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(Stroke. 1996;27:393-397.)
© 1996 American Heart Association, Inc.
Articles |
From the Neurology Service (T.U., M.T.) and Division of Cardiology (T.H., H.K.), Hyogo Brain and Heart Center at Himeji, and Division of Disability Science, Tohoku University Graduate School of Medicine, Sendai (A.Y.), Japan.
Correspondence to Toshiyuki Uehara, MD, Neurology Service, Hyogo Brain and Heart Center at Himeji, 520 Saisho-ko, Himeji, 670, Japan.
| Abstract |
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Methods We performed carotid and intracranial MR angiography (MRA) on 67 patients (49 men, 18 women; age range, 40 to 78 years; mean age, 60.1 years) who had received selective coronary angiography for the clinical diagnosis of IHD. On the basis of these images, degree of stenosis in the regions of the bilateral carotid artery bifurcation and five regions of the intracranial arteries, ie, bilateral intracranial portions of the internal carotid arteries and the middle cerebral arteries and the basilar artery were estimated.
Results Stenosis of more than 25% narrowing of the diameter of the target arteries was found in 15 patients (22.4%) in the extracranial carotid arteries and in 11 patients (16.4%) in the intracranial arteries. Most of the stenotic lesions were mild. The incidence of extracranial carotid stenosis and the severity of coronary atherosclerosis showed a significant correlation. The mean age of the patients with intracranial arterial lesions was statistically higher than those without intracranial lesions.
Conclusions Our data suggest that asymptomatic occlusive lesions in the carotid and intracranial arteries are fairly common in Japanese patients with IHD, although the degree of stenosis is relatively mild. Coexistence of carotid atherosclerosis should be suspected in IHD patients with severe coronary atherosclerosis, and the possibility of atherosclerosis in the intracranial arteries should be considered in aged IHD patients.
Key Words: angiography atherosclerosis cerebral arteries coronary artery disease
| Introduction |
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Previous studies have shown a racial difference in prevalent sites of atherosclerotic lesions.4 5 6 7 8 In whites the extracranial carotid arteries are more affected than the intracranial arteries, while in Asians and blacks the intracranial arteries are more affected. It is also known that in white populations a correlation between the extent of coronary atherosclerosis and extracranial carotid atherosclerosis is strong.4 8 9 10 11 12 13
In Japan, a recent change of lifestyle is believed to have caused an increase of the incidence of extracranial carotid artery disease and IHD.6 7 However, studies investigating the relationship between cerebral and coronary atherosclerosis in Japanese patients are scarce.
We therefore performed carotid and intracranial MRA on patients with IHD to explore the prevalence and extent of asymptomatic cerebral artery occlusive lesions complicating IHD in Japanese patients.
| Subjects and Methods |
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All MRA examinations were performed with a 1.0-T MR system (Magnetom Impact; Siemens). Images were acquired by a three-dimensional, Fourier transform time-of-flight method with a spoiled gradient-echo sequence. For extracranial carotid MRAs, the repetition time was set for 40 milliseconds, echo time for 10 milliseconds, and a flip angle for 20°. The number of excitations per phase encoding was 1. A 128x128x64 matrix was used, with a field of view of 180x180 mm and a partition thickness of 1.6 mm, resulting in a 1.4x1.4x1.6 voxel. We chose this relatively small matrix and field of view to maintain high resolution without increasing the examination time. The axial images thus acquired and magnified to 256x256 with interpolation were used as source data for the construction of projection images with use of a maximum-intensity-pixel projection algorithm. In each case, 10 projection images at 18° increments horizontal over a 180° range were obtained.
The parameters of intracranial MRA were repetition time of 35 to 40 milliseconds, echo time of 7 milliseconds, and a flip angle of 15°. The number of excitations was 1. We used two volume slab orientations, a horizontal section and a section parallel to the clivus, thereby covering the view and compensating the signal attenuation due to flow direction. A 128x128x64 matrix was used, with field of view of 120x120 mm and a partition thickness of 1 mm, resulting in a 0.94x0.94x1-mm voxel. The axial images thus acquired were used as source data for the construction of projection images with use of a maximum-intensity-pixel projection algorithm. In each case, nine projection images at 22.5° increments vertical and horizontal over a 180° range were provided.
Two neurologists (T.U., M.T.), who were blinded to all clinical information, independently reviewed the MRAs. Degree of stenosis was divided into five grades depending on the narrowness of the arteries, ie, normal, mild, moderate, severe, and occluded. Less than 25% reduction of an arterial diameter was graded normal, 25% to 49% reduction mild, 50% to 74% reduction moderate, 75% to 99% reduction severe, and no opening was graded occluded.14 15 The state of the extracranial portion of the ICA was evaluated at the bifurcation site by the carotid MRA, and that of the intracranial arteries at the intracranial portion of the ICA, at the horizontal portion of the MCA, and at the BA by the intracranial MRA. To measure the percent stenosis of extracranial portion of the ICA, we compared the diameter of maximal stenosis with that of the normal-appearing proximal ICA beyond the carotid bulb.16
The severity of coronary artery atherosclerosis was evaluated by CAS, which was defined as the number of affected coronary branches, ie, the right and left anterior descending branches and left circumflexus with more than 75% narrowing of the diameter.17 18
For risk factor evaluation, we investigated the presence or absence of hypertension, diabetes mellitus, hyperlipidemia, and habit of smoking. Hypertension was judged present when systolic pressure was consistently above 160 mm Hg or diastolic pressure consistently above 95 mm Hg or when the patient had a history of treatment for hypertension. Diabetes mellitus was diagnosed when a fasting blood glucose level was above 140 mg/dL or when the patient had a history of treatment for diabetes mellitus. Hyperlipidemia was defined when a serum total cholesterol level was above 220 mg/dL, triglyceride level was above 150 mg/dL, high-density lipoprotein cholesterol level was below 40 mg/dL, or when the patient had a history of treatment.
We used Fisher's exact test for analysis of discrete variables and Student's t test or the Mann-Whitney U test for analysis of continuous variables.
| Results |
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Fig 1
shows the prevalence of arterial
changes in terms of the age group. The number of patients showing
stenosis tended to increase for both extracranial carotid and
intracranial arteries with advancing age. The tendency is clearer for
intracranial arterial lesions.
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Table 2
summarizes the incidence of the risk factors in
terms of CAS score. Among these 67 patients with IHD, 60 had at least
one coronary artery with 75% or more stenosis. Of
these 60 patients, 1 coronary artery was involved in 31
patients, 2 arteries in 22, and 3 in 7 patients. All 7 patients with a
CAS score of 0 had no significant coronary artery
stenosis. The mean age of the CAS 0 group was significantly
younger than that in the other groups. No significant correlation was
found between the incidence of four risk factors and the number of
involved coronary arteries.
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The relationship between the percentage of the number of patients with
affected cerebral arteries and the CAS score is presented in
Fig 2
. The number of the patients showing extracranial
carotid artery lesions increased as the CAS scores increased. The
prevalence of extracranial carotid stenosis in the CAS 3 group
was significantly greater compared with the CAS 0 and 1 groups
(P<.05). Moderate to severe stenosis was found only
in the CAS 2 and 3 groups. The prevalence of intracranial
arterial stenosis was not correlated with the
severity of coronary stenosis.
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The clinical characteristics of the patients with and without cerebral
artery lesions are compared in Table 3
. The mean CAS of
the patients with carotid lesions was significantly higher than that of
the patients without such lesions (P=.011). The incidence of
diabetes mellitus was significantly higher in the patient group with
carotid lesions than in the group without such lesions
(P<.05). The mean age of the patients with intracranial
artery stenosis was statistically higher than that of the
patients without stenosis (P=.003). Incidence of
hypertension was significantly higher in the patient group with
intracranial arterial lesions than in the group without
such lesions (P<.05).
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| Discussion |
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We used MRA as a neuroimaging technique because it is noninvasive and can detect occlusive changes not only in the extracranial but also in the intracranial arteries.14 15 20 21 We have already confirmed the high sensitivity (>95%) and specificity (>85%) of the three-dimensional time-of-flight MRA method for evaluating the status of cranial arteries.14 15 Among 67 IHD subjects, asymptomatic extracranial carotid stenosis of more than 25% narrowing was detected in 15 patients (22.4%) and asymptomatic intracranial arterial stenosis in 11 patients (16.4%). Although the degree of stenosis was relatively mild, it should be considered that asymptomatic occlusive lesions in the cerebral arteries are not uncommon in the population of Japanese IHD patients. The higher prevalence of extracranial carotid lesions compared with intracranial arterial lesions is consistent with the data reported on white populations.
There have been a few studies concerning the frequency and degree of asymptomatic extracranial carotid lesions in IHD patients. Sanguigni et al22 found a reduction in diameter of more than 50% on echo-Doppler ultrasonography in 27.7% of 187 coronary arterial disease patients. Approximately 59% of these patients were completely asymptomatic. Andersen et al23 noted that only 8% of the patients with coronary arterial disease showed hemodynamically significant carotid arterial disease on oculopneumoplethysmography. Barnes et al,24 in their prospective screening of asymptomatic carotid disease in patients undergoing cardiovascular surgery, reported that the prevalence of asymptomatic carotid obstructive lesions, defined as more than 50% diameter reduction by the Doppler ultrasound method, was 12.3% of 324 patients with coronary artery disease.
Tanaka et al25 performed an ultrasonographic study of 92 IHD patients who had received selective coronary angiography and detected silent carotid atheromatous plaques in 50.9% of the group that showed significant stenosis of more than 75% in the coronary arteries and in 34.3% of the group that showed no significant coronary arterial change, demonstrating a correlation between the silent extracranial carotid atheromatous lesion and the severity of coronary atherosclerosis. Unfortunately, details of the carotid stenosis were not described. In the present study we were able to demonstrate that the prevalence of asymptomatic carotid lesions was related to the severity of coronary atherosclerosis.
Although a few autopsy studies confirmed a correlation between intracranial and coronary atherosclerosis,26 27 28 clinical studies on this important issue remained obscure partly because of limited resources in terms of diagnostic tools. Our previous study showed a lack of correlation between these two pathologies.19 To our knowledge there have been no clinical studies of the prevalence and severity of asymptomatic intracranial occlusive lesions in IHD patients. In the present study approximately 16% of the IHD patients were shown to have coexistent intracranial occlusive arterial changes that were asymptomatic and comparatively mild in degree. The prevalence of the intracranial arterial lesions was correlated with age but not with the severity of coronary artery stenosis.
Coronary and cerebral atherosclerosis have been demonstrated to have many common risk factors, ie, age, hypertension, diabetes mellitus, hyperlipidemia, and smoking, but the relative impact of the individual risk factors differs between the two.29 Of all known risk factors, age has the strongest association with atherosclerotic lesions regardless of the site of arteries.10 30 In the present study the prevalence of both extracranial carotid and intracranial arterial lesions tended to increase with advancing age. The mean age of the patients with intracranial lesions was significantly higher than that of the patients without intracranial lesions (P=.003), while the mean age of the patients with extracranial carotid lesions was not significantly different from that of the patients without such lesions.
The fact that only four patients had occlusive lesions in both the extracranial carotid and intracranial arteries may suggest that risk factors related to two arterial territories are different. Among hypertension, diabetes mellitus, hyperlipidemia, and smoking, the incidence of diabetes mellitus was significantly higher in the IHD patients with extracranial carotid lesions than in those without such lesions (P<.05). Handa et al30 found that diabetes mellitus was a possible risk factor for extracranial carotid atherosclerosis in the Japanese. Crouse et al10 reported that diabetes mellitus was a significant risk factor for carotid atherosclerosis when their data were assessed by univariate analysis but was not significant when assessed by multivariate analysis. The prevalence of hypertension in our IHD patients with intracranial arterial lesions was significantly higher than in those without such lesions (P<.05). This association between hypertension and occlusive lesions of the intracranial arteries has been reported.8 31
We conclude that there is a trend that asymptomatic occlusive lesions in the cerebral arterial territories, although mild in degree, are increasing, at least in the Japanese population of patients suffering from IHD. Coexistence of carotid atherosclerosis should be suspected in IHD patients with severe coronary atherosclerosis, and the possibility of atherosclerosis in the intracranial arteries should be considered in aged IHD patients.
| Selected Abbreviations and Acronyms |
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Received July 24, 1995; revision received November 29, 1995; accepted November 29, 1995.
| References |
|---|
|
|
|---|
2.
Toole JF, Yuson CP, Janeway R, Johnston F, Courtland
D, Cordell AR, Howard G. Transient ischemic attacks: a
prospective study of 225 patients. Neurology. 1978;28:746-753.
3.
Graor RA, Hertzer NR. Management of
coexistent carotid artery and coronary artery
disease. Stroke. 1988;19:1441-1444.
4.
Caplan LR, Gorelick PB, Hier DB. Race, sex and
occlusive cerebrovascular disease: a review. Stroke. 1986;17:648-655.
5.
Nishimaru K, McHenry LC Jr, Toole JF. Cerebral
angiographic and clinical differences in carotid system transient
ischemic attacks between American Caucasian and Japanese
patients. Stroke. 1984;15:56-59.
6.
Komachi K, Tanaka H, Shimamoto T, Handa K, Iida M,
Isomura K, Kojima S, Matsuzaki T, Osawa H, Takahashi H, Tsunetoshi
Y. A collaborative study of stroke incidence in Japan:
1975-1979. Stroke. 1984;15:28-36.
7.
Shimamoto T, Komachi Y, Inada H, Doi M, Iso H, Sato S,
Kitamura A, Iida M, Konishi M, Nakanishi N, Terao A, Naito Y, Kojima
S. Trends for coronary heart disease and stroke and
their risk factors in Japan. Circulation. 1989;79:503-515.
8.
Kuller L, Reisler DM. An explanation for
variations in distribution of stroke and
arteriosclerotic heart disease among populations
and racial groups. Am J Epidemiol. 1971;93:1-9.
9.
Ryu JE, Murros K, Espeland MA, Rubens J,
McKinney WM, Toole JF, Crouse JR. Extracranial carotid
atherosclerosis in black and white patients with
transient ischemic attacks. Stroke. 1989;20:1133-1137.
10.
Crouse JR, Toole JF, McKinney WM, Dignan MB, Howard G,
Kahl FR, McMahan MR, Harpold GH. Risk factors for extracranial
carotid artery atherosclerosis.
Stroke. 1987;18:990-996.
11.
Howard G, Ryu JE, Evans GW, McKinney WM, Toole JF,
Murros KE, Crouse JR. Extracranial carotid
atherosclerosis in patients with and without transient
ischemic attacks and coronary artery disease.
Arteriosclerosis. 1990;10:714-719.
12.
Crouse JR, Harpold GH, Kahl FR, Toole JF, McKinney
WM. Evaluation of a scoring system for extracranial carotid
atherosclerosis extent with B-mode ultrasound.
Stroke. 1986;17:270-275.
13.
Craven TE, Ryu JE, Espeland MA, Kahl FR, McKinney WM,
Toole JF, McMahan MR, Thompson CJ, Heiss G, Crouse JR.
Evaluation of the associations between carotid artery
atherosclerosis and coronary artery
stenosis: a case-control study.
Circulation. 1990;82:1230-1242.
14. Uehara T, Mori E, Tabuchi M, Ohsumi Y, Yamadori A. Detection of occlusive lesion in intracranial arteries by three-dimensional time-of-flight magnetic resonance angiography. Cerebrovasc Dis. 1994;4:365-370.
15. Uehara T, Tabuchi M, Ohsumi Y, Yoneda Y, Mori E. Usefulness of 3-dimensional time-of-flight MR angiography for evaluation of carotid artery bifurcation stenosis. Cerebrovasc Dis. 1995;5:199-203.
16.
North American Symptomatic Carotid
Endarterectomy Trial (NASCET) Steering Committee.
North American Symptomatic Carotid
Endarterectomy Trial: methods, patient
characteristics, and progress. Stroke. 1991;22:711-720.
17.
Tanaka H, Nishino M, Ishida M, Fukunaga R, Sueyoshi
K. Progression of carotid atherosclerosis in
Japanese patients with coronary artery disease.
Stroke. 1992;23:946-951.
18.
Tanaka H, Sueyoshi K, Nishino M, Ishida M, Fukunaga R,
Abe H. Silent brain infarction and coronary artery
disease in Japanese patients. Arch Neurol. 1993;50:706-709.
19. Uehara T, Tabuchi M, Hayashi T, Kurogane H. Relationship between atherosclerosis in the cerebral and coronary arteries: cerebral and coronary angiographic findings in 17 patients. Jpn J Stroke. 1994;16:109-116.
20.
Heiserman JE, Drayer BP, Keller PJ, Fram EK.
Intracranial vascular stenosis and occlusion: evaluation with
three-dimensional time-of-flight MR angiography.
Radiology. 1992;185:667-673.
21.
Masaryk AM, Ross JS, DiCello MC, Modic MT, Paranandi L,
Masaryk TJ. 3DFT MR angiography of the carotid bifurcation:
potential and limitations as a screening examination.
Radiology. 1991;179:797-804.
22. Sanguigni V, Gallu M, Strano A. Incidence of carotid artery atherosclerosis in patients with coronary artery disease. Angiology. 1993;44:34-38.
23. Andersen CA, Weiser HC, Greenfield NE. Asymptomatic carotid arterial disease in patients presenting with angiographically proven coronary artery disease. Am J Surg.. 1984;50:473-475.
24. Barnes RW, Liebman PR, Marszalek PB, Kirk CL, Goldman MH. The natural history of asymptomatic carotid disease in patients undergoing cardiovascular surgery. Surgery. 1981;90:1075-1083. [Medline] [Order article via Infotrieve]
25. Tanaka H, Ishida M, Nishino M, Fukunaga R, Yasuno M, Sueyoshi K, Yamada Y, Abe H. Carotid atherosclerosis and silent cerebral infarction in patients with coronary atherosclerosis. J Jpn Coll Angiol. 1991;31:819-824.
26.
Mathur KS, Kashyap SK, Kumar V. Correlation of
the extent and severity of atherosclerosis in the
coronary and cerebral arteries.
Circulation. 1963;27:929-934.
27.
Holme I, Enger SC, Helgeland A, Hjermann I, Leren P,
Lund-Laesen PG, Solberg LA, Strong JP. Risk factors and raised
atherosclerotic lesions in coronary and cerebral arteries:
statistical analysis from the Oslo study.
Arteriosclerosis. 1981;1:250-256.
28.
Leung SY, Ng THK, Yuen ST, Lauder IJ, Ho FCS.
Pattern of cerebral atherosclerosis in Hong Kong
Chinese: severity in intracranial and extracranial vessels.
Stroke. 1993;24:779-786.
29. Nishino M, Sueyoshi K, Yasuno M, Yamada Y, Abe H, Hori M, Kamada T. Risk factors for atherosclerosis and silent cerebral infarction in patients with coronary heart disease. Angiology. 1993;44:432-440.
30.
Handa N, Matsumoto M, Maeda H, Hougaku H, Ogawa S,
Fukunaga R, Yoneda S, Kimura K, Kamada T. Ultrasonic evaluation
of early carotid atherosclerosis.
Stroke. 1990;21:1567-1572.
31.
Yasaka M, Yamaguchi T, Shichiri M. Distribution
of atherosclerosis and risk factors in atherothrombotic
occlusion. Stroke. 1993;24:206-211.
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