Restenosis After Delayed Coronary Angioplasty of the Culprit Vessel in Patients With a Recent Myocardial Infarction Treated by Thrombolysis
Background Clinical follow-up after percutaneous transluminal coronary angioplasty (PTCA) of an infarct-related lesion has demonstrated a low incidence of recurrent symptoms and repeated revascularization. In the absence of systematic angiographic follow-up, this low rate of clinical restenosis may reflect either a truly lower incidence of anatomic restenosis or the lack of recurrent symptoms in patients with extensive infarction in the territory of the restenotic vessel.
Methods and Results We studied 300 consecutive patients who, after a thrombolysis for myocardial infarction, underwent delayed (10.5±6 days after the myocardial infarction) PTCA of the infarct-related lesion. Procedural success was obtained in 253 patients (84%), and angiographic follow-up was performed in 205 of this group (81%) at a mean of 7.3±1.9 months. Restenosis (defined as the recurrence of >50% stenosis) was present in 105 patients (51%). Only 34 of the 105 patients (32%) with angiographic restenosis were symptomatic; the other 68% had clinically silent restenosis. Of these 105 patients, 27 (13% of the total population undergoing follow-up angiography) had reocclusion at the dilated site at follow-up. The severity of the stenosis at follow-up and the late loss in minimal lumen diameter followed a nearly Gaussian distribution if the lesions that were totally occluded at follow-up were excluded. By multivariate analysis, two independent predictors of reocclusion were identified: a small reference diameter (P<.0005) and the presence of collateral vessels before the procedure (P<.01). Only one factor was associated with restenosis in the 178 patients who did not have reocclusion at follow-up: a Thrombolysis in Myocardial Infarction grade ≤2 before the procedure (P<.0001). At follow-up, there was a significantly (P<.01) higher ejection fraction in patients without restenosis (56.1±13.4%) and in patients with restenosis without total occlusion (56.0±13.8%) than in patients with reocclusion (46.4±13.0%).
Conclusions Despite a satisfactory clinical outcome, delayed PTCA of an infarct-related lesion is associated with a high rate of angiographic recurrence. Two distinct mechanisms account for recurrent stenosis: progressive luminal renarrowing as documented after angioplasty of stable lesions and reocclusion of the infarct-related lesion. Only reocclusion is associated with a deterioration in left ventricular function at follow-up.
Percutaneous transluminal coronary angioplasty (PTCA) is a widely used technique for revascularization in patients after a thrombolysis for myocardial infarction.1 2 3 4 The experience of coronary angioplasty performed within the Thrombolysis in Myocardial Infarction (TIMI) II study has been recently described1 ; in the overall TIMI PTCA population, the cumulative incidence of repeated revascularization (20%)1 was lower than that reported for elective PTCA patients (32%).5 In the absence of systematic angiographic follow-up, this low rate of repeated revascularization may be related either to a truly lower incidence of anatomic restenosis or to the lack of recurrent symptoms in patients with extensive infarction in the territory of the restenotic vessel. The relatively low number of studies that addressed the problem of angiographic restenosis after PTCA performed for acute myocardial infarction have provided discordant results.6 7
No study has specifically examined with quantitative angiography the angiographic rate of restenosis when an angioplasty is performed in the infarct-related vessel after a thrombolysis for myocardial infarction. We studied the procedural outcome and the angiographic rate of restenosis, assessed by quantitative coronary angiography, in 300 consecutive patients who underwent such a procedure in our institution, where we recommend angiographic follow-up to all patients who undergo successful coronary angioplasty. We also examined whether changes in left ventricular function between PTCA and follow-up were influenced by the status of the dilated vessel at follow-up angiography.
From the records of our catheterization laboratory, we identified 300 consecutive patients, 264 men and 36 women with a mean (±SD) age of 57 (±10) years, who, between January 1989 and December 1991, underwent delayed PTCA at the infarct-related lesion after a thrombolysis for myocardial infarction (Table 1⇓). The infarct-related artery was determined from the entry ECG, ventriculographic contraction abnormalities, and coronary angiographic findings. During the time period of this study, the strategy for patients undergoing coronary angiography after a thrombolysis for myocardial infarction in our institution was to perform immediate angioplasty of the infarct-related vessel, provided that the diameter stenosis was >50% and that the overall anatomy of the coronary vessels did not preclude angioplasty, eg, left main disease and lesions judged nonamenable for angioplasty at the discretion of the operator. Patients having PTCA within 3 days of the myocardial infarction or having multilesion PTCA were excluded.
Angioplasty was performed according to the standard technique in our laboratory as previously described.8 All patients received aspirin (300 mg/d); a bolus dose of heparin (10 000 IU) was administered just before PTCA. The procedure was considered successful when the residual luminal narrowing in the dilated segment immediately after angioplasty was <50% and when no major complication (ECG or enzymatic evidence of myocardial infarction, the need for bypass surgery during hospitalization, or in-hospital death) occurred. Angiography was performed in at least two projections, after the intracoronary injection of isosorbide dinitrate (2 mg) and just before and immediately after angioplasty. These projections were recorded in our database, and the follow-up angiogram was performed after the intracoronary injection of isosorbide dinitrate in the same projections.
We routinely attempt to obtain a follow-up angiogram 6 months after successful angioplasty, regardless of symptomatic status; angiography is performed earlier if there is a clinical indication. Restenosis was defined by quantitative coronary angiography as the recurrence of ≥50% luminal narrowing in a segment that had previously been dilated to <50%. Clinical data were recorded for all patients at the time of hospitalization for angiographic follow-up; the clinical status of the patients who did not undergo the scheduled hospitalization was obtained by contact with the referring cardiologist.
Qualitative Angiographic Analyses
Two experienced interventional cardiologists performed the qualitative analyses independently. Disagreements were resolved by a further joint reading. Lesions were classified as concentric (symmetric narrowing with an identical or almost identical appearance in orthogonal projections) or eccentric (asymmetric narrowing with the stenotic lumen appearing to lie within the outer half of the “normal” lumen of the vessel in at least one projection). The presence of calcification or thrombus (a discrete intraluminal filling defect) was also noted. The anterograde blood flow before angioplasty was graded with the TIMI Study Group classification.9 The collateral circulation was graded with the classification proposed by Sabia et al.10
Quantitative Coronary Angiography
Quantitative computer-assisted angiographic measurements of the dilated lesion were performed on angiograms obtained just before angioplasty, immediately after angioplasty, and at a 6-month follow-up. Measurements were performed on end-diastolic frames with the caesar (Computer Assisted Evaluation of Stenosis And Restenosis) System. A detailed description of this system and the inter- and intraobserver variations of measurements obtained under routine clinical conditions were reported previously.11
Quantitative Evaluation of Global Left Ventricular Function
Ventricular function was evaluated on single-plane left ventricular angiograms obtained before angioplasty and at follow-up. The ventriculogram was performed in a 30° right anterior oblique projection. The left ventricular contours on end-systolic and end-diastolic frames were traced manually by a single observer who was unaware of the design of the study protocol. The tracings were then digitized with a writing tablet and light pen into a PC 486/25 SX microcomputer. The left ventricular end-diastolic volume index (LVEDVI, mL/m2) and the ejection fraction (EF, %) were calculated according to the area-length method.12
Data are presented as mean±SD. Comparisons between groups for continuous data were made with an unpaired Student’s t test or ANOVA followed by the Student-Newman-Keuls test. Differences between proportions were assessed by χ2 analysis. Linear regression was used to analyze the relation between continuous variables. Multivariate correlates of reocclusion and restenosis were determined by stepwise logistic regression (sas Software). A value of P<.05 was considered to indicate statistical significance.
Table 1⇑ lists the baseline characteristics of the study population. Most of the patients were men with a mean age (±SD) of 57±10 years. The majority had single-vessel disease with a mean left ventricular EF of 52.6±12.3%. The dilated lesion was located with almost equal frequency in the left anterior descending artery (42%) and the right coronary artery (43%) and less often in the left circumflex artery (14%). Twenty-two percent of the lesions had TIMI grade ≤2 flow before angioplasty; angiographically visible collateral vessels were observed in 21% of cases.
Procedural success was obtained in 253 patients (Table 2⇓). There were 11 major in-hospital complications: 5 patients had recurrent myocardial infarction, 3 had emergent coronary bypass surgery, and 3 died during hospitalization. Uncomplicated failure (residual stenosis ≥50% by quantitative coronary angiography) occurred in 36 patients. More detailed analysis of these 36 patients with uncomplicated failure revealed that 12 (33%) had total occlusion before angioplasty and that 16 (44%) had a residual stenosis after angioplasty of <60% by quantitative coronary angiography.
All patients who had successful procedures were asked to return for angiographic follow-up at 6 months; 205 (81%) actually underwent angiography at a mean of 7.3±1.9 months after angioplasty. Clinical follow-up data were obtained for 47 of the 48 remaining patients; one patient was lost to follow-up. Table 3⇓ shows that except for a significantly higher proportion of patients dilated at a right coronary artery lesion in the 48 patients without angiographic follow-up, there were no differences in major baseline characteristics between the two groups of patients.
Of the 252 patients, 7 (2.8%) died during the follow-up period, 3 (1.2%) had bypass surgery, and 3 (1.2%) had recurrent myocardial infarction. At 6 months, 188 (74.6%) were asymptomatic or had atypical chest pain, 51 (20.2%) had stable angina, and 6 (2.4%) had unstable angina.
Table 4⇓ summarizes the quantitative angiographic data of the 205 patients with angiographic follow-up. The angioplasty procedure was associated with an immediate increase in mean minimal lumen diameter from 0.82±0.43 to 1.98±0.43 mm. Mean percent diameter stenosis decreased from 72±13% to 32±10%. At follow-up angiography, the mean minimal lumen diameter had decreased to 1.34±0.77 mm, and mean percent stenosis had increased to 55±25%. Restenosis, defined as the presence of ≥50% stenosis in the dilated segment at follow-up, was present in 105 (51%; 95% CI; range, 44% to 58%) of the 205 patients who underwent angiographic follow-up. Of these 105 patients, 27 (13% of the total population undergoing follow-up angiography; 95% CI; range, 8% to 18%) had total occlusion at the dilated site at follow-up.
Fig 1⇓ shows the distribution of the severity of the stenotic lesions at follow-up. If the lesions that were totally occluded at follow-up are excluded, both minimal lumen diameter and percent stenosis follow a nearly Gaussian distribution. When the distribution of the late loss in minimal lumen diameter from immediately after angioplasty to follow-up was analyzed (Fig 2⇓), a similar pattern was observed.
We also analyzed the relation between clinical status at 6 months and the occurrence of restenosis in the 205 patients who underwent angiographic follow-up (Table 5⇓). The majority of patients undergoing follow-up angiography were asymptomatic (148, 72%); 57 (28%) were symptomatic (48 had stable angina, 6 had unstable angina, and 3 had suffered recurrent myocardial infarction before the follow-up angiogram). The percentage of patients with ≥50% diameter stenosis at follow-up was 48% in asymptomatic patients and 60% in symptomatic patients (P=NS). The percentage of patients with total occlusion at follow-up was also similar in asymptomatic and symptomatic patients. Only 34 (32%) of the 105 patients with angiographic restenosis were symptomatic; the other 68% had clinically silent restenosis.
Predictors of Reocclusion and Restenosis
We analyzed predictors of reocclusion and of restenosis in the 205 patients with angiographic follow-up.
Table 6⇓ shows the univariate predictors of reocclusion. The severity of the stenosis before PTCA (percent stenosis and minimal lumen diameter), the minimal lumen diameter after PTCA, the presence of angiographically visible collateral vessels before PTCA, a TIMI grade of ≤2 before angioplasty, and a smaller reference diameter were all associated with a greater risk of reocclusion by univariate analysis. By multivariate analysis, two independent predictors of reocclusion were identified: a small reference diameter (P<.005) and the presence of collateral vessels before the procedure (P<.01).
Table 7⇓ lists the univariate predictors of restenosis in the 178 patients without reocclusion at follow-up. Percent stenosis before PTCA, the presence of collateral vessels before PTCA, and a TIMI grade of ≤2 before PTCA were associated with a greater risk of restenosis by univariate analysis. By multivariate analysis, only one factor was associated with restenosis in patients without total occlusion at follow-up: a TIMI grade of ≤2 (P<.0001).
Table 8⇓ shows the occurrence of restenosis and reocclusion as a function of the TIMI grade before PTCA. Lesions that had TIMI grade 2 flow before angioplasty had a higher risk of reocclusion and restenosis compared with lesions that had TIMI grade 3 flow before angioplasty. Although the number of patients in the groups with TIMI grades of 0 and 1 was too small to draw definite conclusions, restenosis and reocclusion rates were similar among the groups with TIMI grades of 0, 1, and 2.
Changes in Left Ventricular Function
Among the 205 patients with angiographic follow-up, 197 (96%) had paired ventriculograms (before PTCA and at follow-up) that were suitable for determination of left ventricular function (Table 9⇓). In the group as a whole, there was a small but statistically significant (P<.01) increase in EF from 52.7±12.1% before PTCA to 54.7±13.8% at follow-up. The LVEDVI at follow-up (86.2±22.3 mL/m2) was similar to the LVEDVI before PTCA (86.6±21.9 mL/m2, P=NS). If patients were classified into subgroups based on the angiographic findings at the dilated site at follow-up (no restenosis, restenosis without reocclusion, reocclusion), there were no significant differences in EF or LVEDVI among subgroups before PTCA. During the follow-up period, however, there was an increase in EF in both the subgroup that had not developed restenosis (+2.5±10.4 absolute percent) and the subgroup with a restenosed but nonoccluded vessel (+3.4±10.3 absolute percent). In contrast, in the subgroup that had reocclusion of the dilated vessel at follow-up, there was a decrease in EF (−3.3±10.4 absolute percent). These changes resulted in a significantly (P<.01) higher EF in both the no-restenosis group (56.1± 13.4%) and the restenosis-without-reocclusion group (56.0±13.8%) compared with the reocclusion group (46.4±13.0%). The LVEDVI at follow-up was similar in all groups.
We further assessed a possible relation between the severity of the stenosis at follow-up and the changes in EF from angioplasty to follow-up in the 170 patients who had a nonoccluded vessel at follow-up regardless of whether restenosis had occurred (Fig 3⇓). There was no relation between percent stenosis severity or absolute minimal lumen diameter at follow-up assessed by quantitative angiography and the change in EF between angioplasty and follow-up.
The overall results of the PTCA procedure were favorable, with 84% procedural success (ie, residual stenosis <50% by quantitative coronary angiography without in-hospital complication). With a different definition (normal or improved TIMI flow grade with both improvement of the residual stenosis by >20% and a residual stenosis <60%), the angiographic success for the 1414 patients of the TIMI II study who underwent PTCA of the infarct-related vessel within 42 days of a thrombolysis for myocardial infarction was 80.5%.1 The 1% rate of emergent bypass surgery, the 1.7% rate of myocardial infarction, and the 1% mortality rate in the present study are also concordant with those in prior studies.1 This may be explained in part by the timing of the procedure (10.5±6 days after the myocardial infarction) because it has been demonstrated that patients undergoing delayed PTCA in the TIMI II study had a higher rate of procedural success and a lower risk of acute complication than patients undergoing immediate PTCA.1
Reocclusion and Restenosis Rates
Although a large number of reports have analyzed restenosis rates after elective coronary angioplasty, only a few studies have specifically examined restenosis after PTCA for acute myocardial infarction, and those provided discordant results. Honan et al7 reported the angiographic follow-up of 144 patients from a total population of 289 who had successful PTCA within 24 hours of acute myocardial infarction. With restenosis determined visually by use of a grading scale, 40% of patients had ≥75% stenosis at follow-up. Conversely, Simonton et al6 reported on the angiographic follow-up of 79 patients from a total population of 91 who had successful PTCA after acute myocardial infarction. Only 19% of these patients had restenosis defined visually by the recurrence of a >50% stenosis at follow-up. Differences in patient selection, rates of angiographic follow-up, and techniques used to assess the follow-up angiogram may account for this disparity between studies. In our institution, we recommend angiographic follow-up to all patients who have successfully undergone PTCA. The rate of follow-up angiography (81%) in the consecutive patient population reported here is similar to our overall angiographic follow-up for elective PTCA.8 13 Independent observers analyzed the follow-up angiograms with quantitative coronary angiography. Thus, the results reflect, with reasonable accuracy, the angiographic probability of restenosis in our patient population.
We observed a rate of restenosis (defined as the recurrence of a ≥50% stenosis at follow-up) of 51%. This rate is relatively high compared with the 39% to 43% of restenosis encountered during the same time period in our institution after elective PTCA.8 13 14 This rate is also higher than the 28% to 40% of restenosis in recent large clinical trials that examined the effect of various treatments on restenosis15 16 and higher than the rate of restenosis after balloon angioplasty in another recent study that compared restenosis rates after balloon angioplasty with those after atherectomy using the same angiographic definition of restenosis as the present study.17 This rate, however, is similar to that observed after balloon angioplasty in the CAVEAT study18 ; this may be explained by the high prevalence of patients with unstable angina in the CAVEAT population. The overall loss in minimal lumen diameter from after angioplasty to follow-up (late loss) in the present study was 0.64 mm; this value is higher than the 0.27 to 0.50 mm reported in different studies in which most of the patients underwent elective PTCA.15 17 19
Overall, these results suggest that infarct-related lesions have a greater tendency to recur after successful PTCA. However, more detailed analysis of our results suggests that two distinct mechanisms contribute to lesion recurrence after successful PTCA of infarct-related lesions. As Table 4⇑ and Fig 1⇑ show, a relatively high proportion of the patients with restenosis had total occlusion of the dilated vessel at follow-up. Rensing et al19 suggested that in a population undergoing elective coronary angioplasty, although the overall restenotic process followed a nearly Gaussian distribution, the progression toward total occlusion at follow-up may be, at least in part, due to a mechanism other than progressive luminal renarrowing, which appears to be responsible for restenosis without total occlusion. The low number of patients with total occlusion at follow-up in the study of Rensing et al (70 of 1445, 4.8%) compared with the 13% reported in the present study may reflect the different clinical characteristics of the study population and suggests that infarct-related lesions may have a greater propensity to occlusion after angioplasty. In the present study, 27 of 105 patients (26%) with ≥50% stenosis at follow-up had a total occlusion. As Figs 1⇑ and 2⇑ show, the severity of the stenosis at follow-up and the late loss in minimal lumen diameter follow a nearly Gaussian distribution only if the lesions that had progressed toward total occlusion are excluded. Our results therefore suggest that two different and important mechanisms might be involved in lesion recurrence after PTCA of infarct-related lesions: progressive luminal renarrowing, as documented after angioplasty of stable lesions, and reocclusion. It is not clear if reocclusion is related to thrombosis that occurs as a final step after progressive renarrowing has produced a severe stenosis or if silent thrombotic occlusion occurs early after successful angioplasty; however, the high incidence of total occlusion in this series compared with elective angioplasty supports the second hypothesis. Some insights into the natural history of the infarct-related lesion during the months after a thrombolysis for infarction have been provided by the results of the APRICOT study20 ; in this study, 300 patients with a patent coronary artery within 48 hours of a thrombolysis for infarction were randomized to either warfarin, aspirin, or placebo and had angiographic follow-up 3 months after the procedure. The 29% overall rate of reocclusion was not significantly different among the three groups. This very high rate of spontaneous reocclusion in the months after infarction is consistent with the existence of another mechanism of restenosis (ie, thrombosis and occlusion) after angioplasty of infarct-related lesions distinct from the progressive renarrowing that follows coronary angioplasty of stable lesions.
Predictors of Reocclusion and Restenosis
Because of the suspicion that two distinct mechanisms accounted for lumen renarrowing after PTCA of the infarct-related vessel, we performed a two-step analysis to determine first the predictors of reocclusion and second the predictors of restenosis in the patients who had restenosis without occlusion. The severity of the pre-PTCA stenosis, the presence of angiographically visible collateral vessels before the procedure, a low TIMI grade before PTCA, and a small reference diameter were associated with an increased risk of reocclusion by univariate analysis. On multivariate analysis, a small reference diameter and the presence of collateral vessels were found to be independent predictors of reocclusion.
When analyzing the determinants of restenosis in patients without total occlusion at follow-up, we found that a TIMI grade flow of ≤2 before angioplasty was the only independent predictor. It had already been suggested that the rate of restenosis after angioplasty of total occlusions was higher than that of nonoccluded vessels21 ; our data extend this observation to the patient population undergoing delayed angioplasty of an infarct-related vessel after a thrombolysis for infarction and demonstrate that this high rate of restenosis is related not only to an increase in the rate of reocclusion at follow-up but also to an increase in the rate of restenosis without total occlusion. Our data also demonstrate that the rate of reocclusion and restenosis of TIMI grade 2 lesions is comparable to that of TIMI grade 0 and 1 lesions and clearly different from that of TIMI grade 3 lesions (Table 8⇑). Finally, the reference diameter of the vessel appears unrelated to the occurrence of restenosis when patients with reocclusion are excluded. Because this factor was the strongest predictor of reocclusion, this observation provides further evidence for the existence of two different mechanisms to explain luminal narrowing after PTCA of infarct-related vessels.
Changes in Left Ventricular Function
Several studies have investigated whether delayed PTCA has a beneficial impact on recovery in left ventricular function after a myocardial infarction and have provided discordant results.22 23 In the present study, we found a statistically significant improvement in left ventricular EF as a whole from 52.7% before PTCA to 54.7% at follow-up. The nonrandomized nature of our study does not allow us to attribute this improvement to the performance of PTCA; furthermore, the clinical significance of the relatively small benefit observed cannot be determined.
We observed an improvement in EF in patients with or without angiographic restenosis, providing that the dilated vessel was still patent at follow-up; in contrast, in the subgroup of patients with a total occlusion of the dilated vessel at follow-up, there was a decrease in EF. These results are in agreement with the APRICOT study,20 which showed that in patients with a patent coronary artery 48 hours after a thrombolysis for myocardial infarction and randomized to different antithrombotic regimens, there was a significant increase in EF in patients with persistent patency at 3 months but no recovery in patients with reocclusion. These results emphasize the importance of a patent infarct-related vessel 3 to 6 months after the infarction regardless of the chosen therapeutic option.
In a series of 67 patients treated by emergency primary angioplasty for acute myocardial infarction, Rothbaum et al24 reported that restenosis in the absence of reocclusion did not have an adverse effect on the recovery of global left ventricular function. Conversely, Linderer et al25 studied 145 consecutive patients who had successful PTCA of the infarct-related vessel 5±6 months after infarction and found that only patients without restenosis had an improvement in left ventricular function at angiographic follow-up. Differences in patient selection and in time from infarction to PTCA may account for these discrepancies. In the current study, the subgroup of 170 patients who had a patent vessel at follow-up had a significant improvement in EF that was independent of the degree of stenosis at the PTCA site at follow-up (Fig 3⇑).
We found no relation between vessel patency and LVEDVI at follow-up. In a recent study,26 the patency of the infarct-related vessel after a thrombolysis for myocardial infarction was shown to influence left ventricular remodeling; patients with a total occlusion of the infarct-related vessel had a significantly higher LVEDVI at follow-up than patients with a patent vessel. Among the multiple factors that may explain the lack of left ventricular dilation in the 27 patients with reocclusion in the current study are the late timing of reocclusion (between 10 days and 6 months after the infarction), the well-preserved EF at baseline (50%), and the relatively low number of patients (n=14) with an anterior myocardial infarction.
This was a retrospective single-center study; thus, the technique of PTCA and medical management at our institution might have influenced the results. However, the patients were a consecutive group that underwent the angioplasty procedure in an institution where the probability that a patient undergoes follow-up angiography is less dependent on the symptomatic status after angioplasty. The high rate of angiographic follow-up, coupled with the use of quantitative coronary angiography to assess the angiographic outcome, allowed an objective assessment of the angiographic probability of restenosis. In addition, our study included only patients who underwent delayed angioplasty of an infarct-related lesion (≥3 days); it has been reported that emergency coronary angioplasty may represent an interesting alternative to intravenous thrombolysis in patients with acute infarction27 ; reocclusion and restenosis rates after PTCA in this acute setting and without thrombolysis may not necessarily be similar to those observed after a delayed procedure. However, a recent report of the Primary Angioplasty Registry28 demonstrates that there is also a high incidence of reocclusion and restenosis when emergency PTCA is performed without prior thrombolytic therapy.
This study demonstrates that despite a satisfactory clinical outcome, coronary angioplasty of infarct-related lesions is associated with a high incidence of angiographic recurrence that is often silent. Of the patients with a successful angioplasty in this study, 13% had total occlusion of the dilated lesion at follow-up; this rate, which appears extremely high compared with the angiographic outcome of patients undergoing angioplasty of stable lesions, does compare favorably with the very high spontaneous rate of reocclusion of the infarct-related lesion observed in the months after infarction.20 However, the negative impact of reocclusion on left ventricular function at follow-up emphasizes the need for new strategies designed to prevent reocclusion in this setting; whether these strategies should be pharmacological (antithrombotic agents) or mechanical (coronary stenting) remains to be determined.
- Received June 2, 1994.
- Revision received September 14, 1994.
- Accepted October 2, 1994.
- Copyright © 1995 by American Heart Association
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