutaneous intervention of diseased saphenous vein aorto-coronary bypass grafts. Circulation 2003; 108: 548–553.
[Abstract/Free Full Text] - Kuntz RE, Rogers C BaimDS. Percutaneous coronary intervention-induced emboli during primary PCI for STEMI: too little, too much, or too late? Am Heart J 2005; 150: 4–6.[Medline]
- Limbruno U, De Carlo M, Pistolesi S, Micheli A, Petronio AS, Camacci T, Fontanini G, Balbarini A, Mariani M, De Caterina R. Distal embolization during primary angioplasty: histopathologic features and predictability. Am Heart J 2005; 150: 102–108.[CrossRef][ISI][Medline]
- Rogers C, Huynh R, Seifert PA, Chevalier B, Schofer J, Edelman ER, Toegel G, Kuchela A, Woupio A, Kuntz RE, Macon ND. Embolic protection with filtering or occlusion balloons during saphenous vein graft stenting retrieves identical volumes and sizes of particulate debris. Circulation 2004; 109: 1735–1740.
[Abstract/Free Full Text] - Quan VH, Huynh R, Seifert PA, Kuchela A, Chen WH, Sutsch G, Eisenhauer AC, Rogers C. Morphometric analysis of particulate debris extracted by four different embolic protection devices from coronary arteries, aortocoronary saphenous vein conduits, and carotid arteries. Am J Cardiol 2005; 95: 1415–1419.[CrossRef][ISI][Medline]
- De Carlo M, Limbruno U, Pistolesi S, Fontanini G, Petronio AS, Balbarini A, De Caterina R. Distal embolization during angioplasty for acute myocardial infarction: is pharmacological protection enough? Thromb Haemost 2005; 94: 680–681.[Medline]
- Henriques JP, Zijlstra F, Ottervanger JP, de Boer MJ, van't Hof AW, Hoorntje JC, Suryapranata H. Incidence and clinical significance of distal embolization during primary angioplasty for acute myocardial infarction. Eur Heart J 2002; 23: 1112–1117.
[Abstract/Free Full Text] - Yip HK, Chen MC, Chang HW, Hang CL, Hsieh YK, Fang CY, Wu CJ. Angiographic morphologic features of infarct-related arteries and timely reperfusion in acute myocardial infarction: predictors of slow-flow and no-reflow phenomenon. Chest 2002; 122: 1322–1332.
[Abstract/Free Full Text] - Kotani J, Mintz GS, Pregowski J, Kalinczuk L, Pichard AD, Satler LF, Suddath WO, Waksman R, Weissman NJ. Volumetric intravascular ultrasound evidence that distal embolization during acute infarct intervention contributes to inadequate myocardial perfusion grade. Am J Cardiol 2003; 92: 728–732.[CrossRef][ISI][Medline]
- Prati F, Pawlowski T, Gil R, Labellarte A, Gziut A, Caradonna E, Manzoli A, Pappalardo A, Burzotta F, Boccanelli A. Stenting of culprit lesions in unstable angina leads to a marked reduction in plaque burden: a major role of plaque embolization? A serial intravascular ultrasound study. Circulation 2003; 107: 2320–2325.
[Abstract/Free Full Text] - Tanaka A, Kawarabayashi T, Nishibori Y, Sano T, Nishida Y, Fukuda D, Shimada K, Yoshikawa J. No-reflow phenomenon and lesion morphology in patients with acute myocardial infarction. Circulation 2002; 105: 2148–2152.
[Abstract/Free Full Text] - Mizote I, Ueda Y, Ohtani T, Shimizu M, Takeda Y, Oka T, Tsujimoto M, Hirayama A, Hori M, Kodama K. Distal protection improved reperfusion and reduced left ventricular dysfunction in patients with acute myocardial infarction who had angioscopically-defined ruptured plaque. Circulation 2005; 112: 1001–1007.
[Abstract/Free Full Text] - Kotani J, Nanto S, Mintz GS, Kitakaze M, Ohara T, Morozumi T, Nagata S, Hori M. Plaque gruel of atheromatous coronary lesion may contribute to the no-reflow phenomenon in patients with acute coronary syndrome. Circulation 2002; 106: 1672–1677.
[Abstract/Free Full Text] - Heusch G, Schulz R, Haude M, Erbel R. Coronary microembolization. J Mol Cell Cardiol 2004; 37: 23–31.[CrossRef][ISI][Medline]
- Dorge H, Neumann T, Behrends M, Skyschally A, Schulz R, Kasper C, Erbel R, Heusch G. Perfusion-contraction mismatch with coronary microvascular obstruction: role of inflammation. Am J Physiol 2000; 279: H2587–H2592.[ISI]
- Topol EJ. A guide to therapeutic decision-making in patients with non-ST-segment elevation acute coronary syndromes. J Am Coll Cardiol 2003; 41: 123S–129S.
[Abstract/Free Full Text] - Schömig A, Kastrati A. Distal embolic protection in patients with acute myocardial infarction. Attractive concept but no evidence of benefit. JAMA 2005; 293: 1116–1118.
[Free Full Text] - Stone GW, Peterson MA, Lansky AJ, Dangas G, Mehran R, Leon MB. Impact of normalized myocardial perfusion after successful angioplasty in acute myocardial infarction. J Am Coll Cardiol 2002; 39: 591–597.
[Abstract/Free Full Text] - Stone GW, Grines CL, Cox DA, Garcia E, Tcheng JE, Griffin JJ, Guagliumi G, Stuckey T, Turco M, Carroll JD, Rutherford BD, Lansky AJ; Controlled Abciximab and Device Investigation to Lower Late Angioplasty Complications (CADILLAC) Investigators. Comparison of angioplasty with stenting, with or without abciximab, in acute myocardial infarction. N Engl J Med 2002; 346: 957–966.
[Abstract/Free Full Text] - Limbruno U, Genovesi A, Galli M. Filters to prevent distal embolization during coronary artery stenting: the risk of mousetrap. J Invasive Cardiol 2006, in press.
- Yamaguchi K, Hiasa Y, Takahashi T. Formation of a coronary artery aneurysm after inflation of a PercuSurge GuardWire distal protection balloon. Catheter Cardiovasc Interv 2005; 64: 82–84.[Medline]
- Yabushita H, Bouma BE, Houser SL, Aretz HT, Jang IK, Schlendorf KH, Kauffman CR, Shishkov M, Kang DH, Halpern EF, Tearney GJ. Characterization of human atherosclerosis by optical coherence tomography. Circulation 2002; 106: 1640–1645.
[Abstract/Free Full Text] - Kawasaki M, Takatsu H, Noda T, Sano K, Ito Y, Hayakawa K, Tsuchiya K, Arai M, Nishigaki K, Takemura G, Minatoguchi S, Fujiwara T, Fujiwara H. In vivo quantitative tissue characterization of human coronary arterial plaques by use of integrated backscatter intravascular ultrasound and comparison with angioscopic findings. Circulation 2002; 105: 2487–2492.
[Abstract/Free Full Text] - Fukuda D, Tanaka A, Shimada K, Nishida Y, Kawarabayashi T, Yoshikawa J. Predicting angiographic distal embolization following percutaneous coronary intervention in patients with acute myocardial infarction. Am J Cardiol 2003; 91: 403–407.[CrossRef][ISI][Medline]
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  L. Mauri, C. Rogers, and D. S. Baim Devices for Distal Protection During Percutaneous Coronary Revascularization Circulation, June 6, 2006; 113(22): 2651 - 2656. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||