| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 2000;102:2087.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Independent Association of High Blood Pressure and Aortic Atherosclerosis
A Population-Based Study
Presented in part at the 72nd Scientific Sessions of the American Heart Association, Atlanta, Ga, November 7–10, 1999, and published in abstract form (Circulation 1999;100[suppl I]:I-231).
From the Division of Cardiovascular Diseases and Internal Medicine (Y.A., B.K.K., F.G., J.B.S.), the Department of Neurology (I.M., D.O.W.), the Division of Hypertension and Internal Medicine (G.L.S.), and the Department of Health Science Research (T.M.P., W.M.O., J.P.W.), Mayo Clinic and Mayo Foundation, Rochester, Minn.
Correspondence to Bijoy K. Khandheria, MD, Mayo Clinic, 200 First St SW, Rochester, MN 55905. E-mail khandheria{at}mayo.edu
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background—Atherosclerosis of the thoracic aorta is associated with stroke. The association between hypertension, a major risk factor for stroke, and aortic atherosclerosis has not been determined in the general population.
Methods and Results—Transesophageal
echocardiography was performed in 581 subjects, a
random sample of the Olmsted County (Minnesota) population aged 
45
years participating in the Stroke Prevention: Assessment of Risk in a
Community (SPARC) study. Blood pressure was assessed by multiple office
measurements and 24-hour ambulatory blood pressure monitoring. The
association between blood pressure variables and aortic
atherosclerosis was evaluated by multiple logistic
regression, adjusting for other associated variables. Among
subjects with atherosclerosis, blood pressure
variables associated with complex aortic
atherosclerosis (protruding plaques 4 mm thick,
mobile debris, or ulceration) were determined. Age and smoking history
were independently associated with aortic
atherosclerosis of any degree (P
0.001)
and with complex atherosclerosis
(P=0.002), whereas sex, diabetes mellitus, and body mass
index were not. Multiple systolic and pulse pressure
variables (office and ambulatory), but none of the
diastolic blood pressure variables, were associated
with atherosclerosis and complex
atherosclerosis, adjusting for age and smoking. Among
subjects with atherosclerosis, the odds of complex
atherosclerosis increased as ambulatory out-of-bed
systolic blood pressure increased (odds ratio 1.43 per 10
mm Hg increase, 95% CI 1.10 to 1.87) and with hypertension treatment,
adjusting for age and smoking history.
Conclusions—High blood pressure is independently associated with aortic atherosclerosis. Among subjects with atherosclerosis, high blood pressure is associated with complex atherosclerosis.
Key Words: aorta • atherosclerosis • blood pressure • echocardiography • hypertension
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Systemic hypertension is a major risk factor for cardiovascular morbidity in the general population.1 Evidence supporting the role of hypertension as an atherosclerosis risk factor is based on epidemiological data demonstrating an association between high blood pressure and cardiovascular events. Recent studies have also demonstrated an association between hypertension and ultrasonographically defined carotid atherosclerosis in representative samples of the population.2 To date, the association between high blood pressure and aortic atherosclerosis has not been assessed in the general population because of the semi-invasive nature of transesophageal echocardiography (TEE), the procedure of choice for high-resolution real-time imaging of the thoracic aorta.3
Stroke Prevention: Assessment of Risk in a Community (SPARC) is an ongoing population-based study designed to determine the prevalence of potential risk factors for stroke in the general population.4 5 Study participants, a random sample of the Olmsted County (Minnesota) population, were evaluated by TEE, thus defining the prevalence of aortic atherosclerosis in the general population. Blood pressure was assessed comprehensively in the SPARC population by multiple home and office measurements and by 24-hour ambulatory blood pressure monitoring (ABPM). The current analysis was performed to evaluate the association between various components of systemic blood pressure and both the presence and severity of atherosclerosis of the thoracic aorta in the general population.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
SPARC Study
The design and initial results of the SPARC study were recently published.4 5 The SPARC sampling process was designed to randomly select 580 residents of Olmsted County, Minnesota, stratified by sex and 5 age subgroups (45 to 54, 55 to 64, 65 to 74, 75 to 84, and
85 years). Of 1475 residents initially selected, 230 were ineligible
because of predefined exclusion criteria (terminal illness, dementia,
significant disability, or esophageal disease precluding TEE), and 607
refused to participate in the study. Of the 638 who participated in a
home interview, 50 refused to participate further in the study. Thus,
the final SPARC study sample consisted of 588 subjects (47% of
eligible). TEE was performed successfully in 581 subjects (the
present study population). The medical records of a random
sample of 20% of eligible subjects who refused to participate were
reviewed. The comorbidities of this group were not significantly
different from those of the study group,5 confirming that
study participants were a representative sample of the
population. The present study was approved by the Institutional
Review Board. Written informed consent was obtained from all
participants.
Data Collection
Cardiovascular risk factors were assessed by
home interviews and abstracting of medical records at the Mayo
Clinic and Olmsted County Medical Center, the 2 primary healthcare
providers in Olmsted County. Information on serum lipid levels
(obtained within 1 year of TEE) was abstracted from medical
records. Hypertension treatment (defined as use of antihypertensive
drugs) and smoking status were self-reported during the interview.
Blood Pressure Measurements
Multiple blood pressure measurements were obtained during a home
interview and 2 office appointments related to SPARC (all referred to
as "office" blood pressure measurements).5 Blood
pressure was measured with subjects in the sitting position; a mercury
column sphygmomanometer with an appropriate-sized cuff was used.
Korotkoff phases 1 and 5 established the levels of systolic and
diastolic pressures, respectively. Two systolic and
2 diastolic readings from each of the 3 visits (total of 6
systolic and diastolic readings) were averaged.
Ambulatory blood pressure readings were obtained every 10 minutes
during a 24-hour ABPM period with the use of commercially available
instruments. Only technically satisfactory ABPM recordings
obtained within 30 days of the TEE study were used for the present
analysis. Blood pressure readings were averaged for the entire
monitoring period (
24 hours) and separately for daytime (out-of-bed)
and nighttime (in-bed) measurements.
For office blood pressure measurements, hypertension was defined as
mean systolic blood pressure 140 mm Hg or
diastolic blood pressure 90 mm Hg or
antihypertensive drug therapy. For ABPM, out-of-bed hypertension was
defined as mean out-of-bed systolic blood pressure 135
mm Hg or out-of-bed diastolic blood pressure 85
mm Hg; in-bed hypertension was defined as mean in-bed systolic
blood pressure 120 mm Hg or in-bed diastolic blood
pressure 75 mm Hg.6 Pulse pressure, the difference
between systolic and diastolic blood pressures, was
calculated for office, 24-hour, out-of-bed, and in-bed blood pressure
measurements.
Transesophageal Echocardiography
TEE was performed according to standard practice guidelines with
the use of commercially available ultrasonographic instruments. The
ascending aorta, aortic arch, and descending thoracic aorta were imaged
in short- and long-axis views. Atherosclerosis was
defined as irregular intimal thickening with increased echogenicity.
Atherosclerosis was defined as complex in the presence
of protruding atheroma 4 mm thick,4 7 8
mobile atherosclerotic debris,9 or plaque ulceration, and
it was defined as simple in the absence of complex morphological
features (Figure 1
). For the present
analysis, aortic atherosclerosis was defined as
the presence of atherosclerosis (of any degree) in any
(at least 1) segment of the thoracic aorta.8 Complex
aortic atherosclerosis was defined as the presence of
complex atherosclerosis in any aortic
segment.8
|
Statistical Analysis
Two separate series of multivariate
analyses were performed. The first series of analyses
compared subjects with atherosclerosis of any degree
with subjects without atherosclerosis. The second
series of analyses were performed among subjects with
atherosclerosis, comparing subjects with complex
atherosclerosis with those with simple
atherosclerosis. Continuous variables were compared
by unpaired Student t test (normal data) or Wilcoxon
rank sum test (nonnormal data). Categorical data were compared by
2 or Fisher exact test.
Logistic regression was used to assess the impact of age, sex, comorbid conditions, various blood pressure measurements, and hypertension treatment on the odds of aortic atherosclerosis (proportion with atherosclerosis of any degree/proportion without atherosclerosis). Similarly, the odds of complex atherosclerosis among subjects with atherosclerosis (proportion with complex atherosclerosis/proportion with simple atherosclerosis) were assessed. Initially, to assess the impact of various blood pressure measurements and hypertension definitions, each blood pressure variable was examined separately, adjusting for age and other significant comorbid conditions. Subsequently, the final age-adjusted models were identified by stepwise logistic regression, allowing all office blood pressure variables to compete for entry into the models. A value of P=0.05 was required to enter and to leave the stepwise models. All 2-way interactions between resulting variables were analyzed.
Initially, the total study population was examined only with the use of data available for the entire study population (including office blood pressure measurements). Subsequently, the subgroup for which ABPM data were available was examined. The impact of missing ABPM data on the odds of atherosclerosis was assessed by creating an indicator of subjects missing these data. Adjusting for age, the association between this variable and aortic atherosclerosis was examined by use of logistic regression. Likewise, the interactions between this indicator and the independent variables in the final model were examined.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The age and sex distribution of the SPARC population and the percentage of simple and complex aortic atherosclerosis in the various age and sex strata are presented in Figures 2
and 3,
respectively. The distribution of aortic
atherosclerosis and complex aortic
atherosclerosis within the segments of the thoracic
aorta is presented in Figure 4.
Aortic atherosclerosis of any degree was identified in
298 study participants (51.3%). Complex
atherosclerosis was present in 44 subjects (14.8%
of subjects with aortic atherosclerosis, 7.6% of the
total study population).
|
|
|
Descriptive statistics of variables potentially associated with
aortic atherosclerosis and complex
atherosclerosis are presented in Table 1. The estimated odds ratios of
atherosclerosis and complex
atherosclerosis, associated with selected
variables, are presented in Table 2. Age was significantly associated with
increased risk of atherosclerosis and complex
atherosclerosis. In subjects aged <75 years, the odds
of atherosclerosis increased nearly 4-fold for every
10-year increase in age; beyond age 75, there was no significantly
increased risk. Among subjects with atherosclerosis,
the odds of complex atherosclerosis increased >2-fold
for every 10-year increase in age.
|
|
Total Study Population (581 Subjects)
Predictors of Aortic Atherosclerosis
Pulse pressure, systolic blood pressure, and hypertension
treatment were significantly associated with
atherosclerosis, adjusting for age and smoking history,
the 2 non–blood pressure variables associated with
atherosclerosis (all P0.05). Stepwise
logistic regression identified age, smoking history, and office pulse
pressure as independently associated with aortic
atherosclerosis (Table 3). The odds of
atherosclerosis increased by 23% per 10 mm Hg
increase in pulse pressure.
|
Predictors of Complex Aortic Atherosclerosis
Among those with aortic atherosclerosis, the 44
subjects with complex atherosclerosis were compared
with the 254 subjects with simple atherosclerosis.
Pulse pressure, systolic blood pressure, and hypertension
treatment were significantly associated with complex aortic
atherosclerosis, adjusting for age and smoking history
(all P0.01). Stepwise logistic regression identified age,
smoking history, office pulse pressure, and hypertension treatment as
independently associated with complex aortic
atherosclerosis (Table 4). Among those with
atherosclerosis, the odds of complex
atherosclerosis increased by 31% per 10 mm Hg
increase in pulse pressure.
|
Subgroup With ABPM Data (473 Subjects)
Predictors of Aortic Atherosclerosis
Technically adequate ABPM recordings performed within 30
days of TEE were available for 473 study participants. After adjustment
for age, an indicator of missing ABPM data was not significantly
associated with atherosclerosis. Furthermore, this
indicator did not interact with the other variables associated with
atherosclerosis, suggesting that for these
variables the odds of aortic atherosclerosis were
the same in this subgroup as in the total study population.
Age and smoking were significantly associated with aortic
atherosclerosis. The odds ratios of
atherosclerosis for the various blood pressure
variables, adjusted for age and smoking history (the 2 non–blood
pressure variables associated with
atherosclerosis), are presented in Table 5. Twenty-four-hour systolic
blood pressure, out-of-bed systolic blood pressure, in-bed
hypertension, and hypertension treatment were associated with
atherosclerosis, adjusting for age and smoking history.
None of the diastolic blood pressure variables or the
standard definition of hypertension (based on office blood pressure
measurements) was significantly associated with
atherosclerosis. Stepwise logistic regression
identified age, smoking history, in-bed hypertension, and hypertension
treatment as independently associated with aortic
atherosclerosis (Table 6). A significant interaction was
observed between in-bed hypertension and hypertension treatment, the
odds of atherosclerosis depending jointly on in-bed
hypertension and hypertension treatment. Only subjects with both in-bed
hypertension and hypertension treatment had increased odds of
atherosclerosis: the odds were 3.5 times higher for
these subjects than for those with neither of these conditions. The
interaction between in-bed hypertension and hypertension treatment is
probably related, in part, to the higher in-bed blood pressure
(systolic blood pressure and pulse pressures) in treated in-bed
hypertensives than in nontreated in-bed hypertensives (data not shown).
When categorical variables were not included in the stepwise model
(Table 6), out-of-bed systolic blood pressure emerged as
the blood pressure variable independently associated with aortic
atherosclerosis. The odds of
atherosclerosis increased by 18% per 10 mm Hg
increase in out-of-bed systolic blood pressure.
|
|
Predictors of Complex Aortic Atherosclerosis
ABPM data were available for 230 of the 298 subjects with aortic
atherosclerosis. An indicator of missing ABPM data was
not associated with complex atherosclerosis and did not
interact with the other variables associated with complex
atherosclerosis.
Age and smoking were significantly associated with complex aortic
atherosclerosis. The odds ratios of complex
atherosclerosis for the various blood pressure
variables, adjusting for age and smoking history, are
presented in Table 5
. Multiple systolic blood
pressure and pulse pressure variables (office, 24-hour, and
out-of-bed ambulatory blood pressure measurements) and hypertension
treatment were associated with complex atherosclerosis,
adjusting for age and smoking history. None of the
diastolic blood pressure variables or the standard
definition of hypertension (based on office blood pressure
measurements) was significantly associated with complex
atherosclerosis. Stepwise logistic regression
identified age, smoking history, out-of-bed systolic blood
pressure, and hypertension treatment as independently associated with
complex aortic atherosclerosis (Table 7). Among those with
atherosclerosis, the odds of complex
atherosclerosis increased by 43% per 10 mm Hg
increase in out-of-bed systolic blood pressure. The odds of
complex atherosclerosis were >2 times greater for
those with hypertension treatment than for those without hypertension
treatment.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The SPARC study determines the association between high blood pressure and both the presence and severity of aortic atherosclerosis in the general population. Our detailed analysis of multiple blood pressure variables allows us to conclude the following: (1) Elevated systolic blood pressure and pulse pressure (which is quantitatively determined primarily by systolic blood pressure) are associated with aortic atherosclerosis, whereas diastolic blood pressure is not. (2) The association between high blood pressure and aortic atherosclerosis is apparent by both office (nonambulatory) and ambulatory blood pressure measurements. (3) High blood pressure is associated with both the presence of aortic atherosclerosis and its severity (ie, the presence of complex morphological features). (4) Although hypertension treatment is a general marker of hypertension severity, the association between hypertension treatment and atherosclerosis was independent of blood pressure level in some of our models, suggesting that blood pressure measurements alone may underestimate the true association between blood pressure and aortic atherosclerosis in treated hypertensive subjects.
An association between hypertension and aortic atherosclerosis has been demonstrated by autopsy studies.10 11 Previous echocardiographic studies addressing the association between hypertension and aortic atherosclerosis have yielded nonuniform results, probably because of patient selection, nonstandardized blood pressure measurements, and variable definitions of hypertension. An association between hypertension and aortic atherosclerosis and between pulse pressure and aortic atherosclerosis has been observed in selected patients with valvular disease12 and with atrial fibrillation,8 respectively. However, this association was not consistently observed in other studies.13 14 15 In contrast to all previously published TEE studies, the SPARC study enabled us to uniquely assess both aortic anatomy and blood pressure in a large nonreferred population, representative of the general population in a well-defined geographic area. Moreover, blood pressure was assessed in detail by multiple standardized nonambulatory and ambulatory measurements, thus enabling us to determine the association between multiple blood pressure variables and aortic atherosclerosis.
Sex was not associated with aortic atherosclerosis in
the present study, probably because of age distribution of the
SPARC population (mainly postmenopausal women). Diabetes mellitus was
not independently associated with aortic
atherosclerosis, probably because of the strong
association of diabetes with age. We did not observe an association
between serum lipids levels and aortic atherosclerosis.
However, serum lipid levels were available in only a subgroup of our
study population (Table 1); therefore, we could not definitely
exclude an association between hyperlipidemia and
aortic atherosclerosis. An indicator of subjects
missing lipid measurements was not associated with aortic
atherosclerosis and did not interact with the
variables associated with atherosclerosis in the
final models. In addition, there were no significant differences in
blood pressure measurements between subjects with or without serum
lipid measurements (data not shown). These findings suggest that the
associations observed between blood pressure and aortic
atherosclerosis were not affected by the availability
of serum lipid measurements. Similar results were obtained in an
analysis of a larger subgroup of subjects in whom more remote
(within 5 years of TEE) serum lipid measurements were available (data
not shown), further strengthening the validity of our results in a
smaller subgroup (Tables 1 and 2). Although an
association between hyperlipidemia and aortic
atherosclerosis has been previously
described,16 this association was not demonstrated in a
recently published large echocardiographic
study.8
The association between high blood pressure and aortic atherosclerosis does not imply a cause-and-effect relationship. Hypertension may predispose to aortic atherosclerosis, as hypothesized for other atherosclerotic manifestations.17 Alternatively, aortic atherosclerosis may be associated with increased stiffness (reduced compliance) of the proximal aortic segments (the segments examined by TEE), resulting in secondary elevation of systemic blood pressure.13 18 The association between systolic blood pressure and pulse pressure (but not diastolic pressure) and aortic atherosclerosis supports the later hypothesis.
The association between high blood pressure and aortic atherosclerosis and the association between aortic atherosclerosis and stroke3 offer an additional potential mechanism of stroke in association with hypertension. The currently observed associations between systolic blood pressure, pulse pressure, and aortic atherosclerosis support the previously described associations between systolic hypertension and stroke19 and between pulse pressure and cardiovascular events.20 The findings of the present study should form the basis for future studies designed to evaluate the role of hypertension treatment in prevention of aortic atherosclerosis (as currently evaluated for carotid atherosclerosis21 ) and its potential embolic complications.
|
Acknowledgments |
|---|
This study was supported in part by research grants NS06663 and AR30582 from the US Public Health Service.
Received April 18, 2000; revision received June 5, 2000; accepted June 8, 2000.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
-
Kannel WB. Framingham Study insights into
hypertensive risk of cardiovascular disease.
Hypertens Res. 1995;18:181–196.[Medline]
[Order article via Infotrieve]
-
Ebrahim S, Papacosta O, Whincup P, et al.
Carotid plaque, intima media thickness, cardiovascular
risk factors, and prevalent cardiovascular disease in
men and women. Stroke. 1999;30:841–850.
[Abstract/Free Full Text]
-
Tunick PA, Kronzon I. Atheroma of the
thoracic aorta: clinical and therapeutic update. J Am Coll
Cardiol.. 2000;35:545–554.
[Abstract/Free Full Text]
-
Meissner I, Whisnant JP, Khandheria BK, et al.
Prevalence of potential risk factors for stroke assessed by
transesophageal echocardiography
and carotid ultrasonography: the SPARC Study. Mayo Clin
Proc. 1999;74:862–869.[Medline]
[Order article via Infotrieve]
-
Meissner I, Whisnant JP, Sheps SG, et al. Detection
and control of high blood pressure in the community: do we need a
wake-up call? Hypertension. 1999;34:466–471.
[Abstract/Free Full Text]
-
The sixth report of the Joint National Committee on
Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure. Arch Intern Med. 1997;157:2413–2446.[Abstract]
-
Amarenco P, Cohen A, Tzourio C, et al.
Atherosclerotic disease of the aortic arch and the risk of
ischemic stroke. N Engl J Med. 1994;331:1474–1479.
[Abstract/Free Full Text]
-
Blackshear JL, Pearce LA, Hart RG, et al, for the
Stroke Prevention in Atrial Fibrillation Investigators Committee on
Echocardiography. Aortic plaque in atrial
fibrillation: prevalence, predictors, and thromboembolic implications.
Stroke. 1999;30:834–840.
[Abstract/Free Full Text]
-
Karalis DG, Chandrasekaran K, Victor MF, et al.
Recognition and embolic potential of intraaortic atherosclerotic
debris. J Am Coll Cardiol. 1991;17:73–78.[Abstract]
-
Virmani R, Avolio AP, Mergner WJ, et al. Effect of
aging on aortic morphology in populations with high and low prevalence
of hypertension and atherosclerosis. Am J
Pathol. 1991;139:1119–1129.[Abstract]
-
Homma S, Ishii T, Tsugane S, et al. Different effects
of hypertension and hypercholesterolemia on the
natural history of aortic atherosclerosis by the stage
of intimal lesions. Atherosclerosis. 1997;128:85–95.[Medline]
[Order article via Infotrieve]
-
Tribouilloy C, Peltier M, Andrejak M, et al.
Correlation of thoracic aortic atherosclerotic plaque detected by
multiplane transesophageal
echocardiography and cardiovascular
risk factors. Am J Cardiol. 1998;82:1552–1555.[Medline]
[Order article via Infotrieve]
-
Nishino M, Masugata H, Yamada Y, et al. Evaluation of
thoracic aortic atherosclerosis by
transesophageal echocardiography.
Am Heart J. 1994;127:336–344.[Medline]
[Order article via Infotrieve]
-
Davila-Roman VG, Barzilai B, Wareing TH, et al.
Atherosclerosis of the ascending aorta: prevalence and
role as an independent predictor of cerebrovascular events in cardiac
patients. Stroke. 1994;25:2010–2016.[Abstract]
-
The French Study of Aortic Plaques in Stroke Group.
Atherosclerotic disease of the aortic arch as a risk factor for
recurrent ischemic stroke. N Engl J Med. 1996;334:1216–1221.
[Abstract/Free Full Text]
-
Tribouilloy CM, Peltier M, Iannetta-Peltier MC, et al.
Relation between low-density lipoprotein cholesterol and
thoracic aortic atherosclerosis. Am J
Cardiol. 1999;84:603–605.[Medline]
[Order article via Infotrieve]
-
Alexander RW. Hypertension and the pathogenesis of
atherosclerosis. Hypertension. 1995;25:155–161.
[Abstract/Free Full Text]
-
Smulyan H, Safar ME. Systolic blood pressure
revisited. J Am Coll Cardiol. 1997;29:1407–1413.[Abstract]
-
Kannel WB. Elevated systolic blood pressure as
a cardiovascular risk factor. Am J
Cardiol.. 2000;85:251–255.[Medline]
[Order article via Infotrieve]
-
Franklin SS, Khan SA, Wong ND, et al. Is pulse pressure
useful in predicting risk for coronary heart disease?: the
Framingham Heart Study. Circulation.. 1999;100:354–360.
[Abstract/Free Full Text]
-
Zanchetti A. Intermediate endpoints for
atherosclerosis in hypertension. Blood Press
Suppl. 1997;6:97–102.
This article has been cited by other articles:
 |
|
 |
|
  S. Sen, A. Hinderliter, P. K. Sen, J. Simmons, V. A. LeGrys, J. Beck, S. Offenbacher, K. Moss, and S. M. Oppenheimer Association of Leukocyte Count With Progression of Aortic Atheroma in Stroke/Transient Ischemic Attack Patients Stroke, November 1, 2007; 38(11): 2900 - 2905. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. K. Thambidorai, S. J. Jaffer, T. K. Shah, W. J. Stewart, A. L. Klein, and M. S. Lauer Association of atheroma as assessed by intraoperative transoesophageal echocardiography with long-term mortality in patients undergoing cardiac surgery Eur. Heart J., June 6, 2007; (2007) ehm180v1. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. van der Linden, P. Bergman, and L. Hadjinikolaou The Topography of Aortic Atherosclerosis Enhances Its Precision as a Predictor of Stroke Ann. Thorac. Surg., June 1, 2007; 83(6): 2087 - 2092. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Agmon, B. K. Khandheria, I. Meissner, T. M. Petterson, W. M. O'Fallon, D. O. Wiebers, T. J. H. Christianson, J. P. McConnell, J. P. Whisnant, J. B. Seward, et al. C-Reactive Protein and Atherosclerosis of the Thoracic Aorta: A Population-Based Transesophageal Echocardiographic Study Arch Intern Med, September 13, 2004; 164(16): 1781 - 1787. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. Meissner, B. K. Khandheria, S. G. Sheps, G. L. Schwartz, D. O. Wiebers, J. P. Whisnant, J. L. Covalt, T. M. Petterson, T. J.H. Christianson, and Y. Agmon Atherosclerosis of the aorta: Risk factor, risk marker, or innocent bystander?: A prospective population-based transesophageal echocardiography study J. Am. Coll. Cardiol., September 1, 2004; 44(5): 1018 - 1024. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. C. Pasternak, M. H. Criqui, E. J. Benjamin, F. G. R. Fowkes, E. M. Isselbacher, P. A. McCullough, P. A. Wolf, and Z.-J. Zheng Atherosclerotic Vascular Disease Conference: Writing Group I: Epidemiology Circulation, June 1, 2004; 109(21): 2605 - 2612. [Full Text] [PDF]
|
|
|
|
|
|
Y. Agmon, B. K. Khandheria, I. Meissner, G. L. Schwartz, J. D. Sicks, A. J. Fought, W. M. O'Fallon, D. O. Wiebers, and A. J. Tajik Is aortic dilatation an atherosclerosis-related process?: Clinical, laboratory, and transesophageal echocardiographiccorrelates of thoracic aortic dimensions in the populationwith implications for thoracic aortic aneurysm formation J. Am. Coll. Cardiol., September 17, 2003; 42(6): 1076 - 1083. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Agmon, B. K. Khandheria, I. Meissner, T. M. Petterson, W. M. O'Fallon, T. J. H. Christianson, D. O. Wiebers, T. F. Smith, J. M. Steckelberg, and A. J. Tajik Lack of association between Chlamydia pneumoniae seropositivity and aortic atherosclerotic plaques: A Population-Based transesophageal echocardiographic study J. Am. Coll. Cardiol., May 7, 2003; 41(9): 1482 - 1487. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. S.V. Elkind, R. Sciacca, B. Boden-Albala, S. Homma, and M. R. Di Tullio Leukocyte Count Is Associated With Aortic Arch Plaque Thickness Stroke, November 1, 2002; 33(11): 2587 - 2592. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Fasseas, E. S. Brilakis, B. Leybishkis, M. Cohen, A. B. Sokil, N. Wolf, R. L. Dorn, A. Roberts, and W. VanDecker Association of Carotid Artery Intima-Media Thickness with Complex Aortic Atherosclerosis in Patients with Recent Stroke Angiology, March 1, 2002; 53(2): 185 - 189. [Abstract] [PDF]
|
|
|
|
|
|
Y. Agmon, B. K. Khandheria, I. Meissner, J. D. Sicks, W. M. O'Fallon, D. O. Wiebers, J. P. Whisnant, J. B. Seward, and A. J. Tajik Aortic valve sclerosis and aortic atherosclerosis: different manifestations of the same disease?: Insights from a population-based study J. Am. Coll. Cardiol., September 1, 2001; 38(3): 827 - 834. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||