(Stroke. 1999;30:1002-1007.)
© 1999 American Heart Association, Inc.
Original Contributions |
From the Department of Cardiology, Hippokration Hospital, University of Athens, Greece.
Correspondence to Ioannis Kallikazaros, MD, 12 Anapauseos Street, 15126 Marousi, Athens, Greece.
| Abstract |
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MethodsDuplex ultrasonography and quantitative coronary angiography were used to assess carotid and coronary artery atherosclerosis in 225 consecutive patients (mean age, 58±9 years) with chest pain referred for cardiac catheterization.
ResultsCAD was present in 197 patients (88%). Fifty-seven
patients (25%) had 1-vessel disease, 52 (23%) had 2-vessel disease,
53 (24%) had 3-vessel disease, and 35 (16%) had left main stem
CAD (LMS-CAD). The incidence of severe CAD (3-vessel disease or
LMS-CAD) was 24% and 63% in the normal and impaired ejection fraction
(EF) subgroups, respectively (P<0.005). Carotid disease
(lumen diameter stenosis of
50%) was present in 5.3%,
13.5%, 24.5%, and 40% of patients with 1-, 2-, and 3-vessel disease
and LMS-CAD, respectively. Moreover, the incidence of carotid disease
in patients with severe CAD was 31% in the entire study population and
46% and 5% in the subgroups with impaired and normal EF, respectively
(P<0.005). In the entire study population, the presence
of severe CAD was determined by age, male sex, and carotid disease; in
the impaired EF group by age and carotid disease; and in the normal EF
group only by age. Carotid disease has a high negative (92%) and a
high positive (91%) predictive value for the presence of severe CAD in
the subgroup with normal and impaired EF, respectively.
ConclusionsIn patients evaluated for chest pain, carotid disease is significantly correlated with severe CAD. Furthermore, in patients with impaired left ventricular systolic performance the presence of carotid disease reflects the presence of severe CAD, while in patients with normal EF the absence of carotid disease reflects the absence of severe CAD.
Key Words: angiography carotid artery diseases coronary artery disease ultrasonography, Doppler, duplex
| Introduction |
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In the evaluation of patients with suspected CAD, carotid artery intima-media wall thickness has been reported to be a useful marker for the presence of CAD.9 10 However, the precise relationship between the extent of carotid artery atherosclerosis and the severity of CAD has not been well evaluated. For this purpose, we studied by carotid artery ultrasonography the potential role of carotid disease in identifying the presence of severe CAD in patients who had been referred for chest pain evaluation by coronary angiography. In addition, we investigated the accuracy of carotid disease in predicting the presence of severe CAD in the subgroups of patients with normal or impaired left ventricular systolic performance.
| Subjects and Methods |
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Patients with a history of previous myocardial infarction, angiographically documented CAD, cerebrovascular disease, congenital heart disease, cardiomyopathy, valvular heart disease, and any systematic disease were excluded. We also excluded patients with coronary artery bypass graft, percutaneous transluminal coronary angioplasty, or carotid endarterectomy, because the interpretation of the coronary angiogram or the carotid duplex ultrasonogram may be obscured in these cases.
After a careful history was taken, the patients underwent a physical examination, chest x-ray, ECG, and ultrasound examination of the heart. Blood was drawn from fasting patients on the morning of catheterization for assay of glucose and lipid concentrations by standard laboratory methods. The study protocol included an evaluation of risk factors for cardiovascular disease, carotid artery ultrasonography, and coronary artery angiographyleft ventriculography.
The study protocol was approved by the institutional ethics committee of our hospital. Written informed consent was obtained from all patients after a detailed description of the procedure was given.
Evaluation of Risk Factors Variables
The risk factor variables11 12 13 evaluated in
this study included age, sex,
hypercholesterolemia, hypertension, diabetes
mellitus, family history of CAD, and smoking status. The latter was
assessed with smokers defined as those patients consuming at least 1
cigarette daily.
Hypercholesterolemia was defined as total plasma cholesterol of >200 mg/dL in the previous 12 months or documented hypercholesterolemia requiring lipid-lowering drug therapy. Hypertension was coded as present if there was any history of high blood pressure or if the blood pressure measured twice in the hospital exceeded 140 mm Hg systolic or 90 mm Hg diastolic. Diabetes mellitus was defined if the patient had a history of diabetes or if the fasting plasma glucose exceeded 126 mg/dL or 200 mg/dL 2 hours after the meal. Family history was coded as positive if a first-degree relative had had a significant coronary event before the age of 60 years.
Assessment of Carotid Atherosclerosis
Atherosclerosis of both left and right carotid
arteries was assessed by duplex ultrasound scanning with a Hewlett
Packard Sonos 2.500 commercially available machine with a 7.5/5.5-MHz
imaging transducer. The technique for carotid artery ultrasound
scanning has been previously described in detail.12 14 In
brief, the severity of carotid atherosclerosis was
evaluated by using the maximum percentage diameter stenosis
recorded by B-mode ultrasonography in the case of mild
stenoses and by using parameters of the flow
velocity pattern measured by Doppler ultrasonography in the case of
severe stenoses. The maximum stenosis was defined as
the greatest stenosis observed on the right or left side.
Accordingly, our patients were classified into 1 of the following 5
categories: (1) carotid arteries with no signs of atherosclerotic
lesions, (2) 2% to 15% diameter stenosis, (3) 16% to 49%
diameter stenosis, (4) 50% to 79% diameter stenosis,
and (5) 80% to 100% diameter stenosis.
We defined as carotid disease the carotid
atherosclerosis with a lumen diameter stenosis
of
50% (the latter 2 categories). All measurements were performed
over 5 cycles and averaged. Each scanning period averaged 25 minutes
and was recorded on Super VHS videotape for later offline
analysis by 2 independent readers. The interobserver
variability for the percentage of carotid artery stenosis was
low (4.5±3%).
Coronary AngiographyLeft Ventriculography
Coronary angiography and left ventriculography were
performed by the Judkins technique. The percentage of diameter
stenosis was calculated by quantitative coronary
angiography with a commercially available automated coronary
analysis system (DCI-S, Phillips Medical
System).15 CAD was defined as diameter lumen
stenosis of >50% in at least 1 major coronary artery.
According to the number of diseased vessels, our patients were
classified into 1 of the following 5 patient groups: group 1, patients
with no vessel disease; group 2, patients with 1-vessel disease; group
3, patients with 2-vessel disease; group 4, patients with 3-vessel
disease; and group 5, patients with LMS-CAD with or without other
vessel disease.. Groups 4 and 5 were defined as severe CAD.
Also, according to the left ventricular systolic
performance level, our patients were classified into 2 groups
with normal ejection fraction (EF) (>50%) or with impaired EF
(
50%).
Statistical Analysis
2 tests were used to detect
statistically significant relationships between categorical
variables. A value of P<0.05 was considered
statistically significant.
Stepwise multiple logistic regression was used to detect statistically significant associations between a dichotomous dependent variable and a number of independent ones. Sensitivity, specificity, and predictive values were calculated by use of a standard method.
| Results |
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In the group with impaired left ventricular EF, the number of older patients, smokers, hypertensive patients, and hypercholesterolemic patients was higher than in the group with normal EF.
Carotid Artery Duplex Ultrasonography Data
Carotid artery atherosclerosis was present in
164 patients (73%); 61 patients (27%) had normal left and right
normal arteries. The classification of the entire study population as
well as subgroups is listed, according to the severity of carotid
atherosclerosis, in Table 2
. The group with impaired EF had
significantly fewer patients without atherosclerotic signs than the
group with normal EF (P<0.05).
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Carotid artery disease was found in 38 patients (18%): the subgroup with impaired EF had a significantly greater number of patients with carotid artery disease (28 patients, 33%) compared with the group with normal EF (10 patients, 7%) (P<0.005).
Regarding the location of atherosclerotic plaques in the carotid tree, the bulb was the most common site (in 127 lesions), followed by the internal carotid artery (in 88 lesions) and the common carotid artery (in 80 lesions). Carotid artery stenoses were found to be equally distributed between the right and left carotid arteries.
Coronary Angiography Findings
CAD was found in 197 patients (88%), whereas 28 patients (12%)
had coronary arteries without critical stenosis. The
classification, by diseased vessel, of the study population is
presented in Table 3
.
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The group with impaired EF had significantly fewer patients without CAD, as well as patients with 1- and 2-vessel disease, compared with the group with normal EF (4%, 15%, and 18% versus 18%, 31%, and 26%, respectively; P<0.005). In addition, the latter group had a significantly smaller number of patients with 3-vessel disease, LMS, and severe CAD (16%, 9%, and 24% versus 36%, 27%, and 63%, respectively; P<0.005) compared with the group with impaired EF.
Correlation Between Carotid and Coronary Atherosclerosis
The distribution of carotid disease in the groups with different
degrees of CAD is shown in Figure 1
.
There was a stepwise increase in the number of patients with carotid
disease among the patients with increasing severity of CAD, because
carotid disease was present in 5.3%, 13.5%, 24.5%, and 40% of
patients with 1-, 2-, and 3-vessel disease and LMS-CAD, respectively.
In addition, the incidence of carotid disease in patients with severe
CAD was 31% (27 of 88 patients) in the entire study population.
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Furthermore, the incidence of carotid disease in the subgroup of
patients with severe CAD and impaired EF was greater (25 of 54
patients, 46.3%) compared with patients with severe CAD and normal EF
(2 of 34 patients, 5.8%; P<0.005) (Figure 2
).
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Forward stepwise logistic regression analysis was applied to identify factors that were independently associated with the presence of severe CAD. Severe CAD as a dependent variable was entered in a regression model with 8 independent variables.
This analysis revealed that age, male sex, and carotid
disease were independently related to the presence of severe CAD in the
entire study population (Table 4
).
Furthermore, using the same regression model, in the group with
impaired EF it was revealed that age and carotid disease were
independently associated with severe CAD, while in the group with
normal EF only age was independently associated with severe CAD
(P<0.005 for both cases). In the entire study population,
carotid disease has a high negative predictive value (92%), an
acceptable sensitivity (71%) and specificity (68%), and a low
positive predictive value for the presence of severe CAD. In the
subgroup of patients with impaired EF, carotid disease has a high
positive predictive value (91%), a high sensitivity (90%), an
acceptable specificity (50%), and a low negative predictive value for
the presence of severe CAD. In the patients with normal EF, carotid
disease has a high negative predictive value (92%) and an acceptable
specificity (75%) for the presence of severe CAD.
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| Discussion |
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Our main finding was that carotid disease was significantly related to the presence of severe CAD, defined as LMS-CAD or 3-vessel disease. Furthermore, in patients with impaired left ventricular systolic performance, the presence of carotid disease reflects the presence of severe CAD, whereas in patients with normal EF the absence of carotid disease reflects the absence of severe CAD.
Carotid atherosclerosis is important in view of its relationship to cerebrovascular ischemic disease and coronary atherosclerosis.16 17 This relationship is best expressed by the knowledge that the annual mortality rate after transient ischemic attacks is mainly caused by myocardial infarction and is similar to the annual cardiac mortality rate in patients with stable angina pectoris.18
Autopsy studies have demonstrated a strong correlation between the extent of extracranial carotid and coronary atherosclerosis.19 20 Noninvasive measurements that relate to the severity of coronary atherosclerosis have been sought for clinical screening of patients with chest pain syndromes.1 9 10 21 22 Thus, carotid intima-media thickness has been suggested as a surrogate marker for coronary atherosclerosis for use in clinical trials.
Craven et al1 have suggested that B-mode score is strongly and independently associated with CAD in patients aged >50 years and is at least as useful as well-known risk factors for identifying patients with CAD. Furthermore, it is reported21 that carotid intima-media thickness is significantly correlated with the extent and severity of CAD, but this relationship is weak. Salonen and Salonen22 reported that greater common carotid intima media thickness values in middle-aged men may be independently associated with higher subsequent risk of acute coronary events. Recently, the Atherosclerosis Risk in Communities study10 reported that mean carotid intima-media thickness is a noninvasive predictor of future cardiovascular events.
However, possible additional associations between carotid disease and the severity of CAD have not been well addressed. To investigate this issue further, we extended our attention to the exact relationship between carotid disease and CAD. We found that carotid disease could indicate the presence of severe CAD in patients undergoing coronary angiography for chest pain. Moreover, the combination of carotid disease with impaired left ventricular systolic performance could predict the presence of severe CAD. Also, the absence of carotid disease in a patient with normal left ventricular systolic performance may reflect the absence of severe CAD.
In concordance with the above, Hertzer et al2 studied patients with asymptomatic carotid bruits or transient ischemic attacks and revealed severe operable CAD in 37% of patients clinically suspected of having CAD and in 16% of patients without suspected CAD.
Furthermore, it has been demonstrated23 that nearly one half of patients with either symptomatic or asymptomatic cerebrovascular disease had an abnormal 201Tl test; consequently, these patients may be screened for cardiac disease. Similarly, the presence of increases in wall thickness beyond those predicted by age and sex may identify individuals at higher risk for coronary disease and stroke, and internal carotid artery stenosis correlates more strongly with CAD than wall thickness.4 In this study, the prevalence of coronary disease increased from 17% in patients without stenosis in the carotid arteries to 46% in those with stenosis of >75%. Seino et al24 reported the coexistence of carotid artery disease and CAD in 33% of Japanese patients in their study, as assessed by supraorbital Doppler flow analysis.
Several studies have reported a high incidence of LMS-CAD in candidates for carotid endarterectomy and coronary artery bypass. Vigneswaran et al8 reported that postoperative cerebrovascular complications were more common in patients who had coronary artery revascularization for stenosis for LMS-CAD and, consequently, for optimum perioperative management patients with LMS stenosis should be screened for carotid artery disease before bypass surgery. In previously published studies12 25 we found a significant relationship between carotid artery disease and LMS disease in patients undergoing coronary angiography.
In a similar way, the absence of thoracic plaque detected by multiplane transesophageal echocardiography was found26 to be a powerful predictor for absence of significant CAD in valvular patients, even in the elderly. However, it has been reported27 that atherosclerotic aortic plaque detected by transesophageal echocardiography is useful in predicting significant CAD only in a relatively young population and not in elderly patients.
Coronary arteriography is still the "gold standard" for the diagnosis of CAD, although nowadays there are several very useful noninvasive tests (eg, the exercise test and the stress echo test).28 However, patients frequently demonstrate repolarization abnormalities on the resting or the exercise ECG, thus making it difficult to interpret ischemic changes during stress or in the case of chest pain, when performance of a stress test on a patient is not recommended. Also, at times the patient's current treatment did not allow clear results. Ultrasonography, a valid, simple, safe, noninvasive bedside technique for the assessment of extracoronary atherosclerosis, has been widely used to study carotid atherosclerosis.29 In the management of patients with chest pain, carotid duplex scan obviously cannot replace the already-existing, noninvasive tests for evaluation of CAD. Our classification of patients as to low or normal EF was based on ventriculography. However, it is known that equally good information can be acquired through the ultrasonographic, noninvasive evaluation of the patient.
Based on the findings of our study, the knowledge of the EF of a patient referred for chest pain, along with the information about the atherosclerotic state of the carotid arteries, provide significant indications of the presence or absence of severe CAD.
Several factors may have limited the apparent strength of the relationship we found between carotid disease and severe CAD. First, we studied a group of consecutive patients who were referred for coronary angiography for suspected ischemic heart disease. This selection bias means that our findings regarding the relationship of carotid disease with severe CAD are relevant only to this special group of patients and may not be applicable to the general population. Second, regardless of the method of analysis, coronary angiography frequently underestimates the severity of atherosclerotic disease, although it is a reasonable method for measuring the extent and severity of CAD.
Also, classification of the extent of CAD based on the number of diseased vessels may not be as precise as other specific indexes. However, this classification is very common in everyday clinical practice, and consequently the relationship of carotid disease to the diseased vessels is of practical value. Finally, for the evaluation of carotid disease, carotid duplex ultrasonography is considered a reliable and acceptable test, and angiography is required only in special cases.29
Conclusions
In patients being evaluated for chest pain, the presence of
carotid disease is significantly related to the presence of severe CAD.
In particular, in patients with impaired left ventricular
systolic performance, the presence of carotid disease
reflects the presence of severe CAD, whereas in patients with normal EF
the absence of carotid disease reflects the absence of severe CAD.
Received January 5, 1999; revision received February 1, 1999; accepted February 1, 1999.
| References |
|---|
|
|
|---|
2.
Hertzer NR, Young JR, Bevent G, Graor RA, O'Hara PJ,
Ruschhaupt WF, de Wolfe VG, Malgovec LC. Coronary angiography
in 506 patients with extracranial cerebrovascular disease. Arch
Intern Med. 1985;145:849852.
3.
Di Pasquale GD, Andreoli A, Pinelli G, Grazi P, Manini
G, Tognetti F, Testa C. Cerebral ischemia and
asymptomatic coronary artery disease: a prospective
study of 83 patients. Stroke. 1986;17:10981101.
4.
O'Leary DH, Polak JF, Kronmal RA, Kittner SJ, Bond
MG, Wolfson SK, Bommer W, Price TR, Gardin JM, Savage PJ. Distribution
and correlates of sonographically detected carotid artery disease in
the Cardiovascular Health Study. Stroke. 1992;23:17521760.
5.
Biller J, Feinberg WM, Castaldo JE, Whittemore AD,
Harbaugh RE, Dempsey RJ, Caplan LR, Kresowik TF, Matchar DB, Toole JF,
Easton JD, Adams HP Jr, Brass LM, Hobson RW II, Brott TG, Sternau L.
Guidelines for carotid endarterectomy: a statement
for healthcare professionals from a Special Writing Group of the Stroke
Council, American Heart Association. Circulation. 1998;97:501509.
6. Jones E, Craver J, Michalic R, Murphy D, Guyton R, Bone D, Hatcher C, Reichwald N. Combined carotid and coronary operations: when are they necessary? J Thorac Cardiovasc Surg. 1984;87:716.[Abstract]
7. Chaitman, Rogers W, Davis K, Tyras D, Berger R, Bourassa M, Fischer L, Judkins M, Mock M, Killip T. Operative risk factors in patients with left main coronary artery disease. N Engl J Med. 1980;303:953957.[Abstract]
8.
Vigneswaran WT, Sapsford RN, Stanbridge RD. Disease of
the left main coronary artery: early surgical results and their
association with carotid artery stenosis. Br Heart
J. 1993;70:342345.
9.
Geroulakos G, O'Gorman D, Kalodiki E, Sheridon D,
Nikolaides A. The carotid intima-media thickness as a marker of the
presence of severe symptomatic coronary artery
disease. Eur Heart J. 1994;15:781785.
10.
Chambless LE, Heiss G, Folsom AR, Rosamond W, Szkio M.
Association of coronary heart disease incidence with carotid
arterial wall thickness and major risk factors: the
Atherosclerosis Risk in Communities (ARIC) study,
19871993. Am J Epidemiol. 1997;146:483494.
11.
Crouse JR, Toole JF, McKinney WM, Dignan MB, Howard G,
Kahl FR, Mc Mahan MR, Harpold GH. Risk factors for extracranial carotid
artery atherosclerosis. Stroke. 1987;18:990996.
12. Kallikazaros I, Stratos K, Tsioufis C, Stefanadis C, Sideris A, Sideris S, Toutouzas P. Carotid sinus hypersensitivity in patients undergoing coronary arteriography: relation with the severity of carotid atherosclerosis and the extent of coronary artery disease. J Cardiovasc Electrophysiol. 1997;8:12181228.[Medline] [Order article via Infotrieve]
13.
Delcker A, Diener HC, Wilhelm H. Influence of vascular
risk factors for atherosclerotic carotid artery plaque progression.
Stroke. 1995;26:20162022.
14. Zwiebel WJ. Introduction to Vascular Ultrasonography. 3rd ed. Philadelphia, Pa: WB Saunders Co; 1992.
15. Reiber JHC. On-line quantification of coronary angiograms with the DCI system. Medica Mundi. 1989;34:8998.
16. Fuster V, Weinberger J, Kohler T, Glagov S, Imperato A, Goldstone J. Pathology: clinical correlation of carotid, aortic and peripheral vascular disease. In: Fuster V, ed. Syndromes of Atherosclerosis. New York, NY: Futura Publishing Co; 1996:269277.
17. Chimowitz MI, Mancini GBJ. Asymptomatic coronary artery disease in patients with stroke. Stroke. 1991;26:2327.
18. Heyman A, Wilkinson W, Heyden S, Helms M, Bartel A, Karp H, Tyroler HA, Hames CG. Risk of stroke in asymptomatic persons with cervical arterial bruits. N Engl J Med. 1980;302:838841.[Abstract]
19.
Mathur KS, Kashyap SK, Kumar V. Correlation of the
extent and severity of atherosclerosis in the
coronary and cerebral arteries. Circulation. 1963;27:929934.
20. Mitchell JRA, Schwartz CJ. Relationship between arterial disease in different sites: a study of the aorta and coronary carotid and iliac arteries. BMJ. 1962;1:12931301.
21.
Adams M, Nakagomi A, Keech A, Robinson J, McCredie R,
Bailey B, Freedman S, Celermajer D. Carotid intima-media thickness is
only weakly correlated with the extent and severity of coronary
artery disease. Circulation. 1995;92:21272134.
22. Salonen R, Salonen JT. Determinants of carotid intima media thickness: population-based ultrasonography study in Eastern Finish men. J Intern Med. 1991;229:225231.[Medline] [Order article via Infotrieve]
23.
Love B, Grover-McKay M, Biller J, Rezai K, Mckay C.
Coronary artery disease and cardiac events with
asymptomatic and symptomatic cerebrovascular
disease. Stroke. 1992;23:939945.
24. Seino Y, Takita T, Tanaka K, Takano T, Hayakawa H, Okumura H. Clinical features and coronary backgrounds of coexistent peripheral vascular disease in Japanese coronary artery disease patients. Angiology. 1991;42:899907.
25. Kallikazaros I, Stratos C, Tsioufis C,. Stefanadis C, Sideris S, Sideris A, Vassiliadis J, Toutouzas P. Carotid atherosclerosis as a predictor of the extent of coronary artery atherosclerosis. J Am Coll Cardiol. 1997;29(suppl):943. Abstract.
26.
Tribouilloy C, Peltier M, Colas L, Rida Z, Rey J,
Lesbre J. Multiplane transoesophageal
echocardiographic absence of thoracic aortic plaque is
a powerful predictor for absence of significant coronary artery
disease in valvular patients, even in the elderly. Eur
Heart J. 1997;18:14781483.
27.
Matsumura Y, Takata J, Yabe T, Furuno T,
Chikamori T, Doi Y. Atherosclerotic aortic plaque detected by
transesophageal echocardiography:
its significance and limitation as a marker for coronary artery
disease in the elderly. Chest. 1997;112:8186.
28. Schlant RC, Friesinger GC II, Leonard JJ. Clinical competence in exercise testing: a statement for physicians from the ACP/ACC/AHA Task Force on Clinical Privileges in Cardiology. J Am Coll Cardiol. 1990;16:10611065.[Medline] [Order article via Infotrieve]
29.
Blakeley D, Oddone E, Hasselabland V, Simel
DL, Matchar DB. Noninvasive carotid artery testing: a
meta-analysis review. Ann Intern Med. 1995;122:360367.
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