Circulation. 2009;119:1-4
doi: 10.1161/CIRCULATIONAHA.108.191742
(Circulation. 2009;119:1-4.)
© 2009 American Heart Association, Inc.
Clinical Summaries
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Epicardial Border Zone Overexpression of Skeletal Muscle Sodium Channel SkM1 Normalizes Activation, Preserves Conduction, and Suppresses Ventricular Arrhythmia: An In Silico, In Vivo, In Vitro Study
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Reentry accounts for
85% of serious tachyarrhythmias complicating
ischemic heart disease. Current antiarrhythmic therapies attempt
to prevent or treat these arrhythmias by creating bidirectional
conduction block, prolonging refractoriness, or both in combination.
Implantable defibrillators have had great success in terminating
sustained ventricular tachyarrhythmias. However, these therapies
possess drawbacks ranging from incomplete arrhythmia suppression
to overt toxicity, including proarrhythmia, and the psychological
consequence of painful and sometimes inappropriate defibrillation.
A key contributor to many reentrant arrhythmias is slow conduction
within part of the reentrant circuit such as a myocardial infarct
epicardial border zone. We tested the hypothesis that preserving
or speeding conduction through the depolarized surviving myocytes
within the border zone would be antiarrhythmic. We focally introduced
an adenovirus expressing a skeletal muscle sodium channel (SkM1)
that mathematical modeling indicated would operate more efficiently
at depolarized membrane potentials than the native cardiac sodium
channel (SCN5A). SkM1 preserved conduction in the infarct border
zone by increasing the maximum upstroke velocity of action potentials,
reflected in situ by narrowing of wide or fragmented electrograms.
Electrophysiological testing demonstrated that SkM1 administration
significantly decreased the incidence of inducible ventricular
tachyarrhythmias. This proof-of-concept study provides evidence
that preserving or increasing conduction velocity in the infarct
border zone by focal delivery of a gene-based therapy such as
overexpression of SkM1 is antiarrhythmic. Unlike traditional
drugs, gene therapy interventions are not limited to targeting
the native channels expressed by cardiomyocytes but allow delivery
of foreign channels with more favorable biophysical properties.
See p
19.
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Activated Endocannabinoid System in Coronary Artery Disease and Antiinflammatory Effects of Cannabinoid 1 Receptor Blockade on Macrophages
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Obesity is associated with an increased risk of cardiovascular
morbidity and mortality. The recently discovered endocannabinoid
system contributes to the physiological regulation of energy
balance and food intake. In several clinical trials, modification
of this system by blockade of the cannabinoid 1 (CB1) receptor,
one of the receptors in endocannabinoid system, is reported
to reduce body weight and to improve multiple cardiometabolic
risk factors. Furthermore, a recent clinical study using coronary
intravascular ultrasound showed that a CB1 receptor antagonist
may favorably influence the progression of atherosclerosis.
In this study, we investigated the relationship between the
endocannabinoid system and atherogenesis. Results indicated
the presence and activation of the endocannabinoid system in
patients with coronary artery disease and human atherosclerosis.
We demonstrated an increased expression of CB1 receptor in coronary
atheromata, particularly in lesional macrophages. Our data further
indicate that the CB1 receptor antagonist exhibited antiinflammatory
effects on human macrophages. They suggest that CB1 receptor
blockade modulates the inflammatory state in atheromata through
its antiinflammatory effects on macrophages. Our study highlights
the potential role of the CB1 receptor in atherogenesis and
suggests that studies are needed to test the effect of CB1 receptor
blockade in vascular disease. See p
28.
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Multimarker Approach to Evaluate Correlates of Vascular Stiffness: The Framingham Heart Study
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Arterial stiffness increases with age and contributes significantly
to cardiovascular morbidity and mortality in the elderly. A
better understanding of the pathophysiology of vascular ageing
and the biochemical pathways involved might help in the development
of appropriate therapeutic strategies. In 2000 Framingham Offspring
Study participants, we related 7 biomarkers (C-reactive protein,
aldosterone-to-renin ratio, N-terminal proatrial natriuretic
peptide and B-type natriuretic peptide, plasminogen activator
inhibitor-1, fibrinogen, and homocysteine), representing inflammation,
neurohormonal activation, and hemostasis, to a panel of tonometric
measures, which reflect the different components of arterial
stiffness (ie, central pulse pressure [marker of pulsatile arterial
load], mean arterial pressure [marker of steady arterial load],
and carotid-femoral pulse-wave velocity [measure of aortic stiffness]).
In addition, we analyzed the 2 main components of central pulse
pressure: the forward pressure wave amplitude and augmented
pressure. We first related the multibiomarker panel as a whole
to each vascular function measure and then applied a backward
elimination procedure to identify a parsimonious set of markers
that displayed the strongest associations with each arterial
stiffness measure. We identified the aldosterone-to-renin ratio
as a key correlate of pan-arterial stiffness; it was associated
with all 5 tonometric measures (
P
0.002). In addition, plasminogen
activator inhibitor-1 displayed an association with central
vascular stiffness indices, and CRP showed an association with
wave reflection. These observations support the notion that
distinct biological pathways may selectively influence the different
components of vascular stiffness. See p
37.
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Body Mass Index and Vigorous Physical Activity and the Risk of Heart Failure Among Men
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In a prospective cohort of 21094 men (mean age, 53 years) without
known coronary heart disease at baseline in the Physicians’
Health Study, we examined the individual and combined effects
of body mass index (BMI; calculated as weight in kilograms divided
by height in meters squared, an anthropometric surrogate of
surplus body fat) and vigorous physical activity (defined as
exercise to the point of breaking a sweat) on the incidence
of heart failure (HF) from 1982 to 2007. During a mean follow-up
of 20.5 years, 1109 participants developed new-onset HF. After
adjustment for established risk factors for HF, every 1-kg/m
2 increase in BMI was associated with an 11% increase in the risk
of HF. Compared with lean participants (BMI <25 kg/m
2), overweight
or preobese participants (BMI, 25 to 29.9 kg/m
2) had a 49% and
obese participants (BMI
30 kg/m
2) had a 180% increase in HF
risk. Vigorous physical activity (at least 1 to 3 times a month)
conferred an 18% decrease in HF risk. Lean active men had the
lowest and obese inactive men had the highest (290% greater)
risk of HF. Our findings support the existence of causal links
between excess body weight and HF and sedentary lifestyle and
HF. Therefore, given the high prevalence of these 2 modifiable
risk factors of HF in the general population, together with
the substantial morbidity, mortality, and financial costs imposed
by HF, public health measures to curtail excess weight, to maintain
optimal weight, and to promote physical activity may limit the
scourge of HF. See p
44.
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Impact of Statin Therapy on Central Aortic Pressures and Hemodynamics: Principal Results of the Conduit Artery Function Evaluation-Lipid-Lowering Arm (CAFE-LLA) Study
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There has been much interest recently in the impact of cardiovascular
drugs on central aortic pressures because this impact may influence
clinical outcomes. The Conduit Artery Function Evaluation-Lipid-Lowering
Arm was a randomized placebo-controlled trial that prospectively
examined the impact of atorvastatin (10 mg once daily) on central
aortic pressures in hypertensive patients. Atorvastatin did
not influence central aortic pressures or hemodynamics in these
patients. Thus, the favorable effects of statins on cardiovascular
outcomes in hypertensive patients are via mechanisms that are
independent of important effects on large-artery function and
central pressures. For this reason, the benefits of statins
in hypertensive patients are unlikely to be replicated by blood
pressure lowering alone. See p
53.
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Tissue Doppler Imaging in the Estimation of Intracardiac Filling Pressure in Decompensated Patients With Advanced Systolic Heart Failure
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The ratio of early transmitral velocity to tissue Doppler mitral
annular early diastolic velocity (E/Ea) has been correlated
with pulmonary capillary wedge pressure in a wide variety of
cardiac conditions. However, the reliability of the mitral E/Ea
ratio for predicting pulmonary capillary wedge pressure in patients
admitted for advanced decompensated heart failure is unknown.
A total of 106 prospective consecutive patients with advanced
decompensated heart failure (ejection fraction
30%, New Your
Heart Association class III to IV symptoms) underwent simultaneous
echocardiographic and hemodynamic evaluation on admission and
after 48 hours of intensive medical therapy. We found the predictive
value of baseline mitral E/Ea ratio in estimating pulmonary
capillary wedge pressure to be less robust than previously reported,
which appears to be related to larger left ventricular dimensions,
more impaired cardiac output, and the presence of cardiac resynchronization
therapy. In addition, no reliable direct correlation between
baseline or changes in mitral E/Ea ratio and pulmonary capillary
wedge pressure was found. Taken together, our observations provide
an important refinement in the clinical interpretation of the
mitral E/Ea ratio as it applies to patient populations in which
important confounders such as alterations in myocardial structure,
severity of systolic dysfunction, or the presence of synchronized
pacing may pose challenges to the accurate prediction of left
ventricular filling pressures. See p
62.
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Randomized Study of the Crush Technique Versus Provisional Side-Branch Stenting in True Coronary Bifurcations: The CACTUS (Coronary Bifurcations: Application of the Crushing Technique Using Sirolimus-Eluting Stents) Study
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The optimal strategy in the percutaneous treatment of true coronary
bifurcation lesions has not been fully clarified. In this 350-patient
randomized multicenter trial, we compared the "crush" technique
of electively stenting both branches versus stenting only the
main branch, with provisional side-branch stenting if needed,
with sirolimus-eluting stents. Regardless of the technique used,
sirolimus-eluting stent implantation in true bifurcation lesions
results in good clinical and angiographic results with acceptable
midterm safety. The rates of angiographic restenosis, stent
thrombosis, and major adverse cardiovascular events at 6 months
were similar in both groups. Thus, in most bifurcations with
a significant stenosis in both branches, a provisional strategy
of stenting the main branch only is effective, with the need
to implant a second stent on the side branch occurring in approximately
one third of cases. However, if 2 stents are required and are
implanted with the crush technique, there appears to be no increased
risk of adverse events at 6 months. See p
71.
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Critical Role of Transcription Factor Cyclic AMP Response Element Modulator in β1-Adrenoceptor-Mediated Cardiac Dysfunction
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Heart failure, the common end stage of various cardiac diseases,
is defined as the inability of the heart to cover the body’s
blood supply and is associated with a poor prognosis. Supported
by clinical studies and studies on various animal models, chronic
stimulation of the β
1-adrenoceptor (β
1AR) by elevated
plasma catecholamines is regarded as a central pathogenetic
factor of human heart failure, leading to the progression of
the disease. Transcription factors of the cyclic AMP response
element binding protein/cyclic AMP response element modulator
(CREM) family mediate a cyclic AMP-dependent control of gene
expression and may therefore contribute to β
1AR-mediated
detrimental cardiac effects. In the present study, we show that
the inactivation of CREM protects from cardiomyocyte hypertrophy,
fibrosis, and left ventricular dysfunction in mice with heart-directed
expression of the β
1AR, along with the altered expression
of various myocardial proteins including the cardiac ryanodine
receptor, tropomyosin 1
, and cardiac
-actin. These findings
support the notion that the regulation of genes by CREM represents
an important mechanism of β
1AR-induced cardiac damage and
suggest the inhibition of CREM as a promising therapeutic option
for treating heart failure. See p
79.
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Myocardial Adeno-Associated Virus Serotype 6–βARKct Gene Therapy Improves Cardiac Function and Normalizes the Neurohormonal Axis in Chronic Heart Failure
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A number of previous reports have suggested that cardiac G protein-coupled
receptor kinase 2 inhibition, via the use of the peptide inhibitor
βARKct, could be a potential novel gene therapy for heart
failure (HF). However, these studies tested the effects of βARKct
expression in transgenic mice or with short-term gene transfer
experiments, and thus no clinically relevant conclusions about
the long-term efficacy and adverse effects can be drawn. The
present study investigated the long-term nature of βARKct
gene therapy in HF, providing proof of concept for its sustained
therapeutic effects in the context of a relevant experimental
model of HF. Taking advantage of adeno-associated virus-mediated
gene transfer, which enables efficient and sustained transgene
expression, cardiac βARKct gene delivery restored contractile
dysfunction and reversed cardiac remodeling of chronically failing
hearts. Mechanistically, this appears to be mediated by a normalization
of cardiac β-adrenergic receptor signaling as well as lowering
of gene expression associated with adverse left ventricular
remodeling. Moreover, long-term myocardial βARKct expression
leads to neurohormonal feedback decreasing the hyperactivity
of the sympathetic nervous system and renin-angiotensin-aldosterone
axis in HF. Finally, βARKct therapeutic properties were
superior even to metoprolol, a clinically established HF therapy
in humans, which was able only to prevent but not reverse (as
the βARKct did) progressive deterioration of contractile
function. Therefore, this study shows that βARKct gene
therapy can be of long-term therapeutic value in HF, although
testing of βARKct gene therapy in large animals and in
patients will ultimately define its place in the HF therapeutic
armamentarium. See p
89.
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Acute Doxorubicin Cardiotoxicity Is Associated With p53-Induced Inhibition of the Mammalian Target of Rapamycin Pathway
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Anthracyclines are widely used and highly successful anticancer
chemotherapeutic drugs. Unfortunately, these drugs also cause
acute cardiotoxicity, such as arrhythmia and transient depression
of left ventricular function, and higher cumulative doses are
associated with late-onset refractory cardiomyopathy and heart
failure. Because anthracyclines can interfere with many different
intracellular processes, it has proven difficult to determine
the exact mechanisms that give rise to acute versus chronic
cardiotoxicity. This study examined acute cardiotoxicity in
mice treated with the anthracycline doxorubicin. Treated mice
exhibited a marked decrease in cardiac function acutely that
was accompanied by a reduction in cardiac mass. Molecular analyses
suggested that doxorubicin treatment increased levels of the
tumor suppressor protein p53, which in turn inhibited the activity
of mammalian target of rapamycin (mTOR). Inhibition of mTOR
activity is predicted to decrease the translation of new proteins.
In support of this mechanism, genetically modified mice expressing
either dominant-interfering p53 or constitutively active mTOR
exhibited normal cardiac function and mass after doxorubicin
treatment. Interestingly, rescue of cardiac function and structure
during acute cardiotoxicity was not associated with reduction
of doxorubicin-induced cardiomyocyte apoptosis. These data suggest
that coadministration of mTOR activators might decrease acute
doxorubicin cardiotoxicity, thereby permitting a higher dose
of drug per treatment. If so, administration of fewer doses
of anthracycline at higher levels might be a more effective
anticancer strategy. This approach may also allow lower cumulative
doses, which would reduce the incidence of late-onset refractory
cardiomyopathy. See p
99.
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Get With the Guidelines-Stroke Is Associated With Sustained Improvement in Care for Patients Hospitalized With Acute Stroke or Transient Ischemic Attack
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Stroke is the third-leading cause of death and a leading cause
of long-term disability. Despite widely available evidence supporting
clinical interventions that improve health outcomes for patients
hospitalized for acute ischemic stroke or transient ischemic
attack, many patients do not receive these recommended interventions.
Get With the Guidelines-Stroke is a program of the American
Heart Association/American Stroke Association (AHA/ASA) to improve
the quality of care of patients with stroke and transient ischemic
attack. In this study, Get With the Guidelines-Stroke participation
was associated with sustained and substantial improvements in
a wide variety of acute stroke care and secondary prevention
performance measures over >4 years across a spectrum of participating
hospitals. This is the largest report to date of improvements
in acute stroke care and confirms the sustainability and generalizability
of the improvements observed in the pilot phase of the program.
In addition, the analyses suggest that the benefit of the program
was independent of secular trends in acute stroke care. The
study shows the impact of the program on hospitalized stroke
patients and has broad implications for the ability to improve
stroke care across the country. If patients continue to adhere
to secondary prevention regimens after discharge, clinical trial
data suggest a substantial reduction in stroke recurrence applicable
to many tens of thousands of patients each year. Increased support
for stroke quality initiatives would likely yield substantial
improvements in quality of care and clinical outcomes for stroke
and transient ischemic attack and translate into substantial
healthcare savings. See p
107.
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Platelet P2Y12 Receptor Influences the Vessel Wall Response to Arterial Injury and Thrombosis
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The platelet P2Y
12 receptor plays a major role in platelet activation
and the ensuing thrombotic and inflammatory responses. Platelets
are believed to play a role in the neointima formation that
results from arterial injury such as after percutaneous coronary
intervention or as a consequence of vessel wall inflammation,
as occurs with atherosclerosis. We have determined the role
of the P2Y
12 receptor in the vessel wall response after arterial
injury in mouse models using P2Y
12 receptor knockout mice as
well as the P2Y
12 receptor antagonist clopidogrel to investigate
the role of the receptor. We have shown that the P2Y
12 receptor
plays a substantial role in promoting neointima formation and,
through bone marrow transplantation experiments, have demonstrated
that it is specifically the receptors on platelets that mediate
this response. This suggests that more effectively targeting
the platelet P2Y
12 receptor before percutaneous coronary intervention
might prove effective in reducing restenosis and could also
have a beneficial inhibitory effect on atherogenesis during
long-term administration of P2Y
12 antagonists. See p
116.
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Disparity in Outcomes of Surgical Revascularization for Limb Salvage: Race and Gender Are Synergistic Determinants of Vein Graft Failure and Limb Loss
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Racial and ethnic disparities in the prevalence of peripheral
artery disease and its most severe complication, limb loss,
have been described. However, the variability in outcomes for
revascularization therapies such as surgery or angioplasty is
poorly characterized. Surgical bypass using an autogenous vein
is an effective and durable treatment for many patients with
the most advanced form of peripheral arterial disease, critical
limb ischemia. We examined the relationship between patient
demographics (race and gender) and the outcomes of vein bypass
procedures for critical limb ischemia using a large (n=1404)
multicenter randomized trial database from >80 North American
institutions. Aggressive bypass graft surveillance with duplex
ultrasonography was incorporated into the study protocol to
reliably identify significant vein graft lesions. Propensity
score methods were applied to control for covariates while focusing
on the interaction between race and gender. Our findings demonstrate
that black patients, particularly women, are at increased risk
for vein graft failure and limb loss after surgical revascularization
for critical limb ischemia. The data suggest the possibility
of an altered response to vein bypass surgery in this subgroup.
Aggressive medical therapy and close surveillance are mandated
in these higher-risk cohorts to improve the chances of long-term
success. Further studies are indicated to determine the mechanisms
underlying these observations. See p
123.
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Evidence for Statin Pleiotropy in Humans: Differential Effects of Statins and Ezetimibe on Rho-Associated Coiled-Coil Containing Protein Kinase Activity, Endothelial Function, and Inflammation
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Although cholesterol lowering by 3-hydroxy-3-methylglutaryl
coenzyme A reductase inhibitors or statins is clearly linked
to decreased cardiovascular disease, several recent statin trials
suggest additional benefits beyond cholesterol lowering, possibly
by mechanisms involving inhibition of Rho-associated coiled-coil
containing protein kinase (ROCK). These so-called pleiotropic
effects of statins are thought to be responsible for the observed
improvement in flow-mediated vasodilation, the increased numbers
of circulating endothelial progenitor cells, and perhaps the
reduction in vascular inflammation. We hypothesized that ezetimibe,
which inhibits intestinal cholesterol absorption, may not exert
cholesterol-independent or pleiotropic effects similar to those
of statins and, when used with a lower dose of statin, may have
less effect on ROCK activity than a higher dose of statin. In
a prospective randomized study of 60 dyslipidemic subjects without
cardiovascular disease treated with simvastatin 40 mg/d, simvastatin/ezetimibe
10/10 mg/d, or placebo tablets for 28 days (n=20 in each arm),
we found similar low-density lipoprotein lowering and reduction
of high-sensitivity C-reactive protein between the 2 treatment
groups. However, only simvastatin 40 mg reduced ROCK activity
and improved flow-mediated dilation. Reduction in ROCK activity
with simvastatin 40 mg remained significant even after controlling
for changes in low-density lipoprotein cholesterol and correlated
with an improvement in flow-mediated dilation. No correlation
was found between changes in flow-mediated dilation and changes
in low-density lipoprotein cholesterol or C-reactive protein.
These results indicate that high-dose statin monotherapy exerts
greater effects on ROCK activity and endothelial function, but
not CRP, than low-dose statin plus ezetimibe. These findings
provide additional evidence of statin benefits beyond cholesterol
lowering. See p
131.
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Platelet P2Y12 Receptor Influences the Vessel Wall Response to Arterial Injury and Thrombosis
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Tissue Doppler Imaging in the Estimation of Intracardiac Filling Pressure in Decompensated Patients With Advanced Systolic Heart Failure
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Critical Role of Transcription Factor Cyclic AMP Response Element Modulator in β1-Adrenoceptor–Mediated Cardiac Dysfunction
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Acute Doxorubicin Cardiotoxicity Is Associated With p53-Induced Inhibition of the Mammalian Target of Rapamycin Pathway
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Myocardial Adeno-Associated Virus Serotype 6–βARKct Gene Therapy Improves Cardiac Function and Normalizes the Neurohormonal Axis in Chronic Heart Failure
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Body Mass Index and Vigorous Physical Activity and the Risk of Heart Failure Among Men
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Circulation 2009 119: 71-78.
[Abstract]
[Full Text]
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Epicardial Border Zone Overexpression of Skeletal Muscle Sodium Channel SkM1 Normalizes Activation, Preserves Conduction, and Suppresses Ventricular Arrhythmia: An In Silico, In Vivo, In Vitro Study
- David H. Lau, Chris Clausen, Eugene A. Sosunov, Iryna N. Shlapakova, Evgeny P. Anyukhovsky, Peter Danilo, Jr, Tove S. Rosen, Caitlin Kelly, Heather S. Duffy, Matthias J. Szabolcs, Ming Chen, Richard B. Robinson, Jia Lu, Sinhu Kumari, Ira S. Cohen, and Michael R. Rosen
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Activated Endocannabinoid System in Coronary Artery Disease and Antiinflammatory Effects of Cannabinoid 1 Receptor Blockade on Macrophages
- Koichi Sugamura, Seigo Sugiyama, Toshimitsu Nozaki, Yasushi Matsuzawa, Yasuhiro Izumiya, Keishi Miyata, Masafumi Nakayama, Koichi Kaikita, Toru Obata, Motohiro Takeya, and Hisao Ogawa
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Evidence for Statin Pleiotropy in Humans: Differential Effects of Statins and Ezetimibe on Rho-Associated Coiled-Coil Containing Protein Kinase Activity, Endothelial Function, and Inflammation
- Ping-Yen Liu, Yen-Wen Liu, Li-Jen Lin, Jyh-Hong Chen, and James K. Liao
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[Abstract]
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Multimarker Approach to Evaluate Correlates of Vascular Stiffness: The Framingham Heart Study
- Wolfgang Lieb, Martin G. Larson, Emelia J. Benjamin, Xiaoyan Yin, Geoffrey H. Tofler, Jacob Selhub, Paul F. Jacques, Thomas J. Wang, Joseph A. Vita, Daniel Levy, Ramachandran S. Vasan, and Gary F. Mitchell
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