Non-steroidal anti-inflammatory drugs increase risk of atrial fibrillation

Adding to the list of concerns that clinicians and patients should be vigilant about when using non-steroidal anti-inflammatory drugs (NSAIDs), a research published in the British Journal of Medicine offers evidence for a strong increase in risk of atrial fibrillation (a type of cardiac arrhythmia or ‘heart flutter’). The authors state:

Atrial fibrillation is the most common rhythm disorder observed in clinical practice…It is associated with increased mortality and morbidity, mainly due to haemodynamic impairments that exacerbate or even cause heart failure, and a threefold to fourfold increased risk of thromboembolic stroke…Any confirmed association between use of NSAIDs and atrial fibrillation would have major clinical and public health implications. Older people are of special concern because the prevalence of use of NSAIDs and the incidence of atrial fibrillation increase with age. To address the limitations of the existing literature, we conducted a large population based case-control study examining whether and to what extent use of NSAIDs increases the risk of atrial fibrillation or flutter.

In their case-control study they the examined the data for 32,602 patients diagnosed with atrial fibrillation compared to 325,918 age and sex matched control subjects, correlating specifically with current, recent and long term use of NSAIDs. They obtained results that demonstrate a particular concern for new users:

“Compared with no use, the incidence rate ratio associating current drug use with atrial fibrillation or flutter was 1.33 for non-selective NSAIDs and 1.50 for COX 2 inhibitors. Adjustments for age, sex, and risk factors for atrial fibrillation or flutter reduced the incidence rate ratio to 1.17 for non-selective NSAIDs and 1.27 for COX 2 inhibitors. Among new users, the adjusted incidence rate ratio was 1.46 for non-selective NSAIDs and 1.71 for COX 2 inhibitors.”

In other words, atrial fibrillation was increased for new users by 46% for non-selective NSAIDs and 71% for COX 2 inhibitors (17% and 27% respectively for all users taken together). Their conclusions are important for practitioners to bear in mind when designing strategies to control inflammation, especially considering that other evidence-based anti-inflammatory agents without this troubling risk profile are available:

Use of non-aspirin NSAIDs was associated with an increased risk of atrial fibrillation or flutter. Compared with non-users, the association was strongest for new users, with a 40-70% increase in relative risk (lowest for non-selective NSAIDs and highest for COX 2 inhibitors). Our study thus adds evidence that atrial fibrillation or flutter needs to be added to the cardiovascular risks to be considered when prescribing NSAIDs.”

 

Coffee helps atrial fibrillation with high blood pressure

Nutrition, Metabolism & Cardovascular DiseasesI’ve been seeing a lot of studies that document beneficial effects from drinking coffee, but I never expected this paper that was recently published in the journal Nutrition, Metabolism & Cardiovascular Diseases. Atrial fibrillation is the most common arrhythmia (irregular heart rhythm). The authors set out to investigate…

“the influence of coffee and caffeine consumption on atrial fibrillation (AF) in hypertensive patients…with regard to spontaneous conversion of arrhythmia.”

Spontaneous conversion is when the heart rhythm normalizes on its own. Along the way they made some interesting observations:

“Coffee consumption was higher in normotensive (normal blood pressure) patients. High coffee consumers were more frequent in normotensive patients compared with hypertensive patients. On the other hand, the intake of caffeine was similar in hypertensive and normotensive patients, owing to a higher intake in hypertensive patients from sources other than coffee. Within normotensive patients, we report that non-habitual and low coffee consumers showed the highest probability of spontaneous conversion, whereas, within hypertensive patients, moderate but not high coffee consumers had the lowest probability of spontaneous conversion.”

Interestingly, their data show that if you have high blood pressure, more coffee is better for normalizing atrial fibrillation. Their conclusion:

Coffee and caffeine consumption influence spontaneous conversion of atrial fibrillation. Normotensive non-habitual coffee consumers are more likely to convert arrhythmia within 48h from the onset of symptoms. Hypertensive patients showed a U-shaped relationship between coffee consumption and spontaneous conversion of AF, moderate coffee consumers were less likely to show spontaneous conversion of arrhythmia.”

Atrial fibrillation and subclinical hyperthyroidism (and gluten sensitivity)

It’s necessary to bear in mind when dealing with atrial fibrillation that subclinical hyperthyroidism is a common cause. Subclinical means that there are symptoms from excess thyroid hormone activity even though the lab values appear normal. There are a plethora of recent studies that investigate this phenomenon; here are a few. The authors of the first paper state: “Overt and subclinical hyperthyroidism are both well-known independent risk factors for atrial fibrillation.”

  1. High-Normal Thyroid Function and Risk of Atrial Fibrillation
  2. Activation of Electrical Triggers of Atrial Fibrillation in Hyperthyroidism
  3. Atrial fibrillation and heart attack associated with subclinical hyperthyroidism
  4. Atrial fibrillation associated with exogenous subclinical hyperthyroidism
  5. The mechanisms of atrial fibrillation in hyperthyroidism
  6. Effects of Thyroid Hormone on the Cardiovascular System
  7. Association Between Serum Free Thyroxine Concentration and Atrial Fibrillation

Now the plot thickens. Here is a paper recently published in Nature Reviews Endocrinology discussing the link between celiac disease (gluten sensitivity) and autoimmune thyroiditis. Here is another, fresh off the presses, from the journal Gut. One more for now: this paper published in the journal Thyroid demonstrates that the antibodies involved in celiac disease also bind to thyroid follicles.