- Email: [email protected]
Angiographic findings in patients undergoing catheterization for recurrent symptoms within 30 days of successful coronary intervention
Angiographic Findings in Patients Undergoing Catheterization for Recurrent Symptoms Within 30 Days of Successful Coronary Intervention John A. McPherson, MD, Peter S. Robinson, MD, Eric R. Powers, MD, Ian J. Sarembock, MD, Lawrence W. Gimple, MD, and Michael Ragosta, e studied a consecutive group of patients who, after initial hospital discharge, underwent reW peat coronary angiography for chest pain syndromes within 30 days of successful percutaneous coronary intervention (PCI). We hypothesized that the use of coronary stents, which inhibit elastic recoil and arterial remodeling,1 would be associated with a lower incidence of early restenosis in these patients. In addition, we hypothesized that angiographic variables at the time of the index PCI, such as complex lesion morphology, lesion length, and minimum luminal diameter (MLD) after the procedure, would be associated with early restenosis. •••
Between January 1995 and October 1997, 3,309 consecutive patients underwent successful PCI at our institution. We identified 158 patients (4.8%) who underwent repeat coronary angiography within 30 days of the initial PCI. Patients with abrupt vessel closure immediately after percutaneous transluminal coronary angioplasty (PTCA) (n ⫽ 21), subacute stent thrombosis (n ⫽ 9), and chest pain before hospital discharge (n ⫽ 20) were excluded from analysis. Consequently, the study cohort consisted of 108 patients (3.3%) who underwent repeat coronary angiography between 2 and 30 days of the initial PCI. The decision to perform coronary angiography was entirely at the discretion of the patient’s physician and was based on the clinical suspicion of recurrent myocardial ischemia, usually manifested by chest discomfort. Clinical variables were recorded and included age, sex, presence of diabetes, electrocardiographic findings, and nature of clinical syndrome leading to intervention and repeat angiography. Electrocardiographic changes considered suggestive of ischemia included development of new Q waves, new ST-segment deviation ⱖ0.5 mm, or new T-wave changes. Based on a blinded review of the medical record, the patient’s symptoms were classified as suggestive of myocardial ischemia if the symptoms documented were similar in nature to those leading to the index PCI. All angiograms were analyzed by experienced angiographers blinded to the clinical information. Qualitative angiographic variables at the initial PCI included: number of vessels with ⬎50% narrowing, From the Cardiovascular Division, Department of Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia. Dr. Ragosta’s addrress is: Cardiovascular Division, University of Virginia Health Systems, HSC Box 158, Charlottesville, Virginia 22908. Email: [email protected]. Manuscript received February 23, 1999; revised manuscript received and accepted April 22, 1999. ©1999 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 84 September 1, 1999
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index lesion complexity defined by the American College of Cardiology/American Heart Association classification (type A, B1, B2, or C),2 lesion eccentricity, ulceration, lesion calcium, visible thrombus, the presence of dissection or thrombus after the procedure, and use of coronary stents. The pre-PCI, post-PCI, and repeat angiograms were analyzed using a computerassisted quantitative angiographic analysis system (CARS, Sony Medical Systems, Montvale, New Jersey). Quantitative analysis included determination of lesion length, reference vessel diameter, and MLD before and after the procedure. Acute gain after intervention (increase in MLD from pre- to post-PCI), percent stenosis before and after the procedure (ratio of MLD to reference vessel diameter), and ⌬MLD (the difference between MLD after the procedure and MLD at repeat angiography) were calculated. Based on quantitative analysis of the repeat angiograms, the patients were classified into 1 of 2 groups: (1) early restenosis, defined as the presence of ⬎50% luminal narrowing at the site of the index procedure; or (2) no restenosis, defined as the absence of ⬎50% luminal narrowing at the site of the index procedure. Within the no-restenosis group, patients with ⱖ50% luminal narrowing in an artery not treated at the index procedure were also identified. Data were analyzed with RS/1 software (Bolt, Beranek, and Newman, Cambridge, Massachusetts) with a minicomputer (VAX4000-system 90, Digital Equipment Corp., Houston, Texas). All normally distributed data were expressed as mean ⫾ 1 SD; data not normally distributed were expressed as median (25th, 75th percentile). Comparisons between groups were performed, and group differences of continuous factors were compared using Wilcoxon signed-rank tests. Group differences of categorical variables were compared using chi-square tests or, in the cases of small cell sizes, Fisher’s exact test. Stepwise logistic regression techniques were used to determine multivariate predictors of early restenosis. All p values are from 2-sided tests. •••
Of the 3,309 consecutive patients who underwent successful PCI during the specified time period, 2,253 (68%) were treated with PTCA alone and 1,056 (32%) received coronary stents. Among the 108 patients who returned for early repeat angiography, 81 (75%) had undergone PTCA and 27 (25%) had received coronary stents. Thus, a similar proportion of patients after PTCA underwent early repeat coronary angiography compared with patients who received stents (3.6% of all PTCA patients vs 2.7% of all stented patients, p ⫽ 0002-9149/99/$–see front matter PII S0002-9149(99)00384-7
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TABLE II Clinical Variables in Patients With and Without Early Restenosis
TABLE I Clinical Characteristics of 108 Patients Who Underwent Repeat Angiography Within 30 Days of Successful Coronary Intervention Characteristic Age (yrs) Men Diabetes mellitus Syndrome at index procedure Acute myocardial infarction Recent myocardial infarction* Unstable angina Stable angina Positive stress test Time to angiography (d) Typical symptoms† Electrocardiographic changes‡
Patients 58 ⫾ 12 64 27 15 14 65 5 1 14 ⫾ 9 73 44
*Defined as myocardial infarction within 7 days of index intervention. † Symptoms leading to repeat angiography considered typical of myocardial ischemia. ‡ Electrocardiographic changes at the time of repeat angiography considered suggestive of ischemia. Data are expressed as mean ⫾ SD or percentages.
Age (yrs) Men Diabetes mellitus Time to angiography (d) Suggestive symptoms† Electrocardiographic changes‡
Restenosis (n ⫽ 28)
No Restenosis (n ⫽ 80)
58 ⫾ 13 60 43 11 ⫾ 8 80 50
58 ⫾ 12 58 21* 15 ⫾ 9 70 41
*p ⫽ 0.05 (p ⱕ0.05 was considered significant in univariate analysis). † Symptoms leading to repeat angiography considered suggestive of myocardial ischemia. ‡ Electrocardiographic changes at the time of repeat angiography considered suggestive of ischemia. Data are expressed as mean ⫾ SD or percentages.
TABLE III Angiographic Data from Index Intervention in Patients With and Without Early Restenosis Restenosis (n ⫽ 28) Lesion length (mm) Reference diameter (mm) MLD pre-PCI (mm) Pre-PCI stenosis Visible thrombus Visible calcium Eccentric lesion Ulcerated lesion ACC/AHA type B1, B2, or C Acute gain (mm) MLD post-PCI (mm) Post-PCI stenosis Dissection after PCI
⫾5 ⫾ 0.46 ⫾ 0.30 ⫾ 10 23 7 67 7 87 1.64 ⫾ 0.49 2.08 ⫾ 0.44 28 ⫾ 11 23
10 2.84 0.45 84
No Restenosis (n ⫽ 80) ⫾4 ⫾ 0.52 ⫾ 0.38 ⫾ 12 23 4 50 19 73 1.78 ⫾ 0.59 2.39 ⫾ 0.54* 21 ⫾ 11 9
9 2.91 0.57 82
*p ⫽ 0.009 (p ⱕ0.05 was considered significant in univariate analysis). Data are expressed as mean ⫾ SD or percentages. ACC/AHA ⫽ American College of Cardiology/American Heart Association.
FIGURE 1. Bar graph demonstrating proportions of patients with (black) and without (white and hatched) early restenosis at repeat angiography. Patients without early restenosis are divided into those with no significant lesions (hatched) and those with previously untreated coronary stenoses remote from the index lesion (white). “Stent” and “PTCA Alone” ⴝ type of index intervention.
NS). Clinical characteristics of the 108 patients are listed in Table I. All patients received standard anticoagulation with heparin at the index PCI, and 7 patients in the cohort received abciximab. Of the 108 patients studied, 28 (26%) were found to have early restenosis at the treated site (Figure 1). Of the 80 patients without restenosis, 26 (33%) were found to have ⱖ1 significant coronary stenosis at previously untreated sites. None of the 27 patients initially treated with coronary stents were found to have early restenosis compared with 28 of the 81 patients (35%) who underwent PTCA alone (p ⬍0.0001). Table II summarizes the clinical findings at repeat angiography in patients with and without early restenosis. Chest discomfort and electrocardiographic find590 THE AMERICAN JOURNAL OF CARDIOLOGY姞
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ings were not helpful in identifying patients with and without early restenosis. Patients without early restenosis but with stenoses in other vessels did not differ in their clinical presentation at repeat angiography when compared with those with no significant stenoses. Symptoms and electrocardiographic changes suggestive of recurrent ischemia were present in 19 (73%) and 12 (46%), respectively, of the 26 patients with significant stenoses in other vessels compared with 37 (68%) and 21 (39%), respectively, of the 54 patients without any significant coronary stenoses. Diabetic patients had a significantly higher incidence of early restenosis at repeat angiography than nondiabetics (40% vs 21%, p ⫽ 0.05). No other clinical variable, including patient age, gender, index vessel, time to repeat angiography, presence of typical chest pain, or presence of electrocardiographic changes was significantly different between patients with and without early restenosis. The clinical syndrome at the time of index PCI (stable angina, unstable angina, and acute myocardial infarction) was not associated with early restenosis at repeat angiography. SEPTEMBER 1, 1999
TABLE IV Quantitative Angiographic Data in the 81 Patients Who Underwent Balloon Angioplasty Without Stenting at Index Intervention Total (n ⫽ 81) Reference diameter (mm) MLD pre-PTCA (mm) Pre-PTCA stenosis (%) MLD post-PTCA (mm) Post-PTCA stenosis (%) Acute gain (mm) MLD at RA (mm) ⌬MLD (mm)
Restenosis (n ⫽ 28)
No Restenosis (n ⫽ 53)
2.80 ⫾ 0.45 2.85 ⫾ 0.46 2.78 ⫾ 0.45 0.47 ⫾ 0.34 0.44 ⫾ 0.29 0.49 ⫾ 0.37 84 ⫾ 11
84 ⫾ 9
83 ⫾ 12
2.04 ⫾ 0.45 2.05 ⫾ 0.41 2.04 ⫾ 0.46 27 ⫾ 11
28 ⫾ 11
26 ⫾ 11
1.57 ⫾ 48 1.61 ⫾ 49 1.55 ⫾ 57 1.58 ⫾ 0.70 0.89 ⫾ 0.55 2.00 ⫾ 0.39* 0.46 ⫾ 0.38 1.16 ⫾ 0.44 0.04 ⫾ 0.11*
*p ⬍0.0001 when compared to patients with restenosis. Data are expressed as mean ⫾ SD or percentages. RA ⫽ repeat angiography.
Table III summarizes the angiographic data for the cohort. Patients with early restenosis had no differences in lesion length, reference vessel diameter, preprocedure MLD, preprocedure percent stenosis, or acute gain when compared with those without early restenosis. Lesion characteristics, such as the presence of eccentricity, ulceration, thrombus, calcium, and coronary dissection after intervention, were also similar among those with and without early restenosis. Patients with early restenosis at repeat angiography had a significantly smaller postprocedure MLD and significantly larger percent stenosis after the procedure when compared with those without early restenosis. However, in the multivariate analysis, these variables were not found to be independent predictors of early restenosis. Instead, they were associated with the use of coronary stents at index PCI: patients who underwent PTCA alone had a significantly smaller postprocedure MLD (2.04 ⫾ 0.45 mm vs 2.80 ⫾ 0.46 mm, p ⬍0.0001) and larger percent stenosis after the procedure (27 ⫾ 11% vs 14 ⫾ 7%, p ⬍0.0001) than those treated with stents. Quantitative angiographic data for the 81 patients who underwent PTCA alone is summarized in Table IV. Reference vessel diameter, preprocedure MLD, preprocedure percent stenosis, postprocedure MLD, percent stenosis after the procedure, and acute gain were not different in those with and without early restenosis. In the 53 patients without early restenosis, the ⌬MLD (defined as the difference between postprocedure MLD and the MLD at repeat angiography) was negligible, whereas the ⌬MLD in patients with early restenosis was significant. There was no significant difference in early restenosis in patients with complex versus simple index lesions (25 of 80 [31%] vs 3 of 28 [11%]). However, in the 81 patients who underwent PTCA without stenting, type B or C index lesions were associated with a significantly higher rate of early restenosis than type A lesions (25 of 60 [42%] vs 3 of 21 [14%]; p ⫽ 0.03).
When the significant univariate predictors of restenosis were entered into a stepwise logistic regression, the only significant multivariate predictor of early restenosis was the absence of coronary stenting at the index PCI (p ⫽ 0.006). •••
In the present study, 28 of the 108 patients (26%) referred for repeat angiography within 1 month of successful PCI were found to have early restenosis. PTCA without stenting was the only independent predictor of early restenosis. None of the 27 patients treated with stents were found to have early restenosis despite the presence of clinically suspected myocardial ischemia. All 9 patients excluded from the study due to subacute stent thrombosis presented unequivocally with symptoms of acute myocardial infarction and ST-segment elevation. Although the absence of ST-segment elevation does not definitively exclude subacute stent thrombosis, the low likelihood of early in-stent restenosis or vessel closure suggests that angiography may not be the best initial diagnostic strategy for evaluating recurrent symptoms early after coronary stenting. In over 1,000 consecutive patients who underwent successful coronary stent implantation at our institution, the rate of subacute thrombosis was 1.0%, consistent with previous findings.3 The absence of early in-stent restenosis found in our study is likely explained by the reduction in elastic recoil4 and perhaps reduced early pathologic arterial remodeling.5 This finding is not unexpected since the primary cause of in-stent restenosis is neointimal proliferation, which is a complex process that typically occurs several months after intervention.6 Approximately 3% of patients at our institution were referred for coronary angiography within 30 days of successful PCI, consistent with findings at other institutions.7 However, a limitation of our study is that patients who might have undergone early angiography may have died or had myocardial infarction before being studied. Compared with patients who underwent PTCA, a similar proportion of patients who received stents were referred for repeat angiography. Given the lack of early in-stent restenosis, it is unclear why these patients had a similar incidence of recurrent symptoms. A recent study found that chest pain in the first 24 hours after stenting is common, possibly due to “stretch pain” from overdilation of the treated artery.8 We can speculate that some patients may have prolonged discomfort from arterial stretch or have a higher incidence of noncardiac symptoms due to the use of drugs such as ticlopidine, which may cause gastric irritation.
A significant number of patients with early recurrent chest pain referred for angiography within 30 days of balloon angioplasty were found to have early restenosis. In contrast, excluding patients with stent thrombosis, there were no cases of early in-stent restenosis. PTCA without stenting was the BRIEF REPORTS
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only independent predictor of early restenosis in patients with recurrent chest pain early after PCI. These findings suggest that repeat angiography for the evaluation of early recurrent symptoms after successful coronary stenting has a low diagnostic yield. 1. Painter JA, Mintz GS, Wong SC, Popma JJ, Pichard AD, Kent KM, Satler LF,
Leon MB. Serial intravascular ultrasound studies fail to show evidence of chronic Palmaz-Schatz stent recoil. Am J Cardiol 1995;75:398 – 400. 2. Ellis SG, Vandormael MG, Cowley MJ, DiSciascio G, Deligonul U, Topol EJ, Bulle TM. Coronary morphologic and clinical determinants of procedural outcome with multivessel coronary artery disease: implications for patient selection. Circulation 1990;82:1193–1202.
3. Mak KH, Belli G, Ellis SG, Moliterno DJ. Subacute stent thrombosis: evolving issues and current concepts. J Am Coll Cardiol 1996;27:494 –503. 4. Haude M, Erbel R, Issa H, Meyer J. Quantitative analysis of elastic recoil after balloon angioplasty and after intracoronary implantation of balloon-expandable Palmaz-Schatz stents. J Am Coll Cardiol 1993;21:26 –34. 5. Hoffmann R, Mintz GS, Popma JJ, Satler LF, Pichard AD, Kent KM, Walsh C, Mackell P, Leon MB. Chronic arterial responses to stent implantation: a serial intravascular ultrasound analysis of Palmaz-Schatz stents in native coronary arteries. J Am Coll Cardiol 1996;28:1134 –1139. 6. Komatsu R, Ueda M, Naruko T, Kojima A, Becker AE. Neointimal tissue response at sites of coronary stenting in humans: macroscopic, histological, and immunohistochemical analyses. Circulation 1998;98:224 –233. 7. Tan KH, Sulke N, Taub N, Sowton E. Predictors of angiographic findings when chest pain recurs after successful coronary angioplasty. Eur Heart J 1995;16:1593–1602. 8. Jeremias A, Kutscher S, Haude M, Heinen D, Holtmann G, Senf W, Erbel R. Nonischemic chest pain induced by coronary intervention. A prospective study comparing coronary angioplasty and stent implantation. Circulation 1998;98: 2656 –2658.
Clinical Characteristics and Outcome in Postinfarction Pseudoaneurysm Tiong Cheng Yeo,
MRCP,
Joe F. Malouf,
MD,
Guy S. Reeder,
MD,
and Jae K. Oh,
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contrast to a true aneurysm, the walls of a pseuare composed of fibrous tissue devoid Iof ndoaneurysm the structural elements found in the normal wall. A striking feature of a pseudoaneurysm is its propensity for rupture,1,2 often with a fatal outcome.1,3,4 This study presents clinical characteristics and outcomes of 22 consecutive patients with postinfarction pseudoaneurysm diagnosed antemortem between 1980 and 1996. •••
The diagnosis was based on typical morphologic features obtained by each of the following imaging modalities: 2-dimensional Doppler echocardiography and color flow imaging,5–9 angiography,10 computed tomography,11,12 and magnetic resonance imaging.13 Surgical or pathologic confirmation, or both, was available for 16 patients who had surgical repair. After the study group was identified, the clinical records were reviewed, including patients’ demographics, clinical presentation, results of surgical repair, and vital status at the latest follow-up evaluation. Follow-up information was obtained from clinical records and supplemented by direct mail and telephone contact. The cause of death was determined on the basis of clinical records, death certificates, and correspondence. Death was considered possibly due to cardiac rupture if it was sudden or rupture was confirmed by autopsy findings. Videotape recordings of transthoracic (n ⫽ 16) and transesophageal (n ⫽ 7) echocardiographic studies of 16 patients who underwent echocardiography were From the Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minnesota; and Division of Cardiovascular Diseases, Mayo Clinic Jacksonville, Jacksonville, Florida. Dr. Oh’s address is: Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905. Manuscript received December 29, 1997; revised manuscript received August 12, 1998, and accepted April 21, 1999.
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©1999 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 84 September 1, 1999
FIGURE 1. Two-dimensional parasternal long-axis view of a pseudoaneursym of inferolateral wall, showing off-line measurement of widest diameter of the neck (Omax) and maximal parallel internal diameter of the pseudoaneurysm (Dmax). Ao ⴝ aorta; LA ⴝ left atrium; LV ⴝ left ventricle; Ps ⴝ pseudoaneurysm; RV ⴝ right ventricle; TH ⴝ thrombus.
reviewed. Off-line measurements were performed with a commercial digitizing system (TomTec Imaging Inc., Broomfield, Colorado). Echocardiograms were analyzed for the site and maximal internal width of the neck or orifice of the pseudoaneurysm, Omax. The measurement of Omax was obtained using the frame that demonstrated the greatest diameter of the neck regardless of its timing in the cardiac cycle. The maximal parallel internal diameter of the pseudoaneurysm cavity, Dmax, was then measured using the same frame in which Omax was found (Figure 1). Three such measurements were obtained and averaged for each study. Left ventricular ejection fraction was measured as previously described.14,15 0002-9149/99/$–see front matter PII S0002-9149(99)00385-9
Between January 1995 and October 1997, 3,309 consecutive patients underwent successful PCI at our institution. We identified 158 patients (4.8%) who underwent repeat coronary angiography within 30 days of the initial PCI. Patients with abrupt vessel closure immediately after percutaneous transluminal coronary angioplasty (PTCA) (n ⫽ 21), subacute stent thrombosis (n ⫽ 9), and chest pain before hospital discharge (n ⫽ 20) were excluded from analysis. Consequently, the study cohort consisted of 108 patients (3.3%) who underwent repeat coronary angiography between 2 and 30 days of the initial PCI. The decision to perform coronary angiography was entirely at the discretion of the patient’s physician and was based on the clinical suspicion of recurrent myocardial ischemia, usually manifested by chest discomfort. Clinical variables were recorded and included age, sex, presence of diabetes, electrocardiographic findings, and nature of clinical syndrome leading to intervention and repeat angiography. Electrocardiographic changes considered suggestive of ischemia included development of new Q waves, new ST-segment deviation ⱖ0.5 mm, or new T-wave changes. Based on a blinded review of the medical record, the patient’s symptoms were classified as suggestive of myocardial ischemia if the symptoms documented were similar in nature to those leading to the index PCI. All angiograms were analyzed by experienced angiographers blinded to the clinical information. Qualitative angiographic variables at the initial PCI included: number of vessels with ⬎50% narrowing, From the Cardiovascular Division, Department of Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia. Dr. Ragosta’s addrress is: Cardiovascular Division, University of Virginia Health Systems, HSC Box 158, Charlottesville, Virginia 22908. Email: [email protected]. Manuscript received February 23, 1999; revised manuscript received and accepted April 22, 1999. ©1999 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 84 September 1, 1999
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index lesion complexity defined by the American College of Cardiology/American Heart Association classification (type A, B1, B2, or C),2 lesion eccentricity, ulceration, lesion calcium, visible thrombus, the presence of dissection or thrombus after the procedure, and use of coronary stents. The pre-PCI, post-PCI, and repeat angiograms were analyzed using a computerassisted quantitative angiographic analysis system (CARS, Sony Medical Systems, Montvale, New Jersey). Quantitative analysis included determination of lesion length, reference vessel diameter, and MLD before and after the procedure. Acute gain after intervention (increase in MLD from pre- to post-PCI), percent stenosis before and after the procedure (ratio of MLD to reference vessel diameter), and ⌬MLD (the difference between MLD after the procedure and MLD at repeat angiography) were calculated. Based on quantitative analysis of the repeat angiograms, the patients were classified into 1 of 2 groups: (1) early restenosis, defined as the presence of ⬎50% luminal narrowing at the site of the index procedure; or (2) no restenosis, defined as the absence of ⬎50% luminal narrowing at the site of the index procedure. Within the no-restenosis group, patients with ⱖ50% luminal narrowing in an artery not treated at the index procedure were also identified. Data were analyzed with RS/1 software (Bolt, Beranek, and Newman, Cambridge, Massachusetts) with a minicomputer (VAX4000-system 90, Digital Equipment Corp., Houston, Texas). All normally distributed data were expressed as mean ⫾ 1 SD; data not normally distributed were expressed as median (25th, 75th percentile). Comparisons between groups were performed, and group differences of continuous factors were compared using Wilcoxon signed-rank tests. Group differences of categorical variables were compared using chi-square tests or, in the cases of small cell sizes, Fisher’s exact test. Stepwise logistic regression techniques were used to determine multivariate predictors of early restenosis. All p values are from 2-sided tests. •••
Of the 3,309 consecutive patients who underwent successful PCI during the specified time period, 2,253 (68%) were treated with PTCA alone and 1,056 (32%) received coronary stents. Among the 108 patients who returned for early repeat angiography, 81 (75%) had undergone PTCA and 27 (25%) had received coronary stents. Thus, a similar proportion of patients after PTCA underwent early repeat coronary angiography compared with patients who received stents (3.6% of all PTCA patients vs 2.7% of all stented patients, p ⫽ 0002-9149/99/$–see front matter PII S0002-9149(99)00384-7
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TABLE II Clinical Variables in Patients With and Without Early Restenosis
TABLE I Clinical Characteristics of 108 Patients Who Underwent Repeat Angiography Within 30 Days of Successful Coronary Intervention Characteristic Age (yrs) Men Diabetes mellitus Syndrome at index procedure Acute myocardial infarction Recent myocardial infarction* Unstable angina Stable angina Positive stress test Time to angiography (d) Typical symptoms† Electrocardiographic changes‡
Patients 58 ⫾ 12 64 27 15 14 65 5 1 14 ⫾ 9 73 44
*Defined as myocardial infarction within 7 days of index intervention. † Symptoms leading to repeat angiography considered typical of myocardial ischemia. ‡ Electrocardiographic changes at the time of repeat angiography considered suggestive of ischemia. Data are expressed as mean ⫾ SD or percentages.
Age (yrs) Men Diabetes mellitus Time to angiography (d) Suggestive symptoms† Electrocardiographic changes‡
Restenosis (n ⫽ 28)
No Restenosis (n ⫽ 80)
58 ⫾ 13 60 43 11 ⫾ 8 80 50
58 ⫾ 12 58 21* 15 ⫾ 9 70 41
*p ⫽ 0.05 (p ⱕ0.05 was considered significant in univariate analysis). † Symptoms leading to repeat angiography considered suggestive of myocardial ischemia. ‡ Electrocardiographic changes at the time of repeat angiography considered suggestive of ischemia. Data are expressed as mean ⫾ SD or percentages.
TABLE III Angiographic Data from Index Intervention in Patients With and Without Early Restenosis Restenosis (n ⫽ 28) Lesion length (mm) Reference diameter (mm) MLD pre-PCI (mm) Pre-PCI stenosis Visible thrombus Visible calcium Eccentric lesion Ulcerated lesion ACC/AHA type B1, B2, or C Acute gain (mm) MLD post-PCI (mm) Post-PCI stenosis Dissection after PCI
⫾5 ⫾ 0.46 ⫾ 0.30 ⫾ 10 23 7 67 7 87 1.64 ⫾ 0.49 2.08 ⫾ 0.44 28 ⫾ 11 23
10 2.84 0.45 84
No Restenosis (n ⫽ 80) ⫾4 ⫾ 0.52 ⫾ 0.38 ⫾ 12 23 4 50 19 73 1.78 ⫾ 0.59 2.39 ⫾ 0.54* 21 ⫾ 11 9
9 2.91 0.57 82
*p ⫽ 0.009 (p ⱕ0.05 was considered significant in univariate analysis). Data are expressed as mean ⫾ SD or percentages. ACC/AHA ⫽ American College of Cardiology/American Heart Association.
FIGURE 1. Bar graph demonstrating proportions of patients with (black) and without (white and hatched) early restenosis at repeat angiography. Patients without early restenosis are divided into those with no significant lesions (hatched) and those with previously untreated coronary stenoses remote from the index lesion (white). “Stent” and “PTCA Alone” ⴝ type of index intervention.
NS). Clinical characteristics of the 108 patients are listed in Table I. All patients received standard anticoagulation with heparin at the index PCI, and 7 patients in the cohort received abciximab. Of the 108 patients studied, 28 (26%) were found to have early restenosis at the treated site (Figure 1). Of the 80 patients without restenosis, 26 (33%) were found to have ⱖ1 significant coronary stenosis at previously untreated sites. None of the 27 patients initially treated with coronary stents were found to have early restenosis compared with 28 of the 81 patients (35%) who underwent PTCA alone (p ⬍0.0001). Table II summarizes the clinical findings at repeat angiography in patients with and without early restenosis. Chest discomfort and electrocardiographic find590 THE AMERICAN JOURNAL OF CARDIOLOGY姞
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ings were not helpful in identifying patients with and without early restenosis. Patients without early restenosis but with stenoses in other vessels did not differ in their clinical presentation at repeat angiography when compared with those with no significant stenoses. Symptoms and electrocardiographic changes suggestive of recurrent ischemia were present in 19 (73%) and 12 (46%), respectively, of the 26 patients with significant stenoses in other vessels compared with 37 (68%) and 21 (39%), respectively, of the 54 patients without any significant coronary stenoses. Diabetic patients had a significantly higher incidence of early restenosis at repeat angiography than nondiabetics (40% vs 21%, p ⫽ 0.05). No other clinical variable, including patient age, gender, index vessel, time to repeat angiography, presence of typical chest pain, or presence of electrocardiographic changes was significantly different between patients with and without early restenosis. The clinical syndrome at the time of index PCI (stable angina, unstable angina, and acute myocardial infarction) was not associated with early restenosis at repeat angiography. SEPTEMBER 1, 1999
TABLE IV Quantitative Angiographic Data in the 81 Patients Who Underwent Balloon Angioplasty Without Stenting at Index Intervention Total (n ⫽ 81) Reference diameter (mm) MLD pre-PTCA (mm) Pre-PTCA stenosis (%) MLD post-PTCA (mm) Post-PTCA stenosis (%) Acute gain (mm) MLD at RA (mm) ⌬MLD (mm)
Restenosis (n ⫽ 28)
No Restenosis (n ⫽ 53)
2.80 ⫾ 0.45 2.85 ⫾ 0.46 2.78 ⫾ 0.45 0.47 ⫾ 0.34 0.44 ⫾ 0.29 0.49 ⫾ 0.37 84 ⫾ 11
84 ⫾ 9
83 ⫾ 12
2.04 ⫾ 0.45 2.05 ⫾ 0.41 2.04 ⫾ 0.46 27 ⫾ 11
28 ⫾ 11
26 ⫾ 11
1.57 ⫾ 48 1.61 ⫾ 49 1.55 ⫾ 57 1.58 ⫾ 0.70 0.89 ⫾ 0.55 2.00 ⫾ 0.39* 0.46 ⫾ 0.38 1.16 ⫾ 0.44 0.04 ⫾ 0.11*
*p ⬍0.0001 when compared to patients with restenosis. Data are expressed as mean ⫾ SD or percentages. RA ⫽ repeat angiography.
Table III summarizes the angiographic data for the cohort. Patients with early restenosis had no differences in lesion length, reference vessel diameter, preprocedure MLD, preprocedure percent stenosis, or acute gain when compared with those without early restenosis. Lesion characteristics, such as the presence of eccentricity, ulceration, thrombus, calcium, and coronary dissection after intervention, were also similar among those with and without early restenosis. Patients with early restenosis at repeat angiography had a significantly smaller postprocedure MLD and significantly larger percent stenosis after the procedure when compared with those without early restenosis. However, in the multivariate analysis, these variables were not found to be independent predictors of early restenosis. Instead, they were associated with the use of coronary stents at index PCI: patients who underwent PTCA alone had a significantly smaller postprocedure MLD (2.04 ⫾ 0.45 mm vs 2.80 ⫾ 0.46 mm, p ⬍0.0001) and larger percent stenosis after the procedure (27 ⫾ 11% vs 14 ⫾ 7%, p ⬍0.0001) than those treated with stents. Quantitative angiographic data for the 81 patients who underwent PTCA alone is summarized in Table IV. Reference vessel diameter, preprocedure MLD, preprocedure percent stenosis, postprocedure MLD, percent stenosis after the procedure, and acute gain were not different in those with and without early restenosis. In the 53 patients without early restenosis, the ⌬MLD (defined as the difference between postprocedure MLD and the MLD at repeat angiography) was negligible, whereas the ⌬MLD in patients with early restenosis was significant. There was no significant difference in early restenosis in patients with complex versus simple index lesions (25 of 80 [31%] vs 3 of 28 [11%]). However, in the 81 patients who underwent PTCA without stenting, type B or C index lesions were associated with a significantly higher rate of early restenosis than type A lesions (25 of 60 [42%] vs 3 of 21 [14%]; p ⫽ 0.03).
When the significant univariate predictors of restenosis were entered into a stepwise logistic regression, the only significant multivariate predictor of early restenosis was the absence of coronary stenting at the index PCI (p ⫽ 0.006). •••
In the present study, 28 of the 108 patients (26%) referred for repeat angiography within 1 month of successful PCI were found to have early restenosis. PTCA without stenting was the only independent predictor of early restenosis. None of the 27 patients treated with stents were found to have early restenosis despite the presence of clinically suspected myocardial ischemia. All 9 patients excluded from the study due to subacute stent thrombosis presented unequivocally with symptoms of acute myocardial infarction and ST-segment elevation. Although the absence of ST-segment elevation does not definitively exclude subacute stent thrombosis, the low likelihood of early in-stent restenosis or vessel closure suggests that angiography may not be the best initial diagnostic strategy for evaluating recurrent symptoms early after coronary stenting. In over 1,000 consecutive patients who underwent successful coronary stent implantation at our institution, the rate of subacute thrombosis was 1.0%, consistent with previous findings.3 The absence of early in-stent restenosis found in our study is likely explained by the reduction in elastic recoil4 and perhaps reduced early pathologic arterial remodeling.5 This finding is not unexpected since the primary cause of in-stent restenosis is neointimal proliferation, which is a complex process that typically occurs several months after intervention.6 Approximately 3% of patients at our institution were referred for coronary angiography within 30 days of successful PCI, consistent with findings at other institutions.7 However, a limitation of our study is that patients who might have undergone early angiography may have died or had myocardial infarction before being studied. Compared with patients who underwent PTCA, a similar proportion of patients who received stents were referred for repeat angiography. Given the lack of early in-stent restenosis, it is unclear why these patients had a similar incidence of recurrent symptoms. A recent study found that chest pain in the first 24 hours after stenting is common, possibly due to “stretch pain” from overdilation of the treated artery.8 We can speculate that some patients may have prolonged discomfort from arterial stretch or have a higher incidence of noncardiac symptoms due to the use of drugs such as ticlopidine, which may cause gastric irritation.
A significant number of patients with early recurrent chest pain referred for angiography within 30 days of balloon angioplasty were found to have early restenosis. In contrast, excluding patients with stent thrombosis, there were no cases of early in-stent restenosis. PTCA without stenting was the BRIEF REPORTS
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only independent predictor of early restenosis in patients with recurrent chest pain early after PCI. These findings suggest that repeat angiography for the evaluation of early recurrent symptoms after successful coronary stenting has a low diagnostic yield. 1. Painter JA, Mintz GS, Wong SC, Popma JJ, Pichard AD, Kent KM, Satler LF,
Leon MB. Serial intravascular ultrasound studies fail to show evidence of chronic Palmaz-Schatz stent recoil. Am J Cardiol 1995;75:398 – 400. 2. Ellis SG, Vandormael MG, Cowley MJ, DiSciascio G, Deligonul U, Topol EJ, Bulle TM. Coronary morphologic and clinical determinants of procedural outcome with multivessel coronary artery disease: implications for patient selection. Circulation 1990;82:1193–1202.
3. Mak KH, Belli G, Ellis SG, Moliterno DJ. Subacute stent thrombosis: evolving issues and current concepts. J Am Coll Cardiol 1996;27:494 –503. 4. Haude M, Erbel R, Issa H, Meyer J. Quantitative analysis of elastic recoil after balloon angioplasty and after intracoronary implantation of balloon-expandable Palmaz-Schatz stents. J Am Coll Cardiol 1993;21:26 –34. 5. Hoffmann R, Mintz GS, Popma JJ, Satler LF, Pichard AD, Kent KM, Walsh C, Mackell P, Leon MB. Chronic arterial responses to stent implantation: a serial intravascular ultrasound analysis of Palmaz-Schatz stents in native coronary arteries. J Am Coll Cardiol 1996;28:1134 –1139. 6. Komatsu R, Ueda M, Naruko T, Kojima A, Becker AE. Neointimal tissue response at sites of coronary stenting in humans: macroscopic, histological, and immunohistochemical analyses. Circulation 1998;98:224 –233. 7. Tan KH, Sulke N, Taub N, Sowton E. Predictors of angiographic findings when chest pain recurs after successful coronary angioplasty. Eur Heart J 1995;16:1593–1602. 8. Jeremias A, Kutscher S, Haude M, Heinen D, Holtmann G, Senf W, Erbel R. Nonischemic chest pain induced by coronary intervention. A prospective study comparing coronary angioplasty and stent implantation. Circulation 1998;98: 2656 –2658.
Clinical Characteristics and Outcome in Postinfarction Pseudoaneurysm Tiong Cheng Yeo,
MRCP,
Joe F. Malouf,
MD,
Guy S. Reeder,
MD,
and Jae K. Oh,
MD
contrast to a true aneurysm, the walls of a pseuare composed of fibrous tissue devoid Iof ndoaneurysm the structural elements found in the normal wall. A striking feature of a pseudoaneurysm is its propensity for rupture,1,2 often with a fatal outcome.1,3,4 This study presents clinical characteristics and outcomes of 22 consecutive patients with postinfarction pseudoaneurysm diagnosed antemortem between 1980 and 1996. •••
The diagnosis was based on typical morphologic features obtained by each of the following imaging modalities: 2-dimensional Doppler echocardiography and color flow imaging,5–9 angiography,10 computed tomography,11,12 and magnetic resonance imaging.13 Surgical or pathologic confirmation, or both, was available for 16 patients who had surgical repair. After the study group was identified, the clinical records were reviewed, including patients’ demographics, clinical presentation, results of surgical repair, and vital status at the latest follow-up evaluation. Follow-up information was obtained from clinical records and supplemented by direct mail and telephone contact. The cause of death was determined on the basis of clinical records, death certificates, and correspondence. Death was considered possibly due to cardiac rupture if it was sudden or rupture was confirmed by autopsy findings. Videotape recordings of transthoracic (n ⫽ 16) and transesophageal (n ⫽ 7) echocardiographic studies of 16 patients who underwent echocardiography were From the Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minnesota; and Division of Cardiovascular Diseases, Mayo Clinic Jacksonville, Jacksonville, Florida. Dr. Oh’s address is: Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905. Manuscript received December 29, 1997; revised manuscript received August 12, 1998, and accepted April 21, 1999.
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©1999 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 84 September 1, 1999
FIGURE 1. Two-dimensional parasternal long-axis view of a pseudoaneursym of inferolateral wall, showing off-line measurement of widest diameter of the neck (Omax) and maximal parallel internal diameter of the pseudoaneurysm (Dmax). Ao ⴝ aorta; LA ⴝ left atrium; LV ⴝ left ventricle; Ps ⴝ pseudoaneurysm; RV ⴝ right ventricle; TH ⴝ thrombus.
reviewed. Off-line measurements were performed with a commercial digitizing system (TomTec Imaging Inc., Broomfield, Colorado). Echocardiograms were analyzed for the site and maximal internal width of the neck or orifice of the pseudoaneurysm, Omax. The measurement of Omax was obtained using the frame that demonstrated the greatest diameter of the neck regardless of its timing in the cardiac cycle. The maximal parallel internal diameter of the pseudoaneurysm cavity, Dmax, was then measured using the same frame in which Omax was found (Figure 1). Three such measurements were obtained and averaged for each study. Left ventricular ejection fraction was measured as previously described.14,15 0002-9149/99/$–see front matter PII S0002-9149(99)00385-9