European Heart Journal Advance Access originally published online on June 7, 2007
European Heart Journal 2007 28(14):1709-1716; doi:10.1093/eurheartj/ehm184
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Impact of multivessel disease on reperfusion success and clinical outcomes in patients undergoing primary percutaneous coronary intervention for acute myocardial infarction
1 Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic and Mayo Foundation, Rochester, MN, USA
2 Mid Carolina Cardiology, Charlotte, NC, USA
3 Beth Israel Deaconess Medical Center, Boston, MA, USA
4 Department of Cardiology, College of Physicians and Surgeons, Columbia University Medical Center, 161 Fort Washington Avenue, 5th Floor, New York, NY 10032, USA
5 The Cardiovascular Research Foundation, 111 E. 59th St., 11th Floor, New York, NY 10022, USA
6 Moses Cone Health System, Greensboro, NC, USA
7 Duke University Medical Center, Durham, NC, USA
8 William Beaumont Hospital, Royal Oak, MI 48073, USA
Received 20 July 2006; revised 14 April 2007; accepted 25 April 2007; online publish-ahead-of-print 7 June 2007.
* Corresponding author. Tel: +1 212 851 8304; fax: +1 212 851 9396. E-mail address: gstone{at}crf.org or gs2184@columbia.edu
| Abstract |
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Aims: We sought to investigate the impact of multivessel coronary artery disease (CAD) on reperfusion success and prognosis following primary percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI). The influence of multivessel disease on myocardial reperfusion and subsequent survival after primary PCI has not been studied.
Methods and results: In the CADILLAC trial, primary PCI was performed in 2082 patients of any age with AMI within 12 h of symptom onset. Myocardial perfusion post-PCI assessed by ST-segment recovery and myocardial blush and clinical outcomes were stratified by the extent of CAD. Single-, double-, and triple-vessel disease were present in 1066 (51.2%), 692 (33.2%), and 324 (15.6%) patients, respectively. Patients with multivessel disease compared with those with single-vessel disease undergoing primary PCI were significantly more likely to have absent ST-segment recovery (13.3 vs. 7.4%, P = 0.01), though the rates of post-procedural TIMI-3 flow (89.7 vs. 88.9%, P = 0.66) and grade 2 or 3 myocardial blush (51.2 vs. 51.5%, P = 0.91) in the infarct vessel were comparable. By 1 year, the cumulative incidence of death for patients with single-, double-, and triple-vessel disease was 3.2, 4.4, and 7.8%, respectively (P = 0.003), and the composite rate of major adverse cardiac events (MACE) was 14.8, 19.5, and 23.6%, respectively (P = 0.0006). By multivariable analysis, the presence of triple-vessel disease was the strongest predictor of 1-year death [hazard ratio (HR) = 2.60, P = 0.009], death and re-infarction (HR = 1.88, P = 0.03), and MACE (HR = 1.80, P = 0.0009).
Conclusion: Patients with extensive CAD in vessels remote from the infarct-related artery have reduced reperfusion success and an adverse prognosis following primary PCI in AMI. Future studies regarding the optimal treatment of patients with multivessel disease and AMI are warranted.
Key Words: Primary angioplasty Myocardial infarction Prognosis Multivessel disease Coronary artery disease
| Introduction |
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Primary percutaneous coronary intervention (PCI) in acute myocardial infarction (AMI) results in greater patency of the infarct-related artery (IRA) and lower rates of death, re-infarction, and stroke when compared with fibrinolysis alone.13 Yet despite the prompt and successful restoration of antegrade epicardial blood flow by PCI, a significant proportion of patients with AMI remain at increased risk of death and adverse outcomes. Efforts directed towards the identification of these patients prior to hospital discharge have utilized clinical markers such as demographic characteristics and bedside findings, and non-invasive and invasive testing.46
Not uncommonly, concomitant atherosclerosis in coronary vessels other than the IRA is observed in patients undergoing primary PCI. Multivessel disease has typically been reported to be present in 4050% of patients with AMI in both institutional registries and multicentre clinical trials.711 The prognostic impact of multivessel coronary artery disease (CAD) has rarely been considered in prior studies of pharmacologic reperfusion.1214 A potential advantage of primary PCI as a reperfusion modality is the immediate recognition of the extent of CAD, allowing this variable to be considered in risk stratification.1519 The extent of CAD, as a marker of diffuse atherosclerosis and plaque burden, may directly or indirectly exert an adverse impact upon the prognosis of patients with AMI. Whether contemporary reperfusion modalities, including stents and glycoprotein IIb/IIIa inhibitors, are able to mitigate the adverse prognostic implications of multivessel disease is unknown.
The objective of the current investigation was to examine the prognostic impact of multivessel CAD on procedural results and subsequent clinical outcomes in a contemporary cohort of patients with AMI undergoing primary PCI therapy. As recent studies have demonstrated that a large proportion of patients achieving normal antegrade TIMI-3 flow in the infarct vessel have impaired microcirculatory perfusion or ongoing myocardial injury, reperfusion success was measured by angiographic myocardial blush and ST-segment recovery (
STR).20,21
| Methods |
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Study population and protocol
The details of the CADILLAC trial protocol have been previously described.22 Briefly, a total of 2082 non-shock patients with AMI and symptom duration of < 12 h were randomized at 76 international medical centres to balloon angioplasty vs. stenting, each with or without the use of abciximab. Importantly, patients with multivessel disease requiring angioplasty of more than one of the three major epicardial coronary arteries during the index procedure were excluded. Patients with extensive CAD in whom bypass surgery was likely to be required within 30 days were also excluded. However, patients with multivessel disease requiring staged angioplasty procedures were actively recruited. Clinical follow-up was performed at 1, 6, and 12 months. Other details of the angioplasty procedure and protocol have been previously described.22
In a formal sub-study, a subgroup of 1301 patients were analysed for angiographic microcirculatory reperfusion as assessed by the myocardial blush score at an independent core laboratory, as previously described.20 The presence of collateral vessels to the infarct artery were also assessed at the core lab in this sub-study, using the Rentrop classification (Grade 0no collateral filling; Grade 1filling of collaterals without filling of the epicardial coronary; Grade 2filling of collaterals with incomplete filling of the epicardial coronary; and Grade 3filling of collaterals with complete filling of epicardial coronary).23 In a second formal sub-study involving 700 patients, myocardial reperfusion success was assessed by post-angioplasty electrocardiographic summed
STR in a core laboratory as previously described.21 To analyse completeness of myocardial and microvascular reperfusion of the infarct vessel, patients were grouped according to the degree of myocardial blush (3 = normal, 2 = reduced, and 0/1 = absent), and the extent of
STR (<30%, 3070%, and > 70%).20,21
Definitions and endpoints
Significant atherosclerotic CAD was defined as a visually estimated stenosis
50% for the left main (LM) and
70% for other major arteries and/or their epicardial branches. The number of diseased vessels was determined by involvement of the epicardial segments of the three major arteries [right coronary artery, left anterior descending (LAD), and left circumflex]. Significant atherosclerosis involving the LM segment was considered to be two-vessel disease in the presence of right dominance and three-vessel disease in the presence of left dominance. The primary endpoint of the CADILLAC trial was the composite occurrence of major adverse cardiac events (MACE), consisting of death, re-infarction, disabling stroke, and target vessel revascularization (TVR) for ischaemia, the components having been previously defined.20
Statistical analysis
To analyse the prognostic impact of multivessel CAD, patients were classified according to the number of diseased coronary arteries into three groups: single-, double-, and triple-vessel disease. To examine the prognostic impact of revascularization apart from the IRA subsequent to primary PCI, patients with multivessel disease were grouped according to the occurrence of such revascularization within 30 days after primary PCI. Categorical variables were compared using Fisher's exact test for pairwise variables or the
2 for trend for three or four way comparisons. Continuous variables were expressed as medians with interquartile ranges and were compared using the non-parametric KruskalWallis test. Cumulative event rates were evaluated using KaplanMeier estimates and compared with the log-rank test. To examine the impact of the number of diseased coronary arteries in the context of baseline clinical characteristics, Cox proportional hazard models were constructed for the same endpoints with the following candidate predictors: age, male gender, diabetes mellitus, current smoking, left ventricular ejection fraction (LVEF), creatinine clearance, number of diseased vessels, LAD disease, prior AMI, pre-procedural TIMI grade flow of 02, Killip class, and symptom onset to initial balloon inflation time. The significance level was set at P < 0.05 (two-sided).
| Results |
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Baseline characteristics
Compared with those with single-vessel disease, patients with multivessel disease were older and had a higher incidence of prior AMI, previous coronary artery bypass grafting, and multiple atherosclerotic risk factors apart from smoking (Table 1). Multivessel disease was also associated with higher Killip class, lower baseline LVEF, and less frequent involvement of the LAD as the IRA at presentation. Angiographic and procedural associations of multivessel disease included smaller reference diameter of the infarct vessel, a greater number of stents implanted per patient, and a smaller final minimal lumen diameter (Table 2). There were no differences in stent or abciximab usage, procedural success, collateral flow, or TIMI flow before PCI according to the presence of single-, double-, or triple-vessel disease (Table 2).
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Multivessel disease and reperfusion success in the infarct vessel
There was no difference in final TIMI grade 3 flow in patients with single-, double-, and triple-vessel disease (Table 2). Similarly, myocardial perfusion as assessed by myocardial blush was independent of the extent of CAD. In contrast, however, the degree of
STR correlated with the number of diseased vessels (P = 0.02 for group distribution; Figure 1). Among patients with single-, double-, and triple-vessel disease, absent
STR (<30%) occurred in 7.4, 11.1, and 18.4% of patients, respectively (P = 0.005).
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Thirty-day and 1-year clinical outcomes
Clinical follow-up was obtained in 96.8%. Compared with those with single-vessel disease, patients with multivessel disease had a higher frequency of recurrent ischaemia at 30-days and a non-significant trend towards higher rates of 30-day mortality and MACE (Table 3). At 1 year, mortality was markedly higher in patients with triple-vessel disease, intermediate in patients with double-vessel disease, and lowest with single-vessel disease (Figure 2). Multivessel disease also strongly correlated with a higher combined incidence of death and re-infarction, and a greater frequency of MACE (Table 3). Patients with multivessel disease also were more likely to undergo non-TVR. By multivariable analysis, the presence of triple-vessel disease was the strongest independent predictor of death, death and re-infarction combined, and the occurrence of MACE at 1 year (Table 4). However, the presence of double-vessel disease also was an independent predictor of 1 year MACE.
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Impact of randomization on clinical outcomes
Stenting of the infarct vessel was associated with less ischaemia-driven TVR and occurrence of MACE at 1 year for patients with multivessel disease, and at both 30-days and 1 year for patients with single-vessel disease (Table 5). The use of abciximab was associated with less ischaemia-driven TVR at both 30-days and 1 year among patients with single-vessel disease, but not in multivessel disease. There was no association of stenting or abciximab use with occurrence of death, re-infarction, or disabling stroke in either patients with single or multivessel disease. Among patients with single-vessel disease, stenting was associated with a lower incidence of
STR < 30% (3.9 vs. 9.2%; P = 0.04) than balloon angioplasty. Among patients with multivessel disease, stenting was associated with a higher incidence of myocardial blush grade (MBG) 0 or 1. However, there were no other associations of stenting or abciximab use with differences in ST-segment resolution or final MBG in either patients with single or multivessel disease.
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Non-infarct artery revascularization and outcome
For patients with double- and triple-vessel disease, subsequent revascularization of one or more non-IRAs by either PCI or surgical bypass grafting was performed in 5.6 and 0.6% of patients, respectively, within 30 days. Patients with multivessel disease who underwent non-infarct artery revascularization < 30 days after primary PCI had greater 1-year survival that was comparable to the survival of patients with single-vessel disease (Figure 3).
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| Discussion |
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The principal findings from the current investigation are: (i) concomitant CAD in vessels remote from the IRA is associated with reduced myocardial reperfusion success as measured by ST-segment resolution, and increased early and late mortality and MACE after primary PCI for AMI; (ii) after adjustment for differences in baseline clinical and angiographic variables, the presence of multivessel disease (especially when all three epicardial coronary arteries are involved) remained a powerful independent predictor of mortality; (iii) neither abciximab nor use of stents in the infarct vessel ameliorated the adverse prognostic implications of multivessel disease; (iv) patients with multivessel disease who underwent subsequent revascularization of non-infarct-related coronary arteries had greater survival than patients with multivessel disease in whom such revascularization was not performed, and a similar late prognosis to patients with single-vessel disease.
Significant atherosclerotic narrowings in vessels apart from the IRA are found in approximately 50% of patients undergoing primary PCI for AMI.711 The presence of multivessel disease in these patients has been associated with poorer clinical outcomes, though few studies have examined the prognostic impact of the angiographic extent of CAD after primary PCI, especially in the contemporary era in which stents and glycoprotein IIb/IIIa inhibitors have become standard of care.20 In the large present study of patients without cardiogenic shock undergoing primary PCI, the presence of multivessel disease was a powerful independent correlate of mortality, even after adjustment for differences in baseline clinical and angiographic variables. Moreover, the negative prognostic impact of multivessel disease was not impacted by the use of stents or glycoprotein IIb/IIIa inhibitors. These data have important clinical implications when assessing prognosis; in contrast to other methods of risk stratification that incorporate only baseline clinical variables or require pre-discharge exercise testing,46,24 the on-line assessment of the extent of CAD is an integral component of the primary PCI procedure, which cannot be otherwise obtained without routine cardiac catheterization.
The mechanisms through which multivessel disease adversely affects survival is unknown. Patients with multivessel disease have a greater incidence of co-morbid high-risk baseline features that may contribute to an adverse prognosis. The presence of multivessel disease, however, remained an independent predictor of mortality after correction for these differences. Previous studies have shown that patients with AMI presenting with simultaneous rupture of multiple atherosclerotic plaques undergoing acute multivessel PCI are at significantly increased risk for late death and re-infarction.17 The present study extends these observations, however, by demonstrating that multivessel disease is an independent correlate of an adverse long-term prognosis even when intervention is acutely required in only a single coronary artery. Complications may also occur as a result of PCI and bypass surgery procedures required to treat angina in patients with multivessel disease. The fact that greater survival was evident in patients with multivessel disease in whom revascularization of remote non-infarct-artery-related disease was subsequently performed, however, argues more to the deleterious effects of plaque burden and diffuse ischaemia rather than harm from subsequent revascularization procedures.
Another factor that may contribute to the adverse prognosis in patients with multivessel disease is reduced reperfusion success. Despite equivalent rates of epicardial TIMI-3 flow in patients with single-, double-, and triple-vessel disease, myocardial reperfusion success as assessed by ST-segment resolution was impaired in patients with significant disease remote from the infarct artery, an effect especially pronounced in patients with triple-vessel disease. Reduced myocardial perfusion has been demonstrated to result in diminished survival, despite restoration of normal epicardial blood flow.20,21 Whether remote CAD is a marker of more disseminated atherosclerosis with microcirculatory involvement in the infarct vessel that might directly diminish myocardial perfusion, reflects a greater amount of distal embolization with subsequent capillary plugging,25 is a marker of endothelial dysfunction,26 or indicates greater systemic inflammation27 is unknown, and deserves further study. Notably, reference diameter and final minimal lumen diameter were both smaller in patients with multivessel disease.
Despite its high prevalence, a paucity of data exists regarding the optimal management of patients with AMI and multivessel disease. Reports regarding the need for and timing of subsequent revascularization of diseased vessels following acute reperfusion therapy have been limited to retrospective analyses of surgical series, and have not led to a clear consensus.28 In the acute setting, current practice guidelines recommend revascularization of non-IRA stenoses only in the presence of haemodynamic or electrical instability. In the present study, recurrent ischaemia (occurring in > 25% of patients) and death (in 48% of patients) within 1 year after the incident AMI occurred frequently in patients with double- and triple-vessel disease. Analysis for completeness of revascularization of ischaemic territories during follow-up was not available in the current investigation, though further revascularization of diseased vessels remote from the IRA was associated with enhanced survival in the present study, resulting in survival similar to patients with single-vessel disease. Given its non pre-specified, post hoc nature, this observation requires prospective validation, ideally within the framework of a randomized trial.
Study limitations
Firm conclusions regarding the advisability or timing on non-IRA revascularization cannot be drawn from the current retrospective analysis. The rate of revascularization of significant stenoses remote from the IRA early after primary PCI was relatively low in patients with multivessel disease, possibly reflecting current American College of Cardiology/American Heart Association practice guidelines. Moreover, detailed exploration of the relation between subsequent revascularization procedures and mortality would have been facilitated had data regarding the reasons for the performance or deferral of subsequent revascularization, as well as the completeness of revascularization and myocardial viability been available. However, data regarding the extent of CAD was prospectively collected, and all outcomes carefully adjudicated by independent committees and core laboratories blinding to this variable. The strength of the relationship between the number of diseased vessels and mortality after multivariable analysis suggests the relationship is real, though whether this reflects an underlying vasculopathy or systemic disease state is uncertain.
Conclusions and clinical implications
The angiographic extent of disease is a simple prognostic measure that is readily available in patients undergoing primary PCI and should be employed in the risk stratification of these patients in the acute setting. The presence of significant concomitant CAD in vessels remote from the IRA should be recognized as a major adverse prognostic factor in patients with AMI, even after successful angioplasty. Studies to determine whether efforts to improve myocardial reperfusion success (e.g. advanced pharmacologic approaches, distal protection, or thrombectomy) will further improve the prognosis in this high-risk group are underway. Moreover, future prospective studies regarding the timing and extent of revascularization in patients with multivessel disease after acute reperfusion therapy (whether during the index procedure28,29 or delayed for weeks or longer) are also required to determine the impact of complete revascularization on the prognosis of high-risk patients with multivessel disease.
Conflict of interest: none declered.
| References |
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- Grines CL, Browne KF, Marco J, Rothbaum D, Stone GW, O'Keefe J, Overlie P, Donohue B, Chelliah N, Timmis GC, Vlietstra RE, Strzelecki M, Puchrowicz-Ochocki S, O'Neill WW. A comparison of immediate angioplasty with thrombolytic therapy for acute myocardial infarction. N Engl J Med (1993) 328:673679.
[Abstract/Free Full Text] - Michels KB, Yusuf S. Does PTCA in acute myocardial infarction affect mortality and reinfarction rates? A quantitative overview (meta-analysis) of the randomized clinical trials. Circulation (1995) 91:476485.
[Abstract/Free Full Text] - Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomized trials. Lancet (2003) 361:1320.[CrossRef][ISI][Medline]
- Gibbons RJ, Balady GJ, Beasley JW, Bricker JT, Duvernoy WF, Froelicher VF, Mark DB, Marwick TH, McCallister BD, Thompson PD, Winters WL Jr, Yanowitz FG, Ritchie JL, Cheitlin MD, Eagle KA, Gardner TJ, Garson A Jr, Lewis RP, O'Rourke RA, Ryan TJ. ACC/AHA guidelines for exercise testing: executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing). Circulation (1997) 96:345354.
[Free Full Text] - Yamamuro A, Akasaka T, Tamita K, Yamabe K, Katayama M, Takagi T, Morioka S. Coronary flow velocity pattern immediately after percutaneous coronary intervention as a predictor of complications and in-hospital survival after acute myocardial infarction. Circulation (2002) 106:30513056.
[Abstract/Free Full Text] - Moller JE, Hillis GS, Oh JK, Seward JB, Reeder GS, Wright RS, Park SW, Bailey KR, Pellikka PA. Left atrial volume: a powerful predictor of survival after acute myocardial infarction. Circulation (2003) 107:22072212.
[Abstract/Free Full Text] - O'Keefe JH Jr, Rutherford BD, McConahay DR, Ligon RW, Johnson WL Jr, Georgi LV, Crockett JE, McCallister BD, Conn RD, Gura GM Jr, Good TH, Steinhaus DM, Bateman TM, Shimshak TM, Hartzler GO. Early and late results of coronary angioplasty without antecedent thrombolytic therapy for acute myocardial infarction. Am J Cardiol (1989) 64:12211230.[CrossRef][ISI][Medline]
- Waldecker B, Waas W, Haberbosch W, Voss R, Heizmann H, Tillmanns H. Long-term follow-up after direct perutaenous transluminal coronary angioplasty for acute myocardial infarction. J Am Coll Cardiol (1998) 32:13201325.
[Abstract/Free Full Text] - Krikorian RK, Vacke JL, Beauchamp GD. Timing, mode, and predictors of death after direct angioplasty for acute myocardial infarction. Cath Cardiovasc Diag (1995) 35:192196.[ISI][Medline]
- Moreno R, Garcia E, Soriano J, Acosta J, Abeytua M. Early coronary angioplasty for acute myocardial infarction: predictors of a poor outcome in a non-selected population. J Invas Cardiol (2001) 13:202210.[Medline]
- Grines CL, Cox DA, Stone GW, Garcia E, Mattos LA, Giambartolomei A, Brodie BR, Madonna O, Eijgelshoven M, Lansky AJ, O'Neill WW, Morice MC. Coronary angioplasty with or without stent implantation for acute myocardial infarction. N Engl J Med (1999) 341:19491956.
[Abstract/Free Full Text] - Sanz G, Castaner A, Betriu A, Magrina J, Roig E, Coll S, Pare JC, Navarro-Lopez F. Determinants of prognosis in survivors of myocardial infarction: a prospective clinical angiographic study. N Engl J Med (1982) 306:10651070.[Abstract]
- Simoons ML, Vos J, Tijssen JG, Vermeer F, Verheugt FW, Krauss XH, Cats VM. Long-term benefit of early thrombolytic therapy in patients with acute myocardial infarction: 5 year follow-up of a trial conducted by the Interuniversity Cardiology Institute of the Netherlands. J Am Coll Cardiol (1989) 14:16091615.[Abstract]
- Arnold AE, Simoons ML, Detry JM, von Essen R, Van de Werf F, Deckers JW, Lubsen J, Verstraete M. Prediction of mortality following hospital discharge after thrombolysis for acute myocardial infarction: is there a need for coronary angiography. Europ Heart J (1993) 14:306315.
[Abstract/Free Full Text] - Emmerich K, Ulbricht LJ, Probst H, Krakau I, Hoffmeister T, Lurken E, Thale J, Gulker H. Primary mechanical recanalization of occluded coronary arteries without prior thrombolytic therapy in patients with acute myocardial infarction. A single-center study reporting acute results and complications. Z Cardiol (1995) 84:523.
- Kahn JK, Rutherford BD, McConahay DR, Johnson WL, Giorgi LV, Shimshak TM, Ligon R, Hartzler GO. Results of primary angioplasty for acute myocardial infarction in patients with multivessel coronary artery disease. J Am Coll Cardiol (1990) 16:10891096.[Abstract]
- Goldstein JA, Demetriou D, Grines CL, Pica M, Shoukfeh M, O'Neill WW. Multiple complex coronary plaques in patients with acute myocardial infarction. N Engl J Med (2000) 343:915922.
[Abstract/Free Full Text] - Jaski BE, Cohen JD, Trausch J, Marsh DG, Bail GR, Overlie PA, Skowronski EW, Smith SC Jr. Outcome of urgent percutaneous transluminal coronary angioplasty in acute myocardial infarction: comparison of single-vessel versus multivessel coronary artery disease. Am Heart J (1992) 124:14271433.[CrossRef][ISI][Medline]
- Bedotto JB, Kahn JK, Rutherford BD, McConahay DR, Giorgi LV, Johnson WL, O'Keefe JH, Shimshak TM, Ligon RW, Hartzler GO. Failed direct coronary angioplasty for acute myocardial infarction: in-hospital outcome and predictors of death. J Am Coll Cardiol (1993) 22:690694.[Abstract]
- Costantini CO, Stone GW, Mehran R, Aymong E, Grines CL, Cox DA, Stuckey T, Turco M, Gersh BJ, Tcheng JE, Garcia E, Griffin JJ, Guagliumi G, Leon MB, Lansky AJ. Frequency, correlates, and clinical implications of myocardial perfusion after primary angioplasty and stenting, with and without glycoprotein IIb/IIIa inhibition, in acute myocardial infarction. J Am Coll Cardiol (2004) 44:305312.
[Abstract/Free Full Text] - McLaughlin MG, Stone GW, Aymong E, Gardner G, Mehran R, Lansky AJ, Grines CL, Tcheng JE, Cox DA, Stuckey T, Garcia E, Guagliumi G, Turco M, Josephson ME, Zimetbaum P. Prognostic utility of comparative methods for assessment of ST-segment resolution after primary angioplasty for acute myocardial infarction. J Am Coll Cardiol (2004) 44:12151223.
[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. Comparison of angioplasty with stenting, with or without abciximab, in acute myocardial infarction. N Engl J Med (2002) 346:957966.
[Abstract/Free Full Text] - Rentrop KP, Cohen M, Blanke H, Phillips RA. Changes in collateral channel filling immediately after controlled coronary artery occlusion by an angioplasty balloon in human subjects. J Am Coll Cardiol (1985) 5:587592.[Abstract]
- Morrow DA, Antman EM, Parsons L, de Lemos JA, Cannon CP, Giugliano RP, McCabe CH, Barron HV, Braunwald E. Application of the TIMI risk score for ST-elevation MI in the National Registry of Myocardial Infarction 3. JAMA (2001) 286:13561359.
[Abstract/Free Full Text] - Yamada DM, Topol EJ. Importance of microembolization and inflammation in atherosclerotic heart disease. Am Heart J (2000) 140:S90S102.[CrossRef][ISI][Medline]
- Landmesser U, Hornig B, Drexler H. Endothelial function: a critical determinant in atherosclerosis? Circulation (2004) 109(Suppl. 21 1):II27II33.[Medline]
- Willerson JT. Systemic and local inflammation in patients with unstable atherosclerotic plaques. Prog Cardiovasc Dis (2002) 44:469478.[CrossRef][ISI][Medline]
- Sintek CF, Pfeffer TA, Khonsari S. Surgical revascularization after acute myocardial infarction. Does timing make a difference? J Thor Cardiovasc Surg (1994) 107:13171321.
[Abstract/Free Full Text] - Webb JG, Lowe AM, Sanborn TA, White HD, Sleeper LA, Carere RG, Buller CE, Wong SC, Boland J, Dzavik V, Porway M, Pate G, Bergman G, Hochman JS. Percutaneous coronary intervention for cardiogenic shock in the SHOCK trial. J Am Coll Cardiol (2003) 42:13801386.
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