Number Of Atherosclerotic Risk Factors Research Articles

Abstract 214: Predictors of Mechanical Thrombectomy Success and Failure: A Preliminary Analysis

Introduction Mechanical thrombectomy (MT) is now the standard of care in treatment of large vessel occlusion (LVO) in acute ischemic stroke (AIS). However, a significant minority of patients do not achieve successful recanalization. Previous case series’ have reported failed recanalization at a rate of approximately 12% (1). In the present study, we investigated clinical and procedural characteristics predictive of MT success and failure. Methods We conducted a retrospective analysis of MT patients with LVO presenting to our academic comprehensive stroke center from 2015‐2020. Recanalization failure was defined as TICI 0‐2a and success as TICI 2b‐3. We compared all 49 consecutive failure cases to a random selection of 85 successful MT cases. Demographic, clinical, procedural, and outcome data were compared between the two groups. Results In this cohort, there was no statistically significant difference in sex, pre‐stroke modified Rankin score (mRS), admission National Institutes of Health Stroke Scale (NIHSS), door‐to‐groin time, thrombolytic use, or site of occlusion between the two groups. In the success group, patients were older (76 vs 61, p=0.003), and had a higher average number of atherosclerotic risk factors (p=0.002). There was a higher proportion of embolic stroke of undetermined source (ESUS) in the success group compared with the failure group (8.5% vs 0%, p=0.039). A higher proportion of failure cases were due to large artery atherosclerosis (30.6% vs 19.5%, p=0.12) and cardioembolism (55.1% vs 67.1%, p=0.27), though neither of these differences were statistically significant. Stent‐retrieval alone (SR) was a more common first pass technique in failed than in successful MT (14.3% vs 0%, p=0.001). Conclusion This study investigated clinical and procedural factors associated with successful and failed recanalization in MT. In this cohort, stent‐retrieval alone as a first pass technique was more commonly associated with failed MT. Stroke etiology was associated with rates of failure, with a significantly higher proportion of ESUS in successful cases and a trend toward a higher proportion of large vessel atherosclerosis and cardioembolism in failed MT.

Parametric Imaging of Biologic Activity of Atherosclerosis Using Dynamic Whole-Body Positron Emission Tomography

BackgroundFor molecular imaging of atherosclerotic vessel wall activity, tracer kinetic analysis may yield improved contrast versus blood, more robust quantitative parameters, and more reliable characterization of systems biology. ObjectivesThe authors introduce a novel dynamic whole-body positron emission tomography (PET) protocol that is enabled by rapid continuous camera table motion, followed by reconstruction of parametric data sets using voxel-based Patlak graphical analysis. MethodsTwenty-five subjects were prospectively enrolled and underwent dynamic PET up to 90 minutes after injection of 2-[18F]fluoro-2-deoxy-D-glucose (FDG). Two sets of images were generated: 1) the established standard of static standardized uptake value (SUV) images; and 2) parametric images of the metabolic rate of FDG (MRFDG) using the Patlak plot–derived influx rate. Arterial wall signal was measured and compared using the volume-of-interest technique, and its association with hematopoietic and lymphoid organ signal and atherosclerotic risk factors was explored. ResultsParametric MRFDG images provided excellent arterial wall visualization, with elimination of blood-pool activity, and enhanced focus detectability and reader confidence. Target-to-background ratio (TBR) from MRFDG images was significantly higher compared with SUV images (2.6 ± 0.8 vs 1.4 ± 0.2; P < 0.0001), confirming improved arterial wall contrast. On MRFDG images, arterial wall signal showed improved correlation with hematopoietic and lymphoid organ activity (spleen P = 0.0009; lymph nodes P = 0.0055; and bone marrow P = 0.0202) and increased with the number of atherosclerotic risk factors (r = 0.49; P = 0.0138), where signal from SUV images (SUVmaxP = 0.9754; TBRmaxP = 0.8760) did not. ConclusionsAbsolute quantification of MRFDG is feasible for arterial wall using dynamic whole-body PET imaging. Parametric images provide superior arterial wall contrast, and they might be better suited to explore the relationship between arterial wall activity, systemic organ networks, and cardiovascular risk. This novel methodology may serve as a platform for future diagnostic and therapeutic clinical studies targeting the biology of arterial wall disease.

Long-Term Prognosis of Patients With Transient Ischemic Attack or Stroke and Symptomatic Vascular Disease in Multiple Arterial Beds.

Cerebrovascular, coronary, and peripheral vascular disease have common underlying arterial pathology and risk factors, but the clinical significance of multiple-territory disease in patients with transient ischemic attack (TIA)/ischemic stroke is unclear, particularly whether the number of clinically affected territories still predicts long-term outcome on current standard secondary prevention therapies. In a population-based study of 92 728 individuals in Oxfordshire, United Kingdom (Oxford Vascular Study), we studied patients presenting with TIA/ischemic stroke (2002-2014) in relation to the number of other vascular beds (coronary, peripheral) affected by symptomatic (current or previous) disease. We compared the risk factor profile and long-term prognosis in patients with single- versus multiple-territory disease. Among 2554 patients with 10 679 patient-years of follow-up, 1842 (72.1%) had single- (TIA/stroke only), 608 (23.8%) double-, and 104 (4.1%) triple-territory symptomatic vascular disease. The number of affected vascular beds increased with the number of atherosclerotic risk factors (Ptrend<0.0001). Compared with patients with TIA/stroke only, those with multiple-territory disease had more hypertension (age/sex-adjusted odds ratio [OR], 3.43; 95% confidence interval [CI], 2.76-4.27; P<0.0001), diabetes mellitus (OR, 2.89; 95% CI, 2.27-3.66; P<0.0001), hypercholesterolemia (OR, 4.67; 95% CI, 3.85-5.66; P<0.0001), and current or previous smoking (OR, 1.52; 95% CI, 1.26-1.84; P<0.0001). Triple-territory disease was particularly strongly associated with hypercholesterolemia (OR, 6.80; 95% CI, 4.39-10.53; P<0.0001). Despite more intensive secondary prevention in patients with multiple-territory disease, the 5-year risk of vascular death increased steeply with the number of territories affected (17.2% versus 30.0% versus 42.9%; P<0.0001). Compared with patients with single-territory, patients with multiple-territory disease also had higher postacute long-term risks (90 days to 10 years) of recurrent ischemic stroke (age/sex-adjusted hazard ratio, 1.38; 95% CI, 1.04-1.81; P=0.02) and nonstroke acute vascular events (hazard ratio, 3.06; 95% CI, 2.23-4.20; P<0.0001). Number of affected vascular beds appeared to be a simple clinical rule in identifying TIA/ischemic stroke patients who are at high long-term risk of nonstroke vascular events and vascular death.

Abstract 281: Cyclophilin A is a Novel Biomarker for Oxidative Stress and Atherosclerotic Diseases

Background We have recently demonstrated that oxidative stress induces secretion of cyclophilin A (CyPA) from vascular smooth muscle cells, which plays a crucial role in the pathogenesis of atherosclerosis and abdominal aortic aneurysms (AAA) in mice. Thus, we tested our hypothesis that plasma CyPA levels could be a biomarker of atherosclerotic diseases such as coronary artery disease (CAD) and AAA in humans. Methods and Results In consecutive 320 patients undergoing coronary angiography, we examined the relationship between the severity of CAD and plasma CyPA levels measured by an immunoassay. Plasma CyPA levels were significantly higher in patients with significant coronary stenosis (&gt;50%, n=189) compared to those without it (n=131) (P&lt;0.001). A significant positive correlation was noted between plasma CyPA levels and significant coronary stenosis even after adjustment for age, sex, hypertension, diabetes, dyslipidemia and smoking. The average number of coronary arteries with significant stenosis and the need for coronary intervention were significantly increased in the quartiles of higher CyPA levels (both P&lt;0.001). In addition, plasma CyPA levels were significantly correlated with the number of coronary arteries with significant stenosis (P&lt;0.001). Indeed, plasma CyPA levels were a strong predictor of CAD (adjusted odds ratio for CAD, 6.20; 95% confidence interval, 3.14-12.27; P&lt;0.001). Interestingly, plasma levels of CyPA increased according to the number of atherosclerotic risk factors that enhance oxidative stress. Furthermore, plasma CyPA levels significantly reduced after medical treatment of those risk factors. Finally, pathological examinations showed that CyPA was strongly expressed in atherosclerotic coronary plaque of patients with myocardial infarction. In a separate study, we examined the plasma CyPA levels in patients with aortic aneurysms. Plasma CyPA levels were significantly higher in patients with aortic aneurysms (n=58) compared to those without it (n=69) (P&lt;0.001). Importantly, plasma CyPA levels were significantly higher in patients coexisting with CAD (n=18) compared to those only with aortic aneurysms (n=40) (P=0.012). Conclusion Plasma CyPA level is a novel biomarker of atherosclerotic diseases.

The Impact of Cardiovascular Risk-Factor Profiles on Blood Pressure Control Rates in Adults From Canada and the United States

BackgroundIt is unclear whether blood pressure control varies across the spectrum of atherosclerotic risk. MethodsWe used data from nonpregnant adults who had fasted laboratory samples drawn for the 2007-2009 cycle of the Canadian Health Measures Survey (CHMS) or the 2005-2008 US National Health and Nutrition Examination Survey (NHANES). ResultsThe 1692 CHMS subjects and 3541 NHANES participants were demographically similar (aged a mean of 45 years), although NHANES participants exhibited higher obesity rates (33.8% vs 22.2%, P < 0.001). Over 80% of CHMS and NHANES subjects with hypertension had at least 1 other cardiovascular risk factor. As the number of atherosclerotic risk factors increased, hypertension prevalence increased, but blood pressure control rates improved (from 48% among hypertensives with no other risk factors in CHMS to 77% among those with 3 or more risk factors, and from 35% to 53% in NHANES). However, the converse was not true: The distribution of Framingham risk scores for those subjects with “controlled hypertension” was nearly identical to the distribution among those adults with uncontrolled hypertension in both CHMS and NHANES and substantially higher than scores in normotensive subjects. ConclusionsAlthough control of blood pressure was better in patients with multiple atherosclerotic risk factors, hypertensives with controlled blood pressures exhibited risk-factor profiles similar to those of participants with uncontrolled blood pressures. This suggests the need, in educational messaging and therapy decision making, for an increased focus on total atherosclerotic risk rather than just blood pressure control.

Plasma Cyclophilin A Is a Novel Biomarker for Coronary Artery Disease

Oxidative stress induces secretion of cyclophilin A (CyPA) from vascular smooth muscle cells and it plays a crucial role in the pathogenesis of atherosclerosis in mice. Therefore, we tested our hypothesis that plasma CyPA levels are increased in patients with coronary artery diseases (CAD). In 320 consecutive patients undergoing coronary angiography, we examined the relationship between plasma CyPA levels and the severity of CAD. We measured plasma CyPA by an immunoassay based on the sandwich technique. Plasma CyPA levels were significantly higher in patients with significant coronary stenosis compared to those without it (P<0.001). A positive correlation was noted between plasma CyPA levels and significant coronary stenosis. The average number of stenotic coronary arteries and the need for coronary intervention were significantly increased in the quartiles of higher CyPA levels (both P<0.001). Indeed, the plasma CyPA level significantly correlated with the presence of CAD (adjusted odds ratio for CAD, 6.20; 95% confidence interval, 3.14-12.27; P<0.001). Interestingly, plasma levels of CyPA increased according to the number of atherosclerotic risk factors, all of which induce oxidative stress. Furthermore, plasma levels of CyPA significantly reduced after medical treatment of risk factors. Finally, CyPA was strongly expressed in coronary atherosclerotic plaque in patients with myocardial infarction. Plasma CyPA level is a novel biomarker for oxidative stress and CAD in humans.

Arterial Wall Elasticity Measured Using the Phased Tracking Method and Atherosclerotic Risk Factors in Patients with Type 2 Diabetes

The aim of this study was to investigate the relationship between atherosclerotic manifestations and brachial and radial arterial wall elasticity (AWE) measured using the phased tracking method in patients with type 2 diabetes mellitus (T2DM). This study included T2DM patients (n= 220, mean age 59 years) without a history of stroke or coronary artery disease. The brachial AWE, radial AWE, carotid mean intima-media thickness (IMT), max-IMT and flow-mediated vasodilation (FMD) were measured. The patients were classified according to the number of atherosclerotic risk factors, including obesity, dyslipidemia and hypertension. Group 1 included T2DM patients only, group 2 included patients with two risk factors, group 3 included patients with three risk factors and group 4 included patients with four risk factors. The patients were also divided into two groups according to microangiopathic complications, including retinopathy and nephropathy. The between-group differences were analyzed. The brachial AWE (548, 697, 755 and 771 kPa for groups 1, 2, 3 and 4, respectively) and radial AWE (532, 637, 717 and 782 kPa for groups 1, 2, 3 and 4, respectively) significantly increased in association with an increasing number of risk factors. The brachial AWE and radial AWE were significantly higher in the patients with microangiopathic complications than in those without microangiopathic complications (brachial AWE 797 and 694 kPa and radial AWE 780 and 660 kPa, respectively). Receiver operating characteristic curve analyses revealed that, for brachial AWE and radial AWE, the area under the curve was equal to the max-IMT and higher than the mean-IMT and FMD. Upper limb AWE measurement can reflect the degree of atherosclerosis risk overload and may be useful for evaluating vascular complications in T2DM patients.

Modulation of human monocyte CD36 by type 2 diabetes mellitus and other atherosclerotic risk factors

The pathophysiological role of CD36 in atherosclerosis seems to be largely dependent on its pro-inflammatory function and ability to take up oxidized low-density lipoprotein. Controversy exists concerning the potential beneficial/harmful effects of vascular CD36 inhibition in atherosclerosis. However, as atherosclerosis in murine models does not result in clinical end points such as plaque rupture and thrombotic ischaemia, typical of human disease, clinical studies are required to understand the functional role of CD36 in human atherosclerosis. Our aim was to investigate whether CD36 expression in monocytes is modulated by the presence of an increasing number of atherosclerotic risk factors, and specifically by hyperglycaemia because of diabetes mellitus. The study included 33 patients with advanced atherosclerosis and eight healthy blood donors, as controls. The patients were classified according to the presence of atherosclerotic risk factors. Diabetes mellitus was classified as either well-controlled or poorly controlled. Monocytes were exposed in vitro to low (5·5mM) or high glucose (26mM) concentrations for increasing times. Our results demonstrated that protein levels of glycated CD36 were significantly higher in patients with 3-4 atherosclerotic risk factors than in those with 0-2 atherosclerotic risk factors or in subjects with no atherosclerotic symptoms (P=0·04, in both cases). However, when we analysed just the poorly controlled diabetic patients, their glycated CD36 levels were lower. These data were corroborated by in vitro studies demonstrating that increasing glucose concentrations reduced glycated protein levels (P<0·05). Our results demonstrate that CD36 expression is altered by hyperglycaemia in atherosclerotic patients.

Ultrasound-based markers of carotid atherosclerosis correlate well with the number of classical atherosclerotic risk factors

Background and purposeUltrasound-based indicators such as mean or maximal carotid intima-media thickness (CIMT) and cross-sectional plaque area (C-SPA) have been shown to be measurable indices of atherosclerosis. We investigated whether those indicators correlated with the number of atherosclerotic risk factors assessed in routine clinical practice. Materials and methodsThe study involved a group of 150 patients (median age, 65 years). High-resolution ultrasound was used to assess CIMT and C-SPA of their common and internal carotid arteries. The number of risk factors derived from clinical examination (e.g., hypertension, diabetes, smoking), haematological test, acute phase proteins, serum lipoproteins, homocysteine, and body mass index was assessed. ResultsPlaques occurred in 85 patients (57% of participants). The median plaque area was 21 mm2 (10.7–46.5 mm2), and the mean CIMT was 0.88 mm (standard deviation, 0.28 mm). The study found significant associations among most of the single as well as the total number of risk factors and mean and maximal CIMT and C-SPA. The differences among the groups of patients with different numbers of risk factors were more evident in terms of the maximal and mean CIMT than in the case of C-SPA. Assessment of C-SPA could be statistically underpowered because only 57% of the investigated subjects had plaques in their carotid arteries. ConclusionsWe found a significant correlation between the total number of atherosclerosis risk factors and carotid atherosclerosis as measured by ultrasonography. Along with an increase of the number of risk factors, a gradual increase of CIMT and C-SPA was observed.

Dietary intervention with Okinawan vegetables increased circulating endothelial progenitor cells in healthy young women

Objective Circulating endothelial progenitor cells (EPCs) play a critical role in maintaining the integrity of vascular vessels. The number of EPCs inversely correlates with the number of atherosclerotic risk factors. Although nonpharmacological treatment represents the first approach to the primary prevention of atherosclerotic diseases, little is known about the effects of diet on EPCs. We investigated the effect of a dietary intervention with vegetables that are commonly eaten in Okinawa on the number of EPCs. Methods and results Forty-five healthy young women were employed and randomized to a dietary intervention group ( n = 24) or a control group ( n = 21). Subjects in the intervention group received typical Okinawan vegetables through home-parcel delivery for 2 weeks. After the dietary intervention, urinary potassium and magnesium excretion increased only in the intervention group and changes were greater than in the control group ( p = 0.007, 0.010, respectively). The consumption of total vegetables correlated with changes in both urinary potassium and magnesium excretion. Serum folic acid increased and plasma homocysteine decreased in both groups but the change was significant only in the intervention group. The EPCs number significantly increased in the intervention group but did not in the control group. An inverse correlation was observed between EPC number and plasma homocysteine level ( r = −0.272, p = 0.016). Changes in the EPC number inversely correlated with changes in both serum total cholesterol and low-density lipoprotein cholesterol level ( r = −0.555, p = 0.0002; r = −0.626, p < 0.0001, respectively). Conclusions The consumption of vegetables increased the number of circulating EPCs; this change might be associated with a homocysteine-lowering effect.

Role of N-Terminal Pro-B-Type Natriuretic Peptide in Risk Stratification in Patients Presenting in the Emergency Room

Natriuretic peptides are promising markers in diagnosing acute and chronic heart failure and assessing prognosis in these patients. Increasing routine use to unselected patients is challenged by false-positive results. The aims of this study were to assess (a) the distributions of N-terminal B-type natriuretic peptide (NT-proBNP) values in various diagnostic groups, (b) factors that influence NT-proBNP, and (c) the value of NT-proBNP in risk stratification in unselected emergency room (ER) patients. NT-proBNP was measured in 876 unselected consecutive patients [mean (SD) age, 58 (18) years; 53% male] attending the ERs of 2 university hospitals and 1 community hospital. Diagnoses, age, sex, hemoglobin, creatinine (CREA), C-reactive protein (CRP), troponin T, and intensity of care were documented. In a subset consisting of all 417 patients at 1 center, in-hospital follow-up was completed with respect to a complicated clinical course, including intensive care treatment and death. NT-proBNP was significantly increased in patients with cardiac diagnoses or histories compared with patients with only pulmonary or other diagnoses. In patients with other diagnoses, NT-proBNP values increased significantly with the number of atherosclerotic risk factors (P=0.044). Age, renal function, CRP, and to a much lesser extent, hemoglobin significantly influenced NT-proBNP values. The amount of care was positively correlated with NT-proBNP (P<0.001). Classification and regression tree analysis showed a superior impact of NT-proBNP for identification of high-risk patients. NT-proBNP is a promising marker for identification of patients with structural heart disease in the ER and a suitable tool for risk stratification. Its use in the ER should be limited to clearly clinically defined patient groups at present to avoid a potential excess of additional diagnostic procedures in positive but asymptomatic patients.

Age, Gender, and Number of Atherosclerotic Risk Factors are the Independent Factor of Endothelial Dysfunction in Patients with Coronary Atherosclerosis

Background and Objectives:The endothelial function is impaired in patients with atherosclerosis risk factors as well as in those with atherosclerotic disease, such as coronary artery disease. This study was performed to evaluate the impact of individual risk factors and their number in patients with coronary atherosclerosis, who already had an impaired endothelial function. Subjects and Methods:The endothelial function was measured in 884 consecutive patients (mean age; 59 years old, 486 male) undergoing coronary angiography, using highresolution ultrasound. The flow-mediated brachial artery dilation (FMD, %) was used to measure the endothelial function. The risk factors were classified according to the hypertension, diabetes mellitus, smoking and dyslipidemia, and their number classified from 0 to 4. Results:The FMD was lower (3.85±2.1% vs. 4.27±2.1%, p<0.005) in patients with hypertension (n=431) than in those without (n=453); however, no significant difference was shown according to the presence of other risk factors. A multivariate analysis showed age (β=-0.204, p<0.001), gender (β=0.118, p<0.01) and the number of risk factors (β=-0.150, p<0.01) were independent risk factors of the FMD in patients with coronary atherosclerosis. Furthermore, the FMD was significantly associated with the number of risk factors in our study subjects (r=-0.083, p<0.05, n=884). Conclusion:This study suggests that the increased number of risk factors, old age and male are independent factors for endothelial dysfunction, even in patients with coronary atherosclerosis, who already had an impaired endothelial function. (Korean Circulation J 2005;35:302-308)

Quantification of Isoprostanes as Indices of Oxidant Stress and the Risk of Atherosclerosis in Humans

Enhanced oxidant stress occurring either locally in the vessel wall or systemically is implicated in the pathogenesis of atherosclerosis in humans. Nonetheless, evidence that oxidant stress is increased in vivo in association with this disease and that it can be quantified in living human beings has been lacking because of the unavailability of biomarkers to assess oxidant stress in humans. Recently, the development of methods to quantify the F(2)-isoprostanes (IsoPs), prostaglandin (PG)-like compounds derived from the free radical-catalyzed peroxidation of arachidonic acid, has allowed, for the first time to the author's knowledge, a facile and accurate assessment of oxidant stress in vivo. The purpose of this brief review is to discuss the usefulness of quantifying IsoPs as an index of oxidative injury in association with atherosclerosis. F(2)-IsoPs can be measured in human biological fluids, such as plasma and urine, using highly precise assays. They have been shown to be increased in association in with a number of atherosclerotic risk factors, including cigarette smoking, hypercholesterolemia, diabetes mellitus, and obesity, among others. In addition, recent evidence suggests their quantification may represent an independent marker of atherosclerotic risk. A reduction in cardiovascular risk factors is associated with a decrease in IsoP formation in humans. Despite the fact that the role of oxidant stress in the pathogenesis of atherosclerosis is a hotly debated issue, current evidence suggests that the IsoPs represent a biomarker that has the potential to be of great importance in the assessment of human atherosclerotic cardiovascular disease. Enhanced oxidant stress occurring either locally in the vessel wall or systemically is implicated in the pathogenesis of atherosclerosis in humans. Nonetheless, evidence that oxidant stress is increased in vivo in association with this disease and that it can be quantified in living human beings has been lacking. Recently, the development of methods to quantify the F2-isoprostanes (IsoPs) has allowed a facile and accurate assessment of oxidant stress in vivo. The purpose of this brief review is to discuss the usefulness of quantifying IsoPs as an index of oxidative injury in association with atherosclerosis.

Coronary artery calcium volume scores on electron beam tomography in 12,936 asymptomatic adults

We developed age- and gender-specific normative tables of calcium volume scores by using data from 12,936 asymptomatic patients who underwent electron beam tomographic scanning and compared the volume with the Agatston scores obtained in the same subjects. The 2 scores increased as the number of atherosclerotic risk factors increased. The volume scores were statistically smaller than the Agatston scores at the upper quartile level.

Lumbar spine pathology and multiple atherosclerotic risk factors: a 53-year prospective study of 1,337 patients

Nicholas U. Ahn, MD, Darien, IL, USA; Uri M. Ahn, MD, Bedford, NH, USA; Leelakrishna Nailamshetty, BS, Philadelphia, PA, USA; Jacob M. Buchowski, MS, Baltimore, MD, USA; Peter S. Rose, BS, Bethesda, MD, USA; Paul D. Sponseller, MD, Baltimore, MD, USAIntroduction: A great deal of attention has been directed toward the hypothesis that low back pain is caused by vascular insult to the intervertebral discs or joints of the lumbar spine. More specifically, numerous authors have suggested that atherosclerotic occlusion of the lumbar vessels is a primary cause of low back pain and lumbar spondylosis. A previous study examined the relationship between lumbar spine disease and single atherosclerotic risk factors. It was found that smoking, hypertension and hypercholesterolemia were associated with the development of lumbar spondylosis. Smoking and hypertension were associated with the development of chronic low back pain. It is well known that the presence of multiple risk factors dramatically increases the risk of atherosclerotic occlusion of the coronary arteries and small arteries of the extremities. This leads to a nearly exponential increase in risk of heart disease and peripheral vascular disease as the number of risk factors increases. It would thus follow, if atherosclerosis of the lumbar vessels is a cause of lumbar spine disease, that increasing the number of atherosclerotic risk factors in an individual would increase his or her odds of developing low back pain or lumbar spondylosis.This is the only study that investigates the effect of multiple atherosclerotic risk factors on the development of lumbar spine disease. Furthermore, we have been able to study this relationship using a prospective, long-term (53-year) cohort. Should the increase in number of risk factors lead to an increase in the odds of developing lumbar spine pathology, this would provide further evidence that the vascular hypothesis is valid.Materials and methods: Graduates from the medical school classes from 1948 to 1964 at our institution were asked to participate in a longitudinal study that was started in 1949; 1,337 physicians consented to this study. All volunteers had medical records and questionnaires sent in each year, and all data were stored and recorded. Numerous risk factors for atherosclerosis were identified: smoking history, diabetes mellitus, hypertension, hypercholesterolemia, obesity, family history and peripheral vascular disease. The subsequent development of lumbar spine pathology, including chronic low back pain, lumbar herniated nucleus propolsus and lumbar spondylosis, was determined. Logistic regression analyses were used to examine the relationship between the number of risk factors and the development of lumbar spine disease. Because this is a prospective cohort, only those risk factors that existed before the development of the lumbar spine disease were considered in the analyses.Results: The odds of developing chronic low back pain increased significantly as the number of risk factors increased only in those patients who had a smoking history (p=.02) or a history of hypertension (p=.04). The odds of developing lumbar spondylosis increased significantly as the number of risk factors increased in all patients (p=.03). The odds of developing lumbar herniated nucleus propolsus were not significantly associated with an increase in the number of risk factors.Conclusion: An increase in the number of atherosclerotic risk factors was found to significantly increase the odds of developing chronic low back pain and lumbar spondylosis in this prospective, long-term cohort. This suggests that atherosclerosis of the segmental arteris is a cause of lumbar spine disease and that the vascular hypothesis to the cause of low back pain and lumbar spine degeneration is valid.

Association Between Carotid Artery Bifurcation Disease and Risk Factors for Atherosclerosis

Patients referred to the vascular laboratory for carotid duplex scanning may have identifiable risk factors for atherosclerosis. The presence of these risk factors may be associated with a higher risk of significant carotid bifurcation atherosclerosis. Furthermore, physicians have widely varying thresholds for requesting duplex scanning, and patient characteristics are likely to be highly variable from one vascular laboratory to another. The authors examined the relationship between significant carotid disease and atherosclerotic risk factors in patients referred to a community hospital vascular laboratory. Complete information was available for selected atherosclerotic risk factors including gender, diabetes, hypertension, cigarette smoking, cardiac disease, and prior stroke for 68 men and 78 women undergoing initial carotid duplex scanning between 4/1/93 and 11/11/93. The authors examined the possible correlation of these risk factors with the presence of severe carotid disease (&gt; 50% stenosis including internal carotid occlusion) in at least one distal common carotid artery, bulb, or proximal internal carotid. Severe disease was present in 34 (23%) of 146 patients. Patients with severe carotid disease tended to be older (76.2 ± 1.3 vs 73.4 ± 0.9 years, mean ± SEM), but this difference was not significant (P = 0.11). Patients with severe carotid disease tended to have more total risk factors (3.2 vs 2.1, P &lt; 0.01). Hypertension was the best predictor of severe carotid disease (36% with, 10% without hypertension, P &lt; 0.01). Trends toward greater likelihood of severe carotid disease in men, smokers, and in patients with cardiac disease were not significant. Risk factors may be valuable predictors of the presence or absence of significant carotid bifurcation disease. Hypertension and the total number of atherosclerotic risk factors were strong predictors of significant carotid disease in the laboratory. However, patient characteristics in individual vascular laboratories may be highly skewed and vastly different from other vascular laboratories and the population. Individual vascular laboratories should tabulate atherosclerotic risk factors in addition to indications for carotid duplex scanning so that the importance of these risk factors in each laboratory may be determined.