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Advances in Natural and Applied Sciences, 9(3) March 2015, Pages: 8-12
AENSI Journals
Advances in Natural and Applied Sciences
ISSN:1995-0772 EISSN: 1998-1090
Journal home page: www.aensiweb.com/ANAS
Importance of Further Recognition of Atherosclerotic Patients Candidate for CABG:
Predisposing Factors for Postoperative Stroke
1
Mohammad Ali Sheikhi, 2Ahmad Ebadi, 3Hossein Rahmani
1
Assistant Professor of Cardiovascular surgery MD, Department of Cardiac surgery, Atherosclerosis Research Center Golestan Hospital,
Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
2
Associate Professor of Cardiac Anesthesiology MD, Department of Cardiac Anesthesiology, Golestan Hospital, Atherosclerosis Research
Center, Pain Research Center, Ahvaz Jundishapur University, Ahvaz, Iran
3
Department of Anesthesiology, Pain Research Center, student research committee Ahvaz Jundishapur University of Medical Sciences,
Ahvaz, Iran.
ARTICLE INFO
Article history:
Received 4 September 2014
Received in revised form 24 November
2014
Accepted 8 December 2014
Available online 16 December 2014
Keywords:
Recognition, Atherosclerotic Patients,
Predisposing Factors, Postoperative
ABSTRACT
Given the common pathogenesis of atherosclerotic coronary and carotid diseases,
increasing attention has been paid by cardiovascular surgeons for detection, evaluation
and treatment of carotid artery stenosis in patients undergoing Coronary Artery Bypass
Graft (CABG). Coronary artery bypass is a frequent surgery with a global scope; it has
been proven that the presence of carotid artery stenosis in these patients increases the
risk of ischemic stroke before surgery resulting in reduced quality of life and increased
mortality, as well as disability of patients and increased costs and hospitalization. In
fact, preoperative strokes account for about 3% of the CABG complications. Given that
cardiac surgery patients with carotid artery stenosis are at high risk for surgeryassociated neurological events , therefore, the key points in facing with these patients
are introduced in this pilot study, to help treat them better and with a proper prognosis.
© 2015 AENSI Publisher All rights reserved.
To Cite This Article: Mohammad Ali Sheikhi, Ahmad Ebadi, Hossein Rahmani, Importance of Further Recognition of Atherosclerotic
Patients Candidate for CABG: Predisposing Factors for Postoperative Stroke. Adv. in Nat. Appl. Sci., 9(3): 8-12, 2015
INTRODUCTION
Atherosclerosis:
Atherosclerosis is an epidemic in most developed countries, with a less prevalence in Central and South
America, Africa and Asia. Premenopausal women compared with same age men are at lower risk for
atherosclerosis, but the incidence becomes equal in men and women in postmenopausal women (Thomas, G.,
W. Robert, 2010).
In industrialized countries, atherosclerosis often begins in the first few decades of life. So that one out of
every 6 suddenly died American adolescents aged 13-19 has pathological evidence of atherosclerotic coronary
arteries. Accumulation of lipoproteins, endothelial damage and inflammation are of numerous processes that
contribute to the initiation and progression of atherosclerosis (DOV, M., et al., 2000).
The pathogenesis of atherosclerosis:
In the early stages of atherosclerosis, small particles of lipoproteins penetrate the vascular endothelium;
they are oxidized there and accumulate in the tunica intima. This process is accelerated at the site of endothelial
damage. The damage may arise from hypertension, hypercholesterolemia, smoking, or excessive shear forces
(tangential). Lipid accumulation in the tunica intima leads to the expression of adhesion molecules on the
luminal surface of endothelial cells and thereby allows them to attach the circulating monocytes (e.g.,
macrophages) (Alamowitch, S., et al., 2001; Sabeti, S., et al., 2001; Khairi, H.S., M.c. Crowson, 1995;
Tarzamani, M.K., 2007). The monocytes swallow lipoproteins and changes to fat-accumulated monocytes or
foam cells. Accumulation of these foam cells is the first visible evidence of atherosclerosis. Foam cells multiply
and lead to continuation of local inflammation and thus degradation of endothelium through releasing
proinflammatory mediators. Accumulation of fat in foam cells results in their necrosis, but fat remains at the
center of the plaque. Macrophages and mast cells release enzymes such as metalloproteinase (such as
collagenase and gelatinase) which degrade collagen and the proteins of extracellular matrix adjacent to the
plaque. While, T cells inhibit collagen formation by vascular smooth muscle cells through secreting cytokines
(e.g., interferon alpha) (Durand, D.J., et al., 2004; Hennerici, M., et al., 1987). Increased degradation and
Corresponding Author: Hossein Rahmani, Department of Anesthesiology, Pain Research Center, student research
committee Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
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Advances in Natural and Applied Sciences, 9(3) March 2015, Pages: 8-12
reduced formation of collagen predispose the plaque to corrosion and tear. Activated platelets also release some
substances (such as thromboxane, serotonin) which stimulate vasoconstriction and expansion of thrombus.
When the extent of platelet aggregation and thrombus formation in sufficient to halt blood flow (either partial or
full), an acute coronary event occurs (such as unstable angina, non-ST elevation myocardial infarction
[NSTEMI] or ST elevation myocardial infarction [STEMI]) (Berens, S., et al., 1992; Kobayashi, H., et al.,
2010).
Risk factors for atherosclerosis:
Several risk factors have been identified for development of atherosclerosis. Unrecoverable risk factors
include older age, male gender, and family history of premature atherosclerosis. Other modifiable risk factors
and their treatment may reduce the risk of atherosclerosis. These factors include hyperlipidemia, hypertension,
diabetes mellitus, metabolic syndrome, smoking, obesity, sedentary lifestyle, and excessive alcohol
consumption. As a marker of inflammation, CRP may increase the risk of plaque rupture or contribute to clot
formation. Increased serum levels of CPR, if measured by very sensitive methods, is strongly associated with
risk of MI, stroke, peripheral arterial disease, and sudden death. Coronary artery calcification is also a typical
manifestation of coronary atherosclerosis and is associated with the presence and severity of CAD (David
Sutton, Roger Gregson, H.S., 2003).
Carotid Artery:
The common carotid artery originates from the brachiocephalic artery at right and the aortic arch at left. The
artery is divided into internal and external carotid arteries at the upper rim of the thyroid cartilage. The external
carotid artery supplies the structures in neck, face, skull, tongue and cheeks. The internal carotid artery supplies
the brain, eyes, forehead, and a part of the nose (David Sutton, Roger Gregson, H.S., 2003; Durand, D.J., et al.,
2004).
Carotid Artery Stenosis:
Approximately 730 thousand strokes occur in the United States per year, which impose a cost of more than
$ 40 million. Half of these strokes are the consequence of carotid artery atherosclerosis (Alamowitch, S., et al.,
2001).
The signs depend on the brain area involved. Many patients are asymptomatic and stenosis may be detected
during an examination. The disease may present itself as loss of vision, weakness and tingling in the extremities,
muffled speech, inability to articulate words, or eventually coma. In such situations, an emergency consultation
with a physician is essential to avoid a real stroke.
History of cerebrovascular accident, hypertension, smoking, diabetes, obesity, high cholesterol (especially
LDL), age over 60, female gender, and severe coronary artery disease are the most common risk factors
associated with the occurrence of carotid artery stenosis (Sabeti, S., et al., 2001; Khairi, H.S., M.c. Crowson,
1995).
As mentioned, carotid artery stenosis has been highly reported in females (Durand, D.J., et al., 2004) as
well as in patients with rheumatoid arthritis compared with patients without rheumatoid arthritis, because
cardiovascular mortality and morbidity increase in rheumatoid arthritis (Selnes, O.A., et al, 2012).
This disease is treated based on being symptomatic or asymptomatic and may include the followings:
1. Medical procedures or medications
2. Endarterectomy: surgical removal of plaque from the vessel
3. Repair with open surgery
4. Endovascular procedures: insertion of a vascular stent (Sabeti, S., et al., 2001).
The Relationship between Stroke and Carotid Arteries Stenosis:
Stroke is a severely debilitating disease, which extra cranial atherosclerotic disease, specifically carotid
artery stenosis, is its major causes. Atherosclerotic plaques are most often formed in the proximal internal
carotid artery; however, the common carotid artery is also the culprit at times. In patients who have had a carotid
endarterectomy, the distal common carotid artery is a frequent location for plaque formation. Generally, stroke
occurs as the first symptom of the disease, and often a carotid bruit is the only sign that can be seen on physical
examination (Branthwaite, M.A., 1975).
Carotid Artery Stenosis Detection Techniques:
The two main predictors for stroke are previous symptoms (transient ischemic attack and recent stroke) and
severity of stenotic lesions. For this reason, diagnosis is critical for the prevention of stroke. Several imaging
modalities can be used in this regard. CTA has excellent spatial and contrast resolution for plaque detection. It
is able to detect plaque at the bifurcation of the internal and external carotid arteries, and is used to define
vascular anatomy proximal and distal to a stenotic plaque. CT, however, is not used as the initial screening test.
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Vascular ultrasound is easily accessible and can be brought to the patient's bedside. It is inexpensive, risk-free,
and excellent for the evaluation of carotid anatomy and determination of flow dynamics. B-mode ultrasound is
used for the anatomic determination of the arteries, whereas severity of plaques is evaluated by Doppler, which
can measure the velocity and pressure gradients across a lesion (Branthwaite, M.A., 1975). Doppler sonography
is formed from a combination of real time B-mode images and waveform analysis of Doppler wave. The old
Doppler systems were limited to black and white images, but the recent progresses and the possibility of color
images generation have turned Doppler sonography into a powerful instrument for the evaluation of vascular
disorders (Shirani, S., et al., 2006). There are limitations of Doppler imaging, which can give false
measurements. Any factor that decreases the velocity of the blood from the heart to the carotid arteries can
interfere with accurate estimation of carotid stenosis. Most commonly, severe LV dysfunction, valvular heart
disease, and aortic disease are the culprits. Highly calcified plaques also may cause artifact on ultrasound that
may interfere with accurate assessment. Magnetic resonance angiography (MRA) is another tool for carotid
artery assessment. It is more expensive than the previous two modalities, but it is relatively safe and determines
the anatomy well in plaque morphology. Black-blood imaging is a magnetic resonance sequence in which blood
is black and vessel walls are enhanced, which contribute to determination of plaque morphology. Angiography
can be performed without gadolinium contrast by using time-of-flight sequence, which provides high-density
signals for flowing blood. In addition, PC imaging also can give blood flow velocity pressure information across
stenotic lesions. In general, CT and MRI are used only in the cases where vascular ultrasound is limited or when
a patient requires carotid endarterectomy for carotid artery stenosis.
Coronary Blood Flow:
Anatomy:
Most people have two coronary arteries that originate from the left aortic sinus and right aortic sinus in turn.
The left main coronary artery differs in the length before the left anterior descending artery (LDA) and left
circumflex artery (LCX) branches arise from it. In most cases, LAD coronary artery supplies blood to nearly
50% of the left ventricular mass (approximately 150gr), which includes two-third of the intraventricular septum
and the left ventricular anterior wall. The right coronary artery supplies blood to more than 30% of the left
ventricular mass (about 90gr), which includes one-third of the posterior interventricular septum and half of the
posterior wall. The remaining 20% of the left ventricular mass is supplied by LCX coronary artery (Rosa Mp,
Portal Vl., 2010).
B-3-2 Mechanical Determinants of Coronary Blood Flow: Coronary Perfusion Pressure:
Like other perfusion circulations, coronary myocardial blood flow is dependent on existing pressure. In
physiological conditions, the diastolic aortic pressure becomes the input pressure of the coronary perfusion. On
the other hand, the aortic diastolic pressure, along with cardiac dimensions, determines after load of the left
ventricular, and consequently are myocardial oxygen consumption. Therefore, any reduction in aortic pressure
not only increases coronary perfusion pressure but also increases metabolic needs of coronary blood flow. In
elderly patients with reduced arterial compliance which leads to an increase in systolic and diastolic blood
pressure and reduction of its dialectic pressure, especially in relation with arterial hypertension, the created
condition will not be quite suitable for matching coronary blood flow to myocardial oxygen consumption.
Similarly, aortic stenosis (which causes increased left ventricular systolic pressure and relative decrease of the
aortic diastolic pressure) and aortic regurgitation (which causes decreased aortic diastolic pressure) are
conditions that lead to mismatch between coronary blood flow and myocardial oxygen consumption. In the
presence of coronary stenosis, the post-stenotic coronary pressure becomes the input pressure of the myocardial
perfusion (Ebadi, Ahmad, et al, 2014; Firoozabadi, Mehdi Dehghani, and Ebadi. A., 2014; Firoozabadi, Mehdi
Dehghani, et al, 2014).
Coronary artery bypass graft (CABG):
The number of patients who undergo CABG has increased greatly in recent years, so that it is the most
common major surgery performed in the United States today, partly due to advances in heart surgery which in
turn reduce the risk of mortality. Following decreased mortality, morbidity becomes increasingly more
important because of its fundamental role in improving the outcome of surgery and postoperative quality of life.
CABG improves survival in patients with significant left main coronary artery disease (CAD), 3-vessel CAD,
and ventricular dysfunction. CABG also improves the quality of life in patients with “left main equivalent”
CAD (proximal left anterior descending and proximal left circumflex), but does not protect them from the risk
of subsequent infarction. In patients who were candidates for CABG, the severity of angina pectoris reduced
90% after surgery. The most important mechanism of improvement of survival and left ventricular function after
CABG is restoration of achievable perfusion but without or with negligible contraction of myocardium. The
rates of hospital mortality for coronary bypass surgery in low risk patients can be less than 1%. Myocardial
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infarction associated with surgery occurs in less than 3% and 5-year survival rate is about 90% (Rosa Mp, Portal
Vl., 2010).
Concomitant carotid and coronary artery disease:
Although the number of patients with concomitant carotid and coronary disease is not too high, they are at
high risk in comparison to patients with only carotid or coronary disease. CABG is the treatment of ischemic
heart disease. Advances in the field of conservation, CBP technology, and postsurgical care during the past three
decades have been related with reduced CABG-associated morbidity and mortality. However, stroke is remained
as the major non-cardiac complication of CABG and affects patient’s quality of life, economic status, and
survival. Although the overall incidence of CABG-related stroke is approximately 2%, the role of extra cranial
carotid disease on stroke remains unclear. In various studies, the incidence and morbidity of CVA in patients
undergoing CABG is about 2.1-5.2% and 0-38%, respectively, and regardless of mortality, CVA is the most
serious complication of surgery which disables patients and increases the costs and hospitalization (Ebadi,
Ahmad, et al, 2014). There are several mechanisms which can cause perioperative stroke in patients undergoing
CABG. Embolism can arise from a variety of sources, such as arrhythmias, left ventricular thrombus, dissection
of aorta, microemboli, aortic arch, fragile aorta due to its closure, and aortic catheterization, fat and air
(Firoozabadi, Mehdi Dehghani, and Ebadi. A., 2014). In a study, the following risk factors (with odds ratios) are
presented for CABG perioperative stroke; preoperative factors including carotid stenosis (%5.3), history of
subcortical small vessels ischemia (%4.1), history of cerebrovascular disease (including transient ischemic
attack or stroke) (%2.1), history of diabetes (%2.8), atherosclerotic ascending aorta (%2.0), history of peripheral
vascular disease (%2.0), hypertension (%1.8), smoking (%1.6), previous cardiac surgery (%1.4), and history of
high pulse pressure (1.1 for every 10 mm Hg increase); intraoperative factors including hypotension (*8.4),
manipulation of atherosclerotic ascending aorta (%1.8), cardiopulmonary bypass for more than 2 hours (%1.4);
and postoperative factors including atrial fibrillation (0.6 and 2.6 in two different studies) (denotes the adjusted
odds ratios) (Firoozabadi, Mehdi Dehghani, et al, 2014). Concurrent endarterectomy (CEA) and CABG was
first introduced by Bernhard et al. in 1972 to reduce the risk of mortality and disability from concomitant carotid
and coronary disease. Recent attention paid again today to this strategy is arisen from controlled trials which
show the benefits of isolated CEA in both asymptomatic and symptomatic carotid artery severe stenosis. The
post-CABG causes of stroke are multifactorial. Univariate analysis of systematic review of CABG-associated
stroke has been identified the following factors; carotid stenosis 80% or higher, carotid occlusion, previous
stroke or transient ischemic attack (TIA), peripheral vascular disease, post-infarction angina, female gender,
prolonged CPB, aging, previous CEA, diabetes, smoking, hypertension and carotid bruit (Branthwaite, M.A.,
1975). Brent et al. proposed that simultaneous operation of coronary artery graft and CEA in patients with
concomitant coronary and carotid artery disease can reduce mortality and morbidity in these patients (Rockman,
C.B., et al., 2004). Detection of significant stenosis by auscultation is unreliable. Carotid bruit may be heard
with the smallest carotid stenosis or not heard even when the lumen is only 1-2 mm. Combination of carotid
artery ultrasound and risk factors may have predictive value for patients who are at risk of post-CABG stroke
(Berens, E.S., et al., 1992; Auastasiadis, K., et al., 2009; Szabol, S.Z., et al.,1994; Ikuof, Seigo G., S. Jun, 2000;
Rath, P.C., et al., 2001). Carotid artery disease should be considered in all patients with ischemic heart disease.
Faggieli et al. reported the incidence of carotid artery disease, which is defined as carotid stenosis, as 75% in
patients older than 60 years; this was reported 11% in patients who underwent CABG. Recently, ultrasound has
shown higher incidence of patients with severe carotid and coronary disease than previous studies.
Conclusion:
Carotid disease should be evaluated with ultrasound in patients who undergo CABG, because it was shown
that 20% of them may have unilateral or bilateral carotid stenosis. Major systemic studies on stroke and CABG
pointed out the relationship between increase in stroke and higher degrees of carotid stenosis (Branthwaite,
M.A., 1975). But in order to further identify risk factors and inflammatory complications, it is recommended to
perform further clinical trials in this field (Iewis, B., et al., 1995; Rashid, S., et al., 1996; Zayde, H., et al., 2009;
Akhtar, W., et al., 2009; Shuzou, T., et al., 2005).
REFERENCES
Akhtar, W., A. Sabih, A. Ali, 2009. Carotid artery disease in patients undergoing elective coronary artery
bypass surgery. J Coll Physicians Surg Pax., 19(12): 759-762.
Alamowitch, S., M. Eliasziw, A. Algra, 2001. Risks, causes, and prevention of ischemic stroke in elderly
patients with symptomatic carotid stenosis. Lancet., 357: 1154-1160.
Auastasiadis, K., D. Kiskinis, I. Velissaris, 2009. Preoperative screening and management of carotid disease
in patients undergoing cardiac surgery. Perfusion, 24(4): 257-262.
12
Hossein Rahmani et al., 2015
Advances in Natural and Applied Sciences, 9(3) March 2015, Pages: 8-12
Berens, E.S., S.F. Murphy, T.H. Wareing, 1992. Preoperative carotid artery screening in elderly patients
undergoing cardiac surgery. J Vas Surg, 15(2): 313-321.
Berens, S., N.T. Nonchoukos, S.F. Murphy, 1992. Preoperative carotid artery elderly patients undergoing
carotid surgery. J Vasc Sury, 15(2): 313-323.
Branthwaite, M.A., 1975. Prevention of neurological damage during open-heart surgery. Thorax. 30(3):
258-261.
David Sutton, Roger Gregson, H.S., 2003. Arteriography and interventional angiography. David Sutton.
Text book of Radioloy and Imaging. Churchill Livingstone, 7th ed , 1: 464-465.
DOV, M., A. Karl, M. Richard, 2000. Unrecognised Carotid artery stenosis discovered by calcifications on
a panoramic radiograph. J Am Dent Assoc., 131(11): 1593-1597.
Durand, D.J., B.A. Perler, G.S. Roseborough, M.A. Grega, L.M. Borowicz Jr, W.A. Baumgarner, D.D.
Yuh, 2004. Mandatory versus selective preoperative carotid screening: A retrospective analysis. Ann Thorac
Surg, 78: 159-166.
Durand, D.J., B.A. Perler, G.S. Rosenborough, M.A. Grega, L.M. Borowicz Jr, W.A. Baumgarner, D.D.
Yuh, 2004. Mandatory versus selective preoperative carotid screening: A retrospective analysis. Ann Thorac
Surg, 78: 159-166.
Ebadi, Ahmad, et al, 2014. "Effects of Angiotensin Converting Enzyme Inhibitors Before, During and After
Coronary Artery Bypass Graft Surgery on Hemodynamic Responses and Vasoactive Drugs Requirement."
Firoozabadi, Mehdi Dehghani, and Ebadi. A., 2014. "The Effect of Intravenously Administered Tranexamic
Acid on Platelet Level in Patients under CABG." NATIONALPARK-FORSCHUNG IN DER SCHWEIZ
(Switzerland Research Park Journal) 103.2.
Firoozabadi, Mehdi Dehghani, et al, 2014. "Prevalence Risk Factors In Three Vessel Disease Patients
Candidate For Coronary-Artery Bypass Surgery." Life Science, 11: 12s
Hennerici, M., H.B. Hulsbomer, H. Hefter, D. Lammerts, W. Rautenberg, 1987. Natural history of
Asymptomatic extracranial arterial disease. Brain., 110(Pt 3): 777-91.
Iewis, B., M.D. Sch Wartz, H. lbert, 1995. Asymptomatic carotid artery stenosis and stroke in patients
undergoing cardiopulmonary bypass. Journal of vascular surgery, 21(1): 146-153.
Ikuof, Seigo G., S. Jun, 2000.Carotid and aortic screening for coronary artery bypass grafting. Ann Thorac
surg, 70: 2034-2039.
Khairi, H.S., M.c. Crowson, 1995. Carotid bruit: does it matter? Br Hosp Med., 53: 426-427.
Kobayashi, H., J. Giles, J. Polak, 2010. Increased prevalence of carotid artery atherosclerosis in
Rheumatoid arthritis is artery specific. J Rheumatol., 37(5): 890-893.
Rashid, S., G. Iars, J. Deborah, 1996. Screening carotid ultrasonography and risk factors for stroke in
coronary artery surgery patients. Ann Thorac Surg, 62: 1714-1723.
Rath, P.C., M.K. Agrwala, P.K. Dhar, 2001. Carotid artery involvement in patients of atherosclerotic
coronary artery disease undergoing coronary artery bypass grafting. Indian Heart J., 53(6): 761-765.
Rockman, C.B., G.R. Jacobowitz, P.J. Gange, 2004. Focused screening for occult carotid artery disease. J
Vasc Surg, 39(1): 44-51.
Rosa Mp, Portal Vl., 2010. Prevalence of carotid stenosis in patients referred to myocardial
revascularization surgery. Arq Brascardiol 94(2): 74-169.
Sabeti, S., M. Schillinger, W. Mlekusch, 2001. Quantification of internal carotid artery stenosis with
Duplex US: comparative analysis of different flow velocity criteria Radiology, 232(2): 431-439.
Selnes, O.A., et al, 2012. Cognitive and neurologic outcomes after coronaryartery bypasssurgery. New
England Journal of Medicine, 19: 366: 250-7.
Shirani, S., S.H. Abbasi, M.A. Boroumand, 2006. Preoperative carotid artery screening in patients
undergoing coronary artery bypass. Arch Med Res., 37(8): 987-990.
Shuzou, T., I. Yuji, T. Kengo, 2005. Prevalence of carotid artery stenosis in patients with coronary artery
disease in Japanese population. Strok, 36: 2094-2098.
Szabol, S.Z., E. Boder, K. Httl, 1994. Incidence of stenosis of the internal carotid artery among patients
waiting for coronary artery. Orv Hetil, 135(20): 1073-1076.
Tarzamani, M.K., 2007. Low prevalence of significant carotid artery disease in Iranian patients undergoing
elective coronary artery bypass. Cardiovascular ultrasound., 5(3): 1476-1486.
Thomas, G., W. Robert, 2010. Stenting versus Endarterectomy for treatment of carotid – artery stenosis. N
Engl J Med., 78: 363: 11-23.
Zayde, H., A. Ali, O. Wendler, H. Rashid, 2009. Selective screening for asymptomatic carotid artery
disease prior to isolated heart valve surgery. Angelology, 60(5): 633-666.