ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Dietmar Boethig
Dirk Fritzsche
Dieter Horstkotte
Reiner Koerfer
Kazutomo Minami
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yoda, M.
Right arrow Articles by Minami, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yoda, M.
Right arrow Articles by Minami, K.
Related Collections
Right arrow Coronary disease

Ann Thorac Surg 2004;78:549-555
© 2004 The Society of Thoracic Surgeons


Original article: cardiovascular

Operative outcome of simultaneous carotid and valvular surgery

Masataka Yoda, MDa*, Dietmar Boethig, MDa, Dirk Fritzsche, MD, PhDa, Dieter Horstkotte, MD, PhDa, Reiner Koerfer, MD, PhDa, Kazutomo Minami, MD, PhD

a Department of Thoracic and Cardiovascular Surgery, Heart Center North Rhine-Westphalia, University of Bochum, Bad Oeynhausen, Germany

Accepted for publication February 6, 2004.

* Address reprint requests to Dr Minami, Department of Thoracic and Cardiovascular Surgery, Heart Center North Rhine-Westphalia, University of Bochum, Georgstrasse 11, 32545 Bad Oeynhausen, Germany
e-mail: kminami{at}hdz-nrw.de


    Abstract
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
BACKGROUND: Operative outcome of simultaneous carotid endarterectomy and valvular surgery has not been clarified. We retrospectively reviewed short-term and long-term outcomes after carotid endarterectomy combined with valvular replacement.

METHODS: Seventy-nine patients (50 men and 29 women. mean age, 68.9 ± 6.9 years; range, 53.3 to 78.7 years) underwent carotid endarterectomy combined with valve replacement from February 1985 to April 2002. Indication of carotid endarterectomy was more than 75% carotid stenosis with or without ulceration. Thirteen patients had history of stroke. Endarterectomy was performed under mild hypothermia with cardiopulmonary bypass in all cases. Positions of replaced valves were aortic in 64 patients, mitral in 10, and mitral and aortic in 5 patients.

RESULTS: There were 8 early deaths (10.1%). Early neurologic complications occurred in 8 patients (10.1%); two late events were observed. Double valve replacement was an independent risk factor for early death (p = 0.039; odds ratio = 25.6). For early stroke we found no statistically significant risk factor. Myocardial infarction (p = 0.022; odds ratio = 3.0) and age more than 70 years (p = 0.03; odds ratio = 2.5) were independent risk factors for premature death; we found no independent risk factor for late stroke. Permanent impairment or death as a stroke consequence was seen in 5 patients, 3 of them had ipsilateral strokes, 2 had contralateral strokes.

CONCLUSIONS: Endarterectomy can be safely performed combined with aortic valve surgery. Concomitant mitral or double valve replacement cannot be judged reliably because of the small number of patients, but they might be a high risk.


    Introduction
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
Severe neurologic complications after isolated valvular replacement occur in 3.5% to 5.1% of patients [1]. There are several ways to explain neurologic complications after cardiac operations, such as cerebral hypotension, cerebral hypoperfusion, cerebral embolization (air or atheroma), or intracranial or extracranial vascular disease [2, 3].

Severe extracranial artery stenosis is defined as a more than 90% reduction of the lumen area or more than 70% reduction of the vascular diameter [4]. Severe stenosis of extracranial arteries is found in 1.3% to 16% of preoperative patients requiring cardiac surgery [59]. It is demonstrated to be a most important risk factor for postoperative neurologic complications.

Some authors reported their results after simultaneous surgery of coronary artery bypass grafting and carotid endarterectomy, but the operative outcome of combined valvular surgery and carotid endarterectomy has remained undescribed.

In this study, we review operative and late outcomes after simultaneous carotid endarterectomy and valvular replacement.


    Material and methods
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
Patients
From February 1985 to April 2002, 79 consecutively operated on patients underwent valvular replacement combined with carotid endarterectomy at the Heart Center North Rhine-Westphalia in Bad Oeynhausen. Sixty-four patients had aortic valve replacement (AVR), 10 had mitral valve replacement, and 5 had mitral and aortic valve replacement. An overview on their preoperative conditions is given in Table 1. Concomitant carotid endarterectomy was performed in 45 patients on the right side and in 34 patients on the left side.


View this table:
[in this window]
[in a new window]
 
Table 1. Analyses of Risk Factors From Patient Histories

 
Indication for carotid endarterectomy was more than 75% carotid stenosis with or without ulceration by angiographic diagnosis [10]. Preoperative search for carotid artery stenosis was performed by Doppler ultrasound examination in all patients, followed by arterial digital subtraction angiography or selective carotid cineangiography in patients with presumed indication for operation.

Since 1989, in cases of asymptomatic carotid stenosis, the cerebral reserve capacity was tested with transcranial Doppler ultrasound (EME GmbH, Überlingen, Germany) to detect functionally relevant stenoses [11]. A pathologic finding was defined as an increase in flow velocity in the middle cerebral artery of less than 20% after carbon dioxide stimulation induced by hypercapnia [1214]. Patients with reduced middle cerebral artery flow response were operated on, regardless of whether carotid artery stenosis was symptomatic or not. Patients with asymptomatic carotid artery stenosis and normal middle cerebral artery flow velocity without ulcerations were treated with individual anticoagulation or antithrombogenic drugs, and ultrasonographic short interval follow-up was recommended (Fig 1).



View larger version (21K):
[in this window]
[in a new window]
 
Fig 1. Our treatment strategy of patients with heart disease and carotid artery stenosis (TCD = transcranial Doppler; CEA = carotid endarterectomy.)

 
Operation
At first, the carotid artery was exposed. Then, median sternotomy, pericardiotomy, and cannulation for cardiopulmonary bypass (CPB) with synchronized pulsatile perfusion were performed in the usual fashion. A mean arterial pressure was kept at between 60 and 70 mm Hg with the unloaded beating heart. Mild hypothermia was induced (blood temperature 27°C, nasopharyngeal temperature 32°C). Carotid arteries were clamped when nasopharyngeal temperature was 32°C after decreasing blood temperature to 27°C. Carotid endarterectomy with autologous saphenous vein patch was performed using arterial occlusion. After completion of endarterectomy, cardiac arrest was induced by histidine-tryptophan-ketoglutarate solution (Custodiol, Dr. Franz Köhler Chemie GmbH, Alsbach-Hähnlein, Germany). The perfusion pressure of the histidine-tryptophan-ketoglutarate solution was maintained at 60 mm Hg initially, and maintained at 40 mm Hg for a period of 7 minutes after cardiac arrest [15]. This follows a perfusion rate of 1 mL/min per gram of heart weight, up to a total amount of 3,000 to 4,000 mL used for adults [16, 17]. Valve replacement was performed in the usual fashion (17 porcine, 20 bovine, 11 disc, 42 bileaflet valve prostheses). In 53 patients (67%) concomitant coronary artery bypass grafting (CABG) was performed. The neck incision was left open until the end of the cardiac procedure. Cerebral function was monitored by continuous electroencephalogram (EEG; Drägerwerk AG, Lübeck, Germany) [18]. The EEG was recorded from electrodes placed over the frontal and mastoid areas. Data were derived from compressed spectral array and digital display of power band. Pathologic signs were defined as decrease of total power or slowing in frequency developed on one side or both sides without relation to changes in anesthetic depth or temperature. An intraluminal shunt was used only in two cases, when pathologic signs were found in the EEG.

Postoperative assessment
A consultant neurologist assessed each case of suspected postoperative neurologic damage. Postoperative course including neurologic status was extracted from the patients' hospital records; follow-up was obtained by questionnaires compiled by the patients' referring physicians, cardiologists, or the patients themselves.

Statistical analysis
Early death and early stroke with persisting neurologic deficit were defined as events within 30 days postoperatively. Data were expressed as mean ± standard deviation. For univariate early events risk factor analysis, {chi}2 and, if appropriate, the two-tailed Fisher's exact tests were used. For multivariate early event analysis, logistic regression was used. Univariate analyses of time-dependent risk factors were done with the Kaplan-Meier method (log rank test) and followed by Cox regression modeling to find independent risk factors. Odds ratios are given with the multivariate analyses results. We used SPSS release 11.5.1 (SPSS Inc, Chicago, IL) for all statistical calculations.


    Results
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
Early mortality after simultaneous carotid endarterectomy and valve surgery was 10.1% (8 patients): 3 of 64 died after AVR (4.7%), 2 of 10 after mitral valve replacement, and 3 of 5 after double valve replacement (Table 1).

Early death causes were low output syndrome in 2 patients, lethal stroke in 3 patients, multiorgan failure in 1 patient, right ventricular failure in 1 patient, and ventricular fibrillation in 1 patient (Table 2). Double valve replacement was an independent risk factor for early death (p = 0.039; odds ratio = 25.6).


View this table:
[in this window]
[in a new window]
 
Table 2. List of Causes of Early and Late Death

 
Causes of late death were cardiac events in 10 patients (7 patients with cardiac failure, 1 patient with cardiac infarction, and 2 patients with redo valve operation), stroke in 1 patient, carcinoma in 2 patients, and other causes in 6 patients (Alzheimer's disease in 3; pneumonia, ileus, and diabetes mellitus, each in 1; Table 2).

Previous myocardial infarction, diabetes mellitus, concomitant CABG, and age more than 70 years were preoperative risk factors for premature death in the univariate analysis (Fig 2).



View larger version (44K):
[in this window]
[in a new window]
 
Fig 2. Univariate risk factors for survival. Survival of all patients having the risk factor is compared with patients that were free of it. (CABG = coronary artery bypass grafting; DM = diabetes mellitus; MI = myocardiac infarction.)

 
Cox regression models indicated myocardial infarction (p = 0.022; odds ratio = 3.0) and age more than 70 (p = 0.03; odds ratio = 2.5) as independent risk factors for premature death (Table 1).

Actuarial survival was 79.8% ± 0.05%, 58.9% ± 0.08%, and 34.9% ± 0.08% at 5, 10, and 15 years, respectively. See Figure 3 for stratification by valve prosthesis site and overall estimation.



View larger version (20K):
[in this window]
[in a new window]
 
Fig 3. Survival related to valve site. The bold line is the estimation for all patients with combined carotid endarterectomy and valve replacement, the other three lines derive from the same population that was stratified by valve site. (ALL = all patients; AVR = aortic valve replacement; MVR = mitral valve replacement; DVR = double valve replacement.)

 
Perioperative stroke was seen in 8 patients (10.1%), including 3 lethal strokes: 6 of 64 complications after AVR, 0 of 10 after mitral valve replacement, and 2 of 5 after double valve replacement. The strokes were ipsilateral in 4 patients (50%), contralateral in 3 patients (37.5%), and bilateral in 1 patient (12.5%). After AVR, 6 patients (9.4%) experienced complications of perioperative strokes, including 2 with lethal strokes (3.1%) and 4 who mentioned strokes. With time, the symptoms of 2 of those who mentioned strokes reversed partially, 1 completely. For early stroke, we could not identify independent statistically significant risk factors.

Late stroke occurred in 2 patients (1 ipsilateral, 1 contralateral; Table 2). Preoperative absence of sinus rhythm (p = 0.004), double valve replacement (p = 0.040), and contralateral stenosis of 90% or more (p = 0.016) were univariate risk factors. Age more than 70 years and previous myocardial infarction were risk factors for stroke in the entire postoperative course (Table 1); none of them was independent.

Freedom from ipsilateral stroke reached 93.5% ± 2.8% at 7 months; no further ipsilateral stroke was observed throughout the whole follow-up. Freedom from any stroke was 88.4% ± 3.6%, 88.4% ± 3.6%, and 84.1% ± 5.5% at 5, 10, and 15 years, respectively (Fig 4). Stroke causing death or permanent impairment occurred in 5 patients. In the long-term course, we observed 93.5% ± 2.8% freedom from this severe complication. Freedom from both death and permanent impairment was 78.5% ± 5.4%, 57.1% ± 8.0%, and 32.3% ± 8.5% after 5, 10, and 15 years, respectively.



View larger version (36K):
[in this window]
[in a new window]
 
Fig 4. Freedom from stroke. The upper graph divides the observed strokes in ipsilateral (ipsi) and contralateral ones; the lower graphs show the effect of lost or preserved sinus rhythm (SR).

 

    Comment
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
The increasing percentage of elderly patients in cardiac surgery might be the reason for a growing incidence of carotid artery stenosis in this patient group, ranging around 8% [1921]. Carotid artery Doppler ultrasonography is performed as a routine diagnostic method in our cardiac surgery patients. Although results after simultaneous surgery of CABG and carotid endarterectomy have been reported [3, 5, 8], the operative outcome of combined valvular surgery and carotid endarterectomy has remained undescribed.

Astor and colleagues [1] reported that severe neurologic complications after isolated valvular procedure occur in 3.5% to 8.1%. In our institution, between February 1985 and April 2002, valvular procedure was performed in 8,488 patients, and the incidence of perioperative neurologic deficit was 3.5% [22]. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) collaborators reported on data from 659 patients with 70% to 99% stenosis, 328 of whom underwent carotid endarterectomy without concomitant surgery. The 30-day stroke morbidity and mortality rate for the surgical group was 5.8%. Further, the cumulative risk of any ipsilateral stroke at 2 years was 9% for surgical patients and 26% for patients treated without operation. Study investigators concluded that carotid endarterectomy is highly beneficial to patients with recent hemispheric or retinal transient ischemia or nondisabling strokes and ipsilateral severe carotid stenosis [4].

We previously reported good operative outcomes after simultaneous carotid endarterectomy and CABG operations. The rate of perioperative neurologic deficit was 3.2%, and early mortality rate was 2.6%. Furthermore, a risk factor for early neurologic complication was previous stroke, and for early mortality was age more than 70 years. The risk factors for late neurologic complications were symptomatic carotid stenosis, previous stroke, and bilateral carotid stenosis (>90% stenosis), and for late mortality were previous myocardial infarction, age more than 70 years, previous stroke, and bilateral carotid stenosis (>90% stenosis) [5].

In our study, the rate of perioperative early mortality rate was 2.6%, lethal stroke was 3.1%, and fixed stroke was 1.6% after AVR. We thought carotid endarterectomy combined with AVR could be performed safely and effectively. We found no independent risk factors for late stroke; previous myocardial infarction and age more than 70 years were independent risk factors for premature death.

There is a continuing controversy about the management of patients with concomitant occlusive disease of carotid arteries and heart disease. Three treatment options have been considered: carotid endarterectomy followed by delayed CABG, CABG first with carotid endarterectomy delayed, and combined carotid endarterectomy and CABG under a single operation.

There has been no clear advantage proven for one of these options over another. A meta-analysis using the 16 papers that reported on both the combined and staged procedures revealed a significantly increased risk of the composite end point of stroke or death in patients undergoing the combined procedure, however there was no statistically significant difference between the groups for stroke or death alone [23].

Hertzer and colleagues [24] demonstrated that the stroke rate in the staged (carotid endarterectomy first group and CABG first group) and combined procedures was 4.2%, 14%, and 2.8%, respectively, in the group of patients with unilateral, asymptomatic carotid artery disease. The difference in the stroke rate between the CABG first group and combined procedures was statistically significant. The mortality rate in the staged (carotid endarterectomy first group and CABG first group) and combined procedures was 4.2%, 5%, and 4.2%, respectively, and there was no significant difference.

In the group of patients that had bilateral or symptomatic carotid artery disease, the stroke rate for the combined procedure as compared with the staged procedure (CABG first) was 7.1% and 8.7%, respectively, and the mortality rate was 6.1% and 0%, respectively. This study suggested that the staged procedure (CABG first) should be avoided, and the combined procedure can be performed with low stroke and mortality rates.

In studies that report on more than 200 combined procedures, the stroke rate ranges from 1.0% to 5.1%, and the mortality ranges from 0% to 8.9%. In all of these series, the majority of patients had asymptomatic cerebrovascular disease. However, in those centers that limit the combined procedure to patients with symptomatic or severe bilateral carotid artery disease, the outcomes are more variable. Among these series stroke rates range from 1.7% to 18%, and mortality ranges from 0% to 10.8% [25]. These results suggest that the combined procedure can be done with reasonable safety, patient selection significantly affects the results of the combined procedure, and those patients with severe bilateral or symptomatic carotid artery disease in combination with severe or symptomatic coronary artery disease are at high risk for associated complications.

In the combined procedure most authors repair the carotid artery stenosis before full establishment of CPB. In contrast, we have performed carotid endarterectomy after initiation of CPB because we think that hypothermia and controlled pulsatile perfusion are advantageous for the cerebral perfusion.

Hypothermia decreases cerebral metabolism (oxygen consumption and glucose utilization), and increases the tissue content of adenosine triphosphate [26]. Studies reported that a temperature reduction from 37°C to 28°C reduced cerebral oxygen consumption to 31% to 66% [2729]. Croughwell and associates [30] found that during CPB and the reduction of the patient's body temperature from 37°C to 27°C, cerebral blood flow fell less than cerebral oxygen consumption. This was referred to as a situation of "luxurious cerebral blood flow" accompanied by a reduction of the cerebral arteriovenous oxygen difference. Additionally, general heparinization reduces thromboembolic problems.

Pulsatile perfusion increases cerebral blood flow [31, 32]. Minami and coworkers [33] reported that nonpulsatile perfusion resulted in lower cerebral blood flow, increased capillary closure, sludging, and marked venous constriction with consequent decreased venous return. Some reports [31, 32] have demonstrated a 15% to 19% increase in cerebral blood flow by using pulsatile perfusion. Furthermore, in a stroke model cerebral blood flow increased 55% when circulation was changed from nonpulsatile to pulsatile perfusion [31].

The optimal arterial pressure for cerebral perfusion during CPB under hypothermia is not clearly defined. We keep mean perfusion pressure at 60 to 70 mm Hg (perfusion rate 2.5 to 3.0 L x min–1 x m–2) for these patients. Tufo and associates [34] found that lowering of systemic arterial blood pressure below 50 mm Hg for longer than 10 minutes resulted in a fourfold increased risk compared with the risk with higher blood pressure. Tanaka and colleagues [35] suggested that when arterial blood pressure during CPB fell below approximately 40 mm Hg, cerebral blood flow might decline appreciably, with a concomitant decrease in cerebral oxygen consumption. In a recent review of concomitant disease of the carotid and coronary arteries, Lazar and Menzoian [36] concluded that cerebral perfusion during CPB in patients with carotid artery stenosis can be safely maintained as long as pressures are kept at at least 50 mm Hg; further neurologic complications of CPB appear to be related more to arteriosclerotic aortic disease than to low flow caused by carotid artery stenosis.

Two patients were found to have pathologic signs in the intraoperative EEG monitoring, and 6 patients showed false-negative results. Hypothermia was expected to make the analysis of the EEG more difficult than in isolated carotid endarterectomy under normothermia [5]. In our series, minor EEG changes were fairly common during carotid endarterectomy, but they were generally not followed by cerebral sequelae. In contrast, most of the EEG changes that occurred after carotid endarterectomy were associated with perioperative strokes [18]. This suggests that the EEG monitoring is useful when carotid endarterectomy is combined with heart surgery.

In conclusion, carotid endarterectomy could be safely and effectively performed combined with aortic valvular replacement using CPB for both procedures. Because of the small number of patients, the risk of concomitant double valve replacement cannot be judged reliably, but it might be elevated.


    References
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

  1. Astor B.C., Kaczmarek R.G., Hefflin B., Daley W.R. Mortality after aortic valve replacement: results from a nationally representative database. Ann Thorac Surg 2000;70:1939-1945.[Abstract/Free Full Text]
  2. Schwartz L.B., Bridgman A.H., Kieffer R.W., et al. Asymptomatic carotid artery stenosis and stroke in patients undergoing cardiopulmonary bypass. J Vasc Surg 1995;21:146-153.[Medline]
  3. Mehigan J.T., Buch W.S., Pipkin R.D., Fogarty T.J. A planned approach to coexistent cerebrovascular disease in coronary artery bypass candidates. Arch Surg 1977;112:1403-1409.[Abstract/Free Full Text]
  4. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991;325:445-453.[Abstract]
  5. Minami K., Fukahara K., Boethig D., Bairaktaris A., Fritzsche D., Koerfer R. Long-term result of simultaneous carotid endarterectomy and myocardial revascularization with cardiopulmonary bypass used for both procedures. J Thorac Cardiovasc Surg 2000;119:764-773.[Abstract/Free Full Text]
  6. Weiss S.J., Sutter F.P., Shannon T.O., Goldman S.M. Combined cardiac operation and carotid endarterectomy during aortic cross-clamping. Ann Thorac Surg 1992;53:813-816.[Abstract]
  7. Swain J.A. Cardiac surgery and brain. N Engl J Med 1993;329:1119-1120.[Free Full Text]
  8. Breslau L.J., Fell G., Ivey T.D., Bailey W.W., Miller D.W., Strandness D.E. Carotid artery disease in patients undergoing coronary artery bypass operations. J Thorac Cardiovasc Surg 1981;82:765-767.[Abstract]
  9. Hennerici M., Aurich A., Sandmann W., Freund H.J. Incidence of asymptomatic extracranial artery disease. Stroke 1981;12:750-758.[Abstract/Free Full Text]
  10. Biller J.B., Feinberg W.M., Castaldo J.E., et al. Guidelines for carotid endarterectomy. A statement for healthcare professionals from a special writing group of the Stroke Council, America Heart Association. Circulation 1998;97:501-509.[Free Full Text]
  11. Minami K., Damsch R., Inoue K., Koerfer R. Assessment of cerebral perfusion reserve in patients with severe carotid and coronary artery disease by transcranial Doppler sonography: diagnostic and therapeutical consequence. Z Herz Thorax Gefaesschir 1991;5:17-22.
  12. Bishop C.C.R., Powell S., Insall M., Rutt D., Browse N.L. Effect of internal carotid artery occlusion on cerebral artery blood flow at rest in response to hypercapnia. Lancet 1986;1:710-712.[Medline]
  13. Ringelstein E.B., Grosse W., Matentzoglu S., Goeckner W.M. Non invasive assessment of the cerebral vasomotor reactivity by means of transcranial Doppler sonography during hyper- and hypocapnea. Klin Wochenschr 1986;64:194-195.[Medline]
  14. Aaslid R., Markwalder T., Nornes H. Noninvasive transcranial Doppler ultrasound recording of flow velocity in basal cerebral arteries. J Neurosurg 1982;57:769-774.[Medline]
  15. Preuss C.J. Cardioplegia with an intracellular formation. In: Pieper H.M., Preuss C.J., eds. Ischemic-reperfusion in cardiac surgery. Dordrecht: Kluwer, 1993:107-134.
  16. Schulte H.D., Preuss C.J., Groschopp C. Crystalloid cardioplegia: experience with the Bretschneider solution. In: Engelman R.M., Levitzsky S., eds. A textbook of clinical cardioplegia. New York: Futura, 1982:199-210.
  17. Preuss C.J., Schulte H.D. Cardioplegia for repeat valve surgery. In: Engelman R.M., Levitzsky S., eds. A textbook of clinical cardioplegia. New York: Futura, 1982:203-219.
  18. Inoue K., Minami K., Hartmann N., Dallmann G., Reichelt W. EEG and cerebral complications in combined carotid and cardiac operations. J Cardiothorac Anesth 1989;3(Suppl 1):73.[Medline]
  19. Pillai L., Gutierrez I.Z., Curl G.R., Gage A.A., Balderman S.C., Ricotta J.J. Evaluation and treatment of carotid stenosis in open heart surgery patients. J Surg Res 1994;57:312-315.[Medline]
  20. Balderman S.C., Gutierrez I.Z., Makula P., Bhayana J.N., Gage A.A. Non invasive screening for asymptomatic carotid artery disease prior to cardiac operation. Experience with 500 patients. J Thorac Cardiovasc Surg 1983;85:427-433.[Abstract]
  21. Aranki S.F., Rizzo R.J., Couper G.S., et al. Aortic valve replacement in the elderly. Effect of gender and coronary artery disease on operative mortality. Circulation 1993;88(Suppl 2):II-17-23.
  22. Inoue K., Lueth L.U., Pottkaemper D., Strauss K.M., Minami K., Reichelt W. Incidence and risk factors of perioperative cerebral complications: heart transplantation compared to coronary artery bypass grafting and valve surgery. J Cardiovasc Surg 1998;39:201-208.[Medline]
  23. Borger M.A., Fremes S.E., Weisel R.D., et al. Coronary bypass and carotid endarterectomy: does a combined approach increase risk? A meta-analysis. Ann Thorac Surg 1999;68:14-20.[Abstract/Free Full Text]
  24. Hertzer N.R., Loop F.D., Beven E.G., O'Hara P.J., Krajewski L.P. Surgical staging for simultaneous coronary and carotid disease: a study including prospective randomization. J Vasc Surg 1989;9:455-463.[Medline]
  25. Brown K.R. Treatment of concomitant carotid and coronary artery disease: decision-making regarding surgical options. J Cardiovasc Surg 2003;44:395-399.[Medline]
  26. Kirklin JW, Barratt-Boyes BG. Hypothermia, circulatory arrest and cardiopulmonary bypass. In: Cardiac surgery, 2nd ed. New York: Churchill Livingstone, 1993:61–127
  27. Fuhrman F.A. Oxygen consumption of mammalian tissues at reduced temperatures. In: Dripps R.D., ed. The physiology of induced hypothermia. Washington, DC: National Academy of Sciences, National Research Council, 1956.
  28. Holobut W., Modrzejewski E., Stazka W. Blood irrigation and oxygen consumption of various organs at normal temperature and in hypothermia. J Physiol (Paris) 1969;61:507-517.[Medline]
  29. Rosomoff H.L., Holaday D.A. Cerebral blood flow and cerebral oxygen consumption during hypothermia. Am J Physiol 1954;179:85.[Free Full Text]
  30. Croughwell N., Smith L.R., Quill T., et al. The effect of temperature on cerebral metabolism and blood flow in adults during cardiopulmonary bypass. J Thorac Cardiovasc Surg 1992;103:549-554.[Abstract]
  31. Tranmer B.I., Gross C.E., Kindt G.W., Adey G.R. Pulsatile versus nonpulsatile blood flow in the treatment of acute cerebral ischemia. Neurosurgery 1986;19:724-731.[Medline]
  32. Murkin J.M., Farrar J.K. The influence of pulsatile versus nonpulsatile cardiopulmonary bypass on cerebral blood flow and cerebral metabolism. Anesthesiology 1989;71:A41.
  33. Minami K., Vyska K., Korfer R. Role of the carotid sinus in response of integrated venous system to pulsatile and nonpulsatile perfusion. J Thorac Cardiovasc Surg 1992;104:1639-1646.[Abstract]
  34. Tufo H.N., Ostfeld A.M., Shebelle R.E. Central nervous system dysfunction following open-heart surgery. JAMA 1970;212:1333-1340.[Abstract/Free Full Text]
  35. Tanaka J., Shiki K., Asou T., Yasui H., Tokunaga K. Cerebral autoregulation during deep hypothermic nonpulsatile cardiopulmonary bypass with selective cerebral perfusion in dogs. J Thorac Cardiovasc Surg 1988;95:124-132.[Abstract]
  36. Lazar H.L., Menzoian J.O. Coronary artery bypass grafting in patients with cerebrovascular disease. Ann Thorac Surg 1998;66:968-974.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
ANGIOLOGYHome page
H. Zayed, A. Ali, O. Wendler, and H. Rashid
Selective Screening for Asymptomatic Carotid Artery Disease Prior to Isolated Heart Valve Surgery
Angiology, October 1, 2009; 60(5): 633 - 636.
[Abstract] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Dietmar Boethig
Dirk Fritzsche
Dieter Horstkotte
Reiner Koerfer
Kazutomo Minami
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yoda, M.
Right arrow Articles by Minami, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yoda, M.
Right arrow Articles by Minami, K.
Related Collections
Right arrow Coronary disease


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS