(Circulation. 2000;101:948.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Long-Term Follow-Up of Patients With Mild Coronary Artery Disease and Endothelial Dysfunction
From the Center for Coronary Physiology and Imaging, Division of Cardiovascular Diseases, and Department of Internal Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minn.
Correspondence to Amir Lerman, MD, Mayo Clinic, 200 First St SW, Rochester, MN 55905. E-mail lerman.amir{at}mayo.edu
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Abstract |
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Background—Coronary endothelial dysfunction is characterized by vasoconstrictive response to the endothelium-dependent vasodilator acetylcholine. Although endothelial dysfunction is considered an early phase of coronary atherosclerosis, there is a paucity of information regarding the outcome of these patients. Thus, this study was designed to evaluate the outcome of patients with mild coronary artery disease on the basis of their endothelial function.
Methods and Results—Follow-up was obtained in 157 patients with mildly diseased coronary arteries who had undergone coronary vascular reactivity evaluation by graded administration of intracoronary acetylcholine, adenosine, and nitroglycerin and intracoronary ultrasound at the time of diagnostic study. Patients were divided on the basis of their response to acetylcholine into 3 groups: group 1 (n=83), patients with normal endothelial function; group 2 (n=32), patients with mild endothelial dysfunction; and group 3 (n=42), patients with severe endothelial dysfunction. Over an average 28-month follow-up (range, 11 to 52 months), none of the patients from group 1 or 2 had cardiac events. However, 6 (14%) with severe endothelial dysfunction had 10 cardiac events (P<0.05 versus groups 1 and 2). Cardiac events included myocardial infarction, percutaneous or surgical coronary revascularization, and/or cardiac death.
Conclusions—Severe endothelial dysfunction in the absence of obstructive coronary artery disease is associated with increased cardiac events. This study supports the concept that coronary endothelial dysfunction may play a role in the progression of coronary atherosclerosis.
Key Words: atherosclerosis • acetylcholine • endothelium • coronary disease
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Introduction |
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Coronary heart disease is the leading cause of morbidity and mortality in most industrialized societies.1 Cardiac risk factors were shown to cause impairment of endothelial vasodilator function of both the epicardial conductance vessels and coronary resistance arteries,2 3 4 5 6 which is considered an important phase in atherogenesis.7 8 9 We and others10 11 have demonstrated that coronary endothelial dysfunction in humans may be associated with myocardial ischemia. Furthermore, modifications of cardiovascular risk factors that contribute to endothelial dysfunction improve patient outcomes disproportionately to the improvement in coronary atherosclerosis,12 thus implying that these beneficial effects may be mediated in part through improvement in endothelial function. Despite the general concept that endothelial dysfunction may be the earliest stage of coronary atherosclerosis, follow-up study in patients with endothelial dysfunction is unavailable. Thus, the purpose of this study was to evaluate the outcome of patients with mildly diseased coronary arteries and endothelial dysfunction.
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Methods |
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Study Population
Between January 1993 and June 1997, 168 consecutive patients who had been referred for coronary atherosclerosis were studied prospectively. Patients were included in this study if they had angiographically coronary artery lesions <40% lumen diameter stenosis without evidence of coronary spasm. Exclusion criteria included history of myocardial infarction, percutaneous coronary revascularization, CABG, unstable angina pectoris, history of variant angina, uncontrolled hypertension, peripheral vascular disease, ejection fraction
50%, and
valvular heart disease, and/or significant endocrine, hepatic,
renal, or inflammatory disease. Long-acting nitrates or calcium channel
blocking agents were withheld for 36 to 48 hours before study to allow
assessment of baseline coronary physiology. Patient
demographics and laboratory data, including fasting lipid profile and
serum glucose, were obtained at baseline. The Mayo Clinic Institution
Review Board approved the study, and informed consent was obtained from
all patients.
Study Protocol
Diagnostic coronary angiography and
determination of endothelium-dependent and
endothelium-independent flow reserve were performed as
previously described.10 A Doppler guide wire (0.014-in
diameter, FloWire, Endosonics Incorporated) within a 2.2F
coronary infusion catheter (Ultrafuse, SciMed Life System) was
advanced and positioned in the middle portion of the left anterior
descending coronary artery (LAD). Intracoronary bolus
injections of incremental doses (18 to 36 µg) of adenosine
(Fujisawa), an endothelium-independent vasodilator
primarily of the microcirculation,13 were administered
into the guiding catheter until maximal hyperemia was
achieved.
Assessment of the endothelium-dependent coronary flow reserve was performed by selective infusion of acetylcholine into the LAD. Acetylcholine (Iolab Pharmaceuticals) 0.182, 1.82, and 18.2 µg/mL (10-6, 10-5, and 10-4 mol/L, respectively) was infused at 1 mL/min for 3 minutes.10 14 Hemodynamic data (heart rate and mean arterial pressure), Doppler measurements, and coronary angiography were obtained after each infusion. The infusion was terminated when the largest molar concentration of acetylcholine (10-4 mol/L) was reached. Nitroglycerin (200 µg, Abbott Laboratories) was then injected as an intracoronary bolus.15
Quantitative Coronary Angiography
Artery diameter was analyzed from cine films with use of
a modification of a previously described technique from this
institution.10 16 Measurements were made in the segment
5 mm distal to the tip of the Doppler wire by 2 independent
investigators.
Intravascular Ultrasound Examination
Intravascular ultrasound (IVUS) systems were used in this
study to assess changes in early atherosclerosis in 86
of the patients studied. Details of these systems have been described
elsewhere.17 18 After optimization of the ultrasound image
and continuous real-time images were recorded, 4 to 5 LAD segments
were identified.
Assessment of Coronary Blood Flow
Doppler flow velocity spectra were analyzed online
to determine the time-averaged peak velocity. Volumetric
coronary blood flow (CBF) was determined from the following
relation: CBF=cross-sectional areaxaverage peak
velocityx0.5.19 Endothelium-dependent
coronary flow reserve was calculated as percent change in CBF
in response to acetylcholine as previously described. The
endothelium-independent coronary flow reserve
ratio was calculated by dividing the average peak velocity after
adenosine injection by the baseline average peak
velocity.10
Ultrasound Image Analysis
An offline computer-interactive analysis system was used
to digitize the IVUS video images. Measurements of lumen, plaque plus
media, and vessel areas were made at each specific segments of the
artery as previously described.16 17 18 Percent area
stenosis was calculated as the ratio of plaque plus media area
to vessel area. Morphological plaque features were classified as
previously described.16 17 18 These measurements were done
without knowledge of the results of endothelial
function.
Definition of Endothelial Function and
Coronary Flow Reserve
A normal coronary endothelium-dependent
function was defined as an increase in CBF of >50%, ie, a ratio of
>1.5 in response to acetylcholine, calculated by dividing the CBF
after 10-4 mol/L acetylcholine (18.2 µg/mL) by
the baseline. Endothelial dysfunction was classified as
mild (a percent change in CBF between 0% to 50%) or severe (percent
change in CBF <0%). The decision to divide patients into these groups
was based on the association between the changes in CBF in response to
acetylcholine and perfusion defects we previously
reported.10 Moreover, endothelial
dysfunction was also evaluated according the epicardial
coronary artery diameter response to acetylcholine [%
CAD
(Ach)]. Patients were divided into 3 groups: group 1, normal
endothelial function [%CAD (Ach) >20%, n=20];
group 2, mild endothelial dysfunction [%CAD (Ach)
20% to -20%, n=89]; and group 3, severe endothelial
dysfunction [%CAD (Ach) <-20%, n=48], and their outcome at
follow-up was evaluated. Impaired coronary
endothelium-independent function was defined as a ratio
of flow velocity to adenosine of 2.5.20
Follow-Up
All patients received questionnaires concerning the occurrence
of cardiac events (myocardial infarction, heart failure, and surgical
or percutaneous coronary
revascularization). For those who were not followed
up at our institution, attempts were made to contact patients or their
relatives. In addition, hospital records were reviewed. Cardiac
events were defined as myocardial infarction,
percutaneous or surgical
revascularization, and cardiac death. All cardiac
events were confirmed by a review of hospital records.
Interobserver and Intraobserver Variabilities
Two ultrasound sites from 10% of the patients studied were
randomly selected and measured by the same observer at 2 separate
occasions and by a second observer. These measurements were then used
to evaluate intraobserver and interobserver variabilities at the 2
separate occasions and the second observer. From 20% of the patients,
2 coronary flow reserve measurements also were selected to
assess intraobserver variability. These were expressed as linear
regression between the 2 observations and as percent error, derived as
the absolute difference between observations.
Statistical Analysis
Values are expressed as mean±SE. Comparisons of the baseline
cardiovascular risk variables between the 3 groups
were done with Pearson’s 
2 test. Comparisons
of left ventricular ejection fraction, fasting serum
lipids, and blood glucose between the study groups were done with 1-way
ANOVA. Logistic regression analysis was performed to determine
independent predictors of cardiac events. Statistical significance was
accepted when P<0.05.
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Results |
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We studied 168 patients. Eleven patients were excluded because follow-up could not be obtained (4 with normal endothelial function and 4 with mild and 3 with severe endothelial dysfunction). Follow-up was obtained in 157 (93%) of the initial patients studied, and they constituted the study group. There were 104 women (67%) and 53 men (33%) .The mean age of the study population was 52 years (range, 17 to 78 years). Most patients (92%) had
1 risk factor for coronary artery
disease. Patients were divided into 3 groups according to their response to acetylcholine. Group 1 consisted of 83 patients who had normal endothelium-dependent coronary flow reserve; group 2 consisted of 32 patients with mildly abnormal endothelium-dependent coronary flow reserve; group 3 consisted of 42 patients with severely abnormal endothelium-dependent coronary flow reserve.
Patient Characteristics
The clinical characteristics of the patients according to their
response to acetylcholine are shown in Table 1
. Distribution of sex, age, and
other cardiovascular risk factors was similar between
the study groups. Furthermore, there were no significant differences
between the 3 groups in frequency of use of cardiac medications,
including ß-blockers, ACE inhibitors, or lipid-lowering
agents.
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Changes in CBF
The acetylcholine-induced percent changes in CBF in the 3 groups
are shown in Figure 1. There were
significant differences between group 3 (-38.2±4.3%) compared with
groups 1 and 2 (174.5±18.8% and 24.8±2.8% in groups 1 and 2,
respectively). There were also significant differences between groups 1
and 2. The acetylcholine-induced percent changes in coronary
artery diameter also revealed significant differences between the 3
groups (5.7±2.8%, -13.7±2.8%, and -35.5±3.7% in groups 1
through 3). The epicardial vasoconstrictor response to acetylcholine in
these patients was diffuse rather than focal without complete
epicardial constriction. Noninvasive functional studies, including
treadmill exercise test, exercise thallium, or exercise echoes, were
performed in 78% of the patients studied. There were no significant
differences in the prevalence of positive noninvasive functional
studies between study groups. The coronary flow reserve to
adenosine was significantly lower in group 3 (2.6±0.1)
compared with groups 1 and 2. In addition, there were no significant
differences in systemic hemodynamic
parameters (mean arterial pressure and heart
rate) between the 3 study groups.
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P<0.05 vs groups 1 and
2.
IVUS Data
Thirteen segments with technical problems in their video images
were excluded from analysis. Thus, 295 segments were
analyzed (Table 2). There were no
significant differences between study groups in vessel, lumen, and
plaque plus media areas in absolute terms or when indexed to body
surface area or maximal plaque thickness. Furthermore, there were no
significant differences between groups in plaque morphology and no
significant correlation between coronary artery disease
assessed with IVUS and endothelium-dependent or
-independent coronary flow reserve abnormalities assessed with
acetylcholine and adenosine.
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The interobserver variability was 0.4±2.4% and 1.06±4.3% and the intraobserver variability was 0.8±1.9% and 1.5±3.3% for the coronary diameter and area measurements, respectively. The intraobserver variability for flow velocity measurement was 2.0±2.4%.
Follow-Up
Patients were followed up for a mean of 28 months (range, 11 to 52
months). During follow-up, none of the patients in group 1 or 2 had
cardiac events. However, in patients with severe impairment of
endothelium-dependent coronary flow reserve
(group 3), 6 patients (14%) developed cardiac events (Table 3 and Figure 1
). This 14%
incidence of cardiac events in group 3 represents the number of
patients affected or the incidence of the most severe cardiac event in
the group rather than the total number of events (n=10). Further
analysis of the incidence of cardiac events according to the
percent change in coronary artery diameter in response to
acetylcholine was made. Patients were divided into 3 groups: group 1,
normal endothelial function (n=20); group 2, mild
endothelial dysfunction (n=89); and group 3, severe
endothelial dysfunction (n=48). This division produced
results identical to the original classification in that none of the
patients in groups 1 and 2 had cardiac events and all 6 patients who
had cardiac events were in group 3 (13%). The mean age, sex,
cardiovascular risk factors, and left
ventricular ejection fraction of these 6 patients were
comparable to the various groups studied. Noninvasive functional
studies were performed in 4 patients at the time of initial evaluation
and were abnormal in 2 patients. The prevalence of use of ACE
inhibitors and lipid-lowering agents was also comparable
between groups. Furthermore, although the percent change in CBF to
acetylcholine was even more severely reduced (-47±14.0% in this
subgroup), endothelium-independent coronary
flow reserve in these 6 patients was not significantly different from
that in patients with normal endothelial function or
mild endothelial dysfunction (2.8±0.5). Cardiac events
included myocardial infarction (Figure 2)
and percutaneous coronary
revascularization (Figure 3). CABG was performed in 2 patients
because of the development of multivessel obstructive coronary
artery disease. Of these 6 patients, 2 subsequently developed
congestive heart failure caused by systolic dysfunction and 2
died of cardiac causes, 1 secondary to congestive heart failure and the
other a sudden death. Compared with groups 1 and 2,
endothelial dysfunction was the only predictor of
increased cardiac events.
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Discussion |
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The present study demonstrates for the first time that patients with nonobstructive coronary artery disease and severe endothelial dysfunction are at increased risk for cardiac events.
Several studies have demonstrated that treatment of cardiovascular risk factors known to lead to endothelial dysfunction is associated with a decrease in cardiac events in both primary and secondary prevention studies,21 22 underscoring the concept that the reduction in cardiac events in this patient population may be at least in part secondary to improvement in coronary endothelial function. The mechanism by which endothelial dysfunction leads to cardiac events may be multifactorial. One possible mechanism is myocardial ischemia secondary to endothelial dysfunction even in the absence of obstructive coronary artery disease.10 11 Indeed, we have recently demonstrated that the reduction in CBF response to acetylcholine resulting from coronary endothelial dysfunction was associated with myocardial perfusion defects. However, the lack of any correlation between the frequency of abnormal noninvasive tests among the 3 groups may suggest that endothelial dysfunction in the absence of obstructive coronary artery disease may not cause myocardial ischemia that can be detected noninvasively. Another possible mechanism by which coronary endothelial dysfunction may contribute to cardiac events is through acceleration of coronary atherosclerosis, as evidenced by the development of obstructive coronary artery disease. This is also supported by the observation in cardiac transplant patients that coronary endothelial dysfunction precedes the development of coronary atherosclerosis.23 It may be hypothesized that endothelial dysfunction represents the stage of rapid progression of atherosclerosis, which may be secondary to the loss of various protective physiological roles of endothelial cells. The abnormal response to the endothelium-dependent vasodilator acetylcholine may represent a reduction in nitric oxide (NO) bioavailability.9 24 25 We have previously reported that in this patient population the second messenger of NO is reduced in the coronary circulation,14 implying a decrease in NO activity. NO plays a pivotal role in antiatherogenesis; in addition to being a vasodilator, it inhibits platelet adherence and aggregation, smooth muscle proliferation, and endothelial cell–leukocyte interaction, all of which are key events in atherogenesis.26 Pathophysiological states associated with a decrease in NO bioavailability and endothelial adhesion molecules for monocytes are upregulated.27 This could enhance local inflammation of the vessel wall, which may play a critical role in plaque rupture.28 This hypothesis is supported by the observation that L-arginine supplementation, the precursor of NO, improves endothelium-dependent vasorelaxation29 and attenuates the progression of atherosclerosis in an experimental rabbit hypercholesterolemia model.26 Indeed, medical intervention that increases NO bioavailability was shown to improve patient outcome.21 22 The possibility that experimenting on the LAD caused accelerated iatrogenic atherosclerosis can be ruled out because all patients underwent similar procedures; moreover, cardiac events were not restricted to the LAD territory.
IVUS parameters in our study, including plaque plus media area, maximal plaque thickness, and plaque morphology, were not helpful in predicting cardiac events. This finding is consistent with previous studies demonstrating the dissociation between the vasoreactive response to acetylcholine and coronary atherosclerosis as assessed with IVUS.16 The lack of significant differences in cardiovascular risk factors between the various groups may be related to the duration of risk factors between the various groups in that patients with severe endothelial dysfunction possibly had longer exposure to these risk factors. Another potential explanation may be the presence of significant differences in other unmeasured cardiovascular risk factors such as oxidative stress and asymmetric dimethylarginine that have recently been associated with endothelial dysfunction.30
Study Limitations
One of the main limitations of this study is the invasive
method of coronary angiography, which is a potential risk for
the patient and requires special expertise to perform. Thus, this
method cannot be used in asymptomatic patients as a
screening procedure to define their risk for future
cardiovascular events. Future studies may be needed to
develop a more clinically applicable methodology for wider clinical
use.
Clinical Implications
This study extends previous observations that early
coronary atherosclerosis is associated with
endothelial dysfunction and demonstrates for the first
time that severe endothelial dysfunction in patients
with nonobstructive coronary artery disease is associated with
increased cardiac events.
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Acknowledgments |
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This study was supported by the Miami Heart Research Institute, Rappaport Vascular Biology Program, and Mayo Foundation.
Received June 25, 1999; revision received September 14, 1999; accepted September 29, 1999.
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E. Raichlin, A. Prasad, W. K. Kremers, B. S. Edwards, C. S. Rihal, A. Lerman, and S. S. Kushwaha Sirolimus as primary immunosuppression is associated with improved coronary vasomotor function compared with calcineurin inhibitors in stable cardiac transplant recipients Eur. Heart J., June 1, 2009; 30(11): 1356 - 1363. [Abstract] [Full Text] [PDF]
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S. L. Prior, D. R. Gable, J. A. Cooper, S. C. Bain, S. J. Hurel, S. E. Humphries, and J. W. Stephens Association between the adiponectin promoter rs266729 gene variant and oxidative stress in patients with diabetes mellitus Eur. Heart J., May 2, 2009; 30(10): 1263 - 1269. [Abstract] [Full Text] [PDF]
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W A Jaber, E H Yang, R A Nishimura, P Sorajja, C S Rihal, A Elesber, E Eeckhout, and A Lerman Immediate improvement in coronary flow reserve after alcohol septal ablation in patients with hypertrophic obstructive cardiomyopathy Heart, April 1, 2009; 95(7): 564 - 569. [Abstract] [Full Text] [PDF]
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M. Vona, G.M. Codeluppi, T. Iannino, E. Ferrari, J. Bogousslavsky, and L.K. von Segesser Effects of Different Types of Exercise Training Followed by Detraining on Endothelium-Dependent Dilation in Patients With Recent Myocardial Infarction Circulation, March 31, 2009; 119(12): 1601 - 1608. [Abstract] [Full Text] [PDF]
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R. Corti, A. J. Flammer, N. K. Hollenberg, and T. F. Luscher Cocoa and Cardiovascular Health Circulation, March 17, 2009; 119(10): 1433 - 1441. [Abstract] [Full Text] [PDF]
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J. P.J. Halcox, A. E. Donald, E. Ellins, D. R. Witte, M. J. Shipley, E. J. Brunner, M. G. Marmot, and J. E. Deanfield Endothelial Function Predicts Progression of Carotid Intima-Media Thickness Circulation, February 24, 2009; 119(7): 1005 - 1012. [Abstract] [Full Text] [PDF]
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H. R. Schelbert Coronary circulatory function abnormalities in insulin resistance insights from positron emission tomography. J. Am. Coll. Cardiol., February 3, 2009; 53(5 Suppl): S3 - S8. [Abstract] [Full Text] [PDF]
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M. Gossl, U. I. Modder, E. J. Atkinson, A. Lerman, and S. Khosla Osteocalcin Expression by Circulating Endothelial Progenitor Cells in Patients With Coronary Atherosclerosis J. Am. Coll. Cardiol., October 14, 2008; 52(16): 1314 - 1325. [Abstract] [Full Text] [PDF]
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S. Westphal, C. Abletshauser, and C. Luley Fluvastatin Treatment and Withdrawal: Effects on Endothelial Function Angiology, October 1, 2008; 59(5): 613 - 618. [Abstract] [PDF]
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G. Maiolino, M. Cesari, D. Sticchi, M. Zanchetta, L. Pedon, K. Antezza, A. C. Pessina, and G. P. Rossi Plasma Adiponectin for Prediction of Cardiovascular Events and Mortality in High-Risk Patients J. Clin. Endocrinol. Metab., September 1, 2008; 93(9): 3333 - 3340. [Abstract] [Full Text] [PDF]
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B. Fernhall and S. Agiovlasitis Arterial function in youth: window into cardiovascular risk J Appl Physiol, July 1, 2008; 105(1): 325 - 333. [Abstract] [Full Text] [PDF]
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K. Turkmen, H. Oflaz, B. Uslu, A. O. Cimen, A. Elitok, E. Kasikcioglu, S. Alisir, F. Tufan, S. Namli, M. Uysal, et al. Coronary Flow Velocity Reserve and Carotid Intima Media Thickness in Patients with Autosomal Dominant Polycystic Kidney Disease: From Impaired Tubules to Impaired Carotid and Coronary Arteries Clin. J. Am. Soc. Nephrol., July 1, 2008; 3(4): 986 - 991. [Abstract] [Full Text] [PDF]
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S. S. Shankar and H. O. Steinberg Weight Loss and Vascular Function: The Good and the Unknown Hypertension, July 1, 2008; 52(1): 57 - 58. [Full Text] [PDF]
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S. H. Han, J. H. Bae, D. R. Holmes Jr, R. J. Lennon, E. Eeckhout, G. W. Barsness, C. S. Rihal, and A. Lerman Sex differences in atheroma burden and endothelial function in patients with early coronary atherosclerosis Eur. Heart J., June 1, 2008; 29(11): 1359 - 1369. [Abstract] [Full Text] [PDF]
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C. Pizzi, L. Manzoli, S. Mancini, and G. M. Costa Analysis of potential predictors of depression among coronary heart disease risk factors including heart rate variability, markers of inflammation, and endothelial function Eur. Heart J., May 1, 2008; 29(9): 1110 - 1117. [Abstract] [Full Text] [PDF]
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E. Galluccio, P. Piatti, L. Citterio, P. C. G. Lucotti, E. Setola, L. Cassina, M. Oldani, I. Zavaroni, E. Bosi, A. Colombo, et al. Hyperinsulinemia and impaired leptin-adiponectin ratio associate with endothelial nitric oxide synthase polymorphisms in subjects with in-stent restenosis Am J Physiol Endocrinol Metab, May 1, 2008; 294(5): E978 - E986. [Abstract] [Full Text] [PDF]
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A. J. Flammer, I. Sudano, F. Hermann, S. Gay, A. Forster, M. Neidhart, P. Kunzler, F. Enseleit, D. Periat, M. Hermann, et al. Angiotensin-Converting Enzyme Inhibition Improves Vascular Function in Rheumatoid Arthritis Circulation, April 29, 2008; 117(17): 2262 - 2269. [Abstract] [Full Text] [PDF]
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M. Terashima, P. K. Nguyen, G. D. Rubin, C. Iribarren, B. K. Courtney, A. S. Go, S. P. Fortmann, and M. V. McConnell Impaired coronary vasodilation by magnetic resonance angiography is associated with advanced coronary artery calcification. J. Am. Coll. Cardiol. Img., March 1, 2008; 1(2): 167 - 173. [Abstract] [Full Text] [PDF]
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M. I. Yilmaz, M. Saglam, J. J. Carrero, A. R. Qureshi, K. Caglar, T. Eyileten, A. Sonmez, E. Cakir, M. Yenicesu, B. Lindholm, et al. Serum visfatin concentration and endothelial dysfunction in chronic kidney disease Nephrol. Dial. Transplant., March 1, 2008; 23(3): 959 - 965. [Abstract] [Full Text] [PDF]
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A. Imamura, R. Takahashi, R. Murakami, H. Kataoka, X. W. Cheng, Y. Numaguchi, T. Murohara, and K. Okumura The effects of endothelial nitric oxide synthase gene polymorphisms on endothelial function and metabolic risk factors in healthy subjects: the significance of plasma adiponectin levels Eur. J. Endocrinol., February 1, 2008; 158(2): 189 - 195. [Abstract] [Full Text] [PDF]
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F. Rigo, R. Sicari, S. Gherardi, A. Djordjevic-Dikic, L. Cortigiani, and E. Picano The additive prognostic value of wall motion abnormalities and coronary flow reserve during dipyridamole stress echo Eur. Heart J., January 1, 2008; 29(1): 79 - 88. [Abstract] [Full Text] [PDF]
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E. L. Schiffrin Oxidative Stress, Nitric Oxide Synthase, and Superoxide Dismutase: A Matter of Imbalance Underlies Endothelial Dysfunction in the Human Coronary Circulation Hypertension, January 1, 2008; 51(1): 31 - 32. [Full Text] [PDF]
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S. Lavi, E. H. Yang, A. Prasad, V. Mathew, G. W. Barsness, C. S. Rihal, L. O. Lerman, and A. Lerman The Interaction Between Coronary Endothelial Dysfunction, Local Oxidative Stress, and Endogenous Nitric Oxide in Humans Hypertension, January 1, 2008; 51(1): 127 - 133. [Abstract] [Full Text] [PDF]
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M. I. Worthley, R. S. Kanani, Y.-H. Sun, Y. Sun, D. M. Goodhart, M. J. Curtis, and T. J. Anderson Effects of tetrahydrobiopterin on coronary vascular reactivity in atherosclerotic human coronary arteries Cardiovasc Res, December 1, 2007; 76(3): 539 - 546. [Abstract] [Full Text] [PDF]
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E. R. Duncan, S. J. Walker, V. A. Ezzat, S. B. Wheatcroft, J.-M. Li, A. M. Shah, and M. T. Kearney Accelerated endothelial dysfunction in mild prediabetic insulin resistance: the early role of reactive oxygen species Am J Physiol Endocrinol Metab, November 1, 2007; 293(5): E1311 - E1319. [Abstract] [Full Text] [PDF]
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L. Cortigiani, F. Rigo, S. Gherardi, R. Sicari, M. Galderisi, F. Bovenzi, and E. Picano Additional Prognostic Value of Coronary Flow Reserve in Diabetic and Nondiabetic Patients With Negative Dipyridamole Stress Echocardiography by Wall Motion Criteria J. Am. Coll. Cardiol., October 2, 2007; 50(14): 1354 - 1361. [Abstract] [Full Text] [PDF]
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A. de Bree, L. A van Mierlo, and R. Draijer Folic acid improves vascular reactivity in humans: a meta-analysis of randomized controlled trials Am. J. Clinical Nutrition, September 1, 2007; 86(3): 610 - 617. [Abstract] [Full Text] [PDF]
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K. M. Maki-Petaja, A. D. Booth, F. C. Hall, S. M.L. Wallace, J. Brown, C. M. McEniery, and I. B. Wilkinson Ezetimibe and Simvastatin Reduce Inflammation, Disease Activity, and Aortic Stiffness and Improve Endothelial Function in Rheumatoid Arthritis J. Am. Coll. Cardiol., August 28, 2007; 50(9): 852 - 858. [Abstract] [Full Text] [PDF]
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S. D. Robinson, C. A. Ludlam, N. A. Boon, and D. E. Newby Endothelial Fibrinolytic Capacity Predicts Future Adverse Cardiovascular Events in Patients With Coronary Heart Disease Arterioscler Thromb Vasc Biol, July 1, 2007; 27(7): 1651 - 1656. [Abstract] [Full Text] [PDF]
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P. H. McNulty, M. A. Tulli, B. J. Robertson, V. Lendel, L. A. Harach, S. Scott, and J. P. Boehmer Effect of simulated postprandial hyperglycemia on coronary blood flow in cardiac transplant recipients Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H103 - H108. [Abstract] [Full Text] [PDF]
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E. Grad, M. Golomb, I. Mor-Yosef, N. Koroukhov, C. Lotan, E. R. Edelman, and H. D. Danenberg Transgenic expression of human C-reactive protein suppresses endothelial nitric oxide synthase expression and bioactivity after vascular injury Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H489 - H495. [Abstract] [Full Text] [PDF]
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N. R. Ferreri Estrogen-TNF interactions and vascular inflammation Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H2566 - H2569. [Full Text] [PDF]
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S. Lavi, J. P. McConnell, C. S. Rihal, A. Prasad, V. Mathew, L. O. Lerman, and A. Lerman Local Production of Lipoprotein-Associated Phospholipase A2 and Lysophosphatidylcholine in the Coronary Circulation: Association With Early Coronary Atherosclerosis and Endothelial Dysfunction in Humans Circulation, May 29, 2007; 115(21): 2715 - 2721. [Abstract] [Full Text] [PDF]
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S. Lavi, A. Prasad, E. H. Yang, V. Mathew, R. D. Simari, C. S. Rihal, L. O. Lerman, and A. Lerman Smoking Is Associated With Epicardial Coronary Endothelial Dysfunction and Elevated White Blood Cell Count in Patients With Chest Pain and Early Coronary Artery Disease Circulation, May 22, 2007; 115(20): 2621 - 2627. [Abstract] [Full Text] [PDF]
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T. J. Anderson Prognostic Significance of Brachial Flow-Mediated Vasodilation Circulation, May 8, 2007; 115(18): 2373 - 2375. [Full Text] [PDF]
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M. V. Jimenez, R. M. Estepa, R. M. Camacho, R. C. Estrada, F. G. Luna, and F. B. Guitarte Endothelial dysfunction is related to insulin resistance and inflammatory biomarker levels in obese prepubertal children Eur. J. Endocrinol., April 1, 2007; 156(4): 497 - 502. [Abstract] [Full Text] [PDF]
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A. Lerman, D. R. Holmes, J. Herrmann, and B. J. Gersh Microcirculatory dysfunction in ST-elevation myocardial infarction: cause, consequence, or both? Eur. Heart J., April 1, 2007; 28(7): 788 - 797. [Abstract] [Full Text] [PDF]
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U. Landmesser, S. Spiekermann, C. Preuss, S. Sorrentino, D. Fischer, C. Manes, M. Mueller, and H. Drexler Angiotensin II Induces Endothelial Xanthine Oxidase Activation: Role for Endothelial Dysfunction in Patients With Coronary Disease Arterioscler Thromb Vasc Biol, April 1, 2007; 27(4): 943 - 948. [Abstract] [Full Text] [PDF]
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A. Barac, U. Campia, and J. A. Panza Methods for Evaluating Endothelial Function in Humans Hypertension, April 1, 2007; 49(4): 748 - 760. [Full Text] [PDF]
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B. Belay, P. F. Belamarich, and C. Tom-Revzon The Use of Statins in Pediatrics: Knowledge Base, Limitations, and Future Directions Pediatrics, February 1, 2007; 119(2): 370 - 380. [Abstract] [Full Text] [PDF]
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K. Morita, T. Tsukamoto, M. Naya, K. Noriyasu, M. Inubushi, T. Shiga, C. Katoh, Y. Kuge, H. Tsutsui, and N. Tamaki Smoking Cessation Normalizes Coronary Endothelial Vasomotor Response Assessed with 15O-Water and PET in Healthy Young Smokers J. Nucl. Med., December 1, 2006; 47(12): 1914 - 1920. [Abstract] [Full Text] [PDF]
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K W Lee, A D Blann, K Jolly, G Y H Lip, and on behalf of the BRUM Investigators Plasma haemostatic markers, endothelial function and ambulatory blood pressure changes with home versus hospital cardiac rehabilitation: the Birmingham Rehabilitation Uptake Maximisation Study Heart, December 1, 2006; 92(12): 1732 - 1738. [Abstract] [Full Text] [PDF]
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T. Imanishi, K. Kobayashi, A. Kuroi, S. Mochizuki, M. Goto, K. Yoshida, and T. Akasaka Effects of Angiotensin II on NO Bioavailability Evaluated Using a Catheter-Type NO Sensor Hypertension, December 1, 2006; 48(6): 1058 - 1065. [Abstract] [Full Text] [PDF]
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S. Waxman, F. Ishibashi, and J. E. Muller Detection and Treatment of Vulnerable Plaques and Vulnerable Patients: Novel Approaches to Prevention of Coronary Events Circulation, November 28, 2006; 114(22): 2390 - 2411. [Full Text] [PDF]
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