Cardiac catheterization demonstrated nonobstructive. 3-vessel multi-aneurysmal CAD with sluggish antegrade coronary flow (arrowheads in Figure 1A, C, and ...
encompass both coronary artery aneurysms (CAA) and coronary artery ectasia (CAE).1. CAA is defined as a localized irreversible dilatation of the coronary ...
mg. kg'. h' and were 11.8Â±0.5 (INR=1.0), 12.3Â±0.7 (INR=1.1), 13.3Â±+1.2 (INR=1.4), 14.2+0.4 ... KEY WORDs * .... solution at 30 mL/h. ... Therefore, 200 ,uL of the thrombin solution ..... bin, through point mutations in amino acid position 47,.
Nov 11, 2017 - nary intervention (PCI) or coronary artery bypass grafting surgery, an ... were the positive, forward-directed (aorta-derived) compression wave.
Circulation 68, No. 5, 986-997, 1983. BECAUSE OF PROBLEMS in the study of the natural history of coronary disease, many ofwhich are insur- mountable, no ...
Apr 5, 2017 - Nevertheless because nonobstructive CAD is a heterogeneous and prevalent condition, there is the need for tools to quantify total coronary.
Apr 4, 2017 - assessing the presence or extent of obstructive coronary stenosis .... tient had not been evaluated for CAD, had >1 clinical cardiovascular.
From the Division of Cardiology, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, California. Dr. .... ultrasound ... production was also shown to be associated with lower rates ...... Oriji GK, Keiser HR.
Nov 6, 2017 - at least 1 visible stenosis of â¥30% were manually quantified with the .... calibration curves to identify the sensitivity and specificity ...... Hendel RC, Wackers FJ, Berman DS, Ficaro E, DePuey EG, Klein L, ... Am Heart J. 2007;154:
risk of future cardiovascular disease events.1,2 This observa- ... BackgroundâNonobstructive coronary plaques manifesting high-risk morphology (HRM) ...
revascularization in stable CAD? ... CABG patients have less angina @ 5y: 67% vs. ... Optimal Medical Therapy with or without PCI for stable Coronary disease.
and independent arbiter of clinical risk.1 In current practice ... From the Section of Noninvasive Cardiovascular Imaging (E.W., S.A.A., B.H., .... CV/i General Electric Healthcare, Milwaukee, WI) with a 4- or ..... both death (13.8% versus 20.3%) an
Nov 10, 2016 - pulmonary embolus. â pneumothorax. â pneumonia. â pleuritis .... â¢Sinus tach â Try carotid sinus massage. â¢Atrial flutter â can use adenosine to ...
Angiographic definition of chronic total occlusion (CTO) was used: complete ..... fractional flow reserve computed from coronary CT angiography com- pared to ...
Feb 8, 2014 - ne priÃuve (FFR), Ãak i u uvjetima bez znaÃajnije hipertrofi- je lijeve klijetke. Nasuprot tome, uz hipertenzivnu hipertrofi- ju lijeve klijetke dolazi do hipertrofije kardiomiocita, umna-. Ãanja veziva, kao i perivaskularnih promje
non-exercise related events reduce the utility of standard CAD risk assessment in .... nonobstructive or mildly obstructive coronary arteries. The occurrence of ...
taken into account to define prognosis in coronary disease fully. ...... obstructive coronary artery disease: ten-year study of 601 non- surgical cases.
Jun 28, 1993 - was calculated in millimoles per liter using the formula LDL-. C=TC-(HDL-C+Tg/2.18).18 However, if the level of Tg exceeded 3.39 mmol/L, very-low-density lipoprotein choles- terol (VLDL-C) was measured by enzymatic methods19 after ultr
Apr 1, 2001 - chest pain in women without known coro- nary artery disease is presented in Figure 1.4. Coronary risk factors are more prevalent in women ...
PI against important clinical variables, subsequent revascu- larization, and implantable ... Thomas H. Marwick, MD, PhD, MPH; Scott D. Flamm, MD, MBA. Coronary Artery ...... Reprints: document. Permissions and Rights Question and Answer.
Nov 6, 2017 - of Iopamiron 370 (370 mg iodine/mL, rate 5 mL/s, Schering Bayer,. Germany) .... out plaque overlay, using transverse and MPR views. In MPR ...
Nov 6, 2017 - coronary syndrome and multivessel disease managed with percutaneous ... Yanai Ben-Gal, MD; Rephael Mohr, MD; Frederick Feit, MD; E. Magnus Ohman, MD; ..... present study may provide some guidance to choose between ..... 8 Ben-Gal et al
stali na CABG, mogla bi se ponuditi dijagnostiÃka koro- ...... New answers to three questions on the epidemic of coronary mortality in south Asians: incidence or ...
Albiglutide, a long lasting glucagon-like peptide-1 analog, protects the rat heart against isch- emia/reperfusion injury: evidence for improving cardiac metabolic ...
toward the mean in a pediatric population. Pediatrics 64: 197, 1979 30. Kwiterovich PO Jr, Heiss G, Johnson N, Chase GA, Tamir 1, Rifkind B: Assessment of plasma total cholesterol as a test to detect elevated low density (beta) lipoprotein cholesterol levels (type Ila hyperlipoproteinemia) in young subjects from a population-based sample. Am J Epidemiol 115: 192, 1982 31. Moll P, Sing C, Gordon H, Weidman W, Kottke B: Total cholesterol as indicators of heterogeneous CHD risk and sources of lipid variability. Am J Hum Genet 33: 139A, 1981 32. Moll P, Sing C, Weidman W, Gordon H, Kottke B: Childhood cholesterol levels: Indicators of CHD prevalence and mode of cholesterol inheritance in their families. (abstr) Am J Epidemiol 166: 1982 In press 33. Schrott HG, Bucher KD, Lauer RM: Genetic analyses of families selected through a hypercholesterolemic child: The Muscatine Study. Am J Hum Genet 33: 142A, 1979
VOL 67, No 1, JANUARY 1983
34. Bucher KD, Schrott HG, Clarke WR, Lauer RM: The Muscatine Cholesterol Family Study: distribution of cholesterol levels within families of probands with high, low and middle cholesterol levels. J Chronic Dis 35: 385, 1982 35. Goldstein JL, Albers JJ, Schrott HG, Hazzard WR, Bierman EL, Motulsky AG: Plasma lipid levels and coronary heart disease in adult relatives of newborns with normal and elevated cord blood lipids. Am J Hum Genet 26: 727, 1974 36. Miller NE, Nestel PJ, Boulton TJC, Dwyer T, Leitch D: Cord blood high density lipoprotein concentration in 1797 births: relationship to family history of coronary heart disease. J Chronic Dis 34: 119, 1981 37. Snowden CB, McNamara PM, Garrison RJ, Feinleib M, Kannel WB, Epstein FH: Predicting coronary heart disease in siblings. A multivariate assessment: The Framingham Heart Study. Am J Epidemiol 115: 217, 1982
Aneurysmal Coronary Artery Disease Downloaded from http://circ.ahajournals.org/ by guest on May 4, 2017
PAUL S. SWAYE, M.D., LLOYD D. FISHER, PH.D., PAUL LITWIN, B.A., PAUL A. VIGNOLA, M. D., MELVIN P. JUDKINS, M.D., HARVEY G. KEMP, M.D., J. GERARD MUDD, M.D., AND ARTHUR J. GOSSELIN, M.D. SUMMARY To examine the clinical and historical features and the natural history of aneurysmal coronary disease, we reviewed the registry data of the Coronary Artery Surgery Study (CASS). Nine hundred seventy-eight patients, representing 4.9% of the total registry population, were identified as having aneurysmal disease. No significant differences were noted between aneurysmal and nonaneurysmal coronary disease patients when features such as hypertension, diabetes, lipid abnormalities, family history, cigarette consumption, incidence of documented myocardial infarction, presence and severity of angina, and presence of peripheral vascular disease were examined. In addition, no difference in 5-year medical survival was noted between these two groups. These findings suggest that aneurysmal coronary disease does not represent a distinct clinical entity but is, rather, a variant of coronary atherosclerosis.
ANEURYSMAL coronary disease is characterized by abnormal dilatation of a localized or diffuse segment of the coronary arterial tree. This involvement has also been termed coronary ectasia or dilating arteriosclerosis; destruction of the vessel media is the usual histologic feature. Frequently, aneurysmal disease coexists with coronary atherosclerosis and has raised the question of whether aneurysmal disease is a variant of atherosclerotic coronary disease or a distinct entity. The presence of dilated coronary segments, even in the absence of obstructive disease, is believed to result in alterations in blood flow and stasis, which predispose these patients to myocardial ischemia and infarction. Although many reports on aneurysmal coronary disease have been published, the number of patients in each report has been small. 1-14 We therefore evaluated a large group of patients with aneurysmal coronary disease from the registry data of the multiinstitutional Coronary Artery Surgery Study (CASS), sponsored by From the Miami Heart Institute, Miami Beach, Florida; Loma Linda University, Loma Linda, California; St. Luke's Hospital, New York, New York; St. Louis University, St. Louis, Missouri; and the Coordinating Center for Collaborative Studies in Coronary Artery Surgery, University of Washington, Seattle, Washington. Address for correspondence: Paul S. Swaye, M.D., Miami Heart Institute, 4701 North Meridian Avenue, Miami Beach, Florida 33140. Received April 1, 1982; revision accepted July 6, 1982. Circulation 67, No. 1, 1983.
the National Institutes of Health (NIH). 5 We examined the clinical and historical features and the natural history of coronary aneurysmal disease to determine whether it represents a distinct clinical entity or a variant of coronary atherosclerotic disease.
Materials and Methods Between July 1975 and May 1979, clinical, laboratory and angiographic data were collected in a standardized fashion and entered into a registry of consecutive patients undergoing coronary arteriography for clinically suspected coronary artery disease at 15 participating clinical centers of CASS. Patients who were subsequently shown to have normal coronary arteries were included in the registry. Patients studied for suspected coronary artery disease who were found to have another form of heart disease were excluded. Those who underwent coronary angiography for evaluation of other conditions, such as valvular heart disease, cardiomyopathies and congenital heart disease, were also excluded even if subsequent evidence showed that coronary artery disease was a major clinical problem. A total of 20,087 patients from the participating institutions was entered into the CASS registry. The patients who had undergone cardiac surgery were not included. Each patient was interviewed at the time of hospitalization for coronary angiography by a trained data technician or the responsible physician. The base-
ANEURYSMAL CORONARY ARTERY DISEASE/Swaye et al.
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line historical, physical and laboratory data and the results of coronary arteriography and left ventriculography were collected and recorded on appropriate data forms.
disease. The result of this analysis revealed complete agreement in 70.2% of the randomly selected films. In 20.4% there was disagreement with the original interpretation and in 9.4% the findings were equivocal.
Clinical Data Base A number of clinical descriptors were obtained when the patients entered the registry. The predominant symptoms included chest pain, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, palpitations and fatigue. Chest pain was classified by the responsible physician as definitely angina, probably angina, probably not angina or definitely not angina. Functional classification was designated according to the Canadian Cardiovascular Society. Family history was considered positive when there was knowledge of symptoms of angina pectoris or history of myocardial infarction in parents, siblings or aunts or uncles related by blood before age 55 years. A history of cigarette smoking, treated hypertension, diabetes, lipoprotein abnormalities, or documented myocardial infarction was recorded. The arteriographic data forms allowed entry of information on 27 segments of the coronary vasculature bed. The participating sites agreed to use a uniform code to describe coronary artery anatomy. In this way, angiographic data from different clinical sites could be compared. Details of the classifications used have already been reported. 14 Briefly, coronary stenoses were read as the percent narrowing of the maximal luminal diameter for each segment. The criteria for clinically significant coronary artery obstruction were defined as either a 70% or more reduction in the internal diameter of the right, left anterior descending or left circumflex coronary artery or 50% or greater reduction in the internal diameter of the left main coronary artery. The presence of coronary aneurysmal dilatation was recorded. Discrete or diffuse aneurysmal disease was defined as coronary dilatation that exceeded the diameter of normal adjacent segments or the diameter of the patient's largest coronary vessel by 11/2 times (fig. 1). Left ventricular function was assessed from ejection fractions calculated by a single-plane adaptation of the area-length method of Sandler and Dodge. 16 In addition, a left ventricular wall motion score was obtained by analyzing the five left ventricular segments visualized on right anterior oblique ventriculograms. Uniformity of interpretation of angiographic data among the 15 contributing institutions was achieved by designating quality control sites as part of the ongoing CASS project. Each month, the Coordinating Center randomly selected from each clinical site three films depicting coronary lesions. These films were sent to a quality control site to be reinterpreted. The readings from the original site and quality control site were compared and the discrepancies recorded. By the end of enrollment, 871 films were read as part of this study. As part of the present study, three of the authors independently reviewed 54 films, selected at random from the clinical sites, designated as demonstrating aneurysmal disease. They reviewed these films to evaluate the reproducibility of criteria for aneurysmal
Results Of the 20,087 patients, 978 (4.9%) were identified as having aneurysmal coronary dilatation (fig. 2). Twenty-one had aneurysmal disease and no coronary stenosis (group A), 69 had aneurysmal disease and less
B FIGURE 1. Right coronary arteriograms showingft and saccular (B) aneurysmal involvement.
VOL 67, No 1, JANUARY 1983
ANEURYSMAL CORONARY DILATATION 978 PTS. 21
GROUP A AN ALONE
957 AN + STENOSIS 69
GROUP B GROUP C STENOSIS > 70% <70% STENOSIS FIGURE 2. Subgroups ofpatients with aneurysmal (AN) coronary disease.
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than 70% stenosis (group B), and 888 had aneurysmal disease and 70% stenosis or greater (group C). The control population in this study consisted of the 19,109 other patients (95.1%) in the CASS registry. Among the 978 patients in the study group, the proximal and middle segments of the right coronary artery were most frequently involved by aneurysmal disease. The next most frequently involved segments were the proximal left anterior descending and circumflex coronary arteries. The 978 patients with aneurysmal disease were compared with a group of control patients without aneurysmal disease who had any degree of coronary stenoses (n = 15,249). Patients with completely normal coronary arteries were excluded from this comparison group. The percentage of males with aneurysmal disease was significantly greater than that in the control group (88.2% vs 80.1%, p < 0.001). No age differences were noted. No differences were noted with regard to coronary disease risk factors such as hypertension, diabetes, lipid abnormalities and cigarette use. However, a family history of coronary disease was more common in the control group (43.2% vs 38.5%, p < 0.05). Patients with aneurysmal disease had a higher incidence of documented myocardial infarction (52.9% vs 47.0%, p < 0.001). However, no differences were noted with regard to other clinical descriptors such as angina, peripheral vascular disease and
Canadian Heart Association functional classification. The incidence of three-vessel coronary disease was higher in the aneurysmal group (42.3% vs 34.2%, p < 0.001); however, left ventricular function, as measured by ejection fraction and left ventricular wall motion score, was similar in the two groups. Patients with aneurysmal disease and no associated coronary stenosis or nonsignificant coronary stenosis (groups A and B, n = 90) were then compared with a population that did not have aneurysmal disease or signficant coronary stenosis (n = 1893). Patients with normal coronary arteries were excluded from this comparison group. Although the percentage of males in the aneurysmal group was significantly greater than in the controls (75.3% vs 62.2%, p < 0.05), no differences were noted with regard to age, family history of coronary disease, hypertension, diabetes, lipid abnormalities, and cigarette smoking, associated angina, prior myocardial infarction, functional classification, incidence of peripheral vascular disease, left ventricular ejection fraction and left ventricular wall motion score. Cumulative survival curves* demonstrated reduced survival at the 5-year medical follow-up in the patients with aneurysmal disease and any degree of coronary stenosis (groups B and C) compared with patients without aneurysmal disease and any degree of coronary obstruction (74% vs 83%) (fig. 3). Further,analysis of these groups was performed taking into account arteriographic and ventriculographic findings, including the combinations of number of vessels diseased, the number of proximal vessels diseased and the LV score. The survival curve (fig. 4) failed to show a significant difference between the two groups. Similarly, the survival curves of medically treated patients with aneurysmal disease and either no or nonsignificant coronary stenosis (groups A and B) were not different from those in a control group without aneurysmal disease or significant coronary stenosis (fig. 5). *Computed by the life-table or actuarial method; the statistical significance of differences between groups was compared by log-rank test.
B+C vs CONTROLS N 957 100 >
LEGEND .e-&- GROUPS
YEAR a -
100 100 0.0043
P = Log Rank Stat
Five-year cumulative survival
curves of groups B and C compared with control population without aneurysmal disease.
ANEURYSMAL CORONARY ARTERY DISEASE/Swaye et al.13
B±C vs CONTROLS
(9 (9J n~
FiGURE 4. Five-year cumulative survival curves of groups B and C compared with control population adjusted for arteriographic and ventriculographic findings.
100 100 P = 0.4137 Log Rank Stat D.-
4 82 83
0 5 75
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The patients with aneurysmal disease who underbypass surgery (n = 496) were then compared with a population of patients without aneurysmal disease (n = 7622) who also underwent bypass surgery. The 5-year cumulative survival curves showed no significant differences between the two groups. went coronary
Aneurysmal dilatation of the coronary arteries was first described by Bourgon'7 in 1812. In 1929, Packard and Wechsler reviewed 21 previously reported cases. 14
Since then, numerous isolated case reports and small series of patients have been described."'1 The CASS registry, sponsored by the NIH, affords a unique opportunity to study a large group of patients with angiographically documented coronary aneurysmal dilatation so that the clinical and historical features as well as the natural history of this disease can be further elucidated. In the current study, patients with aneurysmal coronary disease had a similar incidence of "coronary"
risk factors such as hypertension, diabetes, lipid abnormalities and cigarette use compared with controls. This finding differs from other studies' 2 in which a higher incidence of sIystemic hypertension was noted in patients with a'neurysmal disease. Markis et al.' speculate that the systemic hypertension might play a role in the pathogenesis of this disease entity. The reason for this difference is not clear but may relate to differe'nces in patient selection. Other investigators also failed to demonstrate a higher incidence of "coronary" risk factors, including hypertension, in patients with aneurysmial coronary disease.3' .In our study, patients with aneurysmal disease had a greater incidence of documented myocardial infarction than the control group, as observed by others.'I However, our patients with aneurysmal disease and nonsignificant coexistent obstructive lesions did not have a greater incidence of infarction. It would be tempting to suggest that an aneur'ysmal segment with its possible altered flow characteristics in assQciation with a significant obstruction predispoe tomoardial infarction. However, the patients with aneurysmal disease
A±B vs CONTROLS N 89
:D FIGURE 5. 0
LEGEND ---GROUPS A+ B OTHERS W/ 0 VESDIS
100 100 P
of groups A and B compared population without aneurysmal
and significant coronary stenoses, who made up the overwhelming majority of the aneurysm group, had a significantly higher incidence of three-vessel involvement. Therefore, the increased incidence of infarction might merely reflect the increased incidence of threevessel disease in this aneurysmal group. Furthermore, when other factors that affect survival, such as percent luminal narrowing and left ventricular wall motion score, were taken into account, no real differences in survival existed between the patients with aneurysmal disease and comparable patients without aneurysmal disease. In conclusion, our findings failed to reveal a clinical picture or pattern of risk factors that would suggest a diagnosis of aneurysmal coronary disease. Aneurysmal coronary disease appears to be a variant of occlusive coronary atherosclerosis, and both lesions frequently coexist in the same vessel. Acknowledgment Downloaded from http://circ.ahajournals.org/ by guest on May 4, 2017
We acknowledge the assistance of Dr. Minor Duggan, John Rothrock, Klara Soos and Eunice K. Paul in the preparation of the manuscript.
4. 5. 6. 7. 8. 9.
Markis JE, Joffe CD, Cohn PF, Feen DJ, Herman MV, Gorlin R: Clinical significance of coronary arterial ectasia. Am J Cardiol 37: 217, 1976 Befeler B, Aranda J, Embi A, Mullin F, El-Sherif N, Lazzara R: Coronary artery aneurysms. Study of their etiology, clinical course and effect on left ventricular function and prognosis. Am J Med 62: 597, 1977 Swanton RH, Thomas ML, Coltart DJ, Jenkins BS, Webb-Peploe MM, Williams BT: Coronary artery ectasia. A variant of occlusive coronary arteriosclerosis. Br Heart J 40: 393,1978 Aintablian A, Hamby RI, Hoffman I, Kramer RJ: Coronary ectasia: incidence and results of coronary bypass surgery. Am Heart J 96: 309, 1978 Daoud AS, Pankin D, Tulgan H, Florentin A: Aneurysms of the coronary artery. Report of ten cases and review of literature. Am J Cardiol 11: 228, 1963 Falsetti HL, Carroll RJ: Coronary artery aneurysm. A review of the literature with a report of 11 new cases. Chest 69: 630, 1976 Berkoff HA, Rowe GG: Atherosclerotic ulcerative disease and associated aneurysms of the coronary arteries. Am Heart J 90: 153, 1975 Sayegh S, Adad W, MacLeod CA: Multiple aneurysms of the coronary arteries. Am Heart J 76: 266, 1968 Oliveros RA, Falsetti HL, Carroll RJ, Heinle RA, Ryan GF: Atherosclerotic coronary artery aneurysm. Arch Intern Med 134: 1072, 1974 Wilson CS, Weaver WF, Forker AD: Bilateral arteriosclerotic coronary arterial aneurysms successfully treated with saphenous vein bypass grafting. Am J Cardiol 35: 315, 1975 Anabtawi IN, deLeon JA: Arteriosclerotic aneurysms of the coronary arteries. J Thorac Cardiovasc Surg 68: 226, 1974 Van den Broek H, Segal BL: Coronary aneurysms in a young woman: angiographic documentation of the natural course. Chest 64: 132, 1973 Mattern AL, Baker WP, McHale JJ, Lee DE: Congenital coronary
VOL 67, No 1, JANUARY 1983 with angina pectoris and myocardial infarction treated with saphenous vein bypass graft. Am J Cardiol 30: 906, 1972 Packard M, Wechsler H: Aneurysms of coronary arteries. Arch Intern Med 43: 1, 1929 Principal Investigators of CASS and their Associates: National Heart, Lung, and Blood Institute Coronary Artery Surgery Study. Circulation 63 (suppl II): Il-1, 1981 Sandler H, Dodge HT: The use of single plane angiocardiograms for the calculation of left ventricular volume in man. Am Heart J 75: 325, 1968 Scott DH: Aneurysm of the coronary arteries. Am Heart J 36: 403, 1948 aneurysms
Appendix Cooperating Clinical Sites University of Alabama in Birmingham: William J. Rogers, M.D.,* Richard 0. Russell, Jr., M.D., Albert Oberman, M.D., and Nicholas T. Kouchoukos, M.D.; Albany Medical College: Julio A. Sosa, M.D.,* Martin F. McKneally, M.D.,* Joseph Maclllduff, M.D., Thomas Older, M.D., and Eric K. Foster, M.D.; Boston University: Thomas Ryan, M.D.,* David Faxon, M.D., Laura Wexler, M.D., Robert L. Berger, M.D., and Carolyn H. McCabe, B.S.; Loma Linda University: Melvin P. Judkins,M.D.* and Joan Coggin, M.D.*; Marshfield Medical Foundation, Inc. and Marshfield Clinic: William Myers, M.D.,* Richard D. Sautter, M.D.,* John N. Browell, M.D., Dieter M. Voss, M.D., and Robert D. Carlson, M.D.; Massachusetts General Hospital: J. Warren Harthorne, M.D. ,* W. Gerald Austen, M.ID. ,* Robert Dinsmore, M.D., Frederick Levine, M.D., and John McDermott, M.D.; Mayo Clinic and Mayo Foundation: Robert L. Frye, M.D.,* Hugh C. Smith, M.D., Ronald E. Vlietstra, M.D., Michael B. Mock, M.D., David R. Holmes, M.D., and Richard Fulton, M.D. Miami Heart Institute: Arthur J. Gosselin, M.D.,* Parry B. Larsen, M.D., and Paul Swaye, M.D.; Montreal Heart Institute: Martial G. Bourassa, M.D.,* Bernard R. Chaitman, M.D., Claude Goulet, M.D., and Jacques Lesperance, M.D.; New York University: Ephraim Glassman, M.D.,* and Michael Schloss, M.D.; St. Louis University: George Kaiser, M.D.,* J. Gerard Mudd, M.D.,* Robert D. Wiens, M.D., Hendrick B. Barner, M.D., John E. Codd, M.D., Denis H. Tyras, M.D., and Vallee L. Willman, M.D.; St. Luke's Hospital Center: Harvey G. Kemp, Jr., M.D.* and Airlie Cameron, M.D.; Stanford University: Edwin Alderman, M.D.,* Francis H. Koch, M.D.,* Paul R. Cipriano, M.D.,* James F. Silverman, M.D.* and Edward B. Stinson, M.D.*; Medical College of Wisconsin: Felix Tristani, M.D.,* Harold L. Brooks, M.D.,* and Robert J. Flemma, M.D.; Yale University: Lawrence S. Cohen, M.D.,* Rene Langou, M.D., Alexander S. Geha, M.D., Graeme L. Hammond, M.D., and Richard K. Shaw, M.D.
Central Electrocardiographic Laboratory University of Alabama: L. Thomas Sheffield, M.D.,* David Roitman,
M.D., and Carol Troxell, B.S.
Coordinating Center University of Washington: Lloyd Fisher, Ph.D.,* Mary Jo Gillespie, M.S., Kathryn Davis, Ph.D., J. Ward Kennedy, M.D., and Richard Kronmal, Ph.D.
Chairman of Steering Committee Thomas Killip, M.D., Henry Ford Hospital.
*Denotes principal investigator.
Aneurysmal coronary artery disease. P S Swaye, L D Fisher, P Litwin, P A Vignola, M P Judkins, H G Kemp, J G Mudd and A J Gosselin
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