Monday, July 30, 2007

 

the future of Atrial Fibbrillatin


What Does the Future Hold? (Slides with Transcript) CME/CE

Patrick J. Tchou, MD James A Reiffel, MD Disclosures


 

AF and nonpharmalogical treatmants

What's New in Nonpharmacologic Therapy (Slides with Transcript) CME/CE

Patrick J. Tchou, MD Robert A. Schweikert, MD, FACC Disclosure

denk aan transcript om de tekst te lezen, bij de dias !

 

comorbidities van Atrial fibrillation zie slides /transcript

Comorbidities (Slides with Transcript) CME/CE

Patrick J. Tchou, MD Jennifer E. Cummings, MD, FACC James A Reiffel, MD Walid I Saliba, MD Robert A. Schweikert, MD, FACC Disclosures


 

voor Ralph van Lieshout

Blindness is hier bedoeld de veel voorkomende macula degeneratie, die je altijd krijgt als je maar oud genoeg wordt. Als het in de familie zit (aanleg) en je zou het met 80 krijgen en je rookt dan krijg je het gemiddeld een paar jaar eerder. Dus niet roken, want met die osteopathische verzorging van jezelf zou je wel eens heel oud kunnen worden. Bovendien een osteopaat die rookt, komt bij mij over als een Papoea die voor de mensenrechten demonstreert en vervolgens een missionaris in de pot doet.
groeten JAN


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Did You Know Smoking Can Cause Blindness?

A survey published recently by the Royal National Institute of Blind People (RNIB) reveals that just 30 percent of people in the UK are aware that smoking can cause blindness. Only one in three know that smokers are twice as likely as non-smokers to one day lose their sight. Smoking is a proven cause of Age-Related Macular Degeneration (ARMD), the UK's leading cause of vision loss.

 

overgewicht

J. Am. Geriatr. Soc. 2007;55 (6): 913-917


Abstract

Objectives: To evaluate the association between body mass index (BMI) and all-cause mortality and cardiovascular disease (CVD) in an 80-year-old population.
Design: Cohort study.
Setting: Community-based.
Participants: Six hundred ninety-seven of 1,282 (54.4%) 80-year-old candidate individuals.
Measurements: The dates and causes of all deaths were followed up for 4 years.
Results: The relative hazard ratios (HRs) for all-cause mortality were lower in overweight subjects (BMI ≥ 25.0) than in underweight (BMI < 18.5) or normal-weight (BMI 18.5–24.9) subjects. Similarly, the HRs for mortality due to CVD in overweight subjects were 78% less (HR=0.22, 95% confidence interval (CI)=0.06–0.77) than those in underweight subjects, and those in normal weight subjects were 78% less (HR=0.22, 95% CI=0.08–0.60) than those in underweight subjects. Mortality due to CVD was 4.6 times (HR 4.64, 95% CI=1.68–12.80) as high in underweight subjects as in normal-weight subjects, and mortality due to cancers was 88% lower (HR=0.12, 95% CI=0.02–0.78) in the overweight group than in the underweight group. There were no differences in mortality due to pneumonia.
Conclusion: Overweight status was associated with longevity and underweight with short life, due to lower and higher mortality, respectively, from CVD and cancer.



 

cannabis en psychosis

Physician's First Watch for July 27, 2007

David G. Fairchild, MD, MPH, Editor-in-Chief

Arrow Cannabis Use Linked to Later Psychosis

Arrow West Nile Virus Rate Seems Higher Than in Previous Years

Cannabis Use Linked to Later Psychosis

A Lancet meta-analysis on the late effects of cannabis use finds that the drug is associated with a 40% increase in the risk for psychotic symptoms, with more use leading to greater risk.

The authors assessed the studies with particular attention to bias and confounding factors, such as intoxication effects and subjects' having experienced psychosis at baseline. In the seven studies evaluated for a link with psychosis, the odds ratio for psychosis in those who had ever used cannabis versus nonusers was 1.41. Among the most frequent users, the odds ratio was 2.09.

The authors say the question is not so much whether cannabis causes psychosis as it is "whether the evidence ... now available can justify policy implications, such as public education campaigns to alert people to the possible risks."

A commentator calls the study "the most comprehensive meta-analysis to date" and concludes that cannabis' "long-term hazardous effects ... with regard to psychosis seem to have been overlooked."

Lancet article (Free abstract; full text requires subscription)

Lancet comment (Subscription required)


 

simvastatin en dementia

This activity is supported by funding from WebMD.

Medscape Medical News

Simvastatin Linked to Reduced Incidence of Dementia, Parkinson's Disease CME

News Author: Caroline Cassels
CME Author: Hien T. Nghiem, MD

Complete author affiliations and disclosures, and other CME information, are available at the end of this activity.

Release Date: July 24, 2007; Valid for credit through July 24, 2008

Credits Available

Physicians - maximum of 0.25 AMA PRA Category 1 Credit(s) for physicians;
Family Physicians - up to 0.25 AAFP Prescribed credit(s) for physicians

All other healthcare professionals completing continuing education credit for this activity will be issued a certificate of participation.
Physicians should only claim credit commensurate with the extent of their participation in the activity.



July 24, 2007 — Research links simvastatin to a reduction in the incidence of both dementia and Parkinson's disease (PD) of greater than 50%.

In contrast, atorvastatin is associated with a modest, but insignificant, reduction in the incidence of the 2 diseases, and lovastatin has no impact on incidence.

"This study suggests brain penetrant statins are more effective at preventing neurodegenerative disease than impenetrant statins," principal investigator Benjamin Wolozin, MD, from Boston University School of Medicine in Massachusetts, told Medscape.

"There are many statins out there. Some are very effective for preventing cardiovascular disease but not all of them cross the blood-brain barrier equally and, therefore, may not have the same impact on neurodegenerative disease.

"Simvastatin crosses into the brain very effectively, whereas atorvastatin just doesn't achieve as high a level [in the brain]. Lovastatin crosses the blood-brain barrier nicely but it is a first generation statin and therefore is just not as potent as some of the newer agents," he added.

The study is published in the July 19 issue of BMC Medicine.

Previous Research Yielded Conflicting Results

According to Dr. Wolozin, previous research looking at a potential protective effect of statins and dementia, including work by his group, has yielded conflicting results. In part, this was because the numbers of study subjects were not sufficiently powered to detect any statistically significant effect of statins on incident dementia.

However, the current study used the Decision Support System database of the US Veterans Affairs medical system. This large population-based database contains diagnostic, medication, and demographic information on 4.5 million subjects, 94.4% of whom are men.

Prescription utilization was tracked for every subject between 2003 and 2005. Lovastatin, simvastatin, and atorvastatin all had large numbers of prescriptions during this period. Data were obtained for 727,128 subjects taking simvastatin, 53,869 subjects taking atorvastatin, and 54,052 who were prescribed lovastatin.

Fluvastatin and pravastatin were also included. However, according to the authors, the number of subjects taking pravastatin was too small to produce reliable data. Furthermore, a marked increase in fluvastatin during the study period meant subjects' duration of exposure to this statin was much less than that for the other 3 agents. As a result, researchers did not pursue further studies of fluvastatin or pravastatin.

Magnitude of Effect Surprising

Using 3 models for analysis, researchers looked at the incidence of dementia and PD among subjects who had continuously used a statin for at least 7 months.

The first model adjusted only for age; the second model, for 3 major dementia risk factors, including cardiovascular disease, hypertension, and diabetes; and the third model, for the Charlson index, which is an index that provides a broad assessment of chronic disease.

With respect to dementia, researchers found simvastatin was associated with significant reduction in the incidence of dementia using any of the 3 models. In addition, said Dr. Wolozin, the study revealed a similar decrease in incident PD associated with simvastatin.

"We were very surprised by the size of the effect associated with simvastatin and that it worked for both Parkinson's disease and dementia. We were also surprised that atorvastatin hardly had any impact on the incidence of either disease," he said.

While a number of researchers have speculated that statins' apparent protective effect against dementia is caused by an amyloid-lowering mechanism, this study refutes that hypothesis.

"Dementia and Parkinson's disease are both neurodegenerative conditions. Dementia is typically characterized by the build-up of β-amyloid plaques, but this is not the case with Parkinson's. If you accept that statins are acting by a similar mechanism in both diseases it makes it very unlikely that it is acting through an amyloid-lowering mechanism. The most likely mechanism, and one that is most commonly accepted, is that statins protect the brain through an anti-inflammatory mechanism," he said.

Potential Mechanisms

On the other hand, he said a "provocative and interesting" animal study conducted by Johnson-Anuna and colleagues at the University of Minnesota and published in the February 2005 issue of the Journal of Pharmacology and Experimental Therapeutics suggests the neuroprotective effect of statins may be related to their ability to increase growth factors in the brain.

Based on the study's results, Dr. Wolozin said clinicians might want to consider an individual patient's family history when choosing a statin.

"If a patient has a family history of dementia, simvastatin may be a better choice than other agents. On the other hand, we know atorvastatin is somewhat better than simvastatin at preventing morbidity from cardiovascular disease, so if a patient has no dementia history but has cardiovascular risk factors, they may be better off taking atorvastatin. It really boils down to personalized medicine," said Dr. Wolozin.

He added that these findings need to be prospectively confirmed in other population-based studies.

BMC Med. Published online July 19, 2007.



 

simvstatin en arterial calcification

Publication Logo

Simvastatin No Help Against Arterial Calcification


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By David Douglas

NEW YORK (Reuters Health) Jul 19 - Compared with placebo, high-dose simvastatin treatment does not appear to reduce the progression of coronary artery calcified plaque or abdominal aortic calcium levels in subjects without symptoms of vascular disease, according to North Carolina-based researchers.

"We believe that our study and other controlled clinical trials indicate that benefits associated with statin medicines are not reflected in changes in coronary artery calcification measured using computed tomography," lead investigator Greg Terry told Reuters Health.

Terry and colleagues at Wake Forest University Health Sciences, Winston-Salem, came to this conclusion after studying 80 subjects with an unfavorable lipid profile and other cardiovascular risk factors, who were randomized to simvastatin 80 mg daily or placebo.

At 1 year, total cholesterol, triglycerides and LDL cholesterol decreased significantly in the active treatment group, but lipids remained unchanged in placebo patients.

However, coronary artery calcium volume increased by 9% in simvastatin patients and such plaque increased by 5% in placebo patients. Measures of abdominal aortic calcium also increased in both groups.

This study and previous blinded randomized trials, the investigators conclude, "do not support the beneficial effects of statin treatment on coronary artery calcium progression suggested by retrospective and open-label studies."

Am J Cardiol 2007;99:1714-1717.



 

statins colon cancer

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http://www.medscape.com/viewarticle/560418



Publication Logo
Statins May Cut Colon Cancer Recurrence

Allison Gandey

Medscape Medical News 2007. © 2007 Medscape

July 26, 2007 (Chicago) — Researchers report that statins decreased the risk for recurrence in patients diagnosed with stage 1, 2, or 3 colon cancer. Presenting at the recent American Society of Clinical Oncology (ASCO) 43rd Annual Meeting, investigators say the popular lipid-lowering agents may have an important role to play in patients with resected disease.

"Just 6 of 89 patients (6.7%) treated with any statin relapsed, as opposed to 43 of 269 (16%) patients with no statin use," lead author Daniel Anderson, MD, from Regions Hospital, in St. Paul, Minnesota, said during his presentation. The Fisher’s exact test resulted in a P value of .03. Kaplan-Meier analysis of relapse curves showed a significant difference in relapse between groups, with a 2-year recurrence rate of 3.7% among statin users and 10.1% among nonusers (log rank P = .03, using age stratification).

The investigators reported that a significant body of research suggests that statin use reduces the risk of developing colon and other cancers. But not all studies have confirmed these findings. As reported by Medscape earlier this week, a study published in the July 31 issue of the Journal of the American College of Cardiology suggests the cardiovascular benefits of achieved levels of low-density lipoprotein cholesterol might be offset by an increased risk for cancer. In the analysis of patients enrolled in large, randomized statin trials, investigators observed a significant and linear relationship between target cholesterol levels and the risk for new cancer cases.

In the study reported at ASCO, Dr. Anderson, working with colleagues from the Health Partners Research Foundation, in Bloomington, Minnesota, conducted a retrospective analysis of patients treated for stage 1, 2, or 3 colon cancer.

Patients were identified through a hospital tumor registry. All cases were then crosschecked against a health maintenance organization (HMO) membership database. Information on statin use was obtained from the HMO outpatient pharmacy database.

Could Lipid-Lowering Agents Play a Role in Resected Disease?

For each patient, investigators obtained all available data from a 5-year period before first diagnosis of cancer until recurrence or most recent documentation. Dr. Anderson and his team combined demographic and survival data from the tumor registry with pharmacy data on statin use. The researchers then analyzed recurrence and time to recurrent disease in statin users and nonusers.

They looked at 358 colon cancer cases. The median follow-up of patients after diagnosis of colon cancer was 49 months. A total of 89 patients (24.9%) used statins for some period of time, with a median of 780 days of use. The median age of all patients enrolled was 69 years (range, 24 – 95 years).

Statin use was higher in older patients. Those aged 61 to 75 years (33%) were more likely to be taking lipid-lowering agents than those aged 24 to 60 years (22%). But older patients were also more likely to be taking statins than their elderly counterparts — those aged 76 to 95 years (19%) (P = .02).

The researchers found that statin use was linked to a reduced risk for colon cancer recurrence. They observed no association between statin use and stage at diagnosis. But Dr. Anderson cautioned, "Further study of statin use in the prevention of colon cancer recurrence is warranted."

American Society of Clinical Oncology 43rd Annual Meeting: Abstract 4114. Presented June 4, 2007.



Thursday, July 26, 2007

 

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New Guidelines in Atrial Fibrillation -- Update and Perspectives (Slides with Transcript) CME/CE


 

vervolg met tekst

What's New in the 2006 Guidelines (Slides with Transcript)

Management of Atrial Fibrillation: What Is New in the 2006 Guidelines. Walid I. Saliba, MD, FACC: Good morning, everybody, and thank you for being here. ...
www.medscape.com/viewarticle/558983 - Gelijkwaardige pagina's

Tuesday, July 24, 2007

 

A F

tik in op Google: atrial fibrillation: the scope of the problem
Dan de dias en de tekst van Prof. james Reiffel. university Columbia
AF: applying the new guidelines in clinical practice.

Monday, July 23, 2007

 

the affirm trial AF (NEJM)

Original Article
PreviousPrevious
Volume 347:1825-1833  December 5, 2002  Number 23
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A Comparison of Rate Control and Rhythm Control in Patients with Atrial Fibrillation
The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators


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ABSTRACT

Background There are two approaches to the treatment of atrial fibrillation: one is cardioversion and treatment with antiarrhythmic drugs to maintain sinus rhythm, and the other is the use of rate-controlling drugs, allowing atrial fibrillation to persist. In both approaches, the use of anticoagulant drugs is recommended.

Methods We conducted a randomized, multicenter comparison of these two treatment strategies in patients with atrial fibrillation and a high risk of stroke or death. The primary end point was overall mortality.

Results A total of 4060 patients (mean [±SD] age, 69.7±9.0 years) were enrolled in the study; 70.8 percent had a history of hypertension, and 38.2 percent had coronary artery disease. Of the 3311 patients with echocardiograms, the left atrium was enlarged in 64.7 percent and left ventricular function was depressed in 26.0 percent. There were 356 deaths among the patients assigned to rhythm-control therapy and 310 deaths among those assigned to rate-control therapy (mortality at five years, 23.8 percent and 21.3 percent, respectively; hazard ratio, 1.15 [95 percent confidence interval, 0.99 to 1.34]; P=0.08). More patients in the rhythm-control group than in the rate-control group were hospitalized, and there were more adverse drug effects in the rhythm-control group as well. In both groups, the majority of strokes occurred after warfarin had been stopped or when the international normalized ratio was subtherapeutic.

Conclusions Management of atrial fibrillation with the rhythm-control strategy offers no survival advantage over the rate-control strategy, and there are potential advantages, such as a lower risk of adverse drug effects, with the rate-control strategy. Anticoagulation should be continued in this group of high-risk patients.


Source Information



The AFFIRM writing group (D.G. Wyse, A.L. Waldo, J.P. DiMarco, M.J. Domanski, Y. Rosenberg, E.B. Schron, J.C. Kellen, H.L. Greene, M.C. Mickel, J.E. Dalquist, and S.D. Corley) assumes overall responsibility for the content of the manuscript.

Address reprint requests to the AFFIRM Clinical Trial Center, Axio Research, 2601 4th Ave., Ste. 200, Seattle, WA 98121, or to leong@axioresearch.com.

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