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

Δευτέρα 1 Απριλίου 2013

Efficacy and safety of colchicine for pericarditis prevention


At present, this is the first comprehensive meta-analysis on this topic, including all published clinical trials up to December 2011.
There are some limitations to be acknowledged. Some of the included trials were open label (1,2), which might have introduced bias; however findings were similar in open-label and placebo-controlled trials (7-9). Moreover all trials have independent blinded outcome assessment with very low or absent participant dropout, thus indicating studies of high quality. An additional potential limitation is that potentially heterogeneous populations (idiopathic, viral, postoperative pericarditis as well as pericarditis related to a systemic inflammatory disease) have been included, however the same treatment and preventive strategies are adopted and recommended for such patients, that are heterogeneous for etiology but homogenous for pericarditis medical therapy. Bacterial and neoplastic pericarditis has been excluded because requiring specific treatments.
Conclusion In conclusion, the present meta- analysis provides a stronger evidence base for the use of colchicine in patients with pericarditis, as outlined in previous recommendations on colchicine use in the 2004 guidelines on the management of pericardial diseases of the European Society of Cardiology (10), based on expert consensus while randomised trials were not available at that time. At present, there are no available updates of 2004 guidelines, and no specific guidelines on the management of pericardial diseases have been issued by the American College of Cardiology, and the American Heart Association. This meta-analysis is useful to summarise data from all published clinical trials on pericarditis prevention by colchicine.
In conclusion, our study found that colchicine 0.5-1.0 mg daily was safe and efficacious for the primary and secondary prevention of pericarditis and should be considered as first line therapy for pericarditis prevention.
Further data are needed to prove its efficacy and safety in the setting of the first episode of acute pericarditis. Ongoing results of the ICAP trial will provide more solid evidence for or against this additional indication (ClinicalTrials.gov Identifier: NCT00128453).source escardio

Πέμπτη 21 Μαρτίου 2013

Insomnia is linked to increased risk of heart failure

Topics: Heart Failure (HF)
Date: 06 Mar 2013
The study, which is published online today in the European Heart Journal [1], followed 54,279 people between the ages of 20-89 for an average of more than 11 years, and found that those who suffered from three symptoms of insomnia had a more than three-fold increased risk of developing heart failure compared to those with no insomnia symptoms.
Dr Lars Laugsand, a post-doctoral fellow in the Department of Public Health, Norwegian University of Science and Technology, Trondheim, Norway, said: “We related heart failure risk to three major insomnia symptoms including trouble falling asleep, problems staying asleep, and not waking up feeling refreshed in the morning. In our study, we found that persons suffering from insomnia have increased risk of having heart failure. Those reporting suffering from all three insomnia symptoms simultaneously were at considerably higher risk than those who had no symptoms or only one or two symptoms.”
However, he stressed that although the study shows that insomnia is linked to an increased risk of heart failure, it does not show that it causes it. “We do not know whether heart failure is really caused by insomnia, but if it is, insomnia is a potentially treatable condition using strategies such as following simple recommendations concerning sleeping habits (often referred to as sleep hygiene), and several psychological and pharmacological therapies. Evaluation of sleep problems might provide additional information that could be used in prevention of heart failure.”
He said further research would be required to establish whether or not insomnia caused the condition. “It is still unclear why insomnia is linked to higher heart failure risk. We have some indications that there might be a biological cause, and one possible explanation could be that insomnia activates stress responses in the body that might negatively affect heart function. However, further research is also needed to find the possible mechanisms for this association.”
Dr Laugsand and his colleagues collected data from men and women enrolled in the Nord-Trondelag Health study (HUNT) between 1995 and 1997 and who were free from heart failure when they joined. Heart failure is a condition in which the heart is unable to pump enough blood around the body at the right pressure. It usually occurs because the heart muscle has become too weak or stiff to work properly. The researchers followed the study participants until 2008, by which time there had been a total of 1412 cases of heart failure.
When participants joined the study they were asked whether they had difficulty going to sleep and staying asleep, with the possible answers being “never”, “occasionally”, “often” and “almost every night”. They were also asked how often they woke up in the morning not feeling refreshed (non-restorative sleep): “never, few times a year”, “one to two times per month”, “once a week”, “more than once a week”.
After adjusting for factors that could affect the results, such as age, sex, marital status, education, shift work, blood pressure, cholesterol, diabetes, body mass index, physical activity, smoking, alcohol, any previous heart attack, depression and anxiety, the researchers found that having difficulties going to sleep and staying asleep almost every night, and having non-restorative sleep more than once a week were associated with an increased risk of heart failure when compared with people who never or rarely suffered from these symptoms. There was a trend showing a link between the frequency of the symptoms and the increased risk, although most of these findings did not reach statistical significance.
When they looked at the number of symptoms, the researchers found a statistically significant three-fold (353%) increased risk of heart failure for people who had all three insomnia symptoms, compared to those with none, after adjusting for most confounding factors apart from depression and anxiety. When they adjusted their findings to include depression and anxiety, the risk was still significant, with a slightly more than four-fold risk (425%) of heart failure.
The authors write in their paper: “We found a moderate risk increase related to the individual insomnia symptoms. However, the risk among those with all the three insomnia symptoms simultaneously was particularly high even after adjustment for established cardiovascular risk factors and psychological distress. This finding may be interpreted as suggesting that compromising some aspects of sleep may be somehow compensated for, and the net effect on cardiovascular disease may be limited. For example, having difficulty falling asleep might be compensated for by a satisfactory depth and a good continuity of sleep. However, if the initiation of sleep is poor and combined with repeated awakenings and superficial sleep, there may not be any compensatory mechanisms.”source escardio
Authors:
For further information, contact (media inquiries only):
Emma Mason
Email: wordmason@mac.com
Tel: +44 (0)1376 563090
Mobile: +44 (0)7711 296 986
ESC Press Office (for independent comment):
Tel: +33 (0) 4 92 94 86 27
Fax: +33 (0) 4 92 94 86 69
Email: press@escardio.org

Digoxin increases deaths in patients with atrial fibrillation

Digoxin, a drug that has been used worldwide for centuries to treat heart disease, is associated with a significant increase in deaths in patients with atrial fibrillation (AF), according to results from a study published online Wednesday 28 November 2012 in the European Heart Journal.1
Graphic
Foxglove flower
Digoxin, originally extracted from the foxglove plant (digitalis), increases force of contraction of cardiomyocytes and helps maintain a more regular rhythm. It is commonly used in AF patients, and those with heart failure. However, it can be problematic to use successfully, as there is a narrow dose range at which it is effective and beyond which, it can be dangerous. High levels of digoxin in the blood have been correlated with an increased death rate in patients.
Researchers led by Samy Claude Elayi, associate professor of medicine at the Gill Heart Institute, University of Kentucky, USA, analysed data from 4060 AF patients who had enrolled in the landmark Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial, in order to determine the relationship between digoxin and deaths in this group of patients.
They found that digoxin was associated with a 41% increase in deaths from any cause, after controlling for other medications and risk factors and that an increase in deaths occurred regardless of gender or the presence or absence of underlying heart failure. Digoxin was also associated with a 35% increase in deaths from cardiovascular causes, and a 61% increase in deaths from arrhythmias.
Prof. Elayi said: ‘These results mean that among AF patients taking digoxin compared to those not on digoxin in the AFFIRM trial, within five years one additional patient out of six will die from any cause, one additional patient out of eight will die from cardiovascular causes, and one additional patient out of 16 will die from arrhythmias.’
‘These findings call into question the widespread use of digoxin in patients with AF, particularly when used for controlling AF rate in a similar way as in the AFFIRM trial’.
Until now, there have been limited data on the use of digoxin in AF patients. ‘Digoxin in AF patients has hardly been studied’, said Prof. Elayi. ‘The main prospective randomized controlled trials available with digoxin were performed in patients with heart failure and sinus rhythm, excluding AF patients’.
As a result of these findings, the authors conclude in their paper: ‘Our study underscores the importance of reassessing the role of digoxin in the contemporary management of AF in patients with or without HF’.
Prof. Elayi said: ‘These findings mean that physicians should try to first control a patient's heart rate by using alternatives such as, beta-blockers or calcium channel blockers; if digoxin is used, use a low dose with careful clinical follow-up, evaluate potential drug interactions when starting new medications, and monitor digoxin levels. Patients should be aware of potential toxicity and see their physicians immediately in specific clinical situations, for instance, if they experience palpitations or syncope, as these may precede arrhythmic death’.
The researchers say that the mechanism by which digoxin increases deaths among patients is unclear. ‘Deaths from classic cardiovascular causes, whether due to arrhythmia or not, can partly but not entirely explain it. This suggests there must be some additional mechanism that remains to be identified’, said Prof. Elayi.
He concluded ‘There is a need for further studies of the drug's use, particularly in systolic heart failure patients and AF – patients that would in theory, benefit the most from digoxin’.source escardio
Andros Tofield

Δευτέρα 18 Μαρτίου 2013

Atrial flutter: common and main atypical forms


Background

Typical atrial flutter cases (AFL-I) make up 22% of all 8,546 ablation procedures in the Spanish National Ablation's Registry (behind atrioventricular nodal reentrant tachycardia, accessory pathways but ahead of atrial fibrillation).
Furthermore, atrial flutter is considered to hold as much risk as atrial fibrillation for thromboembolic events (3-4% per year).(2,3) Atrial flutter also carries a proarrhythmic risk, and additionally, rhythm control and ventricular rate response can only hardly be achieved with medical treatment. In patients with chronic obstructive pulmonary disease with concomitant bronchodilators especially, controlling the ventricular rate could be challenging with an increased risk of 1:1 ventricular response. Loss of atrioventricular synchronisation and physiological rate response to activity can also decrease functional class in patients with ventricular dysfunction.

We present a brief report describing common atrial flutter as well as the main atypical forms, with a focus on description of their circuits, and main electrocardiographic patterns. (4)

Typical atrial flutter

Typical atrial flutter is an organised atrial tachycardia. It can also be defined as a macroreentrant tachycardia confined to the right atrium. This arrhythmia has a 200-260 ms cycle length, although it may fluctuate depending on patient's previous treatment or ablation, congenital heart disease, etc. (4) Ventricular rate response will be limited by the atrioventricular (AV) node conductions, usually presenting a 2:1 or 3:1 response, during atrial flutter.

Typical atrial flutter originates in a well-known circuit around the tricuspid annulus limited by anatomical barriers such as both the superior and inferior cava veins, the coronary sinus and crista terminalis. The wave front may rotate around this circuit counterclockwise (most frequently) or clockwise, resulting in the counterclockwise common atrial flutter or the clockwise atrial flutter, respectively.(4,5) This condition produces continuous electrical activity around the atrial circuit and consequently in the electrocardiogram (f waves). 

The electrocardiogram shows a saw tooth's pattern in inferior leads, with a slow downward slope followed by a fast upward slope explained by electrical forces going through the cavotricuspid isthmus and the septum, and then approaching the inferior leads through the lateral wall (Figure 1).(4,5) This saw tooth’s appearance could be easily registered when the ventricular rate response is controlled.
Some conditions may make the ECG diagnosis difficult:
  • Scarred atria with low areas of voltage could mimic isoelectric baseline despite atrial continuous electrical activity.
  • Concomitant circuits could also change the typical atrial appearance.
  • Both high and irregular ventricular rate responses may make the diagnosis difficult. In the first case, vagal maneuvers or AV node blocking drugs, such as adenosine, may be useful. In the second case, a regular irregularity has to be always ruled out. (6,7)
Electrophysiological studies (EPs) are indicated:
  • In AFL-I recurrences despite medical treatment (Class I indication)
  • After the first episode of AFL-I (Class IIa indication), especially in those presenting with poor hemodynamic tolerance or tachymiocardiopathy. (8)
The ablation procedure's main target is to achieve bidirectional block through the cavotricuspid isthmus (CTI). (For a closer look at ablation, see previous e-journal articles on rhythmologist's view on the patient after the procedure, or surgeons' look at procedure in lone atrial fibrillation. See here, previous article on flutter’s differential diagnoses and treatment approaches). Acute success rate is almost 95% in the registries.(1) However, at 5 year follow-up almost 70% of these patients might develop atrial fibrillation or atypical atrial flutter, which is probably related to the baseline characteristics, structural heart disease and uncontrolled risk factors. (9-11)

Main atypical forms

The definition of atypical atrial flutter includes a broad spectrum of other macroreentrant tachycardias in which the wave front does not travel around the tricuspid annulus.
Atypical right atrial flutter other than reverse typical atrial flutter, includes the following:  lower loop reentry, fosa ovalis flutter, superior vena cava flutter and upper loop reentry (Figure 2). (12-15)

Lower loop reentry atrial flutter uses a circuit that includes the CTI, as common atrial flutter, but it shortens the circuit through a gap in the crista terminalis. The mean cycle length is usually from 170 to 250 ms. Positive forces in inferior leads and V1 will be underpowered as a consequence of the change in the typical up-down depolarisation of the lateral wall. Upper loop reentry was also described using a circuit through a gap in the crista terminalis and then in the posterior right atrium wall. The electrocardiogram pattern mimics a clockwise typical flutter but the cycle length is usually shorter,  as in lower loop reentry. (12,13)

An infrequent form of right atrial atypical flutter is confined within the superior vena cava and from it the atria are passively activated. (14)

A second group could be called incisional flutters which includes those where the circuit uses previous surgery related scars, frequently seen in patients with history of surgical correction of congenital heart diseases. (5,15)

Finally, atypical flutter may originated in the left atrium. In this case, the leading wave front is confined to the left atrium. The most frequent left atrial flutters are perimitral, peripulmonary veins, septal, roof and posterior wall macroreentrys. The surface electrocardiogram usually presents isoelectric baseline or low amplitude and positive regular F waves best in V1 (Figure 3). (13,16)

Eletrophysiological studies are indicated in AFL-II recurrences despite optimised medical treatment. During EPs, the diagnosis and an accurate characterisation of the circuit may be performed by activation and postpacing interval maps, which requires 3D navigation systems. (17,18)
The acute ablation success is inferior to common atrial flutter ablation, probably due to multifactorial issues such as worse clinical baseline characteristics, multiple concomitants atypical atrial flutters, and the instability of the clinical flutter during the procedure. (19,20)Figure 1. Typical electrocardiographic pattern of common atrial flutter
Figure 2. Right atypical atrial flutter's circuits. SVC: superior vena cava; IVC: inferior vena cava; CT: crista terminalis; FO: Foramen ovale.
Figure 3. Electrocardiographic recording of perimitral atrial flutter. Atrial fluter waves are registered in V1 lead (red arrows).
Conclusion Although atypical atrial fibrillation is characterised by a wavefront not travelling around the tricuspid annulus, it can take on many forms.
Similarly, in typical atrial fibrillation, cycle arrhythmia, scarred atria, concomitant circuits, high and irregular ventricular rate responses can render diagnosis difficult.

Better knowledge of the underlying mechanisms will probably help to increase accurate diagnoses of common atrial flutter as well as the main atypical forms by cardiologists and emergency department physicians.

An article from the e-journal of the ESC Council for Cardiology Practice


Κυριακή 17 Μαρτίου 2013

100 Is The New 150: AHA Lowers Optimal Triglyceride Level

Dietary, lifestyle changes can significantly reduce triglycerides
Statement Highlights:
  • Diet and lifestyle changes that include substituting healthy fats for unhealthy saturated and trans fats, engaging in regular physical activity and losing excess weight can reduce triglycerides – a blood fat –  by 20 percent to 50 percent.
  • New clinical recommendations include reducing the optimal triglyceride level from <150 mg/dL to <100 mg/dL, and performing non-fasting triglyceride testing as an initial screen.
DALLAS, April 18, 2011 — Dietary and lifestyle changes significantly reduce elevated triglycerides (a type of blood fat) — which is associated with heart, blood vessel and other diseases — according to an American Heart Association scientific statement.
Changes such as substituting healthy, unsaturated dietary fats for saturated ones, engaging in physical activity and losing excess weight can decrease triglycerides by 20 percent to 50 percent, according to the statement’s authors.  The statement is published in Circulation: Journal of the American Heart Association.
“The good news is that high triglycerides can, in large part, be reduced through major lifestyle changes,” said Michael Miller, M.D., chair of the statement committee and professor of medicine in epidemiology and public health and director of the Center for Preventive Cardiology at the University of  Maryland School of Medicine in Baltimore.
“In contrast to cholesterol, where lifestyle measures are important but may not be the solution, high triglycerides are often quite responsive to lifestyle measures that include weight loss if overweight, changes in diet and regular physical activity.”
Miller and co-authors analyzed more than 500 international studies from the past 30 years to formulate the scientific statement.
Recommended dietary changes for those outside the normal range of triglycerides include limiting:
  • added sugar  to  less than 5 percent to 10 percent of calories consumed – about 100 calories per day for women and 150 calories per day for men.
  • fructose from both processed foods and naturally occurring foods –less than 50 to 100 grams per day
  • saturated fat to less than 7 percent of total calories
  • trans fat to– less than 1 percent of total calories; and
  • alcohol, especially if triglyceride levels are higher greater than 500 mg/dL
The amount of added sugars is not listed on the Nutrition Facts Panel of packaged foods, so it is hard to know exactly how much added sugar is in food. Because the majority of added sugar consumed by Americans comes from sugar-sweetened beverages, the American Heart Association recommends drinking no more than 36 ounces of sugar-sweetened beverages per week, based on a 2000-calorie-per-day diet.  People with high triglycerides should also focus on eating more vegetables, fruits lower in fructose such as cantaloupe, grapefruit, strawberries, peaches, bananas, high fiber whole-grains and “healthier” unsaturated fats, especially omega-3 fatty acids found primarily in fatty fish like salmon, herring, sardines, lake trout, and albacore tuna.
All patients with triglyceride levels in the borderline to high range (150-199 mg/dL) or greater are also encouraged to incorporate physical activities of at least moderate intensity (such as brisk walking) for a total of at least 150 minutes per week, because these activities may contribute an additional 20-30 percent triglyceride-lowering effect. Combining all of these lifestyle measures is likely to have the most pronounced effect – 50 percent or greater in reducing triglyceride levels.
Triglyceride testing involves a simple blood sample, traditionally taken after a 12-hour fast. The authors suggest using non-fasting triglyceride testing as an initial screen. Although the cutoff for elevated triglycerides remains at 150 mg/dL, a new optimal level of 100 mg/dL has now been set to acknowledge the protective benefit of lifestyle in metabolic health. However, it is not a target for drug therapy because there has not been adequate study to show that drug therapy to lower triglycerides to this level is helpful. Many people can reduce their triglycerides as well as other metabolic risk factors such as blood sugar and blood pressure with diet, weight loss and increased physical activity.
“Triglycerides are an important barometer of metabolic health,” said Neil J. Stone, M.D., co-chair of the statement and professor of medicine in the Feinberg School of Medicine at Northwestern University in Chicago. “When the clinician sees an elevated triglyceride level, there needs to be an important conversation about risk factors and the need to eat less, eat smarter, and to move more on a daily basis to improve triglycerides and the metabolic profile.”
In the United States, nearly one-third (31 percent) of adults have elevated triglyceride levels (more than 150 mg/dL). The percentage varies by ethnicity, and is highest among Mexican-Americans at 36 percent. Whites have the second-highest rate at 33 percent, while blacks have the lowest at 16 percent.  Of concern is that triglyceride levels continue to rise in young adults (aged 20-49) and this mirrors the increased rates of obesity and diabetes identified at earlier ages.source cardiobrief

Σάββατο 16 Φεβρουαρίου 2013

the Women's Health Initiative Trials of Menopausal Hormone Therapy

We re-evaluate the Women's Health Initiative findings and their implications for clinical practice. Menopausal hormone therapy (HT) was effective for relief of vasomotor symptoms, and the risk of coronary heart disease (CHD) tended to be reduced in women close to menopause compared with the increased risk in women more distant from menopause. In recently menopausal women, short-term absolute risks of stroke and venous thromboembolism were small. Estrogen plus progestin therapy, but not estrogen therapy, increased the risk of breast cancer with a suggestion of greater risk when initiated close to the menopause. Menopausal HT increased the risk of CHD in women more than 20 years distant from menopause, particularly in women with vasomotor symptoms. It remains unknown whether the suggestive benefit for CHD in younger women will translate into benefits or harms if menopausal HT is continued into older ages. Based on Women's Health Initiative data, the use of menopausal HT for fewer than 5 years is a reasonable option for the relief of moderate to severe vasomotor symptoms. The risks seen with estrogen plus progestin therapy suggest careful periodic reassessment of the ongoing therapy needs for women taking estrogen plus progestin therapy. The more favorable profile of estrogen therapy allows for individualized management with respect to duration of use when symptoms persist. For both estrogen therapy and estrogen plus progestin therapy, the baseline risk profile of the individual woman needs to be taken into account. Menopausal HT is not suitable for long-term prevention of CHD given risks of stroke, venous thromboembolism, and breast cancer (for estrogen plus progestin therapy) found in both clinical trials and in observational studies.
© 2013 The American College of Obstetricians and Gynecologists