Poor Sleep Related to Resistant Hypertension
Sleep and Depression Scores in Women vs Men
Score Women Men p
PSQI score 5.2 3.6 0.03
Poor sleep quality (%) 46 30 0.01
Depression score 4.5 1.8 0.006
Prevalence of depressive symptoms (%) 20 7 0.003

Καταρρίπτεται ο μύθος για τα βιολογικά προϊόντα

Μια νέα αμερικανική έρευνα έρχεται να αλλάξει την ευρέως διαδεδομένη αντίληψη ότι τα βιολογικά προϊόντα είναι πιο υγιεινή από τα συμβατικά και τονίζει ότι είναι εξίσου πιθανό να είναι μολυσμένα με ορισμένα βακτήρια.
Από την άλλη, όμως, σύμφωνα με τους επιστήμονες, τα βιολογικά αγροτικά και κτηνοτροφικά προϊόντα είναι λιγότερο πιθανό να περιέχουν υπολείμματα παρασιτοκτόνων ή να φιλοξενούν μικρόβια ανθεκτικά στα αντιβιοτικά. Αν και από τόπο σε τόπο διαφέρουν οι πρακτικές που εφαρμόζονται στις βιολογικές φάρμες, τα προϊόντα τους σε γενικές γραμμές αναπτύσσονται χωρίς τη χρήση χημικών φαρμάκων, αντιβιοτικών και ορμονών, ενώ δεν περιέχουν γενετικά τροποποιημένους οργανισμούς.
Όμως, η νέα έρευνα δείχνει ότι η αντίληψη των καταναλωτών πως τα βιολογικά προϊόντα είναι πάντα πιο θρεπτικά και ασφαλή για την υγεία, δεν είναι κατ’ ανάγκη σωστή. Έτσι, παραμένουν ασαφή τα συγκριτικά οφέλη για την υγεία από την κατανάλωσή τους, με δεδομένο μάλιστα ότι τα βιολογικά τρόφιμα είναι πολύ ακριβότερα από τα συμβατικά (συχνά έχουν έως διπλάσια τιμή), αναφέρει το Αθηναϊκό Πρακτορείο Ειδήσεων.
Η νέα μελέτη, με επικεφαλής την δρα Κρίσταλ Σμιθ- Σπάνγκλερ της Ιατρικής Σχολής του πανεπιστημίου Στάνφορντ, που δημοσιεύθηκε στο αμερικανικό ιατρικό περιοδικό «Annals of Internal Medicine», σύμφωνα με το πρακτορείο Reuters, αξιολόγησε τα δεδομένα από 237 σχετικές έρευνες που συνέκριναν τη διατροφική αξία των βιολογικών και των συμβατικών τροφών και τις τυχόν διαφορές στο επίπεδο μικροβίων που περιέχουν.
Από τη σύγκριση δεν προκύπτει κάποια αξιοσημείωτη διαφορά ανάμεσα στις δύο κατηγορίες προϊόντων όσον αφορά την περιεκτικότητά τους σε βιταμίνες (με εξαίρεση τον ελαφρώς περισσότερο φώσφορο στα βιολογικά). Επίσης δεν βρέθηκε κάποια διαφορά στην περιεκτικότητα σε πρωτεΐνες και λίπη, αν και υπάρχουν ενδείξεις ότι το βιολογικό γάλα περιέχει περισσότερα ωμέγα-3 λιπαρά οξέα.
Ειδικότερα στα φρούτα και τα λαχανικά, δεν διαπιστώθηκε ότι τα βιολογικά υπερτερούν σε θρεπτική αξία. «Παρά την ευρέως διαδεδομένη αντίληψη ότι τα βιολογικά προϊόντα είναι πιο θρεπτικά από τα συμβατικά, δεν βρήκαμε αξιόπιστα στοιχεία που να υποστηρίζουν αυτή την αντίληψη», όπως αναφέρουν οι ερευνητές.
Από την άλλη, διαπιστώθηκε ότι τα βιολογικά και τα συμβατικά τρόφιμα είναι εξίσου πιθανό να είναι μολυσμένα με παθογόνους μικροοργανισμούς, όπως κολοβακτηρίδια (E.coli) και σαλμονέλα. Περίπου το 7% των βιολογικών προϊόντων και το 6% των συμβατικών βρέθηκαν να περιέχουν κολοβακτηρίδια, ενώ τα αντίστοιχα ποσοστά για τη σαλμονέλα ήσαν 34% (τα βιολογικά) και 35% (τα συμβατικά).
Αντίθετα, υπήρχε αισθητή διαφορά στη μόλυνση με παρασιτοκτόνα- εντομοκτόνα (7% στα βιολογικά έναντι 38% στα συμβατικά) και στα μικρόβια που είναι ανθεκτικά σε αντιβιοτικά (το βιολογικό/οργανικό κρέας είχε κατά μέσο όρο 33% μικρότερη περιεκτικότητα σε αυτά τα βακτήρια σε σχέση με το συμβατικό κρέας). Πάντως, είναι αξιοσημείωτο ότι, αν και σε μικρότερο βαθμό, τα βιολογικά προϊόντα δεν είναι απαλλαγμένα τελείως (100%) από παρασιτοκτόνα- εντομοκτόνα.
«Είναι αδύνατο να πει κανείς, με βάση αυτήν τη μελέτη, αν η μία μέθοδος καλλιέργειας είναι καλύτερη από την άλλη», δήλωσε ο ερευνητής Τζιν Λέστερ, ειδικός στη φυσιολογία των φυτών στην Υπηρεσία Αγροτικών Ερευνών του υπουργείου Γεωργίας των ΗΠΑ. Όπως είπε, αν και τα νέα ευρήματα είναι ενδιαφέροντα, δεν μπορούν να θεωρηθούν οριστικά, με δεδομένη τη μεγάλη ποικιλομορφία στις βιολογικές/ οργανικές πρακτικές και στην υπάρχουσα δυσκολία να γίνουν διαχρονικές συγκρίσεις.
«Δεν υπάρχει μεγάλη διαφορά ανάμεσα στα βιολογικά και στα οργανικά τρόφιμα, όσον αφορά έναν ενήλικο που θέλει να επιλέξει με βάση μόνο την υγεία του», δήλωσε η ερευνήτρια Ντένα Μπραβάτα. Σημειωτέον ότι ακόμα δεν υπάρχουν μακρόχρονες έρευνες (διάρκειας άνω των δύο ετών) που να συγκρίνουν τις τυχόν διαφορές στις επιπτώσεις για την υγεία μεταξύ όσων τρώνε μόνο συμβατικά και όσων τρώνε μόνο βιολογικά προϊόντα.
Σύμφωνα πάντως με τους ερευνητές, πέρα από τα θέματα της υγείας, υπάρχουν άλλοι λόγοι που θα μπορούσε κανείς να προτιμήσει τα βιολογικά προϊόντα, όπως η (πιθανή) καλύτερη γεύση, το ενδιαφέρον του για το περιβάλλον και τα ζώα κ.α.sourse medicalnews.gr

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.
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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

http://dctrs-news.blogspot.gr/2012/10/stroke-and-bleeding-in-atrial.html

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

Σάββατο 27 Οκτωβρίου 2012

Rivaroxaban vs Warfarin for AFib Causes More GI Bleeding

2:10 μ.μ.    No comments
ATLANTA, Georgia — Patients with atrial fibrillation receiving anticoagulant therapy are more likely to experience gastrointestinal (GI) bleeding when treated with rivaroxaban than when treated with warfarin, according to a new analysis of data from ROCKET AF.
Christopher Nessel, MD, from research and development at Johnson & Johnson in Raritan, New Jersey, reported the findings here at CHEST 2012: American College of Chest Physicians Annual Meeting.
"Compared with warfarin, the risk of GI bleeding is increased with rivaroxaban, but the incidence of life-threatening or fatal GI bleeding is lower," Dr. Nessel told Medscape Medical News. "A careful benefit/risk assessment is needed prior to prescribing rivaroxaban for high-risk patients," he added.
The analysis examined the incidence and outcomes of GI hemorrhage in 14,264 patients with nonvalvular atrial fibrillation enrolled in ROCKET AF.
The patients were randomized to either rivaroxaban or dose-adjusted warfarin. All GI bleeding events were recorded during treatment and for 2 days after the last dose was administered. Severity of bleeding was defined by a corresponding drop in hemoglobin or transfusion of more than 2 units of red cells.
The composite principal safety end point for GI bleeding events (upper GI, lower GI, and rectal bleeding) occurred more frequently in the 394 patients receiving rivaroxaban than in the 290 receiving warfarin (3.61% vs 2.60% per year; hazard ratio [HR], 1.39; 95% confidence interval [CI], 1.19 to 1.61). Major bleeding was more frequent with rivaroxaban than with warfarin (2.00% vs 1.24% per year; HR, 1.61; 95% CI, 1.30 to 1.99), as was clinically relevant nonmajor bleeding (1.75% vs 1.39% per year; HR, 1.26; 95% CI, 1.20 to 1.55).
Patients who experienced major GI bleeding were more likely to have experienced GI bleeding in the past, to have mild anemia, to have a lower creatinine clearance, to be previous or current smokers, and to be older than patients who did not experience a GI bleeding during the trial (n = 13,552). They were also less likely to be female and to have previously experienced a stroke or transient ischemic attack.
The incidence of severe bleeding (transfusion of at least 4 units) was similar in the rivaroxaban and warfarin groups (49 vs 47). Six patients developed fatal bleeding: 1 in the rivaroxaban group and 5 in the warfarin group.
Data May Give Clinicians Pause When Considering Rivaroxaban
"The data presented extend the observations from the ROCKET AF clinical study," Dr. Nessel said. "Specifically, the analyses identified characteristics of nonvalvular atrial fibrillation patients that may predispose them to the occurrence of GI hemorrhage. The data also indicated that the overall fatality rates for bleeds of this nature are very low."
Independent commentator James Wisler, MD, from the division of cardiovascular disease at Duke University Medical Center in Durham, North Carolina, pointed out that this study underscores the importance of critically evaluating these newer anticoagulants when considering their use in a given patient.
"The decision regarding which anticoagulant to use for a given patient is complex, and risks and benefits need to be considered thoughtfully," he told Medscape Medical News. He added that the results of this study might give some physicians pause about initiating a newer anticoagulant, such as rivaroxaban, in a given patient with atrial fibrillation and an unfavorable risk profile, such as those with a previous GI bleed.
"While the previously published results from ROCKET AF suggested that the risk profiles were similar between rivaroxaban and warfarin, these results demonstrate that there is indeed a subpopulation of patients who may be better served with warfarin than rivaroxaban," he explained.
According to Dr. Wisler, both this analysis and the initial ROCKET AF study demonstrate that rivaroxaban is associated with fewer episodes of severe or fatal bleeding events, despite the increase in major and clinically relevant nonmajor bleeding observed in the specific subgroup of this study. "Currently, it is unclear why this discrepancy exists," he added.
He recommends that clinicians take a careful patient history to assess bleeding risk factors when considering the initiation of a newer anticoagulant such as rivaroxaban.
"While perhaps more convenient and efficacious, certain patient populations, such as that evaluated in this study, may receive net harm from these newer agents," he said.
The study authors report multiple financial relationships with the following companies: AstraZeneca, Bayer, Boehringer Ingelheim, BMS, Daiichi Sankyo, Eli Lilly, GSK, Johnson & Johnson, Merck, Momenta Pharmaceuticals, Novartis, Portola, Pozen, Regado Biotechnologies, sanofi-aventis, Schering-Plough, The Medicines Company, Ortho/McNeill, Pfizer, Polymedix, Boston Scientific, Medtronic, Forest Laboratories, Janssen Research and Development, and Genzyme. Dr. Wisler has disclosed no relevant financial relationships.source medscape

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Παρασκευή 12 Οκτωβρίου 2012

Lycopene-Rich Diet May Curb Stroke Risk

11:12 π.μ.    No comments

Lycopene-Rich Diet May Curb Stroke Risk
 

October 9, 2012 — A diet rich in lycopene, found in tomatoes and tomato-based products, may reduce the risk for stroke in men, according to a Finnish population-based study.
The study, published October 9 in Neurology, found that men with the highest serum concentrations of lycopene were far less likely to have a stroke over more than a decade than men with the lowest lycopene levels.
"This study supports previous results that eating tomatoes and tomato-based foods is associated with a lower risk of any stroke and ischaemic stroke," Jouni Karppi, PhD, from the Institute of Public Health and Clinical Nutrition, University of Eastern Finland in Kuopio, told Medscape Medical News.
"The results support the recommendation that people get more than 5 servings of fruits and vegetables a day, which would likely lead to a major reduction in the number of strokes worldwide, according to previous research. This may decrease costs of health care in public health," Dr. Karppi said.
Potent Antioxidant
Lycopene is a potent antioxidant that decreases oxidative modification of low-density lipoprotein (LDL) cholesterol, the first pathogenic step of cerebrovascular events, Dr. Karppi explained. "Lycopene is the most efficient quencher of singlet oxygen," he added. "Lycopene reduces inflammation, inhibits cholesterol synthesis, improves immune function, and prevents platelet aggregation and thrombosis and thereby may decrease the risk of stroke."
The study team investigated the association of carotenoids, retinol and alpha-tocopherol, with stroke in 1031 Finnish men aged 46 to 65 years in the longitudinal population-based Kuopio Ischaemic Heart Disease Risk Factor cohort. Serum concentrations of retinol and alpha-tocopherol were measured by high-performance liquid chromatography at baseline.
During a median follow-up of 12.1 years, 67 men had a stroke, including 50 ischemic strokes.
After multivariable adjustment for age, examination year, body mass index, systolic blood pressure, smoking, serum LDL cholesterol, diabetes, and history of stroke, men in the highest quartile of serum lycopene ( > 0.22 µmol/L) were significantly less likely to have any stroke or ischemic stroke than men in the lowest quartile of lycopene (≤0.030 µmol/L).
Table. Risk for Stroke in Highest vs Lowest Quartile of Lycopene
Type Hazard Ratio (95% Confidence Interval) P Value
Any stroke 0.45 (0.21 - 0.95) .036
Ischemic stroke 0.41 (0.17 - 0.97) .042

Concentrations of alpha-carotene, beta-carotene, alpha-tocopherol, and retinol were not related to the risk for stroke.
Limitations Preclude Firm Conclusions
In comments to Medscape Medical News, Larry B. Goldstein, MD, director of the Duke Stroke Center at Duke University Medical Center in Durham, North Carolina, noted that the conclusions are subject to "all of the limitations of this type of study design (for example recall bias and an inability to account for changes in diet or other risk factors that may have occurred over time)."
"In addition, diet may be a marker for other factors that might affect risk (and) the study is based on a one-time dietary questionnaire with subjects then followed over time," Dr. Goldstein added. He was not involved in the study.
He also noted that the study was limited to Finnish men, and whether the findings would be similar in other populations is uncertain.
Nonetheless, Dr. Goldstein said, "The basic result is consistent with current dietary recommendations from the AHA [American Heart Association] — that diet should include 3 to 5 servings of fruits and vegetables daily and limit sodium consumption (for example, the DASH [Dietary Approaches to Stop Hypertension] eating plan). That diet can certainly include tomatoes and tomato-based products."
The study was supported by a grant from the EVO funding of Lapland Central Hospital, Rovaniemi, Finland. The authors and Dr. Goldstein have disclosed no relevant financial relationships.
Neurology. 2012;79:1540-1547. source medscape
 
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Παρασκευή 5 Οκτωβρίου 2012

Stroke and Bleeding in Atrial Fibrillation With Chronic Kidney Disease

10:14 μ.μ.    No comments

Stroke and Bleeding in Atrial Fibrillation With Chronic Kidney Disease

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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Τρίτη 2 Οκτωβρίου 2012

Poor Sleep Related to Resistant Hypertension

3:13 μ.μ.    No comments
The study was presented here at last week's American Heart Association High Blood Pressure Research 2012 Scientific Sessions by Dr Rosa Maria Bruno (University of Pisa, Italy).
"I would say that treating insomnia may improve resistant hypertension, although we need further data before we make firm clinical recommendations on this," Bruno told heartwire .
She commented: "There is lots of evidence that sleep disorders are related to cardiovascular events, but most relate to sleep-disordered breathing such as sleep apnea. Also, there have been many studies showing an association between short sleep duration and the incidence of cardiovascular events or hypertension. But we looked at whether insomnia was linked to the severity of hypertension, and we found poor sleep quality was significantly more prevalent in patients with resistant hypertension."
Quality Rather Than Quantity
The researchers reported that it was the quality of sleep rather than the duration of sleep that seemed to be the important factor in the relationship with resistant hypertension. They also found a large difference between men and women.
Bruno noted: "In women, poor sleep quality was strongly related to anxiety and depression and resistant hypertension, but this was not the case for men. This difference remained after accounting for other confounding factors. In women, we found that poor sleep quality was associated with a fivefold increase in the probability of having resistant hypertension, even after adjustment."
She cautioned that as this was only a cross-sectional study, they can conclude there is an independent association between poor sleep quality and resistant hypertension, but they cannot deduce that this is a causal effect. "This needs to be confirmed in a prospective study. It could also be that the hypertension is causing the insomnia, but we believe that the insomnia is making the hypertension worse."
Experimental evidence supports this view. It is known that interrupted sleep stimulates the sympathetic nervous system and increases cortisol levels, both of which cause an increase in blood pressure.
For the study, data on sleep quality, anxiety/depression, and cardiovascular risk factors were collected for 270 patients from a hypertension outpatient unit. Sleep quality was measured by the Pittsburgh Sleep Quality Index (PSQI), and anxiety and depression with the Beck Depression Inventory (BDI). Poor sleep quality was defined as PSQI >5, mild to severe depressive symptoms as BDI score >10. Patients with obstructive sleep apnea were excluded. Resistant hypertension was defined as a failure to control hypertension with three or more drugs.
Complete data were available for 234 patients, half of whom were women. Mean sleep duration was 6.4 hours, and 49% of participants had short sleep duration (less than six hours), which was similar in both sexes.
However, women had higher PSQI scores and a higher prevalence of poor sleep quality. Women showed also higher depression scores and prevalence of depressive symptoms than men.
Sleep and Depression Scores in Women vs Men
Score Women Men p
PSQI score 5.2 3.6 0.03
Poor sleep quality (%) 46 30 0.01
Depression score 4.5 1.8 0.006
Prevalence of depressive symptoms (%) 20 7 0.003
Resistant hypertension was present in 15% of patients, and these individuals had higher PSQI scores than those without resistant hypertension, a difference shown in women but not in men. The association between depression score and resistant hypertension showed a similar trend.
Sleep Scores (PSQI) Related to Resistant Hypertension
Group Resistant hypertension No resistant hypertension p
Entire population 5.8 4.1 0.03
Women 6.8 4.8 0.04
Men 4.7 3.5 0.37

Depression Scores (BDI) Related to Resistant Hypertension
Group Resistant hypertension No resistant hypertension p
Entire population 3.6 2.8 0.02
Women 5.1 3.7 0.03
Men 2.0 1.9 0.53
In a multiple logistic regression analysis (including age, sex, obesity, diabetes, previous CV events, sleep duration, use of hypnotic drugs) poor sleep quality was independently associated with resistant hypertension (OR 2.2). But this relationship lost significance when depressive symptoms were included in the model.source medscape
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Δευτέρα 1 Οκτωβρίου 2012

No Place for New Anticoagulants in ACS, Says New Review

2:05 μ.μ.    No comments
September 25, 2012 (Pécs, Hungary) — New oral anticoagulant agents have no net clinical benefit when given to patients with acute coronary syndrome (ACS) who are already receiving antiplatelet therapy, a new meta-analysis has concluded [1].
"ACS patients are a very delicate population. There is a small benefit when oral anticoagulants are added to dual antiplatelet therapy, but such administration results in an unacceptably high rate of bleeding," lead author of the meta-analysis, Dr András Komócsi (University of Pécs, Hungary), told heartwire . Komócsi and colleagues report their findings online September 24, 2012 in the Archives of Internal Medicine.
There is a small benefit when oral anticoagulants are added to dual antiplatelet therapy but such administration results in an unacceptably high rate of bleeding.
In an accompanying editorial [2], Dr Adrian V Hernandez (Cleveland Clinic, OH) largely agrees. "The benefit is largely canceled by the harm; therefore, the routine use of newer oral anticoagulants among patients with ACS is unwarranted," he observes.
The newer anticoagulant agents include the factor Xa inhibitors rivaroxaban (Xarelto, Bayer Healthcare/Janssen Pharmaceuticals) and apixaban (Eliquis, Bristol-Myers Squibb/Pfizer) and the direct thrombin inhibitor dabigatran (Pradaxa, Boehringer Ingelheim). While these new drugs have all shown good results as an alternative to warfarin in patients with atrial fibrillation (AF) and are licensed for use in venous thromboembolism (VTE), their use in patients with ACS has been fraught with difficulty, because in this situation they are added to several other anticlotting agents, so the bleeding risk is very high.
The first phase 3 trial of one of these agents in ACS (the APPRAISE-2 trial with apixaban) was stopped early because of bleeding, but a later trial, ATLAS ACS 2 TIMI 51, appeared to have demonstrated success in this indication with rivaroxaban. But the US FDA has failed to clear rivaroxaban for the additional indication of ACS after its Cardiovascular and Renal Drugs Advisory Committee voted against recommending approval, based on concerns about missing data from the trial. So the fate of these agents in the ACS indication remains in limbo, for the time being.
New Oral Anticoagulants Associated With Threefold Increased Risk of Major Bleeding
Komócsi and colleagues identified seven prospective randomized placebo-controlled studies that evaluated the effects of factor Xa or direct thrombin inhibitors in just over 31 000 patients receiving antiplatelet therapy after an ACS, published between January 2000 and December 2011. Five were dose-finding trials, in which the primary outcome was safety, and two were large phase 3 trials--APPRAISE-2 and ATLAS-ACS 2 TIMI 51.
Based on the pooled results, the use of new oral anticoagulants in patients taking antiplatelets after ACS was associated with a "dramatic" threefold increased risk of major bleeding, the researchers note (odds ratio 3.03; p<0.001).
Significant, although moderate, reductions in the risk for stent thrombosis or composite ischemic events were observed, with no significant benefit on overall mortality. For the net clinical benefit, treatment with the new oral anticoagulants "provided no advantage over placebo (odds ratio 0.98; p=0.57)," they observe.
"The inhibition of the coagulation system is already somehow pushed to the limit in these patients, and we have to be very conscious about this delicate balance of bleeding and ischemic events," Komócsi commented to heartwire .
In his editorial, Hernandez discusses some of the limitations of the new review, including the use of death as an end point rather than cardiovascular death, and the fact that Komócsi et al provided only relative risk reductions, not absolute ones. Nevertheless, he observes, "The conclusions of the meta-analysis seem to be robust."
Could New Anticoagulants Be Beneficial in Subpopulations of ACS Patients?
Hernandez goes on to wonder, however, whether the new oral anticoagulants might be useful for specific populations of patients with ACS and says trials are needed to evaluate the use of these agents in such subgroups.
"It is unknown whether the effects of [new oral anticoagulants] differ among patients with unstable angina, ST-elevation myocardial infarction [STEMI], and non-STEMI," he observes. Also, "no data are available to date on the use of [new oral anticoagulants] in patients with ACS taking prasugrel [Effient, Daiichi Sankyo/Lilly] or ticagrelor [Brilinta, AstraZeneca] undergoing percutaneous coronary interventions [PCIs] or having indications for anticoagulation (eg, cancer, mitral stenosis, mechanical prosthetic valves, or prior stroke without AF)."
Komócsi believes by far the biggest subgroup that might benefit from the new oral anticoagulants comprises ACS patients who also have AF, noting that AF patients were excluded from the pivotal trials included in his meta-analysis. This group constitutes about 9% to 11% of ACS patients, he estimates.
Other subpopulations that might also benefit include those with prosthetic valves and those who have had a prior pulmonary embolism who then go on to develop ACS, he says, noting however that these are "much smaller populations."
Komócsi reports receiving lecture fees from DSI/Lilly. Disclosures for the coauthors are listed in the paper. Hernandez reports no conflicts of interest.source medscape
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