Original Article
A Prospective Natural-History Study of Coronary Atherosclerosis
N Engl J Med 2011; 364:226-235January 20, 2011
Comments
open through January 25, 2011
- Abstract
Background
Atherosclerotic plaques that lead to acute coronary syndromes often occur at sites of angiographically mild coronary-artery stenosis. Lesion-related risk factors for such events are poorly understood.
Methods
In a prospective study, 697 patients with acute coronary syndromes underwent three-vessel coronary angiography and gray-scale and radiofrequency intravascular ultrasonographic imaging after percutaneous coronary intervention. Subsequent major adverse cardiovascular events (death from cardiac causes, cardiac arrest, myocardial infarction, or rehospitalization due to unstable or progressive angina) were adjudicated to be related to either originally treated (culprit) lesions or untreated (nonculprit) lesions. The median follow-up period was 3.4 years.
Results
The 3-year cumulative rate of major adverse cardiovascular events was 20.4%. Events were adjudicated to be related to culprit lesions in 12.9% of patients and to nonculprit lesions in 11.6%. Most nonculprit lesions responsible for follow-up events were angiographically mild at baseline (mean [±SD] diameter stenosis, 32.3±20.6%). However, on multivariate analysis, nonculprit lesions associated with recurrent events were more likely than those not associated with recurrent events to be characterized by a plaque burden of 70% or greater (hazard ratio, 5.03; 95% confidence interval [CI], 2.51 to 10.11; P<0.001) or a minimal luminal area of 4.0 mm2 or less (hazard ratio, 3.21; 95% CI, 1.61 to 6.42; P=0.001) or to be classified on the basis of radiofrequency intravascular ultrasonography as thin-cap fibroatheromas (hazard ratio, 3.35; 95% CI, 1.77 to 6.36; P<0.001).
Conclusions
In patients who presented with an acute coronary syndrome and underwent percutaneous coronary intervention, major adverse cardiovascular events occurring during follow-up were equally attributable to recurrence at the site of culprit lesions and to nonculprit lesions. Although nonculprit lesions that were responsible for unanticipated events were frequently angiographically mild, most were thin-cap fibroatheromas or were characterized by a large plaque burden, a small luminal area, or some combination of these characteristics, as determined by gray-scale and radiofrequency intravascular ultrasonography. (Funded by Abbott Vascular and Volcano; ClinicalTrials.gov number, NCT00180466.)
Media in This Article
Figure 1
Time-to-Event Curves for Major Adverse Cardiovascular Events after Successful, Uncomplicated Percutaneous Coronary Intervention in 697 Patients with Acute Coronary Syndromes.Figure 2
Event Rates for Lesions That Were and Those That Were Not Thin-Cap Fibroatheromas, at a Median Follow-up of 3.4 Years.Article Activity
- Article
Approximately 1,350,000 Americans annually have an acute coronary syndrome (unstable angina or myocardial infarction with or without ST-segment elevation).1 Although percutaneous coronary intervention and pharmacologic therapies have improved the prognosis for such patients,1-4 recurrent major adverse cardiovascular events occur in a substantial proportion of cases.
Recurrent cardiac ischemic events can be due to recurrence at the original treatment site, the presence of untreated lesions elsewhere, or progressive lesions. However, prospective, systematic data on the origin of recurrent events are lacking. Moreover, retrospective studies have shown that most atherosclerotic plaques responsible for future acute coronary syndromes are angiographically mild,5,6 and the lesion-related risk factors for major adverse cardiovascular events are poorly understood. Pathological studies have shown that thrombotic coronary occlusion after rupture of a lipid-rich atheroma with only a thin fibrous layer of intimal tissue covering the necrotic core (a thin-cap fibroatheroma) is the most common cause of myocardial infarction and death from cardiac causes.7-9 However, the prospective identification of thin-cap fibroatheromas has not been achieved, in part because the imaging tools to identify them in vivo did not exist until recently.
We therefore performed a prospective, multicenter study of the natural history of coronary atherosclerosis, using multimodality intravascular imaging to identify the clinical and lesion-related factors that place patients at risk for adverse cardiac events.
Methods
Study Design
The Providing Regional Observations to Study Predictors of Events in the Coronary Tree (PROSPECT) study was conducted at 37 sites in the United States and Europe. The study was designed by the principal investigator and the sponsor, Abbott Vascular, and was funded by Abbott Vascular and Volcano. The sponsor participated in site selection and management and in data collection and analysis (see the Supplementary Appendix, available with the full text of this article at NEJM.org). The principal investigator had unrestricted access to the data, maintained the database, prepared all drafts of the manuscript, made the decision to submit the manuscript for publication, and vouches for the integrity of the study. The study was approved by the institutional review board at each participating center.
Study Patients and Protocol
Patients with acute coronary syndromes were enrolled after undergoing successful and uncomplicated percutaneous coronary intervention for the treatment of all coronary lesions believed to be responsible for the index event and after the completion of any other planned interventions. Detailed inclusion and exclusion criteria are listed in Table 1 in the Supplementary Appendix. All patients provided written informed consent. The study was conducted in accordance with the protocol, which is available at NEJM.org.
Angiography was performed, followed by both gray-scale and radiofrequency intravascular ultrasonography of the left main coronary artery and the proximal 6 to 8 cm of each of the major epicardial coronary arteries, with the use of a synthetic-aperture-array, 20-MHz, 3.2-French catheter (Eagle Eye, In-Vision Gold, Volcano) with motorized catheter pullback (0.5 mm per second). In contrast to conventional gray-scale intravascular ultrasonography, radiofrequency intravascular ultrasonography uses spectral (frequency) analysis as well as amplitude data from the intravascular ultrasonographic signal, providing information about tissue composition that has been correlated with data from histologic samples.10,11 The analysis was performed offline and was not used for procedural guidance. Levels of serum creatinine, fasting lipids, glucose, glycated hemoglobin, and high-sensitivity C-reactive protein were measured at baseline. Medication use after discharge was according to local standards. Clinical follow-up occurred at 30 days, at 6 months, and then yearly for at least 2 years.
Imaging Analysis
All baseline angiograms and intravascular ultrasonographic images were prospectively analyzed at independent core laboratories by means of prespecified methods,12,13 without knowledge of subsequent events. Angiographic qualitative and quantitative measurements12 were obtained for the entire length of the coronary tree, including each epicardial vessel and side branch that was at least 1.5 mm in diameter, with the use of proprietary methods modified from Medis CMS software, version 7.0 (Leiden, the Netherlands), which were validated in 78 randomly selected coronary segments. For each 1.5 mm of vessel, we recorded the reference diameter, minimal luminal diameter, and diameter stenosis (the percentage of cross-sectional diameter lost to stenosis). Analysis of all angiographic lesions with at least 30% visible diameter stenosis was also prespecified.
Offline gray-scale and radiofrequency intravascular ultrasonographic analyses were performed in the core laboratory with the use of QCU-CMS software (Medis) for contouring, pcVH 2.1 software (Volcano) for contouring and data output, and proprietary qVH software (Cardiovascular Research Foundation) for segmental qualitative assessment and quantitative data output. External-elastic-membrane and luminal borders were contoured for each frame (median interslice distance, 0.40 mm). Quantitative intravascular ultrasonographic measurements included the cross-sectional areas of the external elastic membrane, the lumen, and the plaque and media (cross-sectional area of the external elastic membrane minus that of the lumen), plaque burden (plaque-and-media cross-sectional area divided by external-elastic-membrane cross-sectional area), and minimal luminal area. On the basis of radiofrequency intravascular ultrasonography, plaque components were identified as dense calcium, necrotic core, fibrofatty tissue, or fibrous tissue, with the cross-sectional area and percentage of total plaque area reported for each component.10
A lesion on intravascular ultrasonographic imaging was defined as at least three consecutive frames with a plaque burden of at least 40%. Such lesions were classified by means of radiofrequency analysis as one of the following: thin-cap fibroatheroma, thick-cap fibroatheroma, pathologic intimal thickening, fibrotic plaque, or fibrocalcific plaque (Figure 1 in the Supplementary Appendix).13 Each gray-scale and radiofrequency intravascular ultrasonographic frame was coregistered with the corresponding frame from the angiographic roadmap with the use of side branches for alignment.
Data, End Points, and Definitions
Independent study monitors verified all data on case-report forms. The prespecified primary end point was the incidence of major adverse cardiovascular events (the composite of death from cardiac causes, cardiac arrest, myocardial infarction, or rehospitalization due to unstable or progressive angina according to the Braunwald Unstable Angina Classification and the Canadian Cardiovascular Society Angina Classification). The primary end point was adjudicated by a clinical events committee that had no knowledge of other patient data and that used original source documents. On the basis of follow-up angiography, major adverse cardiovascular events were further adjudicated as occurring at initially treated sites (culprit lesions) or at previously untreated coronary segments (nonculprit lesions). If follow-up angiography was not performed, the site associated with the event was classified as indeterminate. An example of plaque characterization from an event related to a nonculprit lesion is shown in Figure 2 in the Supplementary Appendix.
Statistical Analysis
Sample size was calculated to provide adequate power to identify variables associated with nonculprit-lesion–related major adverse cardiovascular events on the basis of a range of assumptions about the frequency of high-risk characteristics, their predictive accuracy, the overall rate of such events, and the hazard ratio for the risk factor. For example, if 71% of patients had a high-risk variable with 85% sensitivity and 85% specificity, 700 patients would be needed to provide 83% and 99% power to detect a hazard ratio of 3.0 for nonculprit-lesion–related rates of major adverse cardiovascular events of 5% and 10%, respectively, with a one-sided alpha of 0.025.
Time-to-event data are presented as Kaplan–Meier estimates. Baseline variables that were considered clinically relevant or that showed a univariate relationship with outcome were entered into multivariate Cox proportional-hazards regression models. Variables for inclusion were carefully chosen, given the number of events available, to ensure parsimony of the final models.14 Lesion-level multivariate models were adjusted for patient effects by means of the marginal Cox model,15 and nonsignificant variables were dropped by means of backward selection. Statistical analyses were performed with the use of SAS software, version 9.1.3 (SAS Institute).
Results
Patients
Between October 29, 2004, and June 8, 2006, a total of 697 patients with acute coronary syndromes were enrolled after they had undergone successful percutaneous coronary intervention (Table 1Table 1
Demographic, Clinical, and Procedural Characteristics of the Patients.). The median age was 58.1 years, 24.0% were women, and 17.1% had diabetes mellitus. The median follow-up was 3.4 years. The rate of use of antiplatelet, lipid-lowering, and other medications was high throughout the follow-up period (Table 2 in the Supplementary Appendix).Baseline Imaging
Angiographic images, gray-scale intravascular ultrasonographic images, and radiofrequency intravascular ultrasonographic images from the index procedures could be evaluated in 697 (100%), 673 (96.6%), and 623 (89.4%) of the patients, respectively. Intravascular ultrasonographic imaging was restricted to the proximal and middle portions of the coronary arteries, where the vessel diameter was sufficient to accommodate the imaging catheters (Table 3 in the Supplementary Appendix).
The frequency of residual disease after percutaneous coronary intervention varied substantially depending on the imaging technique. On angiography, 1814 untreated lesions (i.e., those with a visually ascertained diameter stenosis of at least 30%) were identified in the entire coronary vasculature, including 110 with a diameter stenosis of at least 50% and 12 with a diameter stenosis of at least 70%. Gray-scale intravascular ultrasonography identified 3160 lesions in the proximal-to-middle segments of the three major epicardial coronary arteries in 673 patients, including 620 lesions with a minimal luminal area of 4.0 mm2 or less and 283 lesions with a plaque burden of at least 70%. On the basis of radiofrequency intravascular ultrasonography, most lesions were classified as pathologic intimal thickening or fibroatheromas (Table 4 in the Supplementary Appendix); 596 thin-cap fibroatheromas were identified in 313 of 623 patients.
Adverse Events
Eleven patients (1.6%) had complications that were attributed to the three-vessel imaging procedure (10 dissections and 1 perforation). These complications resulted in 3 nonfatal myocardial infarctions (in 0.4% of patients).
During a median follow-up period of 3.4 years, 149 major adverse cardiovascular events occurred in 135 patients (3-year cumulative rate, 20.4%) (Figure 1Figure 1
Time-to-Event Curves for Major Adverse Cardiovascular Events after Successful, Uncomplicated Percutaneous Coronary Intervention in 697 Patients with Acute Coronary Syndromes.). Most events were rehospitalizations for unstable or progressive angina; cardiovascular events (death from cardiac causes, cardiac arrest, or myocardial infarction) occurred in only 31 patients (3-year cumulative rate, 4.9%) within 3 years (Table 2Table 2
Kaplan–Meier Estimates for Cumulative Rates of Major Adverse Cardiovascular Events at 3 Years.). The 3-year cumulative rate of major adverse cardiovascular events that were judged to be recurrent disease at originally treated culprit lesions was 12.9% (118 lesions in 83 patients). The 3-year cumulative event rate judged to be related to nonculprit lesions was 11.6% (104 lesions in 74 patients). The origin of 18 events in 17 patients (2.7%) was indeterminate.Correlates of Events Related to Nonculprit Lesions
The mean angiographic diameter stenosis of the 106 nonculprit lesions subsequently responsible for major adverse cardiovascular events was 32.3±20.6% at baseline and 65.4±16.3% at follow-up (P<0.001). At baseline, 32 of these lesions (30.2%) were angiographically inconspicuous (less than 30% stenosis on the basis of visual assessment). On quantitative angiography, 30 (28.3%) of these 106 lesions were at least 50% stenotic but less than 70% stenotic, and 5 (4.7%) were at least 70% stenotic. Among these 106 nonculprit lesions, 55 were imaged by intravascular ultrasonography, and all were found to have a baseline plaque burden of at least 40%.
The baseline patient-level and lesion-level correlates of nonculprit-lesion–related major adverse cardiovascular events are given in Table 3Table 3
Independent Correlates of Major Adverse Cardiovascular Events Related to Nonculprit Lesions during Follow-up., and Table 5 and Table 6 in the Supplementary Appendix. The strongest patient-level predictor of nonculprit-lesion–related major adverse cardiovascular events at follow-up was insulin-requiring diabetes, whereas a baseline plaque burden of at least 70%, a minimal luminal area of 4.0 mm2 or less, and the presence of thin-cap fibroatheromas were independent predictors of subsequent nonculprit-lesion–related major adverse cardiovascular events. During follow-up, major adverse cardiovascular events originated from lesions that included 0, 1, 2, or all 3 of these variables in 0.3%, 4.8%, 10.5%, and 18.2% of lesions, respectively. Of 51 nonculprit lesions that were evaluated and classified based on radiofrequency intravascular ultrasonographic imaging and that resulted in major adverse cardiovascular events, 26 (51.0%) were thin-cap fibroatheromas, 8 (30.8%) of which had a minimal luminal area greater than 4.0 mm2 and a plaque burden of less than 70% (i.e., thin-cap fibroatheroma was the only independent risk factor for subsequent major adverse cardiovascular events). Nonculprit-lesion–related major adverse cardiovascular events arose more frequently from thin-cap fibroatheromas with a large plaque burden, a small minimal luminal area, or both (Figure 2Figure 2Event Rates for Lesions That Were and Those That Were Not Thin-Cap Fibroatheromas, at a Median Follow-up of 3.4 Years.). In contrast, follow-up events rarely originated from nonfibroatheromas, regardless of lesion severity (Figure 3 in the Supplementary Appendix).Discussion
We used gray-scale and radiofrequency intravascular ultrasonographic imaging prospectively to characterize coronary atherosclerosis before longitudinal follow-up. We found that approximately one in five patients with acute coronary syndromes who were successfully treated with percutaneous coronary intervention and contemporary medical therapy had recurrent major adverse cardiovascular events within 3 years. Events were nearly equally divided between those related to initially treated lesions and those related to previously untreated lesions. Most events were rehospitalizations for unstable or progressive angina; death from cardiac causes, cardiac arrest, and myocardial infarction were less common. Although the nonculprit lesions that led to major adverse cardiovascular events were frequently mild on angiographic assessment, most were characterized by a large plaque burden, a small luminal area, or both, as seen on gray-scale intravascular ultrasonography but not on angiography; no major adverse cardiovascular events arose from untreated segments with a plaque burden resulting in less than 40% loss of cross-sectional luminal area. The prospective identification of nonculprit lesions associated with major adverse cardiovascular events was further enhanced by the use of radiofrequency intravascular ultrasonography to characterize the morphologic features of plaques, with thin-cap fibroatheromas representing the highest-risk phenotype. Conversely, major adverse cardiovascular events related to nonculprit lesions rarely developed from nonfibroatheromas, regardless of the plaque burden or minimal luminal area.
The primary purpose of this natural-history study was to provide prospective in vivo confirmation of the hypothesis that acute coronary syndromes arise from atheromas with certain histopathological characteristics, and that these characteristics are not necessarily dependent on the degree of angiographic stenosis at that site. Although most of the lesions responsible for major adverse cardiovascular events during follow-up were angiographically mild, intravascular ultrasonography showed that most had either a small luminal area, a large plaque burden, or both — findings that are consistent with the results of pathological studies.7-9 Moreover, although actual histologic assessment of the coronary arteries in vivo is not feasible, the development of radiofrequency intravascular ultrasonography makes it possible to characterize the vessel wall with the use of an imaging technique that has been shown to correlate reasonably well with histologic findings. Events related to nonculprit lesions typically occurred at sites that were classified as thin-cap fibroatheromas on the basis of radiofrequency intravascular ultrasonography, a finding that is consistent with the established concept of vulnerable plaque.7-9
Of 51 nonculprit-lesion–related recurrent events occurring in the imaged segments, 26 (51%) occurred at sites with thin-cap fibroatheromas. There may be several explanations for why adverse events were also associated with other plaque types (most commonly thick-cap fibroatheromas). First, some thin-cap fibroatheromas may not have been identified during the study because of equipment limitations. Second, because intravascular ultrasonography was performed only at baseline, it is possible (indeed likely) that some atheromas evolved over time — that is, thick-cap fibroatheromas developed into thin-cap fibroatheromas.18 This concept is supported by the observation that thick-cap fibroatheromas were associated with an intermediate risk of cardiac events — higher than the risk associated with plaques that were not fibroatheromas and lower than the risk associated with thin-cap fibroatheromas. Such a model is consistent with the construct of Virmani et al., whereby the atherosclerotic lesion progresses from a low-risk to a high-risk phenotype before plaque rupture.19
A second objective of this study was to determine prospectively and systematically how often recurrent events occur at the sites of nonculprit lesions as opposed to the sites of previously treated lesions. Of 157 recurrent events for which the lesion location could be determined, 74 (47%) were related to original nonculprit lesions. Despite undergoing successful percutaneous coronary intervention for all coronary stenoses believed to require revascularization, within 3 years after treatment 11.6% of patients had unanticipated major adverse cardiovascular events associated with untreated coronary segments. Most of these sites showed no evidence of severe stenosis on conventional angiography, but we were able to identify three characteristics of lesions that were significant predictors of subsequent events: a small luminal area, a large plaque burden, and the presence of a thin-cap fibroatheroma.
Although the in vivo detection of potentially vulnerable plaque is of considerable mechanistic interest, there are several reasons why the methods we have used are not currently suitable for clinical application as a means of identifying sites in the coronary vasculature for potential intervention. First, the specificity of our methods is insufficient for such a purpose. Of 595 thin-cap fibroatheromas identified on radiofrequency intravascular ultrasonography, only 26 were sites of recurrent events at a median follow-up of 3.4 years (estimated Kaplan–Meier event rate, 4.9%). Specificity was similarly limited for a plaque burden of at least 70% (event rate, 9.6%) and a minimal luminal area of 4.0 mm2 or less (event rate, 5.3%). Even when all three predictive variables were present, the event rate rose to only 18.2%. These figures suggest that although such lesion characteristics are conducive to the occurrence of a subsequent event, they are not sufficient to predict which atheromas will undergo plaque progression in the intermediate term. Second, the intravascular ultrasonographic catheters used in this study cannot be used to evaluate the distal portions of the coronary arteries; in our protocol, we examined only the proximal 6 to 8 cm of the coronary tree. All 106 nonculprit lesions associated with recurrent events were evaluated with the use of baseline angiography, but only 55 of these lesions were seen on gray-scale ultrasonography and only 51 were seen on radiofrequency intravascular ultrasonography. Third, the use of intravascular ultrasonography was associated with serious adverse events in 11 patients, including 10 coronary dissections and 1 perforation, indicating that these procedures are not without risk. Finally, it is unclear what therapeutic approaches might be effective in mitigating the risk associated with specific lesion features.
In summary, we used conventional coronary angiography, gray-scale intravascular ultrasonography, and radiofrequency intravascular ultrasonography to assess the coronary vasculature in patients who had undergone successful percutaneous coronary intervention for an acute coronary syndrome. At 3 years, the rate of recurrent major adverse cardiovascular events was 20.4%; nearly half these events were associated with nonculprit lesions, most of which appeared by angiography to be mild. Lesion characteristics that were predictive of events associated with nonculprit lesions included a large plaque burden, a small luminal area, and thin-cap fibroatheromas.
Supported by Abbott Vascular and by Volcano.
Dr. Stone reports receiving grant support from Abbott Vascular, TherOx, the Medicines Company, Atrium Medical, Boston Scientific, and Volcano, being a board member for Devax, receiving consulting fees from Osprey, Reva Systems, Merck, InfraReDx, CoreValve, Boston Scientific, Abbott Vascular, Xtent, Edwards Lifesciences, Bioabsorbable Therapeutics, Asten BioPharma, Accelerated Technologies, S.B. Medical, Evalve, AstraZeneca, Prescient, Eli Lilly, Bristol-Myers Squibb, Sanofi-Aventis, Biosensors International, Otsuka, the Medicines Company, and Ortho-McNeil, receiving lecture fees from Edwards Lifesciences, Boston Scientific, and Abbott Vascular, and owning stock or stock options in Devax, CoreValve, Savacor, Biostar I and II funds, MedFocus I, II, and Accelerator funds, Xtent, Caliber, FlowCardia, Ovalum Vascular, MediGuide, Guided Delivery Systems, Arstasis, MiCardia, and AccessClosure; Dr. Maehara, receiving grant support from Boston Scientific and lecture fees from Volcano; Dr. Mintz, receiving grant support from Boston Scientific and Volcano, consultancy fees and lecture fees from Boston Scientific and Volcano, and travel or meeting expenses from Cappella; Dr. Mehran, receiving institutional grant support from Bristol-Myers Squibb and Sanofi-Aventis and consulting fees from Abbott Vascular, Cardiva Medical, the Medicines Company, and Regado BioSciences, and institutional grant support to her spouse from AstraZeneca and Cordis; Dr. McPherson, receiving consulting fees from Abbott Vascular and CardioDx and lecture fees from Volcano and CardioDx; Dr. Marso, receiving grant support from Volcano, Terumo, Novo Nordisk, the Medicines Company, and Amylin Pharmaceuticals, consulting fees from Volcano, Abbott Vascular, and Novo Nordisk, lecture fees from the Medicines Company, and payment for manuscript preparation from Novo Nordisk; Mr. Templin and Ms. White report being employees of Abbott Vascular.
Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.
No other potential conflict of interest relevant to this article was reported.
This article (10.1056/NEJMoa1002358) was updated on November 23, 2011, at NEJM.org.
We thank Deborah Kilpatrick and Bob Jones for their contributions during the design and initiation of the study and to Dr. Renu Virmani for her fundamental discoveries and review of the manuscript.
Source Information
From Columbia University Medical Center/New York–Presbyterian Hospital and the Cardiovascular Research Foundation, New York (G.W.S., A.M., A.J.L., E.C., G.S.M., R.M., H.P.); Cardiovascular Center, Onze-Lieve-Vrouwziekenhuis, Aalst, Belgium (B.B.); Vanderbilt University Medical Center, Nashville (J.M.); North Ohio Heart Center/Elyria Memorial Hospital Regional Medical Center, Elyria, OH (N.F.); Mid America Heart Institute, St. Luke's Hospital, Kansas City, MO (S.P.M.); Abbott Vascular, Santa Clara, CA (B.T., R.W., Z.Z.); and Erasmus University, Thoraxcentrum, Rotterdam, the Netherlands (P.W.S.).
Address reprint requests to Dr. Stone at the Columbia University Medical Center, Cardiovascular Research Foundation, 111 E. 59th St., 11th Fl., New York, NY 10022, or at gs2184@columbia.edu.
The investigators, institutions, and research organizations participating in the Providing Regional Observations to Study Predictors of Events in the Coronary Tree (PROSPECT) investigation are listed in the Supplementary Appendix, available at NEJM.org.
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- Comments (6)
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6 Reader's Comments
ALEXANDER D. FRANKE, MBBS | Physician | Disclosure: NonePERTH AustraliaJanuary 22, 2011Potential confounding factor unaddressed.
Stone et al are thanked for their use of intravenous ultrasound to characterize the 'virtual' histologic features that predicted recurrent myocardial infarctions due to lesions in epicardial vessels not treated by percutaneous intervention. The authors indicated that final variables entered into the multivariate analysis used to support the independent association of certain histological features at non-culprit lesion sites and acute coronary syndromes were age, sex, hypertension, insulin-requiring diabetes mellitus, previous percutaneous coronary intervention, baseline C-reactive protein, and family history of premature coronary artery disease. The authors state that there were 106 non-culprit lesion events occurring in 76 patients. Only 6 of the 76 required insulin for their diabetes. However, the authors observed a dose-response between the number of diseased epicardial arteries and the number of non-culprit lesion events with 29 patients with double-vessel disease and 41 patients with triple-vessel disease experiencing non-culprit lesion acute coronary syndromes. Therefore, of the 76 patients experiencing symptoms related to non-culprit lesions, 70 had disease of either two or three coronary arteries. Unfortunately, the authors' multivariate analysis and discussion do not account for this observation.
Without a more complete analysis of their results, it is premature for the authors to present certain ultrasonographic features of coronary arteries as 'independent' correlates of subsequent acute coronary syndromes.Ramakrishna Pinjala | Physician | Disclosure: NoneIndiaJanuary 21, 2011Current coronary imaging is inadequate to predict the clinical events?
The Trials repeatedly confirm that the existing coronary imaging modalities are inadequate and at the same time not free from complications. We need non-invasive lesion (plaque)-enhancing imaging modalities prior to angiography to define the distribution high-risk plaques. Until then we continue to treat lesions based on the mechanical obstruction they produce. A low risk lesion can become a high-risk lesion, and the reverse also can occur in the natural course of atherosclerosis. What we can understand from these trials is that we need better investigations to aid vascular interventions.
Hélcio Giffhorn | Physician | Disclosure: NoneBrazilJanuary 21, 2011HIGH RISK PATIENTS AND CARDIOVASCULAR EVENTS.
Patients having heart disease automatically places them at high CHD risk ( > 20% over 10 years ) - see Framingham Risk Score. In table 1, some goals were not achieved for the high risk patients for HDL (38.6) and LDL (93.6), and 47.7% are still smoking. A lack of adherence contribuitions to the advancement of the disease ? An invasive method (radiofrequency intravascular ultrasonography) could identify nonculprit lesions responsible for future events, but such a nethod is not practical in this moment. The calcium score failures many times. My opinion is that this study shows adverse cardiac events in high risk patients without proper adherence to medications. The atheromas progress and, then, major adverse cardiovascular events occur sooner.
James Marshall | Physician | Disclosure: NoneJanuary 21, 2011Natural History
It is interesting to see that the fundamental clinical and angiographic outcomes today parallel those of the thrombolytic era( AJC 1990 66:773-778).
Gen-Min Lin | Physician | Disclosure: NoneTaiwanJanuary 19, 2011Recalling the COURAGE Study
I appreciate the work by Dr.Stone and colleagues which reminds me the Optimal Medical Therapy with or without PCI for Stable Coronary Disease (COURAGE) study published in NEJM. The intra-coronary ultrasonographic findings of the target lesion without a minimal luminal area (MLA) ≤ 4 mm2 (hazard ratio=3.21) and a thin-cap fibroatheroma (hazard ratio=3.35) may overcome the hazard of a plaque burden ≥70% (hazard ratio=5.03) in patients with stable angina. Therefore the Providing Regional Observations to Study Predictors of Events in the Coronary Tree (PROSPECT) study seems to compitable with the COURAGE study.
In my opinion, the authors could further estimate the hazard ratio of the aforementioned subjects to controls in PROSPECT to correlate the findings in COURAGE. - Letters
better coronary investigations?
Stone and et al have said that at 3 years, the rate of recurrent major adverse cardiovascular events was 20.4%; nearly half these events were associated with nonculprit lesions, most of which appeared by angiography to be mild.This clearly indicates that angiography currently misses a substantial number of lesions responsible for recurrent major adverse cardiovascular events. Intravascular ultrasonography identifies those nonculprit lesions responsible for future events. Its time we start using better investigative procedures like this to make people live longer.