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.
Enlarge Image
image
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

Παρασκευή 9 Νοεμβρίου 2012

IPad optical scanner helps measure blood loss during surgery

5:55 μ.μ.    No comments
IPad optical scanner helps measure blood loss during surgery
Researchers at Stanford University School of Medicine have developed an optical scanner for Apple's iPad tablet computer that can help accurately measure blood loss during surgery. Researchers said that based on confirmation tests using spectrophotometry, the algorithm reduced variability in measuring blood loss compared with standard human visual estimates and performed well with high blood volumes. A startup company called Gauss Surgical is working to further develop the test, with the aim of putting it in the clinical setting late this year or early next year.
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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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Σάββατο 22 Σεπτεμβρίου 2012

FDA Warns of Potential Heart Failure Risk With Pramipexol

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FDA Warns of Potential Heart Failure Risk With Pramipexol

September 19, 2012 — The US Food and Drug Administration (FDA) has notified healthcare professionals about a possible risk for heart failure with pramipexole (Mirapex, Boehringer Ingelheim), a dopamine agonist used for the management of Parkinson's disease and moderate to severe restless legs syndrome.
"Results of recent studies suggest a potential risk of heart failure that needs further review of available data," a statement from the FDA notes. "Because of the study limitations, FDA is not able to determine whether Mirapex increases the risk of heart failure. FDA is continuing to work with the manufacturer to clarify further the risk of heart failure with Mirapex, and will update the public when more information is available."
The FDA notes that it evaluated a pooled analysis of randomized clinical trials and found that heart failure was more frequent with pramipexole than placebo; however, the increase did not reach statistical significance. They also evaluated 2 epidemiologic studies that also suggested an increased risk for new-onset heart failure with treatment. Limitations of the studies, however, make it difficult to determine whether the excess in heart failure was due to pramipexole or other factors.
More information on the specific studies and the relative risks are included in the safety communication.
"At this time, FDA has not concluded that Mirapex increases the risk of heart failure," the FDA notification states. "Healthcare professionals should continue to follow the recommendations in the drug label when prescribing Mirapex." The benefits and risks of the drug should be discussed with patients, and patients should be encouraged to seek medical attention if they experience signs or symptoms of heart failure on treatment, the safety communication adds.
Healthcare professionals and patients are encouraged to report adverse events or side effects related to the use of this product to the FDA's MedWatch Safety Information and Adverse Event Reporting Program by telephone at 1-800-FDA-1088; by fax at 1-800-FDA-0178; online at https://www.accessdata.fda.gov/scripts/medwatch/medwatch-online.htm; with postage-paid FDA form 3500, available at http://www.fda.gov/MedWatch/getforms.htm; or by mail to MedWatch, 5600 Fishers Lane, Rockville,source medscape
 
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Τετάρτη 19 Σεπτεμβρίου 2012

Are Brand-Name and Generic Drugs Really the Same? The Prescriber Perspective

9:50 π.μ.    No comments

Are Brand-Name and Generic Drugs Really the Same? The Prescriber Perspective

Brand-Name vs Generic Agents: The Prescriber Experience

Prescribers and patients often voice concerns about the safety and efficacy of generic drugs that are substituted for brand-name drug products. Love 'em or hate 'em, they are with us to stay. The US Food and Drug Administration (FDA) approves a generic substitute if it has proven to be "identical, or bioequivalent, to a brand-name drug in dosage form, safety, strength, route of administration, quality, performance characteristics, and intended use."[1]
The FDA's Orange Book provides the latest information on generic approvals. Approved generic agents have been demonstrated to have therapeutic equivalence -- although many providers have questioned whether that equivalence extends to all patients and all clinical scenarios. Jenny Van Amburgh, PharmD, an associate clinical professor of pharmacy at Northeastern University in Boston, Massachusetts, reminded prescribers in a previous discussion on Medscape that generic products are only compared with their brand-name products and not with generics made by other manufacturers.
Drugs that are known to exhibit a narrow therapeutic index (NTI), including levothyroxine, warfarin, phenytoin, and digoxin, are of greatest concern. Switching between generic NTI products made by different manufacturers may require particular vigilance to recommended monitoring.
James Lindon, PharmD, PhD, JD, in an earlier article on Medscape, noted that the product liability law applied to prescription drug products usually only requires the manufacturer to disclose "adequate warning and instruction" to the prescriber or dispenser. There may be no duty for the drug product manufacturer to warn the patient.[2] In contrast, the prescriber and pharmacist may have a duty to counsel the patient when a particular generic product is prescribed or selected by the pharmacy. Laws regarding substitution vary by state.
What if the generic substitution is required by a patient's insurance carrier? Or the switch to a generic drug from a different manufacturer is made at the pharmacy and the prescriber is not aware of it? Is the prescriber liable? Prescribers may not know which generic product was dispensed at the pharmacy or why that agent was chosen. They may not be aware of any concerns about the product selected.
We asked our prescribing readers to participate in a survey describing their experience with generic agents and their opinions on the appropriateness of their use. Here is what they had to say.

Who Participated?

Over 1400 physicians (64% of the sample), nurse practitioners (32%), and physician assistants (4%) completed the survey. Respondents were fairly equally divided in their practice settings. Approximately 27% indicated that they practiced in a private primary care practice, 27% in a private specialty practice, and 27% in a nonprivate clinic (hospital, federally qualified health center, or public health); the remaining 19% were hospital-based (emergency medicine or hospitalist). The respondents were an experienced bunch: More than one half -- 56% -- had been in practice for over 16 years. An additional 16% reported 6-15 years' experience. Only 8% reported practicing for 2 years or less.source medscape.com
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Δευτέρα 17 Σεπτεμβρίου 2012

Ασφαλέστερο το ηλεκτρονικό τσιγάρο σε σχέση με το συμβατικό

1:50 μ.μ.    No comments

Ασφαλέστερο το ηλεκτρονικό τσιγάρο σε σχέση με το συμβατικό

 
Στο συμπέρασμα ότι το ηλεκτρονικό τσιγάρο ίσως ν’ αποτελεί μία πιο ασφαλή μέθοδο καπνίσματος σε σχέση με το κανονικό τσιγάρο, η οποία μπορεί να μειώσει τον κίνδυνο που προκαλεί η επιδημία του καπνίσματος κανονικών τσιγάρων, καταλήγει μελέτη του πραγματοποιήθηκε σε συνεργασία των Πανεπιστημίων Θεσσαλίας και Κρήτης και των τμημάτων ΤΕΦΑΑ και Βιοχημείας (Θεσσαλίας) και Ιατρικής (Κρήτης).
Η μελέτη, η οποία δημοσιεύτηκε πριν από λίγες ημέρες στο επίσημο περιοδικό Τοξικολόγων της Ευρωπαϊκής Ένωσης «Food and Chemical Toxicology», προέβη σε σύγκριση της επίδρασης του κανονικού και του παθητικού καπνίσματος συμβατικού τσιγάρου με το κάπνισμα (κανονικό και παθητικό) ηλεκτρονικού τσιγάρου. Το ηλεκτρονικό τσιγάρο που επιλέχθηκε ήταν από τα πιο διαδεδομένα στην ελληνική αγορά, το δε υγρό γεμίσματος φίλτρων είχε γεύση καπνού και περιεκτικότητα νικοτίνης 11mg/ml. Αυτή είναι μια μέτρια περιεκτικότητα, καθώς τα υγρά γεμίσματος φίλτρων των ηλεκτρονικών τσιγάρων περιέχουν νικοτίνη από 0 έως 36 mg/ml. Εξετάστηκαν 15 καπνιστές και 15 μη καπνιστές άνδρες και γυναίκες. Όσον αφορά το κανονικό κάπνισμα, μελετήθηκαν οι επιπτώσεις καπνίσματος δύο τσιγάρων σε σχέση με την αντίστοιχη χρήση του ηλεκτρονικού τσιγάρου.
Σχετικά με το παθητικό κάπνισμα, μελετήθηκαν οι επιπτώσεις της έκθεσης για μία ώρα σε συνθήκες παθητικού καπνίσματος κοινού τσιγάρου και ηλεκτρονικού τσιγάρου. Χρησιμοποιήθηκε ένα ειδικά διαμορφωμένο εργαστήριο στο οποίο αναπαράχθηκαν οι συνθήκες που συνήθως απαντώνται σε κοινά μπαρ/εστιατόρια της χώρας. Βρέθηκε ότι μετά το κάπνισμα δύο κανονικών τσιγάρων, καθώς επίσης κι έπειτα από παθητικό κάπνισμα κανονικού τσιγάρου τα κύτταρα του αίματος που ενεργοποιούνται στη φλεγμονή αυξήθηκαν στατιστικά σημαντικά σε σχέση με τα άτομα που κάπνισαν (κανονικά και παθητικά) ηλεκτρονικό τσιγάρο.
Αυτό δείχνει ότι ενώ το κανονικό τσιγάρο ενεργοποιεί την διαδικασία της φλεγμονής, κάτι που είναι κύρια υπεύθυνο για την ανάπτυξη παθήσεων όπως ο καρκίνος και τα καρδιαγγειακά νοσήματα. Αντίθετα, το κανονικό και το παθητικό κάπνισμα ηλεκτρονικού τσιγάρου δεν έδειξαν ανάλογα αποτελέσματα. Τα αποτελέσματα αυτά συνάδουν με τη σκέψη ότι το ηλεκτρονικό τσιγάρο ίσως αποτελεί μια πιο ασφαλή μέθοδο καπνίσματος σε σχέση με το κανονικό τσιγάρο, η οποία μπορεί να μειώσει τον κίνδυνο που προκαλεί η επιδημία του καπνίσματος κανονικών τσιγάρων, επισημαίνεται στη σχετική μελέτη.
Το γεγονός ότι κάθε χρόνο πεθαίνουν 6 εκατ. άνθρωποι σε όλο τον κόσμο από το κάπνισμα έχει δημιουργήσει την ανάγκη για μεθόδους εναλλακτικού καπνίσματος για τη μείωση του κινδύνου στη δημόσια υγεία και μία τέτοια μέθοδος, για την οποία έχει γίνει παρουσίαση πληθώρας ερευνών, από διάφορα εργαστήρια ανά τον κόσμο, τον τελευταίο χρόνο, είναι το ηλεκτρονικό τσιγάρο.sourse medical news.gr
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Τρίτη 11 Σεπτεμβρίου 2012

Nonalcoholic Red Wine Reduces Blood Pressure

5:01 μ.μ.    No comments

 
 
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
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Παρασκευή 7 Σεπτεμβρίου 2012

Latest From PURE: 40% of Adult Population Worldwide Has Hypertension

9:29 π.μ.    No comments

Latest From PURE: 40% of Adult Population Worldwide Has Hypertension




Hypertension is truly a global epidemic, being highly prevalent in all communities worldwide, according to new data from the Prospective Urban Rural Epidemiology (PURE) study. Other findings show that awareness is very low and that once patients are aware, most are treated, but control is very poor.
The hypertension cohort of the PURE study was presented at last week's European Society of Cardiology (ESC) 2012 Congress by Dr Rafael Diaz (Instituto Cardiovascular de Rosario, Argentina). The study aimed to assess the prevalence, awareness, and control of hypertension worldwide by measuring blood pressure in 153 000 individuals from 528 urban and rural communities in 17 countries from five continents.
The mean age of the participants was 50.4, 60% were female, and 46% were from rural communities.
The prevalence of hypertension was lowest in lowest-income countries (around 30%) and highest in upper-middle-income economies (around 50%), with high-income and low-middle-income economies having an intermediate level (around 40%).
Only 13% controlled
Only 30% of the population had optimal blood pressure, with another 30% found to be in the prehypertension range. Of the 40% with hypertension, 46% of these individuals were aware of their condition, 40% were treated, but only 13% were controlled.
In low-income countries, there were higher rates of hypertension in urban areas than in rural areas, but this was reversed in upper-income countries, where hypertension was more prevalent in rural communities.
Men were more likely to be hypertensive than women in high- and middle-income countries, but women were more likely to be hypertensive than men in low-income countries.
Low levels of education were association with increased prevalence of hypertension in high- and middle-income economies, but the reverse was true in low-income countries, where hypertension was actually more common in better-educated people.
Awareness, treatment, and control was higher in urban than in rural communities across all incomes, and women had higher rates of awareness, treatment, and control than men again across the board.
The use of multiple antihypertensive drugs was very low, at just 14%, and "practically nonexistent" in low-income countries, Diaz reported.
He concluded that better screening methods are required and increased use of combination medications is needed.
More cooperation needed
Designated discussant Dr Georg Ertl (Wurzburg University, Germany) said the study had the strengths of being very large and truly international, covering a wide spectrum of social and cultural backgrounds.
"For me, the most interesting data are those that show that awareness, treatment, and control are very low all over the world and are virtually absent in rural communities in low-income countries," Ertl commented. Noting that lessons learned in high-income countries may help low-income countries, he suggested that cooperation needs to be fostered between medical institutions in the two economies.sourse medscape
 
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Πέμπτη 6 Σεπτεμβρίου 2012

Hot Cocoa May Boost Seniors' Brain Power

11:59 π.μ.    No comments

Hot Cocoa May Boost Seniors' Brain Power

By Kristina Fiore, Staff Writer, MedPage Today

Cocoa flavanols have shown some benefits for the heart, but they may also be good for cognitive function in older people, researchers found.
In a double-blind study, elderly patients with mild cognitive impairment who consumed high or moderate levels of cocoa flavanols for 2 months had significant improvements on certain cognitive assessment tests compared with those who took in only small amounts, Giovambattista Desideri, PhD, of the University of L'Aquila in Italy, and colleagues reported online in Hypertension.
"Although additional confirmatory studies are warranted, the findings...suggest that the regular dietary inclusion of flavanols could be one element of a dietary approach to the maintaining and improving not only cardiovascular health but also specifically brain health," they wrote.
Evidence suggests eating flavonoids, polyphenic compounds from plant-based foods, may confer cardiovascular benefits. Flavonols are a subclass of these compounds that are abundant in tea, grapes, red wine, apples, and cocoa products including chocolate.
So to assess whether cocoa flavanols could improve cognitive function in elderly patients with mild cognitive impairment (MCI), Desideri and colleagues assessed 90 elderly patients with MCI who were randomized to drink varying levels of a dairy-based cocoa containing flavanols per day for 8 weeks: 990 mg (high), 520 mg (intermediate), or 45 mg (low).
The researchers found that scores on the Mini Mental State Examination didn't change significantly in any of the groups ( P=0.13), a finding that was likely due to the low sensitivity of the test to detect small changes at the upper end of cognitive performance over time, they wrote.
There were, however, changes in the time required to complete Trail Making Tests A and B, with significantly greater improvements for those on high or intermediate doses of flavonols compared with those who had a low intake (P<0.05):
  • High: -14.3 seconds for A, -29.2 seconds for B
  • Intermediate: -8.8 seconds for A, -22.8 seconds for B
  • Low: +1.1 second for A, +3.8 seconds for B
Scores on the verbal fluency test improved significantly for all groups, but, improvements were significantly greater for those who had a high versus low intake (P<0.05):
  • High: +8.0 words per 60 seconds
  • Intermediate: +5.1 words per 60 seconds
  • Low: +1.2 words per 60 seconds
Also, the composite cognitive z-score significantly changed over the study period for the high and intermediate intake groups (P<0.0001), but did not change for those with the lowest intake, they reported.
Desideri and colleagues also observed improvements in several metabolic parameters, including blood pressure and insulin resistance, for those on high and intermediate doses of cocoa flavanols.
For blood pressure, the high flavanol group saw mean reductions of 10 mm Hg for systolic and 4.8 mm Hg for diastolic (P<0.0001) while the intermediate group saw a mean drop of 8.2 mm Hg for systolic and 3.4 mm Hg for diastolic pressures. There were no significant changes for those taking a low dose of flavanols.
Plasma glucose fell a mean 0.6 mmol/L for those in the highest group and by 0.5 mmol/L for those on the mid-level dose (P<0.0001) with no differences for low intake, and both the high and intermediate groups also had significant reductions in homeostasis model assessment–insulin resistance (HOMA-IR) scores (-1.7 and -0.9 points, respectively).
Changes in HOMA-IR were found to be the main determinant of changes in cognitive function, explaining about 40% of composite z-score variability through the study period, the researchers reported (P<0.0001).
Thus the effect on cognition appears to be mediated in part by improvement in insulin sensitivity, the researchers wrote.
They noted that there were no changes in cholesterol or triglycerides in any of the groups.
The study was limited because its short time-frame didn't allow for conclusions about the extent of cognitive benefits and their duration. Nor can it establish whether the observed benefits are a consequence of the cocoa itself or a secondary effect related to general improvements in cardiovascular function or health. Also, participants were in good health overall and without known cardiovascular disease, so the population may be representative of all subjects with MCI.
Still, the researchers concluded that the data "are suggestive of a possible clinical benefit derived from the regular dietary inclusion of cocoa flavanol-containing foods in subjects with MCI."
The study was supported by a grant from Mars, Inc., which supplied the standardized powdered cocoa drinks used in the study.
A co-author is an employee of Mars, Inc.
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Τετάρτη 5 Σεπτεμβρίου 2012

Καταρρίπτεται ο μύθος για τα βιολογικά προϊόντα

11:40 π.μ.    No comments

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
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Τρίτη 4 Σεπτεμβρίου 2012

Q: Will an Inhaler Enhance My Performance?

4:02 μ.μ.    No comments

Q: Will an Inhaler Enhance My Performance? asthma athlete misuse

Until recently, the World Anti-Doping Association (WADA) considered the asthma medication salbutamol (a.k.a. albuterol) a banned substance requiring medical proof of need because it was thought the medication might provide a competitive advantage, likely in the form of increased oxygen consumption (VO2 max). But late in 2009, WADA announced that salbutamol would be allowed in doses recommended for asthmatics. And starting in 2012, WADA took another asthma medication called formoterol off of the prohibited list.
Why would notoriously strict WADA downgrade these meds? Because several studies over the past few years concluded that asthma medications, also referred to as beta-2 agonists, had no significant, positive effects on performance. For example, a 2011 review of 26 studies on the effects of inhaled beta-2 agonists found that the medications did not improve “endurance, strength or sprint performance in healthy athletes.” In another study published in 2011, Belgian researchers wrote that taking salbutamol “does not affect exercise capacity in normal subjects.”
Leading up to the Beijing Olympics, news outlets suggested that the large number of elite athletes using inhalers, including silver medalist swimmer Dara Torres and gold medalist triathlete Emma Snowsill, signaled a potential abuse of asthma meds to get ahead. Amateur athletes, it seemed, were following suit, leaving a record numbers of inhalers behind at triathlon start lines.
Now, however, it’s speculated that the intense training Olympic athletes do might actually cause asthma symptoms. Olympic athletes with asthma regularly beat their non-asthmatic competitors, redorbit.com reports—not because they’re using inhalers, but possibly because the athletes that trained the most did the most damage to their lungs. Or because asthmatic athletes train harder to make up for their pulmonary deficit.
BOTTOM LINE: If you don’t have asthma, don’t use an inhaler. It won’t make you faster, stronger, or last longer, and you could unnecessarily subject yourself to performance-hindering side effects including dizziness, headaches, and nausea. source outside

                                        

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Apixaban: A Good Choice for AF Patients With Renal Dysfunction?

10:32 π.μ.    No comments
August 29, 2012 (Munich, Germany) — A new prespecified analysis of the ARISTOTLE study has shown that the new oral anticoagulant apixaban (Eliquis, Bristol-Myers Squibb/Pfizer) was better than warfarin at preventing the primary outcome, stroke or systemic embolism, in atrial-fibrillation patients, regardless of renal function [1]. And patients with kidney disease seemed to have the greatest reduction in major bleeding with apixaban.
These findings are important, because patients with renal insufficiency pose a problem for any kind of anticoagulant treatment due to their increased risk for both thromboembolic and bleeding events. Up to 20% of those with AF have some renal dysfunction, making treatment decisions difficult in this patient group.
These new results suggest that "apixaban may be particularly suited to address the unmet need for more effective and safer stroke prevention in patients with AF and renal dysfunction," say Dr Stefan H Höhnloser (JW Goethe University, Frankfurt, Germany) and colleagues in their paper published online August 29, 2012 in the European Heart Journal. Höhnloser also reported the results today in a clinical trial and registry update session at the European Society of Cardiology (ESC) 2012 Congress.
In a commentary accompanying the paper [2], Dr Jan Steffel (University Hospital Zurich, Switzerland) and Dr Gerhard Hindricks (University of Leipzig–Heart Center, Germany) concur. "This new substudy of ARISTOTLE provides solid evidence for the superiority of apixaban in patients with atrial fibrillation and chronic kidney disease. In the light of these data, apixaban appears to be a very appealing option for these individuals." However, they caution that this conclusion does not necessarily extend to those with severe renal disease (estimated glomerular filtration rate [eGFR] of <30 mL/min), since they made up only 1.5% of the study population.
And discussant of the trial at the ESC meeting, Dr Keith AA Fox (University of Edinburgh, Scotland), agrees: "In my view, ARISTOTLE provides a treatment option and advantages over warfarin in patients with moderate renal dysfunction, a group that is currently suboptimally treated."
Doctors Torn Deciding on Anticoagulation in AF With Renal Impairment
The main ARISTOTLE results were first reported at the ESC meeting last year and published simultaneously in the New England Journal of Medicine; they were widely viewed as the "most positive" data among the major randomized trials comparing new oral anticoagulants with warfarin for prevention of stroke in AF. Despite this, the US FDA has failed to yet approve apixaban for this indication for reasons that remain unclear. Apixaban is not approved for AF in the European Union, either, although it was cleared for marketing there for prevention of venous thromboembolism.
Steffel and Hindricks say doctors are torn when having to decide whether or not--and if so, how--to anticoagulate patients with atrial fibrillation and renal insufficiency. A recent study has even shown, for instance, that the net clinical benefit of warfarin is unclear in patients with AF and renal disease.
ARISTOTLE provides a treatment option and advantages over warfarin in patients with moderate renal dysfunction, a group that is currently suboptimally treated.
And the initial enthusiasm associated with the novel anticoagulants--such as dabigatran (Pradaxa, Boehringer Ingelheim) and rivaroxaban (Xarelto, Bayer/Johnson & Johnson)--"was dampened shortly after their introduction, when reports of major hemorrhages surfaced," they note. "Indeed, it quickly became clear that especially dabigatran, which is 80% renally cleared, has a significant potential for severe bleeding in patients with reduced renal function."
To try to address this problem, Höhnloser and colleagues evaluated the ARISTOTLE data, comparing apixaban--which is partially excreted by the renal system--with warfarin in relation to renal function. They note that a reduced dose of apixaban (2.5 mg twice daily instead of the usual 5 mg twice daily) was given to patients with two of the following criteria: age >80 years, weight <60 kg, and serum creatinine >133 mmol/L (1.5 mg/dL).
There were 7518 patients (42%) with no renal dysfunction (eGFR of >80 mL/min), 7587 (42%) with eGFR between 50 and 80 mL/min, and 3017 (15%) with an eGFR of <50 mL/min.
The rate of cardiovascular events and bleeding was higher in those with impaired renal function (<80 mL/min), as would be expected.
"The present analysis represents the largest experience of anticoagulation therapy in patients with AF and impaired renal function, and the superiority of apixaban relative to warfarin for preventing stroke or systemic embolism was consistent, irrespective of degree of renal impairment," say the researchers.
Those With Worse Kidney Function Had the Least Major Bleeding on Apixaban
Apixaban was also associated with fewer major bleeding events across all ranges of eGFR, with the relative risk reduction in major bleeding being greater in patients with an eGFR of <50 mL/min (hazard ratio 0.50; 95% CI 0.38–0.66' interaction p=0.005].
To examine whether the reduction in bleeding in patients with impaired renal function was due to the more frequent use of the lower apixaban dose (2.5 mg twice daily), two sensitivity analyses were conducted, first by adjusting for dose and second by excluding all patients on low-dose apixaban and repeating the analysis only in the patients on the standard dose. In both, the interaction between treatment and renal function remained statistically significant for major bleeding.
Steffel and Hindricks seem convinced by this analysis: "The finding of a statistically significant greater reduction in major bleeding in patients with impaired renal function implies a particularly pronounced benefit of apixaban compared with warfarin in this patient population," they observe.
Further Analysis Of Existing Studies Will Provide More Guidance
They then wonder, "Should every patient with atrial fibrillation and renal insufficiency hence be anticoagulated with apixaban?" and "How does apixaban compare with rivaroxaban and dabigatran in these patients?"
Unfortunately, comprehensive cross-trial comparisons with the other novel anticoagulants are impossible to perform, given--among other factors--the different study designs, different patient populations, and (partly)
Περιγραφή αναζήτησης
different bleeding definitions, they state. But as all three trials compared the respective novel agent with warfarin, it would be interesting to compare matched subsets of patients from each trial; "such data, however, are not yet available."
Nevertheless, data from large registries and from real-world use will provide additional evidence for further guidance, they note.
Höhnloser has served as a consultant, member of steering committee, or speaker for Bayer Healthcare, Bristol-Myers Squibb, Boehringer Ingelheim, Boston Scientific, Cardiome, Forest RI, Johnson & Johnson, Medtronic, Pfizer, Portola, Sanofi, and St Jude Medical. Disclosures for the coauthors are listed in the paper. Steffel has received consulting and/or speaker's fees from AstraZeneca, Bayer HealthCare, Boehringer Ingelheim, Bristol-Myers Squibb, and Pfizer and research support from Bayer Healthcare. Hindricks declared no conflicts of interest. Fox has received grant funding and honoraria from Sanofi, Lilly, Bayer, Johnson & Johnson, AstraZeneca and Boehringer Ingelheim.source medscape
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Κυριακή 2 Σεπτεμβρίου 2012

Choosing Oral Contraceptives With Lowest Thrombotic Risk

7:01 μ.μ.    No comments

Oral Contraceptive Pills

The most widely used form of contraception is the combined oral contraceptive pill. However, progestin-only pills, implants, depot medroxyprogesterone acetate (DMPA) injections, and medicated intrauterine devices are other contraceptive options, along with combined preparations available as transdermal patches and vaginal rings.
The combined pill contains 20-50 µg of ethinylestradiol and a progestin. Norethisterone was the first active progestin used in oral contraceptive pills and is classified as a first-generation progestin. Norgestrel and levonorgestrel are second-generation progestins, and desogestrel, gestodene, and norgestimate are the newer, third-generation progestins. Drospirenone is the latest progestogen component (fourth-generation) used in combined pills.
The combination pill works through multiple mechanisms: Negative feedback lowers follicle-stimulating and luteinizing hormone levels and prevents ovulation. The progestin component affects the cervical mucus, endometrium, and tubal motility and contributes significantly to the pill's contraceptive properties. The overall efficacy of the combination pill is user-dependent, but even with less-than-perfect use, it is among the most effective contraceptive options.

Risk for Venous Thromboembolism

In addition to providing effective contraception, use of the combined oral contraceptive pill is associated with multiple noncontraceptive benefits (including decreased blood loss, reduced dysmenorrhea, less cyst formation, and lower risk for ovarian/endometrial cancer). It is not, however, without adverse effects. It was recognized early on that the risk for venous thromboembolism (VTE) was increased among combination pill users.[1] This risk was attributed to its estrogen component, which affects the synthesis of clotting factors.
To mitigate this risk, the dose of the estrogen component was reduced, and later, new progestins were incorporated into the pill. Although the new progestins may be associated with a more favorable clinical profile, reports suggest a higher risk for VTE with these agents.
Many factors influence the risk for VTE. The incidence of VTE increases with age and body mass index. Family history, hematologic problems, immobilization, varicose veins, and pregnancy all affect a woman's risk for VTE. Therefore, these factors need to be controlled for when assessing the risk associated with different forms of hormonal contraception and generations of combination pills. Nonusers of hormonal contraception have a baseline risk for VTE of 1-3 per 10,000 woman-years.
A universal finding of existing research is an increased risk for VTE with the combination pill. The risk was somewhat reduced when the dose of ethinylestradiol was lowered. Most studies that compared pills from various generations found a higher risk with the third- and fourth-generation combined pills compared with the second-generation pills. Studies that failed to find a difference typically drew conclusions on the basis of a small number of VTE events.

Article Summary

This review by Lidegaard and colleagues summarizes the latest findings on VTE risk associated with hormonal contraceptives. In previous research, the investigators found the risk for VTE to be the highest (8 times the baseline risk) during the first year of contraceptive use compared with that of nonusers.[2] The risk, however, was still 3 times higher after 4 years of pill use. On the basis of findings from studies performed in different countries, the risk for VTE is 3 times higher with second-generation pills and 6-7 times higher with third- and fourth-generation pills. The absolute risk is small but cannot be ignored.
The investigators recommended the use of second-generation pills with the lowest estrogen content as the first choice of contraceptive pills. If adverse effects occur, a switch can be made to a third- or fourth-generation pill. Patients at risk for VTE should use a progestin-only pill, DMPA injections, or an intrauterine device. Older women, who have a higher risk for VTE as a result of age, also should use second-generation pills.

Viewpoint

Under normal physiologic conditions, the mechanisms responsible for clotting and spontaneous bleeding are controlled, and the risks for both are low. However, many factors can disrupt this equilibrium. Vascular problems, inherited risk for thrombosis, immobility, obesity, and hormones, in addition to contraceptive pill use, all can influence the clotting cascade and increase the risk for VTE.
Combined oral contraceptive pills containing newer progestins are associated with a doubling of the risk for VTE compared with second-generation pills. Lidegaard and colleagues explain this finding as a differential effect on sex-hormone-binding globulin levels. Newer progestins induce much higher levels, and this affects the total estrogenicity of the pill.
However, other possible explanations exist. Newer preparations are more likely to be prescribed to new users of hormonal contraception. Most VTE occurs during the first year of use, so new users are at higher risk. Newer medications are considered safer overall, and therefore newer-generation pills may be prescribed preferentially to women who are at higher risk for VTE.
Drospirenone has antiandrogenic properties and is commonly prescribed to take advantage of this noncontraceptive benefit. Women with hyperandrogenemia (mainly polycystic ovary syndrome) are more likely to have underlying vascular problems and are at a higher baseline risk for VTE.
The message of this review is that care must be taken in the selection of a combined oral contraceptive pill and the choice has to be individualized, taking into account age, body mass index, family history, and other risk factors. The combined pill carries about the same risk for VTE as the pregnancy it is designed to prevent. Patients should be counseled about the signs of VTE to avoid more severe complications.sourse medscape
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Σάββατο 1 Σεπτεμβρίου 2012

The Pathophysiology of Atrial Fibrillation (AF) and the Importance of Sinus Rhythm

12:40 π.μ.    No comments
Remodeling of the atria caused by atrial fibrillation makes it more difficult to return to sinus rhythm, more difficult to respond to treatment, and increases vulnerability to relapse.1

Classification

  • The American College of Cardiology (ACC), the American Heart Association Task Force (AHA), and the European Society of Cardiology Committee (ESC), in collaboration with the Heart Rhythm Society have established guidelines for the classification of AF2
  • First-detected episode of AF – may or may not be symptomatic; the actual duration of the episode and previous undetected episodes may be uncertain2
  • Recurrent AF - 2 or more episodes2
    • Paroxysmal AF - self-terminating, spontaneously converts to sinus rhythm2
    • Persistent AF - lasts longer than 7 days, is not self-terminating and usually requires medical intervention2
  • Permanent AF – refractory to cardioversion or has persisted for a long period of time2
  • Lone AF – occurring in a patient younger than 60 years who has no clinical or echocardiographic evidence of cardiopulmonary disease, including hypertension2
  • Valvular and nonvalvular AF – occurs in a patient who has evidence or history of rheumatic mitral valve disease, who has a prosthetic heart valve, or who has valve repair; all other forms of AF are classified as nonvalvular AF2

Atrial Fibrillation Begets Atrial Fibrillation

  • One of the main challenges of atrial fibrillation is the tendency of the disease to become chronic over time, during which a combination of molecular and structural changes make it difficult to achieve and maintain sinus rhythm3

Electrical Remodeling

  • The concept that AF is self-perpetuating has been studied extensively in a goat model using an automatic atrial fibrillator that detected spontaneous termination of AF and reinduced AF by electrical stimulation. At first, the electrically induced AF terminated spontaneously. However, with repeated inductions, AF episodes became progressively more sustained until AF persisted and at a more rapid rate. The increasing propensity to AF was associated with progressive shortening of the effective refractory period as well as with increasing episode duration2 (See Figure)
  • Electrophysiological remodeling has led to the phrase “atrial fibrillation begets atrial fibrillation,” originally coined by Wijffels and colleagues2,3
  • In addition to remodeling and changes in electrical refractoriness, prolonged AF disturbs atrial contractile function. After a period of persistent AF, recovery of atrial contraction can be delayed for days or weeks following the restoration of sinus rhythm2

Figure 2-1
Figure. Posterior view of principal electrophysiological mechanisms of atrial fibrillation. A. Focal activation. The initiating focus (indicated by the star) often lies within the region of the pulmonary veins. The resulting wavelets represent fibrillatory conduction, as in multiple-wavelet reentry. B. Multiple wavelet reentry. Wavelets (indicated by arrows) randomly reenter tissue previously activated by the same or another wavelet. The routes the wavelets travel vary. LA indicates left atrium; PV, pulmonary vein; ICV, inferior vena cava; SCV, superior vena cava; and RA, right atrium. Adapted from Konings.2,4

  • Electrophysiological remodeling occurs on 2 time scales: rapid (seconds or minutes) and slower (days or weeks)3
    • Rapid electrophysiological remodeling involves translational modulation of Ica and ITO ionic currents by altered pH, intracellular Ca2+, phosphorylation and oxidation state, and metabolic regulation of pore forming alpha and beta subunits3
    • Slower changes are due to changes in the rate of translation, synthesis, and degradation of ion channel subunits in the myocyte membrane3

Structural Remodeling

  • The most frequent structural changes in AF are atrial fibrosis and loss of atrial muscle mass2
  • Atrial fibrosis may precede the onset of AF. Nonhomogeneity of conduction may result from the juxtaposition of patchy fibrosis with normal atrial fibers2
  • Interstitial fibrosis may be triggered by atrial dilation in any type of heart disease associated with AF. Also, interstitial fibrosis may result from apoptosis leading to replacement of atrial myocytes, loss of myofibrils, disruption of cell coupling gap junctions and organelle aggregates, or accumulation of glycogen granules2
  • Apoptosis, or programmed cell death, provides temporal and spatial control of a cell and determines the cell’s lifetime. Apoptosis may occur inappropriately under pathophysiological conditions. When this happens in the heart, myocytes die and contractile capacity as well as electrical activity is permanently lost. The pathways of electrical activation may be altered due to replacement fibrosis. The presence of apoptotic myocytes in the atrial tissues of patients with chronic AF was documented by Aime-Sempe and colleagues3
  • Structural changes in AF occur at a slow rate, significantly slower than electrophysiological remodeling, and probably most structural changes are irreversible3

Molecular Changes in AF

  • In atrial tissue specimens from a total of 53 explanted hearts of transplantation recipients with dilated cardiomyopathy, 18 had persistent, 19 had permanent, and 16 had no documented AF. Extracellular matrix remodeling including selective upregulation of matrix metalloproteinase 2 (MMP-2), type 1 collagen volume fraction (CVF-1) and downregulation of insulin-like growth factor II mRNA-binding protein 2 (IMP-2) were associated with sustained AF2
  • The concentration of membrane-bound glycoproteins that regulate cell-cell and cell-matrix interactions (disintegrin and metalloproteinases) in human atrial myocardium has been reported to double during AF, potentially contributing to atrial dilation. Dilation of the atria activates several molecular pathways including the renin-angiotensin-aldosterone system (RAAS). Angiotensin II is upregulated in response to stretch, and atrial tissue from patients with persistent AF demonstrates increased expression in angiotensin-converting enzyme (ACE). Angiotensin inhibition and angiotensin II receptor blockage may prevent AF by reducing fibrosis2
  • A genetic defect, such as mutations in lamin AC gene, has been associated with AF. Other triggers of fibrosis include inflammation as seen in cardiac sarcoidosis and autoimmune disorder2

Long-term Impact of AF

  • A retrospective analysis demonstrated that 20% of patients with intermittent AF were in permanent AF after 4 years5
  • 77% of patients with paroxysmal AF were in permanent AF after a mean of 14 years.5 Independent risk factors for early progression to permanent AF included age, dilated left atrium, MI, and valvular disease5
  • The longer one waits to initiate a rhythm treatment strategy, the harder it is to regain sinus rhythm. Patients who converted to sinus rhythm within 3 months of onset of AF were more likely to remain in sinus rhythm at 6 months than patients who converted more than 12 months after onset of AF (67% versus 27%)6
  • By shortening the atrial refractory period, reducing conduction velocity and provoking contractile and structural remodeling, AF sets the stage for self-perturbationSOURCE,MEDSCAPE
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Πέμπτη 30 Αυγούστου 2012

ABO Blood Type Is a Risk Factor for Coronary Heart Disease

10:30 π.μ.    No comments

From Heartwire

ABO Blood Type Is a Risk Factor for Coronary Heart Disease

Michael O’Riordan
\  
August 14, 2012 (Boston, Massachusetts) — Data from two prospective cohort studies have identified the ABO blood group as a risk factor for the development of coronary heart disease [1]. Individuals with blood groups A, B, or AB were 5% to 23% more likely to develop coronary heart disease compared with subjects with O blood type, and the associations were not altered by multivariate adjustment of other risk or dietary factors.
The analysis, led by Dr Meian He (Harvard School of Public Health, Boston, MA), included 62 073 women from the Nurses' Health Study (NHS) and 27 428 men from the Health Professionals Follow-up Study (HPFS) and is published in the September 2012 issue of Arteriosclerosis, Thrombosis, and Vascular Biology.
In the NHS and HPFS, the incident rates of coronary heart disease per 100 000 person-years were 125, 128, 142, and 161 for women with type O, A, B, and AB, respectively, and 373, 382, 387, and 524 for men with type O, A, B, and AB, respectively. Compared with individuals with O blood type, individuals with blood group A, B, or AB had a respective 5%, 11%, and 23% increased risk of developing coronary heart disease in an age-adjusted model. These associations were not significantly altered in the multivariable-adjusted risk model.
Age-Adjusted Hazard Ratios (95% CI) for Coronary Disease by ABO Blood Type
Cohort Blood group O Blood group A Blood group B Blood group AB
NHS 1.0 1.04 (0.94–1.15) 1.14 (1.00–1.30) 1.20 (1.02–1.40)
HPFS 1.0 1.07 (0.96–1.18) 1.10 (0.95–1.27) 1.26 (1.07–1.48)
Combined NHS and HPFS 1.0 1.05 (0.98–1.13) 1.11 (1.01–1.23) 1.23 (1.10–1.37)
The researchers also performed an analysis examining the risk of coronary heart disease in patients with non-O blood type. Compared with individuals with O blood type, those with A, B, and AB had a 9% increased risk of developing coronary heart disease, and this risk was unaltered after adjustment for other risk factors. Similarly, a combined analysis of NHS and HPFS with four other prospective studies, an analysis that included 114 648 subjects, found there was a 6% increased risk of coronary heart disease for those with non-O blood type compared with individuals with O blood.
In total, just over 6% of the coronary heart disease cases were attributable to the A, B, or AB blood types, according to the researchers.
In terms of possible underlying mechanisms for the increased risk, He et al note that in non-O individuals, plasma levels of factor VIII-von Willebrand factor (vWF) are approximately 25% higher than in individuals with type O blood type. Elevated levels of factor VIII-vWF have been previously identified as a risk factor for coronary heart disease.
"The vWF has an important role in hemostasis and thrombosis by mediating platelet adhesion to the vascular wall, especially under high shear stress conditions," explain He and colleagues. "Along with fibrinogen, vWF also participates in platelet aggregation and plays a role in the development of atherosclerosis." In addition, the A blood group has been shown to have higher levels of total and LDL cholesterol.
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Τρίτη 28 Αυγούστου 2012

The Management of Atrial Fibrilliation and the Value of Sinus Rhythm

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The Management of Atrial Fibrilliation and the Value of Sinus Rhythm

Dr. Prystowsky

EXPERT INTERVIEW With Eric Prystowsky, MD

Medscape recently had the opportunity to discuss the management of atrial fibrillation (AF) and the value of sinus rhythm with Eric Prystowsky, MD — Consulting Professor of Medicine, Duke University Medical Center, Durham, NC and Director of the Electrophysiology Laboratory, St. Vincent's Hospital, Indianapolis, IN.


Question: What factors affect the overall management strategy for atrial fibrillation?
Dr Prystowsky:  I approach this from several viewpoints.  As one of the writers of the first international guidelines for the management of patients with AF and also the updated guidelines, and sprinkling into this the personal experience of several decades of managing patients with AF, it is important to have a game plan about the present and future management of that individual.
For example, is this paroxysmal or persistent AF? Are there concomitant medical illnesses that may affect your long-term and even short-term game plan? Is this postop management of atrial fibrillation versus somebody who has been in AF for years? These issues affect whether you're going to do rate or rhythm control, drugs, ablation and so forth.
The next set of issues relate to rate control, rhythm control and the risk of stroke.
The first thing you have to make sure about right away is the risk of stroke and need for risk reduction.
Then, you have to be sure you can control their heart rate. Regardless if you select a rate or rhythm treatment strategy, you have to at least be sure that when they do have episodes of AF that they are not going so fast as to get themselves into trouble.
The third thing is the rate versus rhythm question. Is this a person who will do better in sinus rhythm or is this a person who will do very well just staying in good rate control?
Once you've considered the issues and answered all those questions, you can then lay out a reasonable treatment goal for that individual.

Question: What are the short- and long-term goals you set for your patients?
Dr Prystowsky:  The short-term goal is to ensure you've covered stroke risk, whether or not sinus rhythm is your long-term goal. Managing stroke risk to cover the period of time around the cardioversion is important, because patients who have been in persistent AF for 48 hours or more develop atrial myopathy. They're known to be at risk for developing thrombi that can embolize and cause strokes and other problems, and require three weeks of stroke risk management before and at least four weeks after cardioversion.
Short-term, you must be sure that you also take care of rate control. By short-term, I mean during the first few days of treatment to be sure that the patient will not develop a tachycardia-mediated cardiomyopathy.
Long-term goals are very different. If my long-term goal for a patient is to maintain sinus rhythm, then I know I am going to try to cardiovert the patient. My immediate concern is risk of stroke, but I don't want to postpone cardioversion for too long since it may be more difficult to achieve sinus rhythm.
On the other hand, if it's a 75-year-old with newly discovered AF who is truly totally asymptomatic and you feel he or she is an excellent candidate for rate control, once you've covered the stroke risk, you need to be sure this patient has a long-term goal of good, adequate rate control.
The short-term goal is to stabilize the patient, make sure he or she is not in a risk situation, and then you can determine where the fork in the road is, that is rhythm or rate control long-term.


Question: Which patients are best suited for a rhythm control strategy?
Dr Prystowsky: It is clear that some people can do well with either a rate or rhythm control strategy. There have been a series of randomized, prospective trials published in the last few years that have addressed this issue. The one that is most often quoted—and clearly the biggest trial—was the AFFIRM study. 
The AFFIRM study asked the question, "Do people have a better or worse chance or no difference in survival if they have rate control versus rhythm control?" Patients did equally well whether they were rate or rhythm controlled. That conclusion has been misrepresented, or at the very least misunderstood as physicians have extended the trial results to other groups of patients.
The entry point in this trial was patients who were suitable for either rhythm or rate control and who were at high risk for events such as stroke. It turned out to be a patient population averaging about 70 years old.
The issue is, can you apply the AFFIRM data to a 30-year-old, a 40-year-old and a 50-year-old? I say you certainly cannot.
That kind of data migration, or conclusion migration, is really not appropriate. You have to stick to the question asked and the population in whom it was asked.
The other major issue is that there was a substantial number of patients who were potential candidates but not enrolled because either the treating physician or the trialist did not think they were adequate candidates for rate control. In other words, they needed sinus rhythm, or they weren't going to tolerate just being out of sinus rhythm.
That's a large group of excluded patients even in the elderly patient population. In an AFFIRM type of patient population, I think they have clearly shown rate and rhythm are equivalent treatment strategies, as long as rate control gets the patient to a point of feeling good.
There are three types of patients that I would initially target for sinus rhythm.
In patients who have not been studied, my own bias is that sinus rhythm is best, until someone shows me that rate control in a person in the younger age group is better. Until we know more, I think that sinus rhythm is the preferred initial approach.
Sinus rhythm is also clearly the approach for a second group of patients, in whom you've tried rate control and there are still substantial symptoms. You get them back into sinus rhythm and suddenly they feel much better.
The third group of patients are individuals in whom AF, if not now, but in the future, could be a problem for them. These typically are people who have diastolic compliance problems in their left ventricle.
If a person has ventricular hypertrophy and is on the borderline of diastolic dysfunction or has, even mild to moderate dysfunction that's going to worsen over time, I think leaving them in AF may be an unwise thing to do. At a point in time when there is a problem, it may be too late to restore sinus rhythm.   


Question: Do you believe that being in sinus rhythm has an impact on disease progression?
Dr Prystowsky: First of all, let's look at the heart itself. Will keeping somebody in sinus rhythm make a difference as to whether or not that person's heart stays the same? It's well known if you stay in AF, you will have progressive changes in the atrial tissue that can become permanent. These changes are both anatomic, for example atrial dilatation, as well as electrophysiologic, such as shortening of action potentials in the atrium, and can promote the continuation of AF and make it difficult, even several years later, to maintain and restore sinus rhythm. Persistence of AF can change the atria. 
The next question is, "Will that change affect the cardiovascular state of that person?" That question is difficult to predict. In some patients who have heart failure, it's been shown even with good rate control they just simply don't do as well because of the AF. When you restore sinus rhythm, they literally feel better and do better.
The same holds true for people who have substantial left ventricular diastolic compliance problems. Again, will they actually get worse if you leave them in AF? I don't think we have data to support that.
I think there are people in whom maintaining sinus rhythm will prevent further deterioration of left ventricular function, and I believe there are some data to suggest that's true. I don't think there are any data to suggest that's true for hypertrophy. 


Question: Do you think AF is an under-recognized cardiovascular risk factor?
Dr Prystowsky:  Atrial fibrillation, I believe, is felt by many people to be more of a nuisance than a real problem.
There are a number of patients with AF who will call you for even four seconds of AF. Their chart is on your desk the next morning: Mrs. Smith had a brief run of AF yesterday. 
No matter what you do, you're never going to make that person happy, so doctors don't necessarily want to deal with AF. They don't want to find out if a patient has it. They'd rather it just simply go away.
AF can cause strokes. It can cause heart failure. It can cause deterioration in health. In study after study it's been associated with increased mortality. It is a problem, regardless of being a nuisance.
I think it is totally unrecognized in a large part of the medical community how serious AF can be. What makes it worse is that AF can disguise itself because it is frequently asymptomatic. A patient has a stroke or a TIA, and his or her doctor doesn't do the appropriate workup, which is long-term monitoring to see if, indeed, the person in that age group might have unrecognized AF, and if so needs to be aggressively managed  to prevent future strokes. This goes on all the time.
It's a nuisance and therefore avoided, but it's also grossly unrecognized because of its very frequent asymptomatic presentation.
Atrial fibrillation has a very important effect on the health of our citizens. If you look at the major expenditure for hospitalizations in arrhythmias, it's usually AF. People get admitted to the hospital when it can be totally outpatient managed.
Our job to educate on AF is dramatically important, not only for the individual health of the patient, but for the health of the entire medical healthcare system. 


Question: Please just comment on the public health challenge of atrial fibrillation.
Dr Prystowsky:  From a global perspective there is a need to identify the causes of AF and find ways to minimize its occurrence.
Let's look at risk factors. Probably the most important risk factor, certainly in western civilization, is hypertension. Hypertension is associated with at least 40%-50% of the patients who have AF. Patients with hypertension tend to get left ventricular diastolic dysfunction, which often translates to increased pressure in the left atrium.
Data published in the Journal of Cardiovascular Electrophysiology have shown pulmonary veins are largest in a subgroup of patients who have both hypertension and AF versus hypertension alone, and versus patients without hypertension.
Most patients with AF have their triggers in the pulmonary veins, and one could hypothesize that there are stretch receptors that cause increased automaticity that are more actively engaged in patients who have significant hypertension, pressure changes, and so forth.
Also general cardiovascular care, such as minimizing heart failure and coronary disease, will again minimize the risk of AF. Conditions such as sleep apnea can increase the risk of AF. Attention to patients with these problems will minimize the occurrence of AF.  
We're never going to totally eradicate it based on just those risk factors, but we could hopefully have a substantial reduction in the numbers of AF patients.
The second thing is how can we best manage AF in a cost effective way. First of all, most people with AF do not have to be hospitalized. Clearly, there are exceptions, such as for patients starting drugs that might be somewhat risky for proarrhythmia, which you feel more comfortable starting in a hospital under observation.
There are some people whose AF has caused worsening of heart failure. But for the most part, AF does not require a person to be hospitalized, including cardioversion. In most people, you can perform cardioverversion as an outpatient and send the patient home the same day. An exception is a patient who has started on treatment that prolongs the QT interval, and in that case you would want to monitor the QT interval in sinus rhythm for at least 24 hours.
If we can learn to tailor outpatient therapy and only admit people who really need hospitalization, it's good for the patient and it's good for the general health bill for the country.
I think if we pay attention to both these areas, preventing the episodes as best we can by paying more attention to preventive medicine, and once the patient has been diagnosed with AF, really thinking it through carefully on how to minimize occurrences and avoid admittance to the hospital, I think will make a large step forward in the management of AF for the patient and society.sourse medscape
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