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
Two major clinical trials are testing for the first time whether treating inflammation can reduce the risk of a heart attack or stroke, potentially opening up a new line of attack in the battle against cardiovascular disease.
Brigham and Women's Hospital
'This goes beyond simply asking, is inflammation a marker of risk to asking if it's a target for therapy,' said Paul M. Ridker, who is leading the two trials.
Until now, strategies to fight these killers have focused largely on well-known risk factors such as high blood pressure and cholesterol. The new studies, one sponsored by the National Institutes of Health and the other by pharmaceutical giant Novartis SA, NOVN.VX-1.06% will test the hypothesis that inflammation plays a crucial role in the underlying biology that makes heart disease and stroke the No. 1 and No. 4 causes of death in the U.S., respectively.
Inflammation is part of the body's normal healing response to injury. When the walls of the coronary arteries or the vessels that carry blood to the brain suffer injury from the effects of smoking, obesity and abnormal cholesterol, for instance, the immune system as part of the inflammatory response dispatches cells to repair the damage, researchers say. But in the face of a constant assault by such irritants over decades, possibly abetted by genetics, that system can go into overdrive. Instead of protecting the vessels, inflammation becomes chronic, leading to the accumulation and potential rupture of arterial deposits called plaque that can cause heart attacks and strokes.
Research over two decades has shown that people with chronic inflammation—detectable at low levels, for instance, with a high-sensitivity test for a marker called C-reactive protein—are at significantly higher risk of heart attack and stroke compared with those with evidence of little or no such inflammation.
But whether the risk can be mitigated by inhibiting or shutting down the process with anti-inflammatory drugs isn't known.
"This goes beyond simply asking, is inflammation a marker of risk (for cardiovascular disease) to asking if it's a target for therapy," said Paul M. Ridker, director of the center for cardiovascular-disease prevention at Harvard-affiliated Brigham and Women's Hospital in Boston, who is leading both trials.
Significant progress has been made against heart attacks and strokes in recent years, thanks to what researchers believe is the cumulative impact of prevention strategies that include more aggressive use of cholesterol and blood pressure drugs, anti-smoking initiatives and better exercise and dietary habits. Heart attack admissions among the elderly fell by nearly 25% in the five years ended in 2007, a recent study showed, while stroke deaths declined by nearly 20% in the decade ended in 2008.
Still, both problems exact a heavy toll. More than 1.25 million Americans suffer a heart attack each year, according to the American Heart Association, while nearly 800,000 have a stroke.
"If you could find a way to dramatically reduce the incidence of heart attacks by blocking inflammation, that would change the practice of medicine," said Mark Fishman, a cardiologist and president of the Novartis Institutes for BioMedical Research.
The new trials mark the latest effort to take prevention efforts beyond conventional strategies.
The NIH study will test whether the widely used generic anti-inflammatory drug methotrexate can reduce major cardiovascular events in 7,000 patients with a history of heart attack—who also have either diabetes or a cluster of prediabetic risk factors known as the metabolic syndrome. Enrollment is expected to begin at more than 350 sites in the U.S. and Canada next March.
These are especially high-risk patients for whom current optimal treatment often fails. "We've kind of run out of our tool kit for these individuals and yet they're still having events," said Gary Gibbons, director of the NIH's National Heart, Lung and Blood Institute, which officially funded the study.
The Novartis trial, which is testing the company's anti-inflammatory antibody called canakinumab, has already enrolled 3,000 patients of a planned 17,000 patients with stable cardiovascular disease and elevated levels of inflammation. (The drug is marketed under the brand name Ilaris for a rare inflammatory disease called Muckle-Wells Syndrome.) In proof-of-concept studies, it yielded what Dr. Fishman called "provocative" evidence of benefit in coronary arteries.
But it will take the much-larger study to determine whether it actually prevents serious complications of cardiovascular disease.
Both drugs directly target certain inflammatory pathways with little if any effect on other cardiovascular risk factors. Current preventive medications, including aspirin, which inhibits blood clotting, and cholesterol-lowering statins, which reduce LDL or bad cholesterol, a key heart- and stroke-risk factor, also lower inflammation. Thus in studies showing benefits of both drugs, "we can't tease apart whether lowering inflammation alone has an incremental benefit," Dr. Ridker said.
Finding a benefit may be a challenge in the big trials. All participating patients will be treated with optimal therapy, meaning that those in the anti-inflammatory arms of each study will also be given statins and be compared against patients who are on aggressive statin and other therapies that may also reduce inflammation.
"The question is how difficult will it be to get above and beyond" the benefit of current treatments, said Michael Miller, director of the center for preventive cardiology at University of Maryland Medical Center. "The problem is the placebo group is going to be very well treated."
Indeed, many researchers believe the effectiveness of current therapy has proved a daunting hurdle to efforts to develop new cardiovascular drugs. Niacin and an experimental drug known as a CETP inhibitor—both of which raise HDL or good cholesterol—failed in recent studies to reduce heart risk when added to statin treatment. Other studies intending to show benefit from raising HDL cholesterol are in progress.
One of the first hints that treating inflammation might reduce cardiovascular disease risk came in 1997 in a report led by Dr. Ridker from the so-called Physicians Health Study—the study that a decade earlier had demonstrated the benefit of daily aspirin in preventing heart attacks. Dr. Ridker found that elevated inflammation as measured by levels of C-reactive protein was associated with a threefold risk of heart attack and a doubling of stroke risk. Those with the highest C-reactive protein levels got the most benefit from aspirin.
The findings and subsequent research led to development of a high-sensitivity test for C-reactive protein that many doctors now use to help assess patients' heart and stroke risk. (Dr. Ridker is listed as an inventor on patents held by Brigham and Women's Hospital for such a test, but he said neither he nor the hospital will receive royalties for any of the tests used in either of the two new studies.)
How useful the test is in assessing heart risk has provoked controversy among cardiologists, but there is broad consensus that inflammation is an important player in the development of cardiovascular disease.
"So the question becomes, if we inhibit inflammation, can we get benefit?" Dr. Ridker says. "And we'll see."source wsj

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

Πέμπτη 30 Αυγούστου 2012

ABO Blood Type Is a Risk Factor for Coronary Heart Disease

From Heartwire

ABO Blood Type Is a Risk Factor for Coronary Heart Disease

Michael O’Riordan
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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.

Τρίτη 28 Αυγούστου 2012

The Management of Atrial Fibrilliation and the Value of Sinus Rhythm

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

Παρασκευή 24 Αυγούστου 2012

Perioperative Beta-Blockade: Atenolol Is Associated With Reduced Mortality When Compared to Metoprolol

Wallace AW, Au S, Cason BA
Anesthesiology. 2011;114:824-836

Summary

Studies have suggested that perioperative beta-blockade reduced postoperative adverse cardiac events in both the short and long term, and current guidelines recommend prophylactic beta-blockade for high-risk patients undergoing noncardiac surgery.[1,2] However, it is still unclear whether the protective effect differs among beta-blockers.
In this retrospective study, 3787 patients who underwent perioperative beta-blockade were divided into 2 groups: one that received atenolol and one that received metoprolol. The authors performed logistic regression analysis to investigate mortality among patients continuously managed with either one of these agents.
The results indicated that 30-day mortality (1% in the atenolol group vs 3% in the metoprolol group; P < .001) and 1-year mortality (7% vs 13%, respectively; P < .001) differed between the 2 beta-blockers. Propensity matching that corrected for cardiac risk factors found an odds ratio of 2.1 (95% confidence interval, 1.5-2.9; P < .001) for an increase in 1-year mortality with the use of metoprolol. The investigators concluded that perioperative beta-blockade using atenolol is associated with reductions in both short- and long-term postoperative mortality compared with metoprolol.

Viewpoint

In 2009, on the basis of evidence from many studies, the American College of Cardiology/American Heart Association updated their guidelines, stating that perioperative beta-blockade is a class IIa recommendation for patients with cardiac risk and should be considered during surgery.[1] However, few studies have compared different beta-blockers or characterized their dose effect in the perioperative setting.
Wallace and colleagues' study provides evidence suggesting a difference in effectiveness among beta-blockers. Indeed, not all beta-blockers may be equal. A decrease in sudden death after myocardial infarction has been demonstrated only for the more lipophilic beta-blockers, whereasmetoprolol and propranolol have been shown to prevent ventricular fibrillation in clinical trials.[3] Atenolol has a long duration of action and difference in metabolism compared with metoprolol, and this suggests that a long-acting beta-blocker may be superior to a short-acting one.[4,5] More prospective randomized trials are necessary to validate these observational findings sourse.medscape

Πέμπτη 23 Αυγούστου 2012

Vanishing-Polymer DES Beat Bare-Metal Stents in STEMI

 Use of a biolimus-eluting stent with a biodegradable polymer (BioMatrix, Biosensors Europe) in patients with ST-elevation MI (STEMI) results in an almost 50% lower rate of major adverse cardiovascular events (MACE) compared with using a bare-metal stent, according to the COMFORTABLE AMI study, which has just been published in the August 22, 2012 issue of the Journal of the American Medical Association [1].The findings, which look at outcomes to one year and also hint at superior safety of this newer-generation drug-eluting stent (DES) over bare-metal stents in this setting, were first presented at the EuroPCR 2012 meeting earlier this year, by Dr Lorenz Räber (Berne University Hospital, Switzerland), who is lead author on the current paper.
Senior author Dr Stephan Windecker (Berne University Hospital, Switzerland) told heartwire the COMFORTABLE AMI results, together with other studies looking at newer-generation DES for this patient population, seem to be tipping the scales away from the tradition to opt for bare-metal stents in STEMI.
It's an important paradigm shift, because . . . now we suddenly see that maybe the newer-generation DES is even better in terms of safety.
And this is not least because worries about adverse effects seem to be abating, he observes. "It's an important paradigm shift, because so far we haven been concerned about the safety [with DES in STEMI], but now we suddenly see that maybe the newer-generation DES are even better in terms of safety [than bare-metal stents]," he commented.
In an accompanying editorial [2], Drs Salvatore Cassese and Adnan Kastrati (Deutsches Herzzentrum, Munich, Germany) broadly agree. "The COMFORTABLE AMI trial should make cardiologists feel more comfortable with the use of new-generation DES in patients with STEMI. The efficacy of DES vs [bare-metal stents] in STEMI is already established, and therefore further studies comparing these interventions might not be needed."
Worries about late safety issues with DES "are mostly related to first-generation DES," they note, adding that "larger randomized trials with longer follow-up and head-to-head comparisons of the [newer] available DES technologies are, however, required to completely eliminate these concerns."
Not Known How Newer-Generation Stents Compare With Each Other
Windecker explains that the newer DES, such as the Xience everolimus-eluting stent and the Resolute zotarolimus-eluting stent, release antiproliferative drugs from more biocompatible polymers than the older ones or they have biodegradable polymers--such as the BioMatrix employed in COMFORTABLE AMI--which degrade after the drug has been released to leave a stent surface more closely resembling a bare-metal stent.
In his institution they currently use just four newer-generation DES, the Xience, the Resolute, the BioMatrix, and another investigational stent with a biodegradable polymer, but this time sirolimus-eluting, called Orsiro (Biotronic).
He notes that the EXAMINATION trial comparing the Xience stent with bare-metal stents in STEMI patients also showed very favorable results for the newer stent, so "another question is whether there is a difference between newer-generation DES with durable and biodegradable polymers," he says. Currently, he notes, "we alternate [the newer DES] on a daily basis for all patient populations or we study them in a protocol. At this point in time, we couldn't say one is better or worse than the other."
We alternate [the newer DES] on a daily basis for all patient populations or we study them in a protocol. At this point in time we couldn't say one is better or worse than the other.
Cassese and Kastrati say any studies comparing newer DES should take advantage of intravascular imaging techniques "to provide mechanistic insight into the clinical findings."
But they also add that bare-metal stents should not be forgotten. "Although there is almost no rationale for performing DES vs bare-metal stent studies anymore, it might be conceivable to expect studies that test the hypothesis of noninferiority of new, improved bare-metal stents to available DES," they note.
COMFORTABLE AMI: A Suggestion of Superior Safety for Newer DES
Windecker says the published results of COMFORTABLE AMI are "very much what we presented at EuroPCR." In the study, 1161 patients presenting with STEMI at 11 sites in Europe and Israel between September 2009 and January 2011 were randomized 1:1 to receive the BioMatrix biolimus-eluting stent (n=572) or a bare-metal stent (n=582). The primary end point was the rate of MACE, a composite of cardiac death, target vessel–related reinfarction, and ischemia-driven target lesion revascularization (TLR) at one year.
MACE at one year occurred in 24 patients (4.3%) receiving the BioMatrix stent and 49 (8.7%) receiving a bare-metal stent (hazard ratio 0.49; p=0.004). This was mainly driven by the lower risk of target vessel reinfarction (0.5% vs 2.7%, HR 0.20; p=0.01) and ischemia-driven TLR (1.6% vs 5.7%, HR 0.28: p<0.001) in those receiving the BioMatrix compared with the bare-metal stent. Rates of cardiac death were not significantly different.
Windecker cautioned, however, that care must be taken in interpretation of the 80% relative risk reduction in target vessel reinfarction, a novel finding, because target vessel reinfarction "was not the primary end point."
We need a definitive trial to explore whether in fact [newer] DES may be superior in terms of safety.
Definite stent thrombosis occurred in five patients treated with BioMatrix (0.9%) and 12 (2.1%) of those receiving a bare-metal stent (HR 0.42, p=0.10).
In their editorial, Cassese and Kastrati caution that COMFORTABLE AMI "has neither the required sample size nor the sufficient length of follow-up to provide the definitive answer about the long-term safety of the new biodegradable DES in this setting."
Windecker concurs, although he points to previous four-year findings with this BioMatrix stent in the LEADERS trial, also performed at University of Bern, but this time comparing the newer stent with the older, now-defunct Cypher (sirolimus-eluting) DES in all-comers. The BioMatrix was noninferior and potentially better than Cypher in terms of MACE, with an 80% reduced risk of stent thrombosis.
The COMFORTABLE AMI findings, "in terms of safety, [are] comforting and reassuring, but we need a definitive trial to explore whether in fact DES may be superior in terms of safety," he comments.
GLOBAL-LEADERS Trial Will Compare Ticagrelor With Conventional DAPT
One of the issues that currently helps determine whether doctors use newer DES or bare-metal stents in STEMI patients is expected compliance with antiplatelet therapy. Newer DES are thought to have the edge in acute-STEMI cases if the patient adheres to dual antiplatelet therapy for up to a year. But if there is any question about compliance, clinicians may opt for a bare-metal stent instead.
Windecker and colleagues are now exploring whether single antiplatelet therapy with a more potent agent (ticagrelor [Brilinta, AstraZeneca]) for two years, with just a month's aspirin treatment, will be better than conventional dual antiplatelet therapy with aspirin and clopidogrel for one year in 16 000 patients receiving the BioMatrix stent in a trial called GLOBAL LEADERS.
"We would like to see the balance between ischemia and bleeding in this more simplified regimen. Really, what it's asking is whether we can live without aspirin with a more modern antiplatelet," he says.
Windecker reports receiving research contracts to his institution from Abbott, Boston Scientific, Biosensors, Biotronik, Coris, Medtronic, and St Jude Medical. Räber has no conflicts of interest. Disclosures for the coauthors are listed in the paper. Kastrati holds a patent related to polymer-free sirolimus and probucol coating and reports receiving honoraria from Abbott, Biosensors, Cordis, and Medtronic. Cassese reports no conflicts of interest.sourse medscape

Τετάρτη 22 Αυγούστου 2012

Statins May Lower Risk for Pancreatitis



 Despite opposing results from early observational studies, a new meta-analysis suggests that statins may reduce the risk of developing pancreatitis among patients with normal to slightly elevated triglyceride levels. Findings from the study, conducted by David Preiss, MD, PhD, from BHF Glasgow Cardiovascular Research Centre in the United Kingdom, and colleagues, were published in the August 22/29 issue of JAMA.
Patients with pancreatitis can experience a range of outcomes, from mild, self-limiting episodes to severe or fatal events. Hypertriglyceridemia is the third most common cause of pancreatitis, but the medicines prescribed to lower triglyceride levels carry their own worries. Studies have linked pancreatitis to use of statins, which, as a class, represented $20.1 billion in US sales last year, according to IMS Health, a healthcare information company.
In addition, fibrates, which are prescribed to patients with moderate to severe hypertriglyceridemia, may increase the risk for pancreatitis for patients whose triglyceride levels fall below 400 mg/dL, the threshold used for the prescribing guidelines.
Dr. Preiss and colleagues sought to determine the association between incident pancreatitis and lipid-lowering statins and fibrates by conducting meta-analyses of relevant, published and unpublished, large, randomized clinical trials.
The researchers included 28 randomized clinical trials (21 statin-related trials and 7 studies evaluating fibrates) that involved at least 1000 patients, with a minimum follow-up of 1 year. Unpublished data from the Helsinki Heart Study and its smaller ancillary study were included in the analysis.
Results From Statin and Fibrate Studies
Twenty-one randomized clinical trials of statin therapy provided data on 153,414 participants who were followed up for a mean of 4.3 years. Some 465 participants developed pancreatitis, of whom 204 were assigned statins (risk ratio [RR], 0.79; 95% confidence interval [CI], 0.65 - 0.95; I 2, 0%; P = .01) compared with 261 who received placebo.
In 7 randomized clinical trials of fibrate therapy involving 40,162 participants who were followed up for a mean of 5.3 years with baseline averages of triglycerides ranging from 145 to 184 mg/dL; 144 participants developed pancreatitis, of whom 84 were assigned fibrates (RR, 1.39; 95% CI, 1.00 - 1.95; I 2, 0%; P = .053)
"This report of pooled randomized trial data demonstrates that use of statin therapy was associated with a reduction in the number of patients developing pancreatitis," the authors write. "However, we did not demonstrate an association between use of fibrate therapy and risk of pancreatitis," they add.
Vijay P. Singh, MD, an assistant professor in the Division of Gastroenterology, Hepatology, and Nutrition at the University of Pittsburgh's School of Medicine in Pennsylvania, told Medscape Medical News it is "an interesting study."
"It simply says control your triglycerides and your risk of pancreatitis goes down," Dr. Singh said. "The statins are showing their benefit.... They're doing what they're supposed to do."
Dr. Singh questioned why Dr. Preiss and colleagues focused their discussion on a narrow band of slightly elevated triglyceride levels (145 - 184 mg/dL) when some of the studies' inclusion criteria admitted patients with levels as high at 750 mg/dL.
Focus on Pancreatic Cancer?
Although the authors suggest that their "hypothesis generating" results could be followed up with a trial comparing fibrates and statins for preventing pancreatitis in patients with severe hypertriglyceridemia, Dr. Singh says chronic pancreatitis also carries the risk of causing pancreatic cancer.
"Maybe they should look at pancreatic cancer," he told Medscape Medical News. "That is the thing that has no treatment and is a 99% killer."
Among the study's limitations, pancreatitis was not a prespecified end point in the trials, which had been designed to investigate the effect of lipid-modifying therapies on cardiovascular events. The study authors were unable to separate reports of pancreatitis into acute and chronic cases, and they lacked access to individual patient data. Because the trials under study tended to exclude patients with marked hypertriglyceridemia, the findings may not be generalizable to those patients.
"In those with slightly elevated triglyceride levels, statins appear better supported by the available data than fibrates for preventing pancreatitis," the authors conclude. "Lifestyle modifications also remain important to improve lipid profiles in such individuals."
Although the meta-analysis was not funded by external sources, one author received grant support from the British Heart Foundation and the majority of trials included in the meta-analysis were funded partly or wholly by industry. Authors report receiving honoraria from Pfizer; receiving consultant fees from Amgen Inc, Pfizer, Merck, Genzyme, Vascular Biogenics, ISIS, Boston Diagnostics, and AstraZeneca; receiving speakers' honoraria, honoraria for advisory board participation, consulting fees, or research or travel grants from Abbott/Solvay, Schering Plough, Pfizer Canada, Merck, AstraZeneca, Amgen, Roche, Sharpe & Dohme, Bristol-Myers Squibb, Eli Lilly, Pfizer, Solvay, and Novartis; participating in clinical trials funded by Pfizer; and being listed as a co-inventor on patents held by the Brigham and Women's Hospital that relate to the use of inflammatory biomarkers in cardiovascular disease and diabetes that have been licensed to AstraZeneca and Siemens. Dr. Singh has disclosed no relevant financial relationships.source.medscape

Η σοκολάτα μειώνει την αρτηριακή πίεση

 
Νέα επισκόπηση έδειξε ότι η σοκολάτα μπορεί ενδεχομένως να μειώσει την αρτηριακή πίεση. Ανάλυση 20 ερευνών έδειξε ότι η κατανάλωση σκούρας σοκολάτας καθημερινά, οδήγησε σε ελαφριά μείωση της αρτηριακής πίεσης.

Η έρευνα του Cochrane Group, αναφέρει ότι χημικές ουσίες στο κακάο, το κύριο συστατικό της σοκολάτας, χαλαρώνουν τα αγγεία. Ωστόσο υπάρχουν πιο υγιεινοί τρόποι για να υποχωρήσει η αρτηριακή πίεση.
Η θεωρία είναι ότι το κακάο περιέχει φλαβανόλες, που παράγουν μια χημική ουσία στον οργανισμό, το μονοξείδιο του αζώτου. Αυτό χαλαρώνει τα αγγεία καθιστώντας πιο εύκολο να περάσει από αυτά, χαμηλώνοντας την πίεση.
Ωστόσο έρευνες έδειξαν μεικτή εικόνα. Η ανάλυση Cochrane συνδύασε προηγούμενες έρευνες για να διαπιστώσει αν υπάρχει επίδραση.
Υπήρχε ευρεία ακτίνα στην ποσότητα κακάο που καταναλώθηκε, από 3 έως 105 γρ. την ημέρα σε κάθε συμμετέχοντα. Ωστόσο η γενική εικόνα ήταν μικρή μείωση στην αρτηριακή πίεση.
Συστολική πίεση κάτω από 120mmHg θεωρείται φυσιολογική. Το κακάο οδήγησε σε μείωση 2-3mmHg. Ωστόσο το διάστημα των δοκιμών ήταν μόνο 2 εβδομάδες, έτσι είναι άγνωστα τα μακροπρόθεσμα αποτελέσματα.
Η ερευνήτρια Karin Ried, από το National Institute of Integrative Medicine στη Μελβούρνη, δήλωσε ότι αν και δεν έχουμε ακόμα ενδείξεις για διατηρήσιμη μείωση στην αρτηριακή πίεση, η μικρή υποχώρηση που παρατηρήθηκε βραχυπρόθεσμα θα μπορούσε να συμπληρώσει ενδεχομένως άλλες αγωγές και να συμβάλει πιθανόν στη μείωση του κινδύνου για καρδιαγγειακή νόσο.
Ωστόσο η σοκολάτα περιέχει άφθονα λιπαρά και ζάχαρη, όπως και το κακάο, επομένως δεν είναι ο ιδανικός τρόπος για τη μείωση της αρτηριακής πίεσης.
Υπάρχει επίσης προειδοποίηση στο περιοδικό ‘Lancet’, ότι η σκούρα σοκολάτα μπορεί ενδεχομένως να περιέχει λιγότερες φλαβανόλες από ότι θα περίμενε κάποιος. Η σκούρα σοκολάτα περιέχει υψηλότερη ποσότητα και σε σχέση με τη σοκολάτα γάλακτος, έτσι θα έπρεπε να περιέχει περισσότερες φλαβανόλες, ωστόσο μπορεί επίσης να αφαιρεθούν αυτές, καθώς έχουν πικρή γεύση.
Πηγή: iatronet.gr

Τρίτη 21 Αυγούστου 2012

Δείτε από τι κινδυνεύουν όσοι ροχαλίζουν


roxalitoΕκείνοι που ροχαλίζουν με μεγάλη ένταση και συχνότητα έχουν σχεδόν διπλάσιες πιθανότητες να παρουσιάσουν ρευματοειδή αρθρίτιδα – η οποία ανήκει στα αυτοάνοσα νοσήματα – σύμφωνα με νέα έρευνα.

Η έρευνα διεξήχθη από το πανεπιστήμιο της Taipei στην Ταιβάν και είναι η πρώτη που εστιάζει στη σχέση ανάμεσα στο ροχαλητό και τα αυτοάνοσα νοσήματα όπως η ρευματοειδής αρθρίτιδα, ο ερυθηματώδης λύκος και η αγκυλωτική σπονδυλαρθρίτιδα.

Οι ερευνητές παρακολούθησαν 1411 ασθενείς με υπνική άπνοια – χαρακτηριστικά συμπτώματα της οποίας είναι το ροχαλητό και η διακοπή της αναπνοής κατά τη διάρκεια της νύχτας – και 7.000 υγιείς ενήλικες. Κατά τη διάρκεια πέντε ετών οι ειδικοί κατέγραψαν πόσοι από τους συμμετέχοντες παρουσίασαν τα παραπάνω νοσήματα. Διαπίστωσαν ότι οι ασθενείς με άπνοια είχαν 91% περισσότερες πιθανότητες να παρουσιάσουν κάποια από αυτές τις παθήσεις.

Ωστόσο, οι ερευνητές επισημαίνουν ότι ο απόλυτος κίνδυνος είναι μικρός π.χ., στην ομάδα όσων είχαν άπνοια δηλαδή, το 2,91% παρουσίασαν συμπτώματα ρευματοειδούς αρθρίτιδας.

Η έρευνα δημοσιεύθηκε στο επιστημονικό περιοδικό Sleep Medicine.πηγη spirospero.gr

Τρίτη 14 Αυγούστου 2012

Βρισκόμαστε κοντά σε νίκη επί του Αλτσχάιμερ;



Βρισκόμαστε κοντά σε νίκη επί του Αλτσχάιμερ;
Δυο νέες επιστημονικές ανακαλύψεις έρχονται να προστεθούν στο οπλοστάσιο κατά του Αλτσχάιμερ και αυτή τη φορά οι επιστήμονες εκφράζουν..
. περισσότερη αισιοδοξία από ποτέ. Οι νέοι δρόμοι που άνοιξαν θεωρούνται σημαντικότατοι. Η 1η ανακάλυψη διαπίστωσε ότι η ασθένεια μπορεί να διαγνωστεί μέχρι και 25 χρόνια πριν εκδηλωθεί και η 2η ανακάλυψη έχει να κάνει με τον εντοπισμό μίας μετάλλαξης γονιδίου που παρέχειπροστασία από την ανίατη αυτή, νευροεκφυλιστική νόσο,η οποία πλήττει πολλά εκατομμύρια ανθρώπους σε όλο τον κόσμο.
Στην πρώτη μελέτη, οι ερευνητές της Ιατρικής Σχολής του πανεπιστημίου της Ουάσινγκτον, με επικεφαλής τον καθηγητή νευρολογίας Ράνταλ Μπέιτμαν, που δημοσίευσαν τη σχετική μελέτη στο ιατρικό περιοδικό New England Journal of Medicine, κατάφεραν να δημιουργήσουν ένα «χρονολόγιο» της αφανούς προόδου της νόσου πολύ πριν αυτή εκδηλωθεί.
Οι επιστήμονες μελέτησαν επί χρόνια οικογένειες (συνολικά 128 μέλη) που έχουν γενετικό κίνδυνο εμφάνισης Αλτσχάιμερ και διαπίστωσαν ότι ο οργανισμός αυτών των ατόμων εμφάνισε τα πρώτα σημάδια της νόσου έως και 25 χρόνια πριν τα πρώτα ορατά συμπτώματα. Στα άτομα με τη σχετική γενετική προδιάθεση, που έχουν κληρονομήσει μία από τις τρεις μεταλλάξεις, οι οποίες σίγουρα προκαλούν τη νόσο, αυτή αρχίζει να εμφανίζεται μετά την ηλικία των 30 ή 40 ετών αντί για τη συνήθη ηλικία των 65 - 75 ετών. Αυτή η σπάνια γενετική και κληρονομική μορφή του Αλτσχάιμερ αφορά λιγότερο από το 1% των συνολικών περιστατικών.
Οι ερευνητές έκαναν σε αυτά τα άτομα διαδοχικά τεστ αίματος και εγκεφαλονωτιαίου υγρού, καθώς επίσης απεικονίσεις εγκεφάλου και νοητικά τεστ. Έτσι, διαπίστωσαν ότι το πρώτο σημάδι (μία πτώση του επιπέδου του βήτα αμυλοειδούς στο εγκεφαλονωτιαίο υγρό) μπορεί να ανιχνευθεί πολύ πρόωρα, ακόμα και 25 χρόνια πριν τα πρώτα συμπτώματα.
Το επόμενο σημάδι, περίπου 15 χρόνια πριν την αρχική εκδήλωση των συμπτωμάτων, είναι η ανίχνευση αυξημένων επιπέδων της πρωτεΐνης Ταυ, που βρίσκεται στα εγκεφαλικά κύτταρα και επίσης μπορεί να εντοπιστεί στο εγκεφαλονωτιαίο υγρό. Παράλληλα, αρχίζει η συρρίκνωση σε τμήματα του εγκεφάλου, καθώς και η εμφάνιση των χαρακτηριστικών εγκεφαλικών «πλακών».
Δέκα χρόνια πριν την κανονική εκδήλωση της νόσου, εμφανίζεται μείωση στο επίπεδο της γλυκόζης του σακχάρου στον εγκέφαλο, ενώ παράλληλα κάνουν την εμφάνισή τους τα πρώτα αδιόρατα προβλήματα μνήμης.
Είναι όμως αβέβαιο κατά πόσο το ίδιο «χρονολόγιο» βιοχημικών αλλαγών στον οργανισμό ισχύει και για τους ανθρώπους που πρόκειται να εμφανίσουν την μη κληρονομική μορφή του Αλτσχάιμερ, γι' αυτό οι ερευνητές επεσήμαναν την ανάγκη να γίνουν περαιτέρω έρευνες.
Στη δεύτερη μελέτη, επιστήμονες της ισλανδικής εταιρίας γενετικής deCODE, με επικεφαλής την Κάρι Στέφανσον, που έκαναν τη σχετική δημοσίευση στο περιοδικό Nature, ανακάλυψαν μία σπάνια γενετική μετάλλαξη που προστατεύει από τη νόσο Αλτσχάιμερ την μειονότητα των ανθρώπων, που την έχουν στο γονιδίωμά τους. Οι ερευνητές ευελπιστούν ότι θα μπορούσαν να αξιοποιήσουν δεόντως το εύρημα, αναπτύσσοντας φάρμακα που θα μιμούνται την προστατευτική δράση του εν λόγω γονιδίου.
Οι επιστήμονες εκτιμούν ότι όσοι είναι άνω των 85 ετών και διαθέτουν την μετάλλαξη, είναι επτάμιση φορές λιγότερο πιθανό να έχουν Αλτσχάιμερ. Σύμφωνα με τους ερευνητές, πρόκειται για την πρώτη γενετική μετάλλαξη που έχει βρεθεί να παρέχει ισχυρήπροστασία κατά της νόσου. Οι ερευνητές, κάνοντας περαιτέρω έρευνες, κατέληξαν μάλιστα στο συμπέρασμα ότι η εν λόγω γονιδιακή ποικιλομορφία προστατεύει γενικότερα από την άνοια και την έκπτωση των νοητικών λειτουργιών που παρατηρείται στην τρίτη ηλικία.
Βασική αιτία για τη νόσο Αλτσχάιμερ θεωρείται η σταδιακή δημιουργία πρωτεϊνικών «πλακών» που καταστρέφουν τα εγκεφαλικά κύτταρα. Οι πλάκες αποτελούνται κυρίως από το πεπτίδιο του βήτα αμυλοειδούς, το οποίο παράγεται από μία πρόδρομη πρωτεΐνη (που ελέγχεται από το γονίδιο ΑΡΡ), όταν η τελευταία διασπάται από ορισμένα ένζυμα (BACE).
Η γενετική μετάλλαξη που ανακαλύφθηκε (και αφορά μόνο ένα «γράμμα» του γενετικού αλφαβήτου, δηλαδή ένα νουκλεοτίδιο στο γονίδιο ΑΡΡ), μειώνει σχεδόν κατά το ήμισυ την ποσότητα του βήτα αμυλοειδούς που παράγεται μετά τη διάσπαση της πρωτεΐνης ΑΡΡ. Αυτό επιτρέπει στους ηλικιωμένους να αποφεύγουν σε σημαντικό βαθμό τη συσσώρευση σε επικίνδυνα επίπεδα των εγκεφαλικών «πλακών».
Η ανακάλυψη ενισχύει την πεποίθηση των επιστημόνων ότι μια υπό ανάπτυξη κατηγορία φαρμάκων -οι λεγόμενοι «αναστολείς BACE», θα μπορούσαν να δράσουν προστατευτικά, αρκεί να χορηγηθούν έγκαιρα.
tromaktiko

Χτυπά» τον καρκίνο η καθημερινή λήψη ασπιρίνης

 
Όσοι παίρνουν καθημερινά ασπιρίνη και δεν αντιμετωπίζουν κάποιο πρόβλημα υγείας μειώνουν κατά 16% τον κίνδυνο θανάτου από καρκίνο. Παράλληλα η καθημερινή λήψη ασπιρίνης φαίνεται πως επιβραδύνει την εξάπλωση της νόσου στους καρκινοπαθείς.
Αυτό ήταν το βασικό συμπέρασμα μίας νέας αμερικανικής επιστημονικής έρευνας, η οποία έρχεται μεν να επιβεβαιώσει προηγούμενες μελέτες, που είχαν κάνει ανάλογες διαπιστώσεις, όμως εκτιμά ότι η ωφέλεια της ασπιρίνης είναι τελικά μικρότερη από αυτήν (έως 37%) που είχαν βρει οι παλαιότερες έρευνες. Οι ερευνητές, με επικεφαλής τον επιδημιολόγο Έρικ Τζέικομπς της Αμερικανικής Εταιρίας Καρκίνου, που έκαναν τη σχετική δημοσίευση στο περιοδικό του Εθνικού Ινστιτούτου Καρκίνου των ΗΠΑ, σύμφωνα με το πρακτορείο Ρόιτερ και τη βρετανική «Γκάρντιαν», παρακολούθησαν την εξέλιξη της υγείας άνω των 100.000 ανδρών και γυναικών, χωρίς προηγούμενο ιστορικό καρκίνου, που έπαιρναν καθημερινά μία χαμηλή δόση ασπιρίνης (75 μιλιγκράμ) για χρονικό διάστημα έως 11 ετών.
Οι θάνατοι από ορισμένες μορφές καρκίνου (εντέρου, στομάχου, οισοφάγου κ.α.) ήταν σημαντικά μειωμένοι σε ποσοστό έως 40%, ενώ σε άλλους καρκίνους οι θάνατοι εμφάνιζαν μικρότερη μείωση, της τάξης του 12% κατά μέσο όρο. Συνολικά, η μέση μείωση των θανάτων ήταν περίπου 16% τόσο για όσους έπαιρναν την ασπιρίνη για πάνω από πέντε χρόνια, όσο και για εκείνους που το έκαναν για λιγότερα χρόνια.
Στον καρκίνο των πνευμόνων πάντως η ασπιρίνη δεν φαίνεται να έχει κάποια προστατευτική δράση, πιθανότατα επειδή η νικοτίνη του τσιγάρου ακυρώνει τα οφέλη της στους καπνιστές. Από την άλλη, η προστατευτική δράση της ασπιρίνης εμφανίζεται αρκετά μεγαλύτερη στους άνδρες (υπερδιπλάσια μείωση των θανάτων από καρκίνο) σε σχέση με τις γυναίκες.
Τον Μάρτιο, μία άλλη έρευνα, με επικεφαλής τον Πίτερ Ρόθγουελ του πανεπιστημίου της Οξφόρδης, είχε αναφέρει ότι ο κίνδυνος θανάτου από καρκίνο είναι μικρότερος κατά 37% κατά μέσο όρο για όσους παίρνουν καθημερινά ασπιρίνη για διάστημα μεγαλύτερο των πέντε ετών και περίπου 25% για όσους παίρνουν την ασπιρίνη για τρία χρόνια.
Η νέα μελέτη επιβεβαιώνει μεν την επωφελή δράση της ασπιρίνης, όμως, καταλήγει στο συμπέρασμα ότι η καθημερινή λήψη σχετίζεται με μία σχετικά μικρότερη μείωση του κινδύνου, αν και επισημαίνει ότι ακόμα και μία μικρή προστατευτική δράση έχει νόημα.
Οι επιστήμονες δεν είναι ακόμα βέβαιοι μέσω ποιου μηχανισμού η ασπιρίνη δρα προστατευτικά, αλλά υποθέτουν ότι βοηθά στην καταστολή των φλεγμονών στον οργανισμό ή επιβραδύνει τις προκαρκινικές μεταλλάξεις στα κύτταρα. Αν και συνεχώς νέες έρευνες δείχνουν ότι ακόμα και σε χαμηλή δοσολογία η ασπιρίνη μειώνει τον κίνδυνο του καρκίνου, τόσο στους υγιείς, όσο και στους ασθενείς, οι γιατροί προς το παρόν διστάζουν να εισηγηθούν την ευρεία χρήση της ως προληπτικού αντικαρκινικού φαρμάκου. Μία αιτία είναι οι πιθανές στομαχικές παρενέργειές της (εσωτερική αιμορραγία) λόγω της τακτικής λήψης, οι οποίες είναι πιθανό να αποβούν θανατηφόρες σε σπάνιες περιπτώσεις, ιδίως σε άτομα άνω των 70 ετών.  πηγη¨medicalnews.gr

Οι παγίδες της παραλίας για τους καρδιοπαθείς

 
Η θάλασσα και ο ήλιος κρύβουν παγίδες για τους καρδιοπαθείς. Γι’ αυτό πριν ξεκινήσουν για τις καλοκαιρινές τους διακοπές πρέπει να συμβουλευτούν το γιατρό τους.
H καρδιά δεν αγαπά τις υψηλές θερμοκρασίες της παραλίας αλλά ούτε και τις χαμηλές του θαλασσινού νερού. Γι’ αυτό το λόγο όσοι ανήκετε στις ομάδες υψηλού κινδύνου για καρδιαγγειακή νόσο θα πρέπει να είστε προσεκτικοί, ειδικά στα πρώτα σας μπάνια. Στην παραλία
Ο ήλιος είναι εχθρός της καρδιάς. Αν ανήκετε στις ομάδες υψηλού κινδύνου, πρέπει να αποφεύγετε τις άσκοπες μετακινήσεις ιδίως τις ώρες που ο ήλιος είναι δυνατός (11 π.μ. – 3 μ.μ.).
Το καλύτερο είναι να επισκέπτεστε την παραλία τις πρωινές ή τις απογευματινές ώρες, όταν η θερμοκρασία είναι πιο χαμηλή.
Όταν κάνει πολλή ζέστη, είναι καλύτερα να παραμένετε σε κλιματιζόμενους χώρους και, αν υπάρχει ανάγκη να μετακινηθείτε, φροντίστε να φοράτε ανοιχτόχρωμα ρούχα και καπέλο.
Δείξτε προσοχή
Η μεγάλη ζέστη είναι το ίδιο βλαβερή όπως και το πολύ κρύο. Ιδιαίτερη προσοχή χρειάζεται να δείξετε σε περίπτωση που έχετε ιστορικό στηθάγχης, εμφράγματος, καρδιακής ανεπάρκειας οποιασδήποτε αιτιολογίας ή άλλες σπανιότερες καρδιακές παθήσεις.
Στη θάλασσα
Το κολύμπι –με την προϋπόθεση ότι σας το έχει επιτρέψει ο γιατρός– είναι ιδανική άσκηση. Ωστόσο είναι απαραίτητο να τηρείτε πάντα κάποιους κανόνες.
– Πριν μπείτε στη θάλασσα κάντε μια μικρή προθέρμανση με ήπιες ασκήσεις χεριών και ποδιών, ένα ελαφρύ τροχάδην ή λίγο περπάτημα επί πέντε λεπτά.
– Όταν η θερμοκρασία είναι υψηλή, αποφύγετε το κολύμπι. Η ζέστη αυξάνει τους παλμούς και ανοίγει τα αγγεία του δέρματος προκαλώντας εφίδρωση με αποτέλεσμα να κουράζει την καρδιά.
Ιδανική ώρα για κολύμπι είναι είτε νωρίς το πρωί, είτε το απόγευμα.
– Αποφύγετε όμως τα κρύα νερά και προτιμήστε να κολυμπήσετε όταν η θάλασσα είναι πιο ζεστή.
– Απαγορεύεται να κολυμπήσετε αν έχετε φάει, έστω και ελαφριά.
Πηγή: myworld.gr