| Nonalcoholic Red Wine Reduces Blood Pressure |
September 7, 2012 (Barcelona, Spain) — Nonalcoholic red
wine was associated with a greater reduction in blood pressure than
regular red wine in a new study [1].
The researchers, led by
Dr Gemma Chiva-Blanch (University of
Barcelona, Spain), conclude that the polyphenols found in red wine are
the likely mediators of the blood-pressure reduction and that alcohol
appears to weaken their antihypertensive effect.
They suggest that daily consumption of nonalcoholic red wine may be useful for the prevention of mild to moderate hypertension.
For the study, published online in
Circulation Research on
September 6, 2012, 67 men at high cardiovascular risk were randomized
into three four-week treatment periods in a crossover clinical trial.
Each participant followed a common background diet and also drank red
wine (30 g alcohol/day), the equivalent amount of dealcoholized red
wine, or gin (30 g alcohol/day). Blood pressure and plasma nitric-oxide
(NO) concentration were measured at baseline and between each
intervention. The men were moderate alcohol consumers before the study,
but they abstained from drinking any alcohol for a two-week run-in
period at the start of the study.
Results showed that both systolic and diastolic blood pressure
decreased significantly after the dealcoholized red wine intervention,
and these changes correlated with increases in plasma NO. During the
red-wine phase, the men had a small reduction in blood pressure and a
small increase in NO, while there was no change in blood pressure and a
small reduction in NO while drinking gin.
Changes in blood pressure and nitric oxide with the different beverages
| Change in BP/NO
|
Red wine
|
Nonalcoholic red wine
|
Gin
|
| Systolic blood pressure (mm Hg) |
-2.3 |
-5.8 |
-0.8 |
| Diastolic blood pressure (mm Hg) |
-1.0 |
-2.3 |
-0.1 |
| Nitric oxide (µmol/L) |
+0.6 |
+4.1 |
-1.4 |
The researchers note that although the blood-pressure reduction
associated with nonalcoholic red wine was modest, reductions of this
magnitude have been associated with a 14% decrease in coronary heart
disease and 20% reduction in stroke risk.source medscape
Trying a New Line of Attack in Heart Disease
Two major clinical trials are testing for the first
time whether treating inflammation can reduce the risk of a heart attack
or stroke, potentially opening up a new line of attack in the battle
against cardiovascular disease.
Brigham and Women's Hospital
'This goes beyond simply
asking, is inflammation a marker of risk to asking if it's a target for
therapy,' said Paul M. Ridker, who is leading the two trials.
Until now, strategies to fight these
killers have focused largely on well-known risk factors such as high
blood pressure and cholesterol. The new studies, one sponsored by the
National Institutes of Health and the other by pharmaceutical giant
Novartis SA,
NOVN.VX-1.06%
will test the hypothesis that inflammation plays a crucial role in the
underlying biology that makes heart disease and stroke the No. 1 and
No. 4 causes of death in the U.S., respectively.
Inflammation is
part of the body's normal healing response to injury. When the walls of
the coronary arteries or the vessels that carry blood to the brain
suffer injury from the effects of smoking, obesity and abnormal
cholesterol, for instance, the immune system as part of the inflammatory
response dispatches cells to repair the damage, researchers say. But in
the face of a constant assault by such irritants over decades, possibly
abetted by genetics, that system can go into overdrive. Instead of
protecting the vessels, inflammation becomes chronic, leading to the
accumulation and potential rupture of arterial deposits called plaque
that can cause heart attacks and strokes.
Research over two decades has shown that people with chronic
inflammation—detectable at low levels, for instance, with a
high-sensitivity test for a marker called C-reactive protein—are at
significantly higher risk of heart attack and stroke compared with those
with evidence of little or no such inflammation.
But whether the risk can be mitigated by inhibiting or shutting down the process with anti-inflammatory drugs isn't known.
"This goes beyond simply asking, is inflammation a marker of risk
(for cardiovascular disease) to asking if it's a target for therapy,"
said Paul M. Ridker, director of the center for cardiovascular-disease
prevention at Harvard-affiliated Brigham and Women's Hospital in Boston,
who is leading both trials.
Significant progress has been made
against heart attacks and strokes in recent years, thanks to what
researchers believe is the cumulative impact of prevention strategies
that include more aggressive use of cholesterol and blood pressure
drugs, anti-smoking initiatives and better exercise and dietary habits.
Heart attack admissions among the elderly fell by nearly 25% in the five
years ended in 2007, a recent study showed, while stroke deaths
declined by nearly 20% in the decade ended in 2008.
Still, both problems exact a heavy toll. More than 1.25 million
Americans suffer a heart attack each year, according to the American
Heart Association, while nearly 800,000 have a stroke.
"If you could find a way to dramatically reduce the incidence of
heart attacks by blocking inflammation, that would change the practice
of medicine," said Mark Fishman, a cardiologist and president of the
Novartis Institutes for BioMedical Research.
The new trials mark the latest effort to take prevention efforts beyond conventional strategies.
The NIH study will test whether the widely used generic
anti-inflammatory drug methotrexate can reduce major cardiovascular
events in 7,000 patients with a history of heart attack—who also have
either diabetes or a cluster of prediabetic risk factors known as the
metabolic syndrome. Enrollment is expected to begin at more than 350
sites in the U.S. and Canada next March.
These are especially high-risk patients for whom current optimal
treatment often fails. "We've kind of run out of our tool kit for these
individuals and yet they're still having events," said Gary Gibbons,
director of the NIH's National Heart, Lung and Blood Institute, which
officially funded the study.
The Novartis trial, which is testing the company's anti-inflammatory
antibody called canakinumab, has already enrolled 3,000 patients of a
planned 17,000 patients with stable cardiovascular disease and elevated
levels of inflammation. (The drug is marketed under the brand name
Ilaris for a rare inflammatory disease called Muckle-Wells Syndrome.) In
proof-of-concept studies, it yielded what Dr. Fishman called
"provocative" evidence of benefit in coronary arteries.
But it will take the much-larger study to determine whether it
actually prevents serious complications of cardiovascular disease.
Both drugs directly target certain inflammatory pathways with little
if any effect on other cardiovascular risk factors. Current preventive
medications, including aspirin, which inhibits blood clotting, and
cholesterol-lowering statins, which reduce LDL or bad cholesterol, a key
heart- and stroke-risk factor, also lower inflammation. Thus in studies
showing benefits of both drugs, "we can't tease apart whether lowering
inflammation alone has an incremental benefit," Dr. Ridker said.
Finding a benefit may be a challenge in the big trials. All
participating patients will be treated with optimal therapy, meaning
that those in the anti-inflammatory arms of each study will also be
given statins and be compared against patients who are on aggressive
statin and other therapies that may also reduce inflammation.
"The question is how difficult will it be to get above and beyond"
the benefit of current treatments, said Michael Miller, director of the
center for preventive cardiology at University of Maryland Medical
Center. "The problem is the placebo group is going to be very well
treated."
Indeed, many researchers believe the effectiveness of current therapy
has proved a daunting hurdle to efforts to develop new cardiovascular
drugs. Niacin and an experimental drug known as a CETP inhibitor—both of
which raise HDL or good cholesterol—failed in recent studies to reduce
heart risk when added to statin treatment. Other studies intending to
show benefit from raising HDL cholesterol are in progress.
One of the first hints that treating inflammation might reduce
cardiovascular disease risk came in 1997 in a report led by Dr. Ridker
from the so-called Physicians Health Study—the study that a decade
earlier had demonstrated the benefit of daily aspirin in preventing
heart attacks. Dr. Ridker found that elevated inflammation as measured
by levels of C-reactive protein was associated with a threefold risk of
heart attack and a doubling of stroke risk. Those with the highest
C-reactive protein levels got the most benefit from aspirin.
The findings and subsequent research led to development of a
high-sensitivity test for C-reactive protein that many doctors now use
to help assess patients' heart and stroke risk. (Dr. Ridker is listed as
an inventor on patents held by Brigham and Women's Hospital for such a
test, but he said neither he nor the hospital will receive royalties for
any of the tests used in either of the two new studies.)
How useful the test is in assessing heart risk has provoked
controversy among cardiologists, but there is broad consensus that
inflammation is an important player in the development of cardiovascular
disease.
"So the question becomes, if we inhibit inflammation, can we get benefit?" Dr. Ridker says. "And we'll see."source wsj
Atrial fibrillation and chronic kidney
disease are each linked to increased risk for stroke and systemic
thromboembolism. The goal of this large cohort study was to examine
these risks and the effects of antithrombotic therapy in patients with
both conditions, which has not been fully studied to date. The
investigators identified all patients who were discharged with a
diagnosis of nonvalvular atrial fibrillation between 1997 and 2008, as
listed in Danish national registries.
Time-dependent Cox regression analyses allowed determination of the
risk for stroke or systemic thromboembolism and bleeding associated with
non-end-stage chronic kidney disease and with end-stage chronic kidney
disease (defined as the need for renal replacement therapy). The
investigators also compared the effects of treatment with warfarin,
aspirin, or both in patients with chronic kidney disease vs those
without renal disease.
Non-end-stage chronic kidney disease was present in 3587 (2.7%) of
132,372 patients included in the analysis, and end-stage chronic kidney
disease in 901 (0.7%).
Risk for stroke or systemic thromboembolism was increased in patients
with non-end-stage chronic kidney disease compared with those without
renal disease (hazard ratio [HR], 1.49; 95% confidence interval [CI],
1.38-1.59;
P < .001). Severity of renal disease, as
determined by the intensity of treatment with loop diuretics, did not
affect this risk.
In patients with end-stage chronic kidney disease, the risk for
stroke or systemic thromboembolism was even higher (HR, 1.83; 95% CI,
1.57-2.14;
P < .001). In both groups of patients, treatment
with warfarin alone, but not in combination with aspirin, significantly
reduced this risk.
The risk for bleeding was also increased in both groups and was
further increased with warfarin alone, aspirin alone, or both in
combination. Among patients with non-end-stage chronic kidney disease,
the risk for bleeding was associated with the dose of loop diuretics and
with the cause of the chronic kidney disease.
Viewpoint
Study limitations include an observational
cohort design with possible residual confounding, possible
underestimation of frequencies of risk factors, inclusion of only
hospitalized patients with atrial fibrillation, bleeding outcome
restricted to events resulting in hospitalization or death, and lack of
brain imaging data. Nonetheless, the findings of this large cohort
study suggest that chronic kidney disease was associated with an
increased risk for stroke or systemic thromboembolism and bleeding in
patients with atrial fibrillation. Although warfarin therapy was
associated with a reduction in risk for stroke or systemic
thromboembolism in patients with chronic kidney disease, both warfarin
and aspirin were associated with an increased risk for bleeding.
The risks and benefits of warfarin therapy should be carefully
weighed in patients with chronic kidney disease and atrial fibrillation.
Patients who take warfarin should have close monitoring of the
international normalized ratio. Clinical trials could help determine the
role of warfarin or of other anticoagulants in this patient
population.source medscape
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