Aggressive Lipid-Lowering Therapy Compared with Angioplasty in Stable Coronary Artery Disease
Bertram Pitt, M.D., David Waters, M.D., William Virgil Brown, M.D., Ad J. van Boven, M.D., Ph.D., Leonard Schwartz, M.D., Lawrence M. Title, M.D., Daniel Eisenberg, M.D., Linda Shurzinske, M.S., Lisa S. McCormick, Pharm.D., for The Atorvastatin versus Revascularization Treatment Investigators
Background Percutaneous coronary revascularization is widelyused in improving symptoms and exercise performance in patientswith ischemic heart disease and stable angina pectoris. In thisstudy, we compared percutaneous coronary revascularization withlipid-lowering treatment for reducing the incidence of ischemicevents.
Methods We studied 341 patients with stable coronary arterydisease, relatively normal left ventricular function, asymptomaticor mild-to-moderate angina, and a serum level of low-densitylipoprotein (LDL) cholesterol of at least 115 mg per deciliter(3.0 mmol per liter) who were referred for percutaneous revascularization.We randomly assigned the patients either to receive medicaltreatment with atorvastatin, at 80 mg per day (164 patients),or to undergo the recommended percutaneous revascularizationprocedure (angioplasty) followed by usual care, which couldinclude lipid-lowering treatment (177 patients). The follow-upperiod was 18 months.
Results Twenty-two (13 percent) of the patients who receivedaggressive lipid-lowering treatment with atorvastatin (resultingin a 46 percent reduction in the mean serum LDL cholesterollevel, to 77 mg per deciliter [2.0 mmol per liter]) had ischemicevents, as compared with 37 (21 percent) of the patients whounderwent angioplasty (who had an 18 percent reduction in themean serum LDL cholesterol level, to 119 mg per deciliter [3.0mmol per liter]). The incidence of ischemic events was thus36 percent lower in the atorvastatin group over an 18-monthperiod (P=0.048, which was not statistically significant afteradjustment for interim analyses). This reduction in events wasdue to a smaller number of angioplasty procedures, coronary-arterybypass operations, and hospitalizations for worsening angina.As compared with the patients who were treated with angioplastyand usual care, the patients who received atorvastatin had asignificantly longer time to the first ischemic event (P=0.03).
Conclusions In low-risk patients with stable coronary arterydisease, aggressive lipid-lowering therapy is at least as effectiveas angioplasty and usual care in reducing the incidence of ischemicevents.
Coronary revascularization by percutaneous techniques is widelyused in the treatment of patients with stable angina pectoris,inducible myocardial ischemia, or both. Studies comparing medicaltreatment and percutaneous revascularization suggested thatpatients who underwent revascularization had an improvementin their quality of life, exercise performance, or both.1,2,3However, the effect of medical treatment, as compared with percutaneousrevascularization, on the incidence of ischemic events and theneed for subsequent revascularization was less certain. Lipid-loweringtreatment has been shown to reduce significantly the incidenceof cardiovascular events, overall mortality, and the need forrevascularization.4,5 We postulated that in patients with one-or two-vessel coronary artery disease, relatively normal leftventricular function, and no severe symptoms of angina pectoris,treatment with atorvastatin could delay or prevent the needfor revascularization without increasing the risk of ischemicevents. In a randomized, controlled study, we compared the outcomesin patients who received atorvastatin with the outcomes in similarpatients who underwent percutaneous revascularization, withor without stenting, and then received usual medical treatment,which could include lipid-lowering medication.
Methods
Study Design
The design of the Atorvastatin versus Revascularization Treatmentstudy has been reported previously.6 The study was an 18-month,open-label, randomized, multicenter study of patients with stablecoronary artery disease, a serum level of low-density lipoprotein(LDL) cholesterol of at least 115 mg per deciliter (3.0 mmolper liter), and a serum level of triglycerides of no more than500 mg per deciliter (5.6 mmol per liter). The patients hadstenosis of 50 percent or more in at least one coronary arteryand had been recommended for treatment with percutaneous revascularization.The patients were asymptomatic or had Canadian CardiovascularSociety (CCS) class I or II angina (four patients had more severeangina) and were able to complete at least four minutes of atreadmill test conducted according to the Bruce protocol ora bicycle exercise test at 20 W per minute without marked electrocardiographicchanges indicative of ischemia.7,8,9 Major criteria for exclusionfrom the study were left main coronary artery disease, triple-vesseldisease, unstable angina or myocardial infarction within theprevious two weeks, and an ejection fraction of less than 40percent. Informed consent was obtained from the study patients,and the research protocol was approved by the appropriate institutionalreview boards.
Treatment
The patients were stratified according to whether they had single-or double-vessel disease (defined as stenosis of 50 percentor more in one or two coronary arteries, respectively) and werethen randomly assigned either to receive medical treatment with80 mg of atorvastatin (Lipitor, Parke-Davis, Ann Arbor, Mich.)per day or to undergo the recommended percutaneous revascularizationprocedure (angioplasty), followed by usual care, which couldinclude lipid-lowering treatment. There was no washout periodfor patients already receiving lipid-lowering medication. Patientsassigned to receive atorvastatin discontinued any other lipid-loweringmedication they might have been taking and began taking atorvastatin(80 mg per day), whereas patients assigned to angioplasty andusual care were allowed to continue their current drug regimen.
Statistical Analysis
An independent end-points committee, the members of which wereunaware of the treatment assignments, reviewed all ischemicevents, and all analyses were based on the committee's classificationof ischemic events.
The CochranMantelHaenszel test, with stratificationaccording to the participating center and the extent of disease,was used in an intention-to-treat analysis to compare the twotreatment groups in regard to the proportion of patients withischemic events. We defined an ischemic event as at least oneof the following: death from cardiac causes, resuscitation aftercardiac arrest, nonfatal myocardial infarction, cerebrovascularaccident, coronary-artery bypass grafting, angioplasty, andworsening angina with objective evidence resulting in hospitalization.We used a Cox proportional-hazards analysis and KaplanMeiercurves to examine the time to a first ischemic event.
The sample size was planned to provide the study with 85 percentpower, with a two-sided level of significance of 5 percent forthe detection of a difference between treatment groups in theproportion of patients with ischemic events. Assumptions includedevent rates of 20 percent and 35 percent over a period of 18months in the atorvastatin and angioplasty groups, respectively.
Because of concern about the safety of patients not undergoingpercutaneous revascularization as the initial treatment, weperformed two interim analyses, using the O'BrienFlemingstopping rule. Consequently, the significance level for thefinal analysis of the incidence of ischemic events was adjustedfrom 5 percent to 4.5 percent.10 All remaining variables weretested with a 5 percent level of significance.
Results
Patients
A total of 341 patients at 37 centers in North America and Europewere randomly assigned to treatment groups between July 1995and December 1996. The characteristics of the patients in thetwo treatment groups were similar at base line (Table 1). Therewere small but significant differences between the groups interms of sex, concurrent use of aspirin or other anticoagulants,and the presence of left anterior descending coronary arterydisease. Separate analyses for each sex and for patients withand without left anterior descending coronary artery diseaseshowed the trends within these subgroups to be similar to theoverall results. In no subgroup was there a result favoringangioplasty.
Table 1. Base-Line Characteristics of the Patients.
One patient in the atorvastatin group never received atorvastatin,and 11 of the patients in the angioplasty group (6 percent)did not undergo revascularization as assigned because of refusalby the patient (8 patients), disease progression (1, who underwentcoronary-artery bypass grafting), regression of the lesion (1),and a procedure that was unsuccessful because of technical difficulty(1); these patients remained in the study. Four of the patientsin the atorvastatin group (2 percent) and two of the patientsin the angioplasty group (1 percent) withdrew from the studybecause of an adverse event (mild impotence in one patient inthe atorvastatin group) or a decision by the patient (threepatients in the atorvastatin group and two in the angioplastygroup). In addition, eight of the patients in the atorvastatingroup discontinued the study treatment (two because of elevationsin the level of liver enzymes, five because of adverse events,and one because of a decision by the patient); these patientsremained in the study. Overall, at least 95 percent of the patientswere considered to be compliant with the atorvastatin regimenat each visit to the clinic. Follow-up information was collectedon all patients at least 18 months after randomization; no patientswere lost to follow-up.
Overall, 166 patients in the angioplasty group underwent theassigned procedure (with a total of 213 treated lesions). Concomitantstenting was used in 64 of the lesions, and atherectomy in 4.The mean percentages of stenosis in the target lesions beforeand after revascularization were 81 percent and 20 percent,respectively. The mean percentage of stenosis at base line inthe atorvastatin group was 80 percent.
The patients' smoking status did not change throughout the study,whereas patients in both treatment groups made similar improvementsin their eating and exercise habits.
Concurrent Medication
At screening, 75 patients (22 percent) were taking medicationthat modifies lipid levels. In the angioplasty group, 130 patients(73 percent) received lipid-lowering medication at some timeduring the study, of whom 125 (71 percent of the total group)received a statin (median dose, 20 mg per day), and 123 (69percent) were receiving lipid-lowering medication at the endof the study. Atorvastatin received approval from U.S. and Europeanregulatory authorities while the study was under way; as a result,17 of the patients in the angioplasty group (10 percent) receivedprescriptions for atorvastatin (median dose, 20 mg per day).In the atorvastatin group, 153 patients (93 percent) continuedto receive atorvastatin until the end of the study. During thestudy, aspirin was taken by 135 patients in the atorvastatingroup (82 percent) and 158 in the angioplasty group (89 percent),although significantly more patients in the angioplasty grouphad been taking aspirin at base line.
Lipoprotein Levels
The patients who were randomly assigned to receive atorvastatinhad significantly lower levels of LDL cholesterol, total cholesterol,and triglycerides than the patients in the angioplasty group(P<0.05) (Figure 1). Because 22 percent of all patients werealready receiving lipid-lowering medication at base line andthere was no washout period, the changes in lipid levels reflectincremental changes from base-line values.
Figure 1. Changes in Lipoprotein Levels in the Atorvastatin Group and the Angioplasty Group.
An asterisk denotes that the reduction was significantly different from that in the angioplasty group (P<0.05). To convert values for cholesterol to millimoles per liter, multiply by 0.02586. To convert values for triglycerides to millimoles per liter, multiply by 0.01129. LDL denotes low-density lipoprotein, and HDL high-density lipoprotein.
Ischemic Events
Twenty-two of the patients in the atorvastatin group (13 percent)and 37 in the angioplasty group (21 percent) had ischemic events,a difference of 36 percent (P=0.048) (Table 2). Although thisdifference did not reach the level of significance as adjustedfor interim analyses (P=0.045), it did reach the conventional5 percent level of significance. Twenty of the patients in theatorvastatin group (12 percent) underwent a revascularizationprocedure, either coronary-artery bypass grafting or percutaneousangioplasty, during the follow-up period, as compared with 29of the patients in the angioplasty group (16 percent) who hada subsequent revascularization. Fourteen of the follow-up proceduresin the angioplasty group (48 percent) involved the placementof at least one stent, whereas nine of the follow-up proceduresin the atorvastatin group (41 percent) included stenting.
Table 2. Occurrence of Ischemic Events According to Treatment Group.
When the data on ischemic events were analyzed according totime, there was a greater difference between treatment groupsafter the first six months of treatment. Twelve of the patientsin the atorvastatin group (7 percent) and 17 of the patientsin the angioplasty group (10 percent) had a first event withinsix months after treatment was begun (P=0.45). After the firstsix months, 10 patients in the atorvastatin group (6 percent)and 20 patients in the angioplasty group (11 percent) had afirst event (P=0.09).
Of the 23 patients in the atorvastatin group and the 28 patientsin the angioplasty group who had a target lesion of the proximalleft anterior descending coronary artery at base line (14 percentand 16 percent, respectively), 2 of the patients in the atorvastatingroup (9 percent) had ischemic events, as compared with 7 ofthe patients in the angioplasty group (25 percent).
Treatment with atorvastatin, as compared with angioplasty, wasassociated with a significantly longer time to a first ischemicevent (P=0.03) and with a reduction in risk of 36 percent (Figure 2).
Figure 2. Cumulative Incidence of First Ischemic Events.
The time to an ischemic event was significantly longer in the atorvastatin group (P=0.03), and the risk reduction was 36 percent (95 percent confidence interval, 5 to 67 percent).
Angina
At the end of the study, 67 patients in the atorvastatin group(41 percent) had an improvement in the CCS classification ofangina symptoms, 78 (48 percent) had no change, and 19 (12 percent)had a deterioration. Of the patients in the angioplasty group,95 (54 percent) had an improvement in the CCS classification,70 (40 percent) had no change, and 12 (7 percent) had a deterioration.This difference between treatment groups significantly favoredangioplasty (P=0.009 by the CochranMantelHaenszeltest). However, this outcome variable was the only one not reviewedby the end-points committee.
The percentage of patients receiving antianginal medicationwas similar in the treatment groups both at base line and atthe end of the study, although in many cases the nitrates prescribedwere only nitroglycerin to be taken as needed (Table 3). Morepatients started to use or increased their doses of antianginalmedications in the angioplasty group (18 percent) than in theatorvastatin group (8 percent), and fewer patients stopped usingantianginal medications or decreased their doses in the angioplastygroup (16 percent) than in the atorvastatin group (21 percent).
Table 3. Use of Antianginal Medication at Base Line and at the End of the Study.
At base line, 25 percent of the patients in the atorvastatingroup and 24 percent of the patients in the angioplasty groupwere receiving two antianginal drugs, and 15 percent and 12percent, respectively, were receiving three. At the end of thestudy, 24 percent of each group were receiving two antianginaldrugs, and 12 percent and 13 percent, respectively, were receivingthree.
Quality of Life
The patients' quality of life was assessed at base line andat 6 and 18 months after randomization with use of the 36-itemMedical Outcomes Study Short-Form General Health Survey.11,12Both treatment groups had a mean increase in the summary scoresfor physical and mental health at both the 6-month and 18-monthassessments, denoting an improvement in the quality of lifefrom base line. Mean increases in scores ranged from 2.9 to6.3; the increases were slightly larger in the angioplasty group.Given the variability and the small sample, we could not determineany differences between the two groups in terms of quality oflife.
Safety
The adverse events reported were similar in the two treatmentgroups. Seventeen of the patients in the atorvastatin group(10 percent) reported serious adverse events, none of whichwere considered to be related to atorvastatin therapy. In 13patients, the serious events led to, or resulted from, diagnosticor surgical procedures (colectomy [2 patients], cholecystectomy[2 patients], gastrectomy, appendectomy [2 patients], dilationand curettage, placement of hip screws, repair of a right femoralartery, magnetic resonance imaging and radiography of the femur,pacemaker implantation, and electrophysiologic study of an implantedpacemaker). The other four patients had bronchopneumonia; abdominalpain, constipation, and atypical chest pain; a urinary tractinfection and prostate cancer; and rheumatoid arthritis.
Twenty-eight of the patients in the angioplasty group (16 percent)had serious adverse events. Six of these patients (21 percent)had events that were considered to be related to the angioplastyprocedure (thrombosis at the access site, dissection, arteriovenousfistula, coronary occlusion, occlusion of iliac stenosis, andfemoral hematoma). Four of the patients in the atorvastatingroup (2 percent) had persistent, clinically important elevationsin the level of aspartate or alanine aminotransferase (definedas a level that was more than three times the upper limit ofnormal). No patient in either treatment group had persistent,clinically important elevations in the creatine kinase level(defined as a level that was more than 10 times the upper limitof normal). Seven cancers were diagnosed during the study: threein patients in the atorvastatin group and four in patients inthe angioplasty group.
Discussion
Our study suggests that aggressive lowering of LDL cholesterollevels with atorvastatin (to a mean level of 77 mg per deciliterin our study group) is at least as effective as angioplastyfollowed by usual care (which reduced the LDL cholesterol levelto 119 mg per deciliter in our study) in reducing the incidenceof ischemic events in low-risk patients who have been referredfor revascularization.
We found a 36 percent lower incidence of ischemic events overa period of 18 months in patients treated with atorvastatinas compared with angioplasty followed by usual medical care.This result narrowly missed the level of significance as adjustedfor interim analyses. Nonetheless, our findings are important.This is particularly true given the significantly longer timeto a first ischemic event in the patients treated with atorvastatinthan in those who underwent angioplasty (Figure 2). Most angioplasty-relatedevents and restenoses occur within six months after revascularization.However, in this study, 20 of the patients in the angioplastygroup (11 percent) had a first ischemic event after six months,as compared with 10 of the patients in the atorvastatin group(6 percent). The greater difference in the incidence of ischemicevents after the first six months (Figure 2) suggests that thechief explanation for the difference in the occurrence of ischemicevents is the effect of the lowering of lipid levels with atorvastatin.In previous trials, lipid-lowering treatment has been shownto have a beneficial effect only after six or more months.4,5This finding is supported by the KaplanMeier analysis(the time to the first ischemic event) in the present study,which showed a greater divergence between the two treatmentgroups after six months. Although it is possible that many ischemicevents that occurred after six months among patients in theangioplasty group could have been related to complications ofangioplasty, an analysis of individual angiograms indicatedthat restenosis could account for only a small percentage ofthe events. This finding suggests a delayed effect of lipidlowering, possibly due to an improvement in endothelial function(vasomotor tone).
Major coronary events were infrequent in both treatment groups;their incidence was only 2 percent per year. Fewer patientsin the atorvastatin group than in the angioplasty group werehospitalized with worsening angina and objective evidence ofmyocardial ischemia (11 vs. 25), and fewer patients in the atorvastatingroup underwent bypass surgery or angioplasty during follow-up(20 vs. 29). Of the patients randomly assigned to receive atorvastatin,87 percent continued to receive medical therapy without havingan ischemic event during 18 months of follow-up. As in previoustrials comparing medical therapy with angioplasty, there wasa small but significant improvement in the CCS angina classin patients randomly assigned to undergo angioplasty,1,2,3 albeitwith an increase in antianginal treatment. However, this improvementin the severity of angina among patients in the angioplastygroup was more than offset by the reduction in ischemic eventsand the longer time to a first event among patients in the atorvastatingroup.
The 46 percent reduction in the LDL cholesterol level, to amean level of 77 mg per deciliter, with the use of atorvastatinin this study was not associated with an increase in adverseevents. The adverse events reported were similar in the twotreatment groups, and only four of the patients in the atorvastatingroup (2 percent) had persistently elevated aspartate or alanineaminotransferase levels.
It is unlikely that a longer follow-up period would have showna benefit of angioplasty in comparison with medical treatment.Serial angiographic studies have shown that myocardial infarctionoccurs most often in lesions that originally appear to be hemodynamicallyunimportant and that would therefore not be subject to angioplasty.13Thus, we postulate that the aggressive lowering of lipid levelsis more likely than angioplasty of high-grade lesions to preventfurther progression of these minimal coronary-artery lesionsand thereby prevent plaque rupture.14 In cholesterol-loweringtrials, there was little benefit of medical treatment over placeboin the first two years of treatment, and outcome curves beganto diverge after this time.4,5 It could thus be argued thatlonger follow-up in our study might further favor medical treatmentwith atorvastatin.
Our results do not provide evidence in regard to the value ofangioplasty in patients who have severe symptoms and whose qualityof life has been severely affected or in high-risk patientswith left ventricular dysfunction, left main coronary arterydisease, or triple-vessel disease or in patients with anginapectoris who have less exercise tolerance. However, one mightanticipate that aggressive lowering of lipid levels would complementangioplasty in such patients, particularly by stabilizing untreatedlesions.
Until the results of additional long-term trials in a largernumber of patients are available, aggressive lipid loweringwith atorvastatin appears to be as safe and as effective asangioplasty and usual care in reducing the incidence of ischemicevents. Moreover, it appears that in patients with relativelynormal left ventricular function who do not have severe symptoms,an initial strategy of aggressive lipid lowering with atorvastatinmay reduce the likelihood of ischemic events and thereby delayor prevent the need for revascularization. If at any time symptomsworsen or exercise performance deteriorates to the extent thatit interferes with the quality of life, patients may elect toundergo revascularization without any apparent penalty for theirinitial decision.
Supported by a grant from Parke-Davis Pharmaceutical Research,a division of Warner-Lambert Company.
Drs. Pitt, Waters, and Brown are consultants to Parke-Davis.Ms. Shurzinske and Dr. McCormick are employees and stockholdersof Parke-Davis.
We are indebted to D. McDougal, C. Justice, W. Foley Eggleston,and R. Overhiser for assistance in managing the study and toT. Stern, Ph.D., for statistical support.
* Other investigators are listed in the Appendix.
Source Information
From the Department of Medicine, University of Michigan School of Medicine, Ann Arbor (B.P.); the Division of Cardiology, Hartford Hospital, Hartford, Conn. (D.W.); the Department of Medicine, Emory University School of Medicine, Atlanta (W.V.B.); Thoraxcentre, University Hospital, Groningen, the Netherlands (A.J.B.); the Department of Medicine, Toronto Hospital, Toronto (L. Schwartz); the Division of Cardiology, Queen Elizabeth II Health Sciences Centre, Halifax, N.S. (L.M.T.); Providence Saint Joseph Medical Center, Los Angeles (D.E.); and Parke-Davis Pharmaceutical Research Division, Warner-Lambert Company, Ann Arbor, Mich. (L. Shurzinske, L.S.M.).
Address reprint requests to Dr. Pitt at the Division of Cardiology, University of Michigan Medical Center, 3910 Taubman, 1500 E. Medical Center Dr., Ann Arbor, MI 48109-0366, or at bpitt{at}umich.edu.
References
Parisi AF, Folland ED, Hartigan P. A comparison of angioplasty with medical therapy in the treatment of single-vessel coronary artery disease. N Engl J Med 1992;326:10-16. [Abstract]
Hueb WA, Bellotti G, de Oliveira SA, et al. The Medicine, Angioplasty or Surgery Study (MASS): a prospective, randomized trial of medical therapy, balloon angioplasty or bypass surgery for single proximal left anterior descending artery stenoses. J Am Coll Cardiol 1995;26:1600-1605. [Abstract]
Coronary angioplasty versus medical therapy for angina: the second Randomised Intervention Treatment of Angina (RITA-2) trial. Lancet 1997;350:461-468. [CrossRef][Medline]
Scandinavian Simvastatin Survival Study Group. Randomized trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet 1994;344:1383-1389. [CrossRef][Medline]
Sacks FM, Pfeffer MA, Moye LA, et al. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. N Engl J Med 1996;335:1001-1009. [Free Full Text]
McCormick LS, Black DM, Waters D, Brown WV, Pitt B. Rationale, design, and baseline characteristics of a trial comparing aggressive lipid lowering with Atorvastatin Versus Revascularization Treatments (AVERT). Am J Cardiol 1997;80:1130-1133. [CrossRef][Medline]
Campeau L. Grading of angina pectoris. Circulation 1976;54:522-523. [Medline]
Janicki JS, Weber KT. Equipment and protocols to evaluate the exercise response. In: Janicki JS, Weber KT, eds. Cardiopulmonary exercise testing. Section 9. Philadelphia: W.B. Saunders, 1986:147.
Brasseur LA, Mairaux PH, Kandouci AB, Detry JM. Respiratory and metabolic parameters during submaximal and maximal exercise in normal men. In: Rulli V, Messin R, Denolin H, eds. Normal values in adult ergometry according to age, sex, and training. Torino, Italy: Schiapparelli Farmaceutici, 1983:3-14 (pamphlet).
Geller NL, Pocock SJ. Design and analysis of clinical trials with group sequential stopping rules. In: Peace KE, ed. Biopharmaceutical statistics for drug development. New York: Marcel Dekker, 1988:489-508.
Ware JE Jr, Sherbourne CD. The MOS 36-item short-form health survey (SF-36). 1. Conceptual framework and item selection. Med Care 1992;30:473-483. [Medline]
Ware JE Jr, Snow KK, Kosinski M, Gandek B. SF-36 health survey: manual and interpretation guide. Boston: Health Institute, New England Medical Center, 1993.
Forrester JS, Shah PK. Lipid lowering versus revascularization: an idea whose time (for testing) has come. Circulation 1997;96:1360-1362. [Free Full Text]
Waters D. Plaque stabilization: a mechanism for the beneficial effect of lipid-lowering therapies in angiographic studies. Prog Cardiovasc Dis 1994;37:107-120. [CrossRef][Medline]
Appendix
In addition to the authors, the principal investigators of theAtorvastatin versus Revascularization Treatment study were asfollows: United States D.M. Black and M. Pressler, AnnArbor, Mich.; A.S. Brown, Lombard, Ill.; M.D. Ezekowitz, WestHaven, Conn.; R.L. Feldman, Ocala, Fla.; C.M. Gibson, West Roxbury,Mass.; S.W. Halpern, Santa Rosa, Calif.; M.A. Kellett and L.Keilson, Portland, Me.; D. Lu, Washington, D.C.; B. MacCallisterand R. VandenBelt, Ypsilanti, Mich.; M. Miller, Baltimore; W.O'Neill, Royal Oak, Mich.; C.J. Pepine, Gainesville, Fla.; A.L.Pucillo, Valhalla, N.Y.; and R. Wilensky, Philadelphia; Canada T.J. Anderson, Calgary, Alta.; R.G. Carere, Vancouver,B.C.; G. Cote, Montreal; J. Ducas, Winnipeg, Man.; S. Lepage,Sherbrooke, Que.; L. Schwartz, Toronto; B. O'Neill and L. Title,Halifax, N.S.; Europe France: J.L. Guermonprez, Paris;J. Puel, Toulouse; Germany: A. Frey, Bad Krozingen; F.X. Kleber,Berlin; H. Mudra, Munich; B. Wagner, Freiburg; A. Zeiher, Frankfurt;Italy: P. Zardini, Verona; Spain: E. Domingo, Barcelona; C.Macaya, Madrid; Switzerland: W. Kiowski, Zurich; the Netherlands:P. de Feyter, Rotterdam; A.J. van Boven, Groningen; United Kingdom:N.H. Brooks, Manchester; A.R. Rickards and A.D. Timmis, London;and D.H. Roberts, Blackpool.
The committees that participated in the study were as follows:AdvisoryData and Safety Monitoring Committee B. Pitt, W.V. Brown, and D. Waters; End-Points Committee R. DiBianco (chairperson), K. Eagle, A. Maseri, and C.M. O'Connor.
Bastarrika, G., Lee, Y. S., Huda, W., Ruzsics, B., Costello, P., Schoepf, U. J.
(2009). CT of Coronary Artery Disease. Radiology
253: 317-338
[Abstract][Full Text]
Horst, B., Rihal, C. S., Holmes, D. R. Jr, Bresnahan, J. F., Prasad, A., Gau, G., Lennon, R., Lerman, A.
(2009). Comparison of Drug-Eluting and Bare-Metal Stents for Stable Coronary Artery Disease. J Am Coll Cardiol Intv
2: 321-328
[Abstract][Full Text]
SHISHEHBOR, M. H., HAZEN, S. L.
(2009). JUPITER to Earth: A statin helps people with normal LDL-C and high hs-CRP, but what does it mean?. Cleveland Clinic Journal of Medicine
76: 37-44
[Abstract][Full Text]
Crea, F., Camici, P. G., De Caterina, R., Lanza, G. A.
(2009). CHAPTER 17 Chronic Ischaemic Heart Disease. ESC Textbook of Cardiovascular Medicine
2: med-9780199566990-chapter-med-9780199566990-chapter
[Abstract][Full Text]
Jacobson, T. A., Wertz, D. A., Hoy, T., Kuznik, A., Grochulski, D., Cziraky, M.
(2008). Comparison of Cardiovascular Event Rates in Patients Without Cardiovascular Disease in Whom Atorvastatin or Simvastatin Was Newly Initiated. Mayo Clin Proc.
83: 1316-1325
[Abstract][Full Text]
Lin, G. A., Dudley, R. A., Lucas, F. L., Malenka, D. J., Vittinghoff, E., Redberg, R. F.
(2008). Frequency of Stress Testing to Document Ischemia Prior to Elective Percutaneous Coronary Intervention. JAMA
300: 1765-1773
[Abstract][Full Text]
Schomig, A., Mehilli, J., de Waha, A., Seyfarth, M., Pache, J., Kastrati, A.
(2008). A Meta-Analysis of 17 Randomized Trials of a Percutaneous Coronary Intervention-Based Strategy in Patients With Stable Coronary Artery Disease. J Am Coll Cardiol
52: 894-904
[Abstract][Full Text]
Weintraub, W. S., Boden, W. E., Zhang, Z., Kolm, P., Zhang, Z., Spertus, J. A., Hartigan, P., Veledar, E., Jurkovitz, C., Bowen, J., Maron, D. J., O'Rourke, R., Dada, M., Teo, K. K., Goeree, R., Barnett, P. G., on Behalf of the Department of Veterans Affairs Co,
(2008). Cost-Effectiveness of Percutaneous Coronary Intervention in Optimally Treated Stable Coronary Patients. Circ Cardiovasc Qual Outcomes
1: 12-20
[Abstract][Full Text]
Weintraub, W. S., Spertus, J. A., Kolm, P., Maron, D. J., Zhang, Z., Jurkovitz, C., Zhang, W., Hartigan, P. M., Lewis, C., Veledar, E., Bowen, J., Dunbar, S. B., Deaton, C., Kaufman, S., O'Rourke, R. A., Goeree, R., Barnett, P. G., Teo, K. K., Boden, W. E., the COURAGE Trial Research Group,
(2008). Effect of PCI on Quality of Life in Patients with Stable Coronary Disease. NEJM
359: 677-687
[Abstract][Full Text]
Coylewright, M., Blumenthal, R. S., Post, W.
(2008). Placing COURAGE in Context: Review of the Recent Literature on Managing Stable Coronary Artery Disease. Mayo Clin Proc.
83: 799-805
[Abstract][Full Text]
Holmes, D. R. Jr, Gersh, B. J., Whitlow, P., King, S. B. III, Dove, J. T.
(2008). Percutaneous coronary intervention for chronic stable angina a reassessment.. J Am Coll Cardiol Intv
1: 34-43
[Abstract][Full Text]
Brown, M. L., Sundt, T. M. III, Gersh, B. J.
(2008). Indications for Revascularization. Card Surg Adult
3: 551-572
[Full Text]
Cheng, S., Jarcho, J.
(2007). Management of Stable Coronary Disease -- Polling Results. NEJM
357: e28-e28
[Full Text]
Kereiakes, D. J., Teirstein, P. S., Sarembock, I. J., Holmes, D. R. Jr, Krucoff, M. W., O'Neill, W. W., Waksman, R., Williams, D. O., Popma, J. J., Buchbinder, M., Mehran, R., Meredith, I. T., Moses, J. W., Stone, G. W.
(2007). The Truth and Consequences of the COURAGE Trial. J Am Coll Cardiol
50: 1598-1603
[Abstract][Full Text]
Bax, J. J., Young, L. H., Frye, R. L., Bonow, R. O., Steinberg, H. O., Barrett, E. J.
(2007). Screening for Coronary Artery Disease in Patients With Diabetes. Diabetes Care
30: 2729-2736
[Abstract][Full Text]
Lipson, A. H., Fallis, W. M., Wang, X., Yi, Y.
(2007). Are patients with hyperlipidemia undertreated?: Study of patients admitted to hospital with coronary events. cfp
53: 1502-1507
[Abstract][Full Text]
Lin, G. A., Dudley, R. A., Redberg, R. F.
(2007). Cardiologists' Use of Percutaneous Coronary Interventions for Stable Coronary Artery Disease. Arch Intern Med
167: 1604-1609
[Abstract][Full Text]
Stein, E. A.
(2007). Statins and Children: Whom Do We Treat and When?. Circulation
116: 594-595
[Full Text]
Scolari, F., Ravani, P., Gaggi, R., Santostefano, M., Rollino, C., Stabellini, N., Colla, L., Viola, B. F., Maiorca, P., Venturelli, C., Bonardelli, S., Faggiano, P., Barrett, B. J.
(2007). The Challenge of Diagnosing Atheroembolic Renal Disease: Clinical Features and Prognostic Factors. Circulation
116: 298-304
[Abstract][Full Text]
Merhige, M. E., Breen, W. J., Shelton, V., Houston, T., D'Arcy, B. J., Perna, A. F.
(2007). Impact of Myocardial Perfusion Imaging with PET and 82Rb on Downstream Invasive Procedure Utilization, Costs, and Outcomes in Coronary Disease Management. JNM
48: 1069-1076
[Abstract][Full Text]
Pijls, N. H.J., van Schaardenburgh, P., Manoharan, G., Boersma, E., Bech, J.-W., van't Veer, M., Bar, F., Hoorntje, J., Koolen, J., Wijns, W., de Bruyne, B.
(2007). Percutaneous Coronary Intervention of Functionally Nonsignificant Stenosis: 5-Year Follow-Up of the DEFER Study. J Am Coll Cardiol
49: 2105-2111
[Abstract][Full Text]
Hochman, J. S., Steg, P. G.
(2007). Does Preventive PCI Work?. NEJM
356: 1572-1574
[Full Text]
Boden, W. E., O'Rourke, R. A., Teo, K. K., Hartigan, P. M., Maron, D. J., Kostuk, W. J., Knudtson, M., Dada, M., Casperson, P., Harris, C. L., Chaitman, B. R., Shaw, L., Gosselin, G., Nawaz, S., Title, L. M., Gau, G., Blaustein, A. S., Booth, D. C., Bates, E. R., Spertus, J. A., Berman, D. S., Mancini, G.B. J., Weintraub, W. S., the COURAGE Trial Research Group,
(2007). Optimal Medical Therapy with or without PCI for Stable Coronary Disease. NEJM
356: 1503-1516
[Abstract][Full Text]
Patel, T. N., Shishehbor, M. H., Bhatt, D. L.
(2007). A review of high-dose statin therapy: targeting cholesterol and inflammation in atherosclerosis. Eur Heart J
28: 664-672
[Abstract][Full Text]
Mahmarian, J. J., Dakik, H. A., Filipchuk, N. G., Shaw, L. J., Iskander, S. S., Ruddy, T. D., Keng, F., Henzlova, M. J., Allam, A., Moye, L. A., Pratt, C. M., for the INSPIRE Investigators,
(2006). An Initial Strategy of Intensive Medical Therapy Is Comparable to That of Coronary Revascularization for Suppression of Scintigraphic Ischemia in High-Risk But Stable Survivors of Acute Myocardial Infarction. J Am Coll Cardiol
48: 2458-2467
[Abstract][Full Text]
Gibbons, R. J., Miller, T. D.
(2006). Noninvasive Risk Stratification After Myocardial Infarction: New Evidence, New Questions. J Am Coll Cardiol
48: 2468-2470
[Full Text]
Dzau, V. J., Antman, E. M., Black, H. R., Hayes, D. L., Manson, J. E., Plutzky, J., Popma, J. J., Stevenson, W.
(2006). The Cardiovascular Disease Continuum Validated: Clinical Evidence of Improved Patient Outcomes: Part I: Pathophysiology and Clinical Trial Evidence (Risk Factors Through Stable Coronary Artery Disease). Circulation
114: 2850-2870
[Full Text]
Bonovas, S., Filioussi, K., Tsavaris, N., Sitaras, N. M.
(2006). Statins and Cancer Risk: A Literature-Based Meta-Analysis and Meta-Regression Analysis of 35 Randomized Controlled Trials. JCO
24: 4808-4817
[Abstract][Full Text]
Kennedy, D. J., Burket, M. W., Khuder, S. A., Shapiro, J. I., Topp, R. V., Cooper, C. J.
(2006). Quality of life improves after renal artery stenting.. Biol Res Nurs
8: 129-137
[Abstract]
Smith, P. K., Califf, R. M., Tuttle, R. H., Shaw, L. K., Lee, K. L., Delong, E. R., Lilly, R. E., Sketch, M. H. Jr, Peterson, E. D., Jones, R. H.
(2006). Selection of surgical or percutaneous coronary intervention provides differential longevity benefit.. Ann. Thorac. Surg.
82: 1420-1429
[Abstract][Full Text]
Authors/Task Force Members, , Fox, K., Garcia, M. A. A., Ardissino, D., Buszman, P., Camici, P. G., Crea, F., Daly, C., De Backer, G., Hjemdahl, P., Lopez-Sendon, J., Marco, J., Morais, J., Pepper, J., Sechtem, U., Simoons, M., Thygesen, K., ESC Committee for Practice Guidelines (CPG), , Priori, S. G., Blanc, J.-J., Budaj, A., Camm, J., Dean, V., Deckers, J., Dickstein, K., Lekakis, J., McGregor, K., Metra, M., Morais, J., Osterspey, A., Tamargo, J., Zamorano, J. L., Document Reviewers, , Zamorano, J. L, Andreotti, F., Becher, H., Dietz, R., Fraser, A., Gray, H., Antolin, R. A. H., Huber, K., Kremastinos, D. T., Maseri, A., Nesser, H.-J., Pasierski, T., Sigwart, U., Tubaro, M., Weis, M.
(2006). Guidelines on the management of stable angina pectoris: executive summary: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology. Eur Heart J
27: 1341-1381
[Full Text]
Wong, K Y K, McSwiggan, S, Kennedy, N S J, MacWalter, R S, Struthers, A D
(2006). B-type natriuretic peptide identifies silent myocardial ischaemia in stroke survivors. Heart
92: 487-489
[Abstract][Full Text]
Nash, D. T.
(2005). The Case for Medical Treatment in Chronic Stable Coronary Artery Disease. Arch Intern Med
165: 2587-2589
[Full Text]
King, S. B. III
(2005). Angioplasty Is Better Than Medical Therapy for Alleviating Chronic Angina Pectoris. Arch Intern Med
165: 2589-2592
[Full Text]
King, S. B. III
(2005). Rebuttal. Arch Intern Med
165: 2593-2594
[Full Text]
Abrams, J., Thadani, U.
(2005). Therapy of Stable Angina Pectoris: The Uncomplicated Patient. Circulation
112: e255-e259
[Full Text]
Nashed, B., Yeganeh, B., HayGlass, K. T., Moghadasian, M. H.
(2005). Antiatherogenic Effects of Dietary Plant Sterols Are Associated with Inhibition of Proinflammatory Cytokine Production in Apo E-KO Mice. J. Nutr.
135: 2438-2444
[Abstract][Full Text]
Ong, H.T.
(2005). The statin studies: from targeting hypercholesterolaemia to targeting the high-risk patient. QJM
98: 599-614
[Abstract][Full Text]
Kawasaki, M., Sano, K., Okubo, M., Yokoyama, H., Ito, Y., Murata, I., Tsuchiya, K., Minatoguchi, S., Zhou, X., Fujita, H., Fujiwara, H.
(2005). Volumetric Quantitative Analysis of Tissue Characteristics of Coronary Plaques After Statin Therapy Using Three-Dimensional Integrated Backscatter Intravascular Ultrasound. J Am Coll Cardiol
45: 1946-1953
[Abstract][Full Text]
Katritsis, D. G., Ioannidis, J. P.A.
(2005). Percutaneous Coronary Intervention Versus Conservative Therapy in Nonacute Coronary Artery Disease: A Meta-Analysis. Circulation
111: 2906-2912
[Abstract][Full Text]
Mensah, K., Mocanu, M. M., Yellon, D. M.
(2005). Failure to protect the myocardium against ischemia/reperfusion injury after chronic atorvastatin treatment is recaptured by acute atorvastatin treatment: A potential role for phosphatase and tensin homolog deleted on chromosome ten?. J Am Coll Cardiol
45: 1287-1291
[Abstract][Full Text]
Authors/Task Force Members, , Silber, S., Albertsson, P., Aviles, F. F., Camici, P. G., Colombo, A., Hamm, C., Jorgensen, E., Marco, J., Nordrehaug, J.-E., Ruzyllo, W., Urban, P., Stone, G. W., Wijns, W.
(2005). Guidelines for Percutaneous Coronary Interventions: The Task Force for Percutaneous Coronary Interventions of the European Society of Cardiology. Eur Heart J
26: 804-847
[Full Text]
Modest, G. A.
(2005). Medical vs Surgical Management of Left Main Coronary Artery Disease. JAMA
293: 1060-1061
[Full Text]
Kim, J., Henderson, R. A., Pocock, S. J., Clayton, T., Sculpher, M. J., Fox, K. A.A., RITA-3 Trial Investigators,
(2005). Health-related quality of life after interventional or conservative strategy in patients with unstable angina or non-ST-segment elevation myocardial infarction: One-year results of the third randomized intervention trial of unstable angina (RITA-3). J Am Coll Cardiol
45: 221-228
[Abstract][Full Text]
Sabatine, M. S., Braunwald, E.
(2005). Another look at the age-old question: Which came first, the elevated c-reactive protein or the atherothrombosis?. J Am Coll Cardiol
45: 244-245
[Full Text]
Bonetti, P. O., Kaiser, C., Zellweger, M. J., Grize, L., Erne, P., Schoenenberger, R. A., Pfisterer, M. E., TIME Investigators,
(2005). Long-Term Benefits and Limitations of Combined Antianginal Drug Therapy in Elderly Patients with Symptomatic Chronic Coronary Artery Disease. J CARDIOVASC PHARMACOL THER
10: 29-37
[Abstract]
Curtis, J. P., Krumholz, H. M.
(2004). Keeping the Patient in View: Defining the Appropriateness of Percutaneous Coronary Interventions. Circulation
110: 3746-3748
[Full Text]
Claude, J., Schindler, C., Kuster, G. M., Schwenkglenks, M., Szucs, T., Buser, P., Osswald, S., Kaiser, C., Gradel, C., Estlinbaum, W., Rickenbacher, P., Pfisterer, M., for the Trial of Invasive versus Medical therapy i,
(2004). Cost-effectiveness of invasive versus medical management of elderly patients with chronic symptomatic coronary artery disease: Findings of the randomized trial of invasive versus medical therapy in elderly patients with chronic angina (TIME). Eur Heart J
25: 2195-2203
[Abstract][Full Text]
Woodard, L. D., Kressin, N. R., Petersen, L. A.
(2004). Is Lipid-Lowering Therapy Underused by African Americans at High Risk of Coronary Heart Disease Within the VA Health Care System?. AJPH
94: 2112-2117
[Abstract][Full Text]
Hanania, G, Cambou, J-P, Gueret, P, Vaur, L, Blanchard, D, Lablanche, J-M, Boutalbi, Y, Humbert, R, Clerson, P, Genes, N, Danchin, N, for the USIC 2000 Investigators,
(2004). Management and in-hospital outcome of patients with acute myocardial infarction admitted to intensive care units at the turn of the century: results from the French nationwide USIC 2000 registry. Heart
90: 1404-1410
[Abstract][Full Text]
Koren, M. J., Hunninghake, D. B., the ALLIANCE Investigators,
(2004). Clinical outcomes in managed-care patients with coronary heart disease treated aggressively in lipid-lowering disease management clinics: The alliance study. J Am Coll Cardiol
44: 1772-1779
[Abstract][Full Text]
Tunon, J., Blanco-Colio, L. M., Martin-Ventura, J. L., Egido, J.
(2004). Intensive treatment with statins and the progression of cardiovascular diseases: the beginning of a new era?. Nephrol Dial Transplant
19: 2696-2699
[Full Text]
Nissen, S. E.
(2004). High-Dose Statins in Acute Coronary Syndromes: Not Just Lipid Levels. JAMA
292: 1365-1367
[Full Text]
Cannon, C. P.
(2004). Revascularisation for everyone?. Eur Heart J
25: 1471-1472
[Full Text]
Wolber, T., Walther, C., Gielen, S., Mobius-Winkler, S., Hambrecht, R.
(2004). Management of Stable Coronary Disease: Primum Nil Nocere * Response. Circulation
110: e65-e65
[Full Text]
Lazar, H. L.
(2004). Role of statin therapy in the coronary bypass patient. Ann. Thorac. Surg.
78: 730-740
[Abstract][Full Text]
Kaiser, C., Kuster, G. M., Erne, P., Amann, W., Naegeli, B., Osswald, S., Buser, P., Schlapfer, H., Brett, W., Zerkowski, H.-R., Schindler, C., Pfisterer, M., the TIME Investigators,
(2004). Risks and benefits of optimised medical and revascularisation therapy in elderly patients with angina - on-treatment analysis of the TIME trial. Eur Heart J
25: 1036-1042
[Abstract][Full Text]
Yokoyama, I., Inoue, Y., Moritan, T., Ohtomo, K., Nagai, R.
(2004). Impaired myocardial vasodilatation during hyperaemic stress is improved by simvastatin but not by pravastatin in patients with hypercholesterolaemia. Eur Heart J
25: 671-679
[Abstract][Full Text]
Hambrecht, R., Walther, C., Mobius-Winkler, S., Gielen, S., Linke, A., Conradi, K., Erbs, S., Kluge, R., Kendziorra, K., Sabri, O., Sick, P., Schuler, G.
(2004). Percutaneous Coronary Angioplasty Compared With Exercise Training in Patients With Stable Coronary Artery Disease: A Randomized Trial. Circulation
109: 1371-1378
[Abstract][Full Text]
Thadani, U.
(2004). Current Medical Management of Chronic Stable Angina. J CARDIOVASC PHARMACOL THER
9: S11-S29
[Abstract]
Berger, P.
(2004). Ranolazine and Other Antianginal Therapies in the Era of the Drug-Eluting Stent. JAMA
291: 365-367
[Full Text]
Rihal, C. S., Raco, D. L., Gersh, B. J., Yusuf, S.
(2003). Indications for Coronary Artery Bypass Surgery and Percutaneous Coronary Intervention in Chronic Stable Angina: Review of the Evidence and Methodological Considerations. Circulation
108: 2439-2445
[Full Text]
Gadsby, R.
(2003). Review: Diabetic dyslipidaemia -- the case for using statins. British Journal of Diabetes & Vascular Disease
3: 402-407
[Abstract]
Henderson, R. A., Pocock, S. J., Clayton, T. C., Knight, R., Fox, K. A. A., Julian, D. G., Chamberlain, D. A., Second Randomized Intervention Treatment of Angina,
(2003). Seven-year outcome in the RITA-2 trial: coronary angioplasty versus medical therapy. J Am Coll Cardiol
42: 1161-1170
[Abstract][Full Text]
Crea, F, Lanza, G A
(2003). The elusive link between stenosis severity and prognosis in stable ischaemic heart disease. Heart
89: 961-962
[Full Text]
Friday, K. E.
(2003). Aggressive Lipid Management for Cardiovascular Prevention: Evidence from Clinical Trials. Exp. Biol. Med.
228: 769-778
[Abstract][Full Text]
Malik, I.
(2003). JournalScan. Heart
89: 815-816
[Full Text]
Bloomgarden, Z. T.
(2003). Inflammation and Insulin Resistance. Diabetes Care
26: 1922-1926
[Full Text]
Scolari, F., Ravani, P., Pola, A., Guerini, S., Zubani, R., Movilli, E., Savoldi, S., Malberti, F., Maiorca, R.
(2003). Predictors of Renal and Patient Outcomes in Atheroembolic Renal Disease: A Prospective Study. J. Am. Soc. Nephrol.
14: 1584-1590
[Abstract][Full Text]
Chaturvedi, S.
(2003). Should the Multicenter Carotid Endarterectomy Trials Be Repeated?. Arch Neurol
60: 774-775
[Full Text]
Thompson, P. D., Clarkson, P., Karas, R. H.
(2003). Statin-Associated Myopathy. JAMA
289: 1681-1690
[Abstract][Full Text]
Wong, K Y K, Walter, R S M., Douglas, D, Fraser, H W, Ogston, S A, Struthers, A D
(2003). Long QTc predicts future cardiac death in stroke survivors. Heart
89: 377-381
[Abstract][Full Text]
Lau, W. C., Waskell, L. A., Watkins, P. B., Neer, C. J., Horowitz, K., Hopp, A. S., Tait, A. R., Carville, D. G.M., Guyer, K. E., Bates, E. R.
(2003). Atorvastatin Reduces the Ability of Clopidogrel to Inhibit Platelet Aggregation: A New Drug-Drug Interaction. Circulation
107: 32-37
[Abstract][Full Text]
Futterman, L. G., Lemberg, L.
(2003). Seminal Changes in the Management of the Acute Coronary Event: Current Concepts. Am J Crit Care
12: 73-76
[Full Text]
Sundt, T. M. III, Gersh, B. J., Smith, H. C.
(2003). Indications for Coronary Revascularization. Card Surg Adult
2: 541-559
[Full Text]
Pasternak, R. C.
(2002). The ALLHAT Lipid Lowering Trial--Less Is Less. JAMA
288: 3042-3044
[Full Text]
Rashid, S., Uffelman, K. D., Barrett, P. H. R., Lewis, G. F.
(2002). Effect of Atorvastatin on High-Density Lipoprotein Apolipoprotein A-I Production and Clearance in the New Zealand White Rabbit. Circulation
106: 2955-2960
[Abstract][Full Text]
Martin, R M, Hemingway, H, Gunnell, D, Karsch, K R, Baumbach, A, Frankel, S
(2002). Population need for coronary revascularisation: are national targets for England credible?. Heart
88: 627-633
[Abstract][Full Text]
Flansbaum, B. E., Huddleston, J. M.
(2002). Update in Hospital Medicine. ANN INTERN MED
137: 814-822
[Abstract][Full Text]
Fihn, S. D., Williams, S. V., Gibbons, R. J.
(2002). Guidelines for the Management of Patients with Chronic Stable Angina. ANN INTERN MED
137: 549-549
[Full Text]
Modest, G. A.
(2002). Guidelines for the Management of Patients with Chronic Stable Angina. ANN INTERN MED
137: 548-549
[Full Text]
Malik, I.
(2002). JournalScan. Heart
88: 319-320
[Full Text]
Sculpher, M.J., Smith, D.H., Clayton, T., Henderson, R.A., Buxton, M.J., Pocock, S.J., Chamberlain, D.A.
(2002). Coronary angioplasty versus medical therapy for angina. Health service costs based on the second Randomized Intervention Treatment of Angina (RITA-2) trial. Eur Heart J
23: 1291-1300
[Abstract]
Danchin, N, Grenier, O, Ferrieres, J, Cantet, C, Cambou, J-P
(2002). Use of secondary preventive drugs in patients with acute coronary syndromes treated medically or with coronary angioplasty: results from the nationwide French PREVENIR survey. Heart
88: 159-162
[Abstract][Full Text]
Mark, D. B., Hlatky, M. A.
(2002). Medical Economics and the Assessment of Value in Cardiovascular Medicine: Part II. Circulation
106: 626-630
[Full Text]
Keaney, J. F. Jr., Vita, J. A.
(2002). The Value of Inflammation for Predicting Unstable Angina. NEJM
347: 55-57
[Full Text]