Aneurismal disease of different vascular territories: is it a rare association?
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Publications and source records attributed to Hasan Turhan.
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Accessory mitral valve tissue is an extremely rare congenital cardiac anomaly. Most of the cases reported in the literature were associated with left ventricular outflow tract obstruction. In this report, a second cerebrovascular event is presented in the same patient two years after an operation in which septal myectomy was performed but accessory mitral valve tissue was not excised.
OBJECTIVE: Hyperhomocysteinemia is recognized as an independent risk factor for arterial disease including coronary artery disease, cerebrovascular disease and peripheral vascular disease. Previously, an association between increased plasma homocysteine level and peripheral arterial aneurysms has been reported. However, the relationship between coronary artery ectasia (CAE) and plasma homocysteine level has not been investigated. Accordingly, this study was designed to investigate plasma homocysteine level in patients with isolated CAE. METHODS: Thirty-two patients with isolated CAE without significant stenosis and 30 control subjects with angiographically normal coronary arteries were included in this study. Fasting plasma homocysteine concentrations were measured by Fluorescence Polarization Immunoassay method using homocysteine kids. Hyperhomocysteinemia is defined as plasma homocysteine levels above the 95th percentile of the control subjects (13.6 mumol/l). RESULTS: According to the definition of hyperhomocysteinemia, 19 (59%) of patients with isolated CAE had elevated levels of plasma homocysteine compared to 2 (7%) in the control subjects with angiographically normal coronary arteries (p<0.001). In addition, patients with isolated CAE had significantly higher levels of plasma homocysteine compared to control subjects (14.9+/-4.5 micromol/l vs. 8.6+/-1.9 micromol/l respectively, p<0.001). Besides, we detected a significant positive correlation between the number of ectasic segment and plasma homocysteine level (r=0.537, p=0.002). CONCLUSION: We have shown for the first time an association between elevated plasma homocysteine level and isolated CAE. Larger prospective studies are needed to confirm the role of hyperhomocysteinemia in CAE and to evaluate the usefulness of homocysteine-lowering therapies.
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BACKGROUND: Elevated plasma levels of homocysteine are currently considered a major, independent risk factor for cardiovascular diseases. Recently, several investigators have suggested that even mild elevation in plasma homocysteine level can severely disturb vascular endothelial function and subsequently impair coronary blood flow. Accordingly, we investigated plasma homocysteine level in patients with slow coronary flow. METHOD: Study population included 53 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (group I, 21 females, 32 males, mean age=48+/-9 years), and 50 subjects with angiographically proven normal coronary arteries without associated slow coronary flow (group II, 22 females, 28 males, mean age=50+/-8 years). Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction frame count (TIMI frame count). All patients in group I had TIMI frame counts greater than two standard deviations above those of control subjects (group II) and, therefore, were accepted as exhibiting slow coronary flow. The mean TIMI frame count for each patient and control subject was calculated by adding the TIMI frame counts for each major epicardial coronary artery and then dividing the obtained value into 3. Plasma homocysteine level was measured in all patients and control subjects using commercially available homocysteine kits. RESULTS: There was no statistically significant difference between two groups in respect to age, gender, hypertension, diabetes mellitus, hyperlipidemia and cigarette smoking (p>0.05). Plasma homocysteine level of patients with slow coronary flow were found to be significantly higher than those of control subjects (15.5+/-5.7 vs. 8.7+/-4.2 microM/l, respectively, p<0.001). Moreover, we found a significant positive correlation between plasma homocysteine level and mean TIMI frame count (r=0.660, p<0.001). CONCLUSION: We have shown that patients with slow coronary flow have raised level of plasma homocysteine compared to control subjects with normal coronary flow. This data suggests that elevated level of plasma homocysteine may play a role in the pathogenesis of slow coronary flow.
BACKGROUND: Inflammation has been reported to be a major contributing factor to many cardiovascular events. In the present study, we aimed to evaluate plasma soluble adhesion molecules; intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin as possible indicators of endothelial activation or inflammation in patients with slow coronary flow. METHOD: Study population included 17 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (group I, 11 male, 6 female, mean age=48+/-9 years), and 20 subjects with angiographically proven normal coronary arteries without associated slow coronary flow (group II, 11 male, 9 female, mean age=50+/-8 years). Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction frame count (TIMI frame count). All patients in group I had TIMI frame counts greater than two standard deviation above those of control subjects (group II) and, therefore, were accepted as exhibiting slow coronary flow. Serum levels of ICAM-1, VCAM-1, and E-selectin were measured in all patients and control subjects using commercially available ELISA kits. RESULTS: Serum ICAM-1, VCAM-1, and E-selectin levels of patients with slow coronary flow were found to be significantly higher than those of control subjects with normal coronary flow (ICAM-1: 545+/-198 ng/ml vs. 242+/-113 ng/ml respectively, p<0.001, VCAM-1: 2040+/-634 ng/ml vs. 918+/-336 ng/ml respectively, p<0.001, E-selectin: 67+/-9 ng/ml vs. 52+/-8 ng/ml respectively, p<0.001). Average TIMI frame count was detected to be significantly correlated with plasma soluble ICAM-1 (r=0.550, p<0.001), VCAM-1 (r=0.569, p<0.001) and E-selectin (r=0.443, p=0.006). CONCLUSION: Increased levels of soluble adhesion molecules in patients with slow coronary flow may be an indicator of endothelial activation and inflammation and are likely to be in the causal pathway leading to slow coronary flow.
Cardiac hydatid cyst is a rare complication of parasitic infection caused by Echinococcus granulosus. Cardiac involvement occurs in only 0.2-2% of hydatidosis cases. Rupture of hydatid cysts into cardiac chambers is very rare. In this report, we present a case of intracavitary left ventricular hydatid cysts ruptured during cardiopulmonary resuscitation in a patient with acute myocardial infarction.
BACKGROUND: P-wave dispersion (PWD), has been defined as the difference between maximum and minimum P-wave duration. Prolonged P-wave duration and increased PWD have been reported to be related with increased risk for atrial fibrillation (AF). AF is the most common sustained arrhythmia encountered in patients with rheumatic mitral stenosis (MS). Beta-blockers are the mainstay of therapy in patients with rheumatic MS to control ventricular rate both during sinus rhythm and AF. In the present study, we aimed to evaluate the effect of long-term beta-blocker therapy on P-wave duration and PWD in patients with rheumatic MS. METHOD: Study population includes 46 patients (group I, 8 men, 38 women, mean age = 34+/-8 years) with newly diagnosed moderate-to-severe rheumatic MS who have not taken any medication before and prescribed oral beta-blocker therapy and 46 healthy control subjects without any cardiovascular disease (group II, 8 men, 38 women, mean age = 35+/-7 years). Mitral valve area, maximum and mean diastolic mitral gradients, left atrial diameter, and systolic pulmonary artery pressure were evaluated by transthoracic echocardiography before initiation of beta blocker therapy and repeated at the end of the first month. Baseline maximum and minimum P-wave duration and PWD were determined on 12-lead electrocardiogram recorded for each patient and control subject and repeated at the end of the first month after initiation of beta-blocker therapy in patient group. RESULTS: Maximum P-wave duration and PWD were found to be significantly higher in patients with MS than those in control subjects (Maximum P-wave duration: 128+/-7 ms vs. 104+/-4 ms and PWD: 52+/-6 ms vs. 27+/-3 ms, p < 0.001 for both). Both groups had comparable minimum P-wave duration (75+/-4 ms vs. 76+/-4 ms, p = 0.093). Maximum P-wave duration and PWD were found to be significantly decreased by long-term beta blocker therapy (Maximum P-wave duration; 128+/-7 ms vs. 122+/-6 ms, p < 0.001, PWD; 52+/-6 ms vs. 47+/-5 ms, p < 0.001). However, there was no significant difference between the values of minimum P wave duration measured before and at the end of the first month of beta-blocker therapy (75+/-4 ms vs. 75+/-3 ms, p = 0.678). Statistically significant decrease were detected on maximum and mean mitral gradient and systolic pulmonary artery pressure and resting heart rate at the end of the first month of beta-blocker therapy. However, only the change in resting heart rate was found to be significantly correlated with the decrease in maximum P-wave duration and PWD (Maximum P-wave duration: r = 0.327, p = 0.026, PWD: r = 0.378, p = 0.01). CONCLUSION: We have shown for the first time that long-term beta-blocker therapy causes a significant decrease in maximum P-wave duration and PWD in patients with rheumatic MS.
BACKGROUND: Thrombolysis in myocardial infarction (TIMI) frame count is a simple clinical tool for assessing quantitative indexes of coronary blood flow. This technique counts the number of cineangiographic frames from initial contrast opacification of the proximal coronary artery to opacification of distal arterial landmarks. We hypothesized that patients with normal coronary artery (NCA) and myocardial infarction (MI) might have impaired coronary flow. Accordingly, we assessed the TIMI frame counts of patients with NCA and MI and compared to patients with NCA and without MI. MATERIALS AND METHOD: This retrospective study included consecutive patients with MI and who were found to have normal coronary angiograms performed between 1999 and 2003. Fifty patients (group I) with NCA and MI were enrolled in the study. Fifty consecutive patients with NCA and without MI were also enrolled in the study as control group (group II). Mean time interval between MI and coronary angiography was 6 +/- 2 days. RESULTS: There were statistically significant differences between groups I and II in respect to gender (11 females (22%) versus 22 females (44%), p = 0.003, respectively) and smoking status (62% (31/50) versus 38% (19/50), p = 0.02). Comparison of TIMI frame counts between two groups revealed that group I patients had significantly higher TIMI frame counts than group two patients for all three coronary arteries (LAD: 40 +/- 12 versus 23 +/- 7, Cx: 47 +/- 14 versus 27 +/- 7, RCA: 36 +/- 10 versus 26 +/- 10, respectively, p < 0.001 for all). Smokers were significantly younger when compared to non-smokers (44 +/- 5 years versus 51 +/- 9 years, p = 0.008, respectively). TIMI frame counts of smokers did not significantly differ from those of non-smokers in group I patients. There were statistically significant differences between smokers and non-smokers in group II patients regarding TIMI frame counts for all three coronary arteries (LAD: 29 +/- 7 versus 18 +/- 3, LCX: 34 +/- 10 versus 22 +/- 4, RCA: 34+ /- 13 versus 20 +/- 4, respectively, p < 0.001 for all). CONCLUSION: We have shown that patients with MI and NCA have higher TIMI frame counts for all coronary arteries when compared to patients without MI and NCA. Absence of difference between smokers and non-smoker in the myocardial infarction group in respect to TIMI frame count, has suggested that smoking does not lead to further increase of TIMI frame counts. On the other hand, in patients without MI and with NCA, smokers have higher TIMI frame counts than non-smokers have.
BACKGROUND: Diabetic patients have been reported to have impaired coronary collateral vessel growth, although they have excessive neovascularization in the retina. HYPOTHESIS: This study was designed to compare coronary collateral circulation (CCC) in patients with proliferative diabetic retinopathy (PDR) with that in patients without DR. METHODS: Ninety diabetic patients with chronic total occlusion in at least one major epicardial coronary artery were enrolled in the study. Groups 1 and 2 consisted of 48 patients without DR and 42 patients with PDR, respectively. Coronary collateral circulation (CCC) was analyzed according to the Rentrop system. Each group was also divided into two subgroups according to poor and good CCC. Serum vascular endothelial growth factor (VEGF) levels were measured using the enzyme-linked immunosorbent assay (ELISA) kit. RESULTS: The mean Rentrop collateral score was higher in Group 1 than in Group 2 (2.39 +/- 1.07 vs. 1.76 +/- 0.76, respectively, p < 0.001). When the two groups were compared with respect to poor and good CCC, poor CCC was higher in patients with PDR (64 vs. 36%, respectively, p = 0.01). Serum VEGF levels were higher in patients with PDR than in those without DR (219 +/- 99 vs. 139 +/- 98 pg/ml, p < 0.001); however, patients with poor and good CCC had similar VEGF levels. CONCLUSIONS: We have shown that patients with PDR have a lower coronary collateral score than patients without DR. Also, serum VEGF was significantly higher in patients with PDR than in those without DR. These findings have suggested that diabetes mellitus may have a different action on retinal and coronary circulation.
BACKGROUND: The metabolic syndrome is more prevalent with the use of the recently defined National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) criteria and is associated with a greater risk of atherosclerotic cardiovascular disease than any of its individual components. This study evaluated the prevalence of metabolic syndrome in female and male patients with newly diagnosed premature coronary artery disease. METHOD: The study population included 582 consecutive patients (496 men, 86 women) with newly diagnosed premature coronary artery disease (aged < or =45 years). Besides classic major coronary risk factors, all patients were evaluated for the presence of metabolic syndrome based on the NCEP ATP III criteria. RESULTS: The majority of patients were male (85% versus 15%). The overall prevalence of metabolic syndrome was 37%. Women with premature coronary artery disease were found to have a higher prevalence of metabolic syndrome than men (73% versus 31% respectively, p < 0.001). Furthermore, the mean number of components of metabolic syndrome was significantly higher in women compared to men (2.81 +/- 1.09 versus 1.85 +/- 1.08 respectively, p < 0.001). In addition, metabolic syndrome was detected to be the most frequent coronary risk factor in women (73%). Besides, cigarette smoking was found to be significantly higher in males compared to females (70% versus 36% respectively, p < 0.001) and it was the most prevalent coronary risk factor in men with premature coronary artery disease. CONCLUSION: We have shown for the first time a higher prevalence of metabolic syndrome in young females compared with young males with premature coronary artery disease. This data may be useful in directing primary and secondary preventive measures.
UNLABELLED: Plasma soluble adhesion molecules, intercellular adhesion molecule-1 (ICAM)-1, vascular cell adhesion molecule-1 (VCAM-1) and E-selectin leves of patients with isolated coronary artery ectasia (CAE), patients with obstructive coronary artery disease without CAE and subjects with angiographically normal coronary arteries were evaluated. Patients with isolated CAE were detected to have significantly higher levels of plasma soluble ICAM-1, VCAM-1 and E-selectin in comparison with patients with obstructive coronary artery disease without CAE (ICAM, 673 +/- 153 versus 381 +/- 106, respectively, P < 0.001; VCAM-1, 2366 +/- 925 versus 1136 +/- 208, respectively, P < 0.001; E-selectin, 74 +/- 21 versus 61 +/- 18, respectively, P = 0.01) and subjects with normal coronary arteries (ICAM-1, 673 +/- 153 versus 303 +/- 131, respectively, P < 0.001; VCAM-1, 2366 +/- 925 versus 729 +/- 231, respectively, P < 0.001; E-selectin, 74 +/- 21 versus 49 +/- 9, respectively, P < 0.001), suggesting the presence of a more severe and extensive chronic inflammation in the coronary circulation in patients with isolated CAE. BACKGROUND: The common coexistence of coronary artery ectasia (CAE) with coronary artery disease (CAD) suggests that it may be a variant of CAD. However, it is not clear why some patients with obstructive CAD develop CAE whereas most do not. Inflammation has been reported to be a major contributing factor to both obstructive and aneurysmatic vascular disorders and therefore, in the present study, the plasma soluble adhesion molecules, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin levels in isolated CAE were investigated. METHODS: The study population consisted of three groups: the first consisted of 32 patients with isolated CAE without stenotic lesion; the second of 32 patients with obstructive CAD without CAE; and the third group of 30 control subjects with normal coronary arteries. Coronary diameters were measured as the maximum diameter of the ectasic segment by use of a computerized quantitative coronary angiography analysis system. According to the angiographic definition used in the Coronary Artery Surgery Study, a vessel is considered to be ectasic when its diameter is > or =1.5 times that of the adjacent normal segment in segmental ectasia. Plasma soluble ICAM-1, VCAM-1 and E-selectin levels were measured in all patients and control subjects using commercially available enzyme-linked immunosorbent assay kits. RESULTS: Patients with isolated CAE were found to have significantly higher levels of plasma soluble ICAM-1, VCAM-1, and E-selectin in comparison with patients with obstructive CAD without CAE (ICAM, 673 +/- 153 versus 381 +/- 106, respectively; P < 0.001; VCAM-1, 2366 +/- 925 versus 1136 +/- 208, respectively; P < 0.001; E-selectin, 74 +/- 21 versus 61+/-18, respectively; P = 0.01) and control subjects with normal coronary arteries (ICAM-1, 673 +/- 153 versus 303 +/- 131, respectively;, P < 0.001; VCAM-1, 2366 +/- 925 versus 729 +/- 231, respectively; P < 0.001; E-selectin, 74 +/- 21 versus 49 +/- 9, respectively; P < 0.001). In addition, we detected statistically significant positive correlation between the total length of ectasic segments and the levels of plasma soluble ICAM-1 (r = 0.625; P < 0.001), VCAM-1 (r = 0.548; P = 0.001) and E-selectin (r = 0.390; P = 0.027). Multivariate logistic regression analysis revealed a significant independent relation between isolated CAE and ICAM-1 [odds ratio (OR) = 1.023; 95% confidence interval (CI) = 1.0048-1.0414; P = 0.0129] and VCAM-1 (OR = 1.0057; 95% CI = 1.0007-1.0106; P = 0.0240). CONCLUSIONS: We have shown that patients with isolated CAE have raised levels of plasma soluble ICAM-1, VCAM-1 and E-selectin in comparison with patients with obstructive CAD without CAE and control subjects with normal coronary arteries, suggesting the presence of a more severe and extensive chronic inflammation in the coronary circulation in these patients.
BACKGROUND: Coronary artery ectasia (CAE) is defined as localized or diffuse non-obstructive lesions of the epicardial coronary arteries with a luminal dilation exceeding the 1.5-fold of normal adjacent segment or vessel diameter. Varicocele is the dilatation of the pampiniform plexus. Recently increased prevalence of peripheral varicose veins has been shown in patients with CAE. In this study we aimed to assess the prevalence of varicocele, which is dilatation of another venous system, in patients with CAE. MATERIALS AND METHODS: Thirty-five male consecutive patients with coronary artery ectasia in combination with or without coronary artery disease (CAD) and 63 male, age-matched patients with coronary artery disease were included in the study. All patients were evaluated for the presence of varicocele. RESULTS: Twenty-one patients with CAE were found to have varicocele (62% of group I patients). In patients with CAD, 24 patients (38%) were found to have varicocele. The difference between the two groups in respect to presence of varicocele was statistically significant (P=0.02; odds ratio=1.57; 95% confidence interval 1.05- 2.3). CONCLUSION: We have shown that patients with coronary artery ectasia have an increased prevalence of varicocele compared to those with coronary artery disease. The mechanism underlying coronary artery ectasia might further increase the prevalence of varicocele in susceptible patients.
BACKGROUND: The development of coronary collateral vessels is the physiological response of myocardial tissue to hypoxia or ischemia, which results in an increase in blood supply to the tissue. However, a lack of collateral vessels or the presence of poor collateralization in some patients despite the presence of significant coronary stenosis or obstruction and evidence of myocardial ischemia suggest that some other factors may affect the development of collateral circulation. In the present study we aimed to evaluate coronary collateral circulation in patients with metabolic syndrome with advanced coronary artery disease and compare the results with those of patients without metabolic syndrome. METHOD: The study population comprised 102 patients with metabolic syndrome and advanced coronary artery disease (>or=90% diameter stenosis in at least one major epicardial coronary artery) and 102 control participants without metabolic syndrome who also had >or=90% diameter stenosis in at least one major epicardial coronary artery. The diagnosis of metabolic syndrome was based on the National Cholesterol Education Program Adult Treatment Panel III clinical definition. Coronary collateral vessels were analysed according to the Cohen and Rentrop grading system. Both groups were also divided into two additional groups according to the Rentrop collateral score as patients with poor collateral circulation (Rentrop score 0-1) and good collateral circulation (Rentrop score 2-3). RESULTS: The mean Rentrop collateral score for patients with metabolic syndrome was significantly lower than for those without metabolic syndrome (1.38+/-0.79 compared with 1.99+/-1.08, respectively, P<0.001). When two groups were compared with respect to poor and good collateral circulation, poor collateral circulation was found to be significantly higher in the metabolic syndrome group (70% compared with 32%, respectively, P<0.001). Moreover, multivariate logistic regression analysis revealed a significant relationship between poor collateral circulation and metabolic syndrome (odds ratio=4.29, 95% confidence interval=1.73-10.69, P=0.002). CONCLUSION: We have shown for the first time that the development of coronary collateral vessels is poorer in patients with metabolic syndrome with advanced ischemic heart disease than in control participants without metabolic syndrome. Thus, it can be suggested that metabolic syndrome is one of the significant factors affecting the development of coronary collateral vessels adversely.
BACKGROUND: Increased preprocedural C-reactive protein (CRP) levels in patients with acute myocardial infarction (MI) undergoing primary percutaneous coronary intervention (PCI) may affect myocardial perfusion. Accordingly, this study was designed to investigate the impact of admission CRP levels on the development of poor myocardial perfusion after PCI in patients with acute MI. METHODS: The study population consisted of 75 patients (62 men, mean age, 61.6+/-6.68 years), who were admitted to our hospital with acute anterior MI and who underwent primary PCI in the left anterior descending coronary artery. All patients underwent stenting following balloon angioplasty. Myocardial perfusion was evaluated by using Thrombolysis In Myocardial Infarction (TIMI) myocardial perfusion grade (TMPG). Patients were divided into two groups according to TMPG after PCI. Group 1 consisted of 25 patients with TMPG 0-1 and group 2 comprised 50 patients with TMPG 2-3. Admission serum high sensitive CRP (hs-CRP) levels were analysed by using nephelometric method. RESULTS: Admission hs-CRP levels, pain to balloon time and white blood cell count (WBC) of patients in group 1 were significantly higher than those of the patients in group 2 (P<0.001; P<0.001; P=0.002, respectively). Univariate analysis identified ejection fraction, pain to balloon time, WBC and hs-CRP levels as the predictors of poor myocardial perfusion. In multivariate logistic regression analysis, hs-CRP levels and pain to balloon time were found to have statistically significant independent association with poor myocardial perfusion. Adjusted odds ratios were calculated as 1.85 for hs-CRP [P=0.003; 95% confidence interval (CI), 1.23-2.80] and 5.49 for pain to balloon time (P=0.04; 95% CI, 1.08-27.84). CONCLUSIONS: On admission, high CRP level in patients with acute MI undergoing primary PCI is likely to be in the causal pathway leading to the development of poor myocardial perfusion, especially when combined with prolonged pain to balloon time.
BACKGROUND: Cardiovascular risk factors are reported to increase the incidence of aortic valve calcification. Among older women, low bone mineral density appears to be associated with increased prevalence of aortic calcification. We aimed to assess and compare cardiovascular risk factors and bone mineral density of patients with and without aortic valve calcification. MATERIALS AND METHODS: Cardiovascular risk factors and bone mineral density measurements have been assessed in 49 patients with aortic valve calcification and in 65 patients without aortic valve calcification. All patients were subsequently referred to the nuclear medicine department to measure bone mineral density after echocardiographic evaluation. RESULTS: No statistically significant differences were observed between the two groups with respect to sex, body mass index, history of coronary artery disease, diabetes mellitus, hypercholesterolemia, and smoking status. Although height and weight of the patients with aortic valve calcification were significantly lower than those of patients without aortic valve calcification, they were not independent risk factors. Age and hypertension were found to be independent positive risk factors for aortic valve calcification, whereas T score was found to be negatively associated with aortic valve calcification. CONCLUSION: We have shown that aortic valve calcification is positively associated with age and hypertension, whereas bone mineral density is negatively associated with aortic valve calcification. The mechanism underlying the association between decreased bone mineral density and aortic valve calcification remains to be clarified in further studies.
BACKGROUND: Although atherosclerosis is supposed to be responsible for more than 50% of coronary artery ectasia, the precise pathology of coronary artery ectasia is not clearly understood. A histopathological examination of ectatic segments has revealed mainly destruction of the media layer of the artery. In the present study, we assessed carotid intima-media thickness and common carotid artery diameter in patients with and without coronary artery ectasia. MATERIALS AND METHODS: Thirty-five consecutive patients with coronary artery ectasia and coronary artery disease and 35 age and sex-matched patients with coronary artery disease alone were included in the study. The common carotid artery was studied as the longitudinal plane within 10 mm from the bifurcation of the common carotid artery. The intima-media thickness was measured in the far wall at end-diastole from the B-mode screen to a point within the 10-mm segment proximal to the bifurcation by one investigator blinded to clinical data. RESULTS: No significant differences with respect to age, body mass index, hypertension, diabetes mellitus, hypercholesterolemia and smoking habits were observed between the two groups studied. Intima-media thickness of the common carotid artery of the patients with coronary artery ectasia was significantly lower than that of the patients with coronary artery disease alone (0.71 +/- 0.13 vs. 0.77 +/- 0.09 mm, respectively, P = 0.04). CONCLUSION: Decreased intima-media thickness of the carotid artery in patients with coronary artery ectasia and coronary artery disease may have pathogenic mechanisms different from coronary artery disease per se.