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Ann Thorac Surg 1998;66:1-11
© 1998 The Society of Thoracic Surgeons
a Cardiac Surgery Department, Gasthuisberg University Hospital, Leuven, Belgium
Address reprint requests to Dr Sergeant, Cardiac Surgery Department, Gasthuisberg University Hospital, Herestreet, 3000 Leuven, Belgium
Presented at the Thirty-fourth Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 26–28, 1998.
Abstract
Background. This study sought to determine whether extensive arterial grafting reduces the prevalence and consequences of infarct after coronary artery bypass grafting.
Methods. Post-primary coronary artery bypass grafting infarcts and time-related events thereafter were identified by 99.9% complete follow-up of 9,600 patients (1971 to 1992). The contribution of arterial grafting to freedom from infarct was assessed by multivariable hazard function analysis to adjust for other risk factors.
Results. Unadjusted 1-month and 10-year freedom from infarction was 97% and 86%. By multivariable analysis, arterial grafting lowered the prevalence of periprocedural (p = 0.005), intermediate term (p = 0.007 and 0.006), and late infarction (arterial grafting to the left anterior descending coronary artery, p = 0.0006). Unadjusted survival after first infarct after coronary artery bypass grafting was 74% and 52% at 1 and 10 years; arterial grafting improved 10-year survival from 48% to 59% (p = 0.002). An additional benefit or cost of extending arterial grafting (n = 1,727) beyond a single one could not be identified (p > 0.1).
Conclusions. Arterial conduits, particularly to the left anterior descending coronary artery, should be used for coronary artery bypass grafting to reduce early and late myocardial infarction and its consequences. However, use of more than a single arterial graft appears to confer no additional benefit.
Coronary artery bypass grafting has evolved into abundant use of bilateral sequential mammary, radial, and gastroepiploic arteries. The assumption that single arterial grafting to the left anterior descending coronary artery (LAD) [1, 2] improved graft patency and late survival gave rise to the assumption that multiple arterial grafting would contribute further to superior results. However, after adjusting for differences in prevalence of risk factors, we [3] have been unable to identify an additional survival benefit of arterial grafts to other systems. This finding stimulated us to seek possible additional protection of multiple arterial grafting against the morbid event of myocardial infarction after coronary artery bypass grafting (CABG) and its consequences.
Material and methods
Patients
A consecutive series of 9,600 patients underwent isolated first time CABG at the Gasthuisberg University Hospital of the Katholieke Universiteit Leuven (K.U. Leuven) Belgium, from 1971 to 1992. The mean age of the patients increased from 48.9 ± 7 years in 1971 to 62.3 ± 8 years in 1991. Seventeen percent of the patients were women. Single coronary system disease was present in 11%, two-system disease in 29%, and three system disease in 60%. Left main coronary artery stenosis of more than 90% stenosis was identified in 355 patients. Mild mitral and aortic valve regurgitation, insufficient to warrant valvular reconstruction or replacement, was present in 643 and 95 patients, respectively.
The complete data set has been described and characterized in detail in previous publications [3].
Surgical technique
Intermittent aortic cross-clamping, moderate hypothermia at 28°C, and pretreatment with 1 mg/kg of lidoflazine [4] since 1980, have been the technique of choice for managing the ischemic myocardium during operation. Arterial grafting was started using the internal mammary artery (IMA) in 1972. At least one in-situ IMA anastomosis was constructed in 6,074 patients. Bilateral and sequential IMA [5] grafting started in 1973 and 1978, respectively, but the use and the method of use was inconsistent over time. The left IMA was constructed most frequently to the LAD system (n = 4,833 patients). Bilateral IMAs were constructed in 207 patients to a single coronary system and in 985 patients to two coronary systems. The distribution of the patients by in-situ IMA distal anastomoses and by age group is presented in Table 1. The number of patients alive, without having suffered an infarct after CABG, within various follow-up intervals, is presented according to the number of in-situ IMA distal anastomoses in Table 2. In addition to the in-situ IMA anastomoses, IMA free grafting and gastroepiploic artery in-situ grafting were performed in 122 and 43 patients, respectively. In-situ arterial grafting only was achieved in 1,088 patients, of which 442 had multiple system disease.
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Event
The diagnosis of early perioperative infarct was documented by the intensive care specialist (an independent unit) using repeated surface electrocardiogram (ECG) (Minnesota classification) and routine enzymatic measurements. The cut-off value for positive enzymes was a creatinine kinase MB fraction higher than 8% of total creatinine kinase. The diagnosis of later perioperative infarct was based on repeated routine in-house surface ECG and enzymatic measurements on suspicion of the event. The ECG changes were always compared with earlier ECGs of the patient before confirmation of the new event. Surface ECG by the referring cardiologist (an independent unit) at the first visit after CABG confirmed where appropriate the perioperative diagnosis.
The diagnosis of follow-up infarcts was documented by the attending cardiologist. If the ECG changes in follow-up did not correlate with clinical symptoms in the same time frame, the date and time of first occurrence of the ECG changes were considered the relevant date and time for the event. Patients not experiencing the event were censored at the common closing date, at the end of follow-up for those with incomplete follow-up, or at death, whichever occurred earliest.
Characterization of overall freedom from first infarct
Nonparametric estimates of overall nonrisk-adjusted freedom from first infarct were obtained by the method of Kaplan and Meier [6]. A completely parametric method was used to identify the number of hazard phases, identify the form of the equation for each phase, and estimate the parameters that characterize the distribution of times until first infarct [7].
Multivariable analysis of freedom from first infarct
The general methods used to identify incremental risk factors for first infarct have been described previously for the event death [3], including the variables (Appendix 1) and their organization for analysis, and the exploratory analyses accompanying the multivariable analyses, which were conducted in the parametric, multiphase hazard function domain.
In a directed stepwise entry of variables into the multivariable risk factor model, a p value criterion of 0.05 was used for retention of variables in the final analysis. Regression coefficients are presented plus or minus one standard error. Goodness of fit of the patient–procedure–experience model to the data was checked in the two ways previously detailed [8, 9].
Sequential analyses
To facilitate the analysis and better discover and understand the nature and influence of single and multiple arterial grafting in the face of change in prevalence of other variables, the risk factor analysis was conducted in a sequential fashion. First, only patient variables were entered, then procedure variables likely to be known or estimated at the time of decision making were added, including the use of arterial grafts, and finally experience variables. Variables from the isolated and preceding analyses were allowed to enter and leave the model.
Nature and influence of risk factors
Exploration of the influence of arterial grafting was performed by constructing a series of nomograms representing solutions of the final parametric equation for all variables (patient, procedure, and experience). These were risk-adjusted in the sense that all other variables in the model were set to those of a patient of median risk in the last year of the study. Thus, each figure represents the risk-adjusted prediction for a specific, but typical, hypothetical patient (Table 3).
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Results
Nonrisk-adjusted freedom from first infarct
A first infarct after CABG was identified in 1,030 patients (the remaining 8,570 patients were censored at death, the common closing date or, rarely, at incomplete follow-up). The nonrisk adjusted 1-month, 1-, 10-, and 15-year freedom (Fig 1A) from first infarct was 97.3%, 96.7%, 86%, and 73%, respectively. A three-phase hazard function was identified (Fig 1B). It consists of an early hazard phase, corresponding to the perioperative period, that rapidly declined to disappearance by the fifth day after operation, a constant hazard phase and a late hazard phase rising gradually beyond 2 years after operation for as long as the extent of follow-up. Arterial grafting was associated with a lower prevalence of infarction after CABG (p < 0.0001) and this reduction was similar in magnitude for one, two, three, or four IMA distal anastomoses (p < 0.0001) for the full extent of their follow-up (Fig 2).
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Events before and after first infarct
The first infarct was preceded by return of anginal symptoms in 386 patients (37%) of the total of the patients experiencing an infarct after CABG.
After the first infarct and within the follow-up interval after CABG, 400 of the 1,030 patients died. The nonrisk-adjusted parametric survival after first infarct after CABG at 1 month, 5 years, and 10 years was 79%, 65%, and 52%, respectively (Fig 4). Stratified by the presence of an arterial graft, but unadjusted for any residual variability, the 1-month and 10-year survival after first infarct was 77% and 48% without arterial grafting of any kind and 83% and 59% in the presence of an arterial graft (p = 0.002) (Fig 5). An additional benefit of multiple arterial grafting over a single arterial graft was not demonstrated (p = 0.6).
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Limitations of the studied event
First infarct after CABG is nearly always a clinical event with electrocardiographic and often hemodynamic stigmata. The time relatedness of the event might be misdocumented over a few hours in the very early postoperative events, it might have been misdocumented over a few weeks in the rare silent late infarcts but the number of events will be reliable because the event will be identified at the next physician’s visit. Silent infarcts will nearly certainly have been missed in patients with left bundle-branch block.
Limitations of the data set
All statements related to arterial grafting are limited to the techniques of arterial grafting used during the time frame of the study reported. Sequential and bilateral in-situ IMA anastomoses were considered normal practice. A free IMA graft was only constructed when after planning in-situ grafting, the IMA was found to be too short or was damaged proximally. Only a limited number of patients with in-situ gastroepiploic grafting and none with radial artery grafting were performed during this time. Inferences about multiple arterial grafting are also limited by this technique being used more recently. However, even at 9 years of follow-up, more than 1,000 patients with multiple arterial grafts are alive without infarct, and at 10 years, more than 800.
Clinical relevance of the event for the patient
The clinical relevance of infarct after CABG is increased by the fact that few of the patients received anginal warnings of the impending infarct. The hazard function indicates that monitoring for early infarcts is advisable, with diminishing returns, for about 5 days after operation, and the risk of infarction must be weighted against the benefits of early discharge after CABG.
A higher prevalence, early and late, of infarct after CABG was reported in the Bypass Angioplasty Revascularization Investigation trial [10], 80.4% at 5 years. This higher prevalence could have been induced by the absence of single vessel disease, the smaller sample size (n = 914), the higher periprocedural infarct rate of 4.6% and the multicenter aspect of the trial. The results of our study are similar to the 10- (89% ± 2%) and 15-year (77% ± 3%) freedom given for a smaller group (n = 428) of patients but also with very extended and complete follow-up [11], using the anniversary method.
This study gives a first insight in several events after infarct. The first infarct after CABG has a 1-month lethal cost of close to 21% (Fig 2) (uncorrected for patient and procedure variability). This mortality is comparable to mortality after infarct without previous CABG, because it includes patients in all grades of cardiac failure at the moment of infarct. The 30-day mortality in the Gruppo Italiano per lo Studio della Streptochinase nel’Infarto miocardico 1 trial [12] increased from 7% for Killip class I to 81% for Killip class IV. Stratified actuarials explored the relation between some of the patient variability and survival after first infarct after CABG: age more than 65 years of age (p = 0.0007), insulin-treated diabetes (p = 0.0001), and ventricular function (p = 0.0001).
Even if the patient survives, quality of further life will be reduced by the loss of ventricular mass and function, concomitant with myocardial cell necrosis.
Return of angina was noted fairly rapidly in most patients after their first infarct after CABG. This high rate could have been induced by the use of thrombolysis, often reducing the impact of the infarct but not taking away the cause.
Impact of arterial grafting on freedom from first infarct
From the first reports by Kay [13] and Barner [14] and their colleagues emphasizing the good patency rates after direct anastomosis between an internal mammary artery graft and a coronary artery, surgeons have been increasing their expectation in this graft. This was further increased after Siegel and Loop [15] reported higher patency rates compared to saphenous vein grafts, certainly when this was correlated with improved survival [16]. Tector and coworkers [17] insisted in 1983 to use this arterial conduit for grafting the anterior descending coronary artery.
Several investigators reported reduced early postoperative infarction rates in the presence of arterial or more extensive arterial grafting, sometimes without [18], sometimes after correction [19, 20] for patient variability. These findings were confirmed in this study with the first-month reduction of freedom from infarct for the median patient from 97% to 98% by having at least one arterial graft, preferably to the LAD. The additional early benefit of increasing the number of arterial grafts above a single one was lost after correction for patient variability.
Loop and colleagues [1] demonstrated a better late cardiac event-free survival after a left IMA anastomosis, versus a saphenous vein, to the LAD. These findings are confirmed in this study for the event infarct, after correction for patient variability, and are quantified for a median patient (see Table 3) in Figure 3. This benefit is increasing over time and as far as the extent of the follow-up. An additional benefit is identified in the interaction between single vessel disease and the presence of only arterial grafts. This benefit is active over the entire follow-up interval but most visible between a few days and 2 years after operation, because this is the interval when the constant phase is proportionally the most important.
The positive findings for a single mammary artery graft prompted surgeons to use both arteries. In a case-matched study with a follow-up of 15 years, Fiore and colleagues [21] observed, a significant (p = 0.02) reduction (59% to 75% freedom) of late infarcts in increasing the number of mammary artery grafts to two. But the curves for both groups crossed one another at 10 years after operation. These findings were not reconfirmed in this study after correction for patient variability. A median patient (Table 3) improves freedom from infarct at 10 years from 86% to 91% by having one arterial graft, preferably to the LAD. A similar additional increase with a second arterial graft is very unlikely because it would annihilate all other influences. The absence of additional advantage of a second or third IMA anastomosis could have been foreseen as the first IMA anastomosis was most frequently selected for the supply of the left anterior descending artery, the dominant artery responsible for the preservation of the ventricular function and capable of delivery of collateral flow.
Impact of arterial grafting on events after first infarct after coronary artery bypass grafting
In addition to a first insight in the prevalence and time structure of events after-infarct, this study has explored the influence of arterial grafting on these events. An arterial graft protected the patient’s survival after the first infarct after CABG (Fig 5). No additional benefit of single arterial grafting was documented in return of postinfarct angina or reintervention. Double mammary artery reconstruction reduced return of angina after CABG (Fig 7), certainly versus a single or no arterial graft. Further research is warranted to determine whether these benefits remain active after adequate correction for some of the identified patient variability.
Clinical inferences
The first infarct after CABG is a rare event with major clinical relevance for the patient. Patients in whom the demographic, cardiac or noncardiac comorbidity reduces the 10-year survival are unlikely to suffer the event. Only one-third of the patients is warned by preinfarct angina. The occurrence of this first infarct after CABG should be avoided by all therapeutic and procedural means, as well during the primary CABG procedure as in follow-up.
Arterial grafting, certainly to the LAD, seems one of these therapeutic possibilities. No increased risk or benefit was identified with more extensive or complete arterial grafting in any hazard phase. The age of the median coronary bypass patient in 1998 has reached or exceeded 70 years in most surgical programs. The comorbidity has risen in parallel. Therefore, it is unlikely that more extensive arterial revascularization will ever reduce the prevalence of first infarct after CABG due to the rarity of the event, the limited life expectancy of the median patient, and the not yet identifiable benefit of this extensive arterial grafting.
Acknowledgments
We thank Robert Brown (UAB) for his unsurpassed expertise in handling the most complex database, analytic, and graphic requests.
Appendix 1: Variables considered in the multivariable analysis of infarct after coronary artery bypass grafting
Patient variables
Demographics. Sex; age (years) at operation; weight; height; body surface area; body mass index; weight–height ratio, difference and ratio of weight to ideal body weight where ideal weight is (height in cm minus 100) for men and (height in cm minus 110) for women; blood group; rhesus factor.
Preoperative rhythm disturbances. Atrial fibrillation; right hemiblock, left partial or total hemiblock (and either); recent ventricular tachycardia or ventricular fibrillation or intractable ventricular tachycardia or repeated ventricular fibrillation; permanent pacemaker implanted before or at the coronary artery bypass grafting.
Previous procedures. Percutaneous transluminal coronary angioplasty (PTCA) unsuccessful PTCA, successful PTCA, number of previous PTCAs, interval since last PTCA, duration of freedom from angina after last PTCA; previous noncarotid vascular operation, previous carotid endarterectomy, or either.
Acute myocardial infarction. Interval between infarct and operation; location of infarct (coronary distribution); use of preoperative thrombolytic therapy; interval since last thrombolytic therapy.
Hemodynamic status. Cardiogenic shock without or with cardiopulmonary resuscitation; hemodynamic instability (0 = stable, 1 = unstable on medication but not in shock, 2 = shock, 3 = shock with cardiopulmonary resuscitation; unstable (yes/no), and graded with states 2 and 3 combined); New York Heart Association class (limitation by either angina or heart failure); increment of limitation by heart failure above that of angina (0 = none, 1 = mild, 2 = moderate, 3 = severe).
Symptoms of reversible ischemia. K.U. Leuven Angina Class (0 = mild, 1 = mild symptoms, 2 = symptoms with normal activities, 3 = severe with symptoms even at rest, 4 = unstable angina); Canadian Angina Class (0–4, and augmented to grade 5 by unstable angina); duration of anginal symptoms; angina at rest; unstable angina; treatment requirement for unstable angina (0 = no unstable angina, 1 = unstable angina controlled by intravenous medication, 2 = changing ST segment in the hours before operation despite maximal intravenous medication.
Exercise testing. Positive exercise test by electrocardiogram or on clinical grounds, clinically positive test; electrocardiogram positive test.
Distribution of coronary artery disease (limited to those predictable at the time of decision making). Number of coronary systems diseased (70% diameter reduction or more), one, two, or three system disease, left main stenosis (percent, 
50%, 70%, and 90%).
Left ventricular function. Ejection fraction; left ventricular end-diastolic pressure; number of previous myocardial infarcts; left ventricular hypertrophy on electrocardiogram; graded (subjective) ventricular dysfunction (0 = none, 1 = mild, 2 = moderate, 3 = severe).
Coexisting conditions (cardiac). Ischemic mitral incompetence (insufficient to require surgical intervention); aortic valve stenosis; aortic valve insufficiency.
Coexisting vascular disease. Abdominal aortic disease; peripheral vascular disease; cerebral vascular disease; carotid artery disease; internal carotid artery occlusion, internal carotid artery percent stenosis; 80% to 99% uni- or bilateral internal carotid artery stenosis, previous history of vascular operation, previous history of carotid operation, history of stroke; history of transient ischemic attack, calcification of ascending aorta.
Hyperlipidemia. Cholesterol level; HDL level; low-density lipoprotein level; triglyceride level.
Coexisting conditions (noncardiac). Diabetes (graded as 0 = none, 1 = oral treatment, 2 = insulin treatment, and each grade separately); overweight (>10 kg above calculated ideal weight, based on sex and height as defined under demographic variables above); difference from ideal weight; ratio of actual weight versus ideal weight; hypertensive (systolic blood pressure >160 mm Hg or diastolic pressure >100 mm Hg, or on antihypertensive medication); current or history of malignancy; on dialysis; history of severe renal failure; history of renal transplantation; history of nephrectomy; history of hepatic disease (hepatitis or clinical hepatic dysfunction); history of smoking; family history of ischemic heart disease; pulmonary disease (legally confirmed incapacitating anthracosilicosis, important reduction in diffusing capacity, chronic obstructive pulmonary disease, asthmatic bronchitis), chronic obstructive pulmonary disease, pulmonary function (forced vital capacity volumes and 1-second expiratory volumes, these normalized to gender height and age); psychiatric history.
Procedure variables (limited to those predictable at the time of decision making)
Bypassing conduit. Use of saphenous vein conduits (solely or with other conduits), number of saphenous vein conduits used, number of vein graft distal anastomoses, location of coronary systems to which vein grafts are anastomosed; use of internal thoracic artery (solely or with other conduits); number of internal mammary artery arteries used; number of internal mammary artery distals; location and number of coronary systems receiving internal mammary artery conduits; gastroepiploic artery as the conduit; number of distals; and location of systems receiving this conduit; total arterial conduits, distals and location of anastomoses; end-to-end grafts used; prosthetic conduits used; free internal mammary artery used; ratio of total conduits to total distals, and by extent of coronary disease; ratio of arterial conduits to total arterial distals, and by extent of coronary disease; ratio of nonarterial conduits to total nonarterial distals, and by extent of coronary disease; the largest number of distals on an arterial graft, largest number of distals on a nonarterial graft; patch grafts used; completeness of revascularization.
Quality of distal vessels. Proportion of distal anastomoses to small coronary arteries (1 mm or less in size).
Concomitant procedures. Repair of abdominal aortic aneurysm; carotid endarterectomy; plication or resection of left ventricular aneurysm (limited anterior or apical).
Institutional experience variables
Each surgeon; inexperienced surgeons; surgeon’s experience (number of isolated coronary cases operated on previous to that patient); surgeon’s routine (number of isolated coronary cases operated on in the previous calendar year); date of operation (number of years since 1971); month of operation.
Appendix 2: Parameter estimates, selected variables, their mathematical transformation, their coefficients, and their standard error for the final model
Early phase
Intercept = 0.0006341649; Delta = 0; Rho = 0.003259097; Nu = 14.33759; M = 0
Height of the patient (inverse transformation, 170 divided by length in cm) = 5.477461 ± 1.45; Unstable ST-segment but not acute infarct = 0.4786189 ± 0.0946; Infarct within 30 days before operation = -0.946236; Preoperative inferior infarct = -0.639429 ± 0.413; History of peripheral vascular disease = 0.4065837 ± 0.163; Preoperative pulmonary vital capacity as a percent of normal = -0.858741 ± 0.426; Presence of an arterial graft = -0.336324 ± 0.120; Coronary endarterectomy performed = 1.672594 ± 0.160; Planned concomitant pacemaker insertion = 2.506339 ± 0.713; Incomplete revascularization = 0.4348333 ± 0.146; Low-risk-for-infarct-return surgeon = -0.804866 ± 0.158.
Constant phase
Intercept = 4.940636E-06
Height of the patient (inverse transformation, 170 divided by length in cm) = 6.483815 ± 2.99; Presence of an arterial graft = -0.636646 ± 0.236; Incomplete revascularization = 0.89658 ± 0.251; Age at operation (squared 50 divided by age at operation) = 0.9953316 ± 0.205; Stable angina before operation = -0.640694 ± 0.218; Clinical or electrocardiographical positive stress test before operation = -0.6967748 ± 0.280; Percent left main coronary artery stenosis = -1.78812 ± 0.840; Preoperative aortic valve incompetence = 1.50528 ± 0.504; Preoperative history of abdominal aortic disease = 1.193248 ± 0.356; Preoperative blood urea nitrogen higher than 50 mg/dL = 1.155435 ± 0.393; Presence of a patch graft = 2.338759 ± 0.591; One system disease and no arterial grafts constructed = 0.788195 ± 0.288.
Late phase
Intercept = 2.548915E-07; Tau = 1; Gamma = 2.591674; Alpha = 1; Eta = 1
Infarct within 30 days before operation = 0.7825094 ± 0.265; History of peripheral vascular disease = 0.5642084 ± 0.157; Preoperative pulmonary vital capacity as a percent of normal = -1.0873 ± 0.459; Height of the patient = 0.04568757 ± 0.0135; Blood group A = -0.285174 ± 0.112; Two or three coronary system disease = 0.7000357 ± 0.274; Cerebral (noncarotid) vessel disease = 1.232227 ± 0.404; Preoperative cholesterol value (inverse transformation) = -1.04798 ± 0.288355; Higher grade of diabetes (grade 0 = no diabetes; grade 1 = abnormal glucose tolerance test with dietary treatment; grade 2 = diabetic, receiving oral hypoglycemic treatment; grade 3 = insulin-treated diabetes) (the squared transformation is used) = 0.1184553 ± 0.0291; Nonarterial graft to the body of the left anterior descending coronary artery = 0.4023177 ± 0.117.
References
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A. M. Lincoff, L. A. LeNarz, G. J. Despotis, P. K. Smith, J. E. Booth, R. E. Raymond, S. K. Sapp, C. F. Cabot, J. E. Tcheng, R. M. Califf, et al. Abciximab and bleeding during coronary surgery: results from the EPILOG and EPISTENT trials Ann. Thorac. Surg., August 1, 2000; 70(2): 516 - 526. [Abstract] [Full Text] [PDF]
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M. Kawasuji, N. Sakakibara, S. Fujii, T. Yasuda, and Y. Watanabe Coronary artery bypass surgery with arterial grafts in familial hypercholesterolemia J. Thorac. Cardiovasc. Surg., May 1, 2000; 119(5): 1008 - 1013. [Abstract] [Full Text] [PDF]
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R. Dion, D. Glineur, D. Derouck, R. Verhelst, P. Noirhomme, G. El Khoury, E. Degrave, and C. Hanet Long-term clinical and angiographic follow-up of sequential internal thoracic artery grafting Eur. J. Cardiothorac. Surg., April 1, 2000; 17(4): 407 - 414. [Abstract] [Full Text] [PDF]
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J. Tatoulis, B. F. Buxton, J. A. Fuller, and A. G. Royse Total arterial coronary revascularization: techniques and results in 3,220 patients Ann. Thorac. Surg., December 1, 1999; 68(6): 2093 - 2099. [Abstract] [Full Text] [PDF]
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O. Wendler, B. Hennen, T. Markwirth, J. Konig, D. Tscholl, Q. Huang, E. Shahangi, H.-J. Schafers, and S. H. G. Borst T GRAFTS WITH THE RIGHT INTERNAL THORACIC ARTERY TO LEFT INTERNAL THORACIC ARTERY VERSUS THE LEFT INTERNAL THORACIC ARTERY AND RADIAL ARTERY: FLOW DYNAMICS IN THE INTERNAL THORACIC ARTERY MAIN STEM J. Thorac. Cardiovasc. Surg., November 1, 1999; 118(5): 841 - 848. [Abstract] [Full Text] [PDF]
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T. M. Sundt III, H. B. Barner, C. J. Camillo, and W. A. Gay Jr Total arterial revascularization with an internal thoracic artery and radial artery T graft Ann. Thorac. Surg., August 1, 1999; 68(2): 399 - 404. [Abstract] [Full Text] [PDF]
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S. Noda and H. B. Barner Arterial conduits Ann. Thorac. Surg., January 1, 1999; 67(1): 285 - 286. [Full Text] [PDF]
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F. D. Loop Coronary artery surgery: the end of the beginning Eur. J. Cardiothorac. Surg., December 1, 1998; 14(6): 554 - 571. [Abstract] [Full Text] [PDF]
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