We found no evidence of a temporal trend in hazard ratios between newly diagnosed atrial fibrillation and all cause mortality. The hazard ratios for non-cardiovascular death declined over time but no evidence of a temporal trend for cardiovascular death was found. Mortality associated with newly diagnosed atrial fibrillation remained high compared with individuals without atrial fibrillation, despite showing some improvements over the past 45 years. More than 10 years after a diagnosis of atrial fibrillation, individuals with atrial fibrillation lose about two years of life compared with matched referents.
BMJ 2020; 370 doi: https://doi.org/10.1136/bmj.m2724 (Published 11 August 2020)
Cite this as: BMJ 2020;370:m2724
Recurrences of atrial fibrillation lasting 30 seconds or more were less common in the abstinence group (53% vs. 73% of control patients). The median percentage of time spent in atrial fibrillation was also lower in the abstinence group (0.5% vs. 1.2%).
The skeptical cardiologist has been evaluating a demo version of AliveCor’s new KardiaMobile 6L. I have been a huge advocate of Kardia’s single lead ECG and use it with great success in dozens of my afib patients. I’ve written about how this personal ECG monitoring empowers patients and providers and is a crucial component of…
Thanks Doctor for the ECG history lesson and for sharing your insights.
And congratulations on the Stanley Cup!
A majority of patients in the ablation group, about 63%, were in sinus rhythm at the 60-month follow-up, compared with only 22% (P<0.001) in the group with medically managed AF, “which suggests that maintenance of sinus rhythm is beneficial when achieved without the use of antiarrhythmic drugs,” write the authors, led by Dr Nassir F Marrouche (University of Utah Health, Salt Lake City).
Read the source article here.
The past 3 decades have been characterized by an exponential growth in knowledge and advances in the clinical treatment of atrial fibrillation (AF). It is now known that AF genesis requires a vulnerable atrial substrate and that the formation and composition of this substrate may vary depending on comorbid conditions, genetics, sex, and other factors. Population-based studies have identified numerous factors that modify the atrial substrate and increase AF susceptibility. To date, genetic studies have reported 17 independent signals for AF at 14 genomic regions. Studies have established that advanced age, male sex, and European ancestry are prominent AF risk factors. Other modifiable risk factors include sedentary lifestyle, smoking, obesity, diabetes mellitus, obstructive sleep apnea, and elevated blood pressure predispose to AF, and each factor has been shown to induce structural and electric remodeling of the atria. Both heart failure and myocardial infarction increase risk of AF and vice versa creating a feed-forward loop that increases mortality. Other cardiovascular outcomes attributed to AF, including stroke and thromboembolism, are well established, and epidemiology studies have championed therapeutics that mitigate these adverse outcomes. However, the role of anticoagulation for preventing dementia attributed to AF is less established. Our review is a comprehensive examination of the epidemiological data associating unmodifiable and modifiable risk factors for AF and of the pathophysiological evidence supporting the mechanistic link between each risk factor and AF genesis. Our review also critically examines the epidemiological data on clinical outcomes attributed to AF and summarizes current evidence linking each outcome with AF.
Researchers in Connecticut have found that obstructive sleep apnea (OSA) in patients with atrial fibrillation (AF) appears to be an independent predictor of stroke.
Concerns about Pradaxa surfaced 2 years ago, he says, when doctors began reporting a larger number of serious and sometimes fatal bleeding problems in older patients on the drug.
The claim by the company that the drug needs no blood-level monitoring is misguided, Moore says. “It turns out the company has had data for several years, showing the amount of anticoagulation [blood thinning] varied [from patient to patient] more than five-fold.”
That means, Moore says, that “the same dose could produce widely varying effects on blood clotting. Some patients would be at extremely high risk of bleeding. Others would not get a strong enough blood clotting effect to serve its purpose, reduce the risk of stroke.”
Do the phrases “serious and sometimes fatal bleeding problems” combined with the drug maker’s withholding of data bother anyone? And yet another example of putting profits before people.
I found another fine article on the Pradaxa mess. Follow the link to The Poison Review. There you will find more details on this story and more links for further reading, including a link to the full text BMJ article.
The Institute for Safe Medication Practices reported that in 2011 there were 3781 serious adverse effects and 542 patient deaths reported in the United States in association with dabigatran. In comparison, warfarin (Coumadin) was associated with only 72 deaths during that same time period. – See more at: http://www.thepoisonreview.com/2014/07/27/must-read-marketing-vs-medicine-in-the-case-of-pradaxa-dabigatran/#sthash.tpAapuE6.dpuf
If you’re not totally confused by now you should be.
Bisphosphonate use was associated with significantly increased risks of atrial fibrillation and serious atrial fibrillation, researchers found.
A systematic review of randomized controlled studies and observational studies showed use of bisphosphonates was associated with a 27% increased risk of atrial fibrillation (95% CI 1.16-1.39) in observational studies and, in randomized controlled trials alone, with a 40% increased odds of serious atrial fibrillation (95% CI 1.02-1.93), according to Abhishek Sharma, MD, of Maimonides Medical Center in Brooklyn, N.Y., and colleagues.
MRI indicated silent cerebral ischemia lesions in 89% patients with paroxysmal Afib and 92% with persistent Afib compared with 46% of controls, which wasn’t significantly different between the two types of Afib but was for both versus controls (P<0.01).
The number of these lesions averaged 41 in persistent Afib, 33 in paroxysmal Afib, and 12 in controls, which was significantly different for all three groups.
The high prevalence of these lesions in the control group compared with what has been reported in the general population may have reflected the moderate to high cardiovascular risk among these patients referred for cardiovascular prevention or treatment, the researchers suggested.
The lesions can have either ischemic and embolic origins, but the peculiar “spotted” distribution of “small sharply demarcated lesions, often in cluster, with bilateral distribution, prevalently in the frontal lobe” seen in 50% and 67% of the paroxysmal and persistent Afib patients, respectively, strongly supported an embolic mechanism, they noted.
If these findings are replicated in future studies, the question for underwriters is should any Afib risk be Standard mortality?