[FEMORAL HEAD FRACTURE IN PATIENTS 65 YEARS AND OLDER WITH ATRIAL FIBRILLATION: THE EFFECT OF ANTI-COAGULATION ON COMPLICATIONS AND PROGNOSIS].

BACKGROUND: Atrial fibrillation and hip fractures are common problems in elderly patients. Delay in the timing of surgical repair can lead to increased complications and anti-coagulation could be a reason for delay. OBJECTIVES: To assess morbidity and mortality in patients 65 years and older with atrial fibrillation (AF) and hip fracture in relation to the type of anti-coagulation. METHODS: A retrospective cross-sectional study of patients with AF and hip fracture aged 65 and older was conducted in a tertiary hospital. Data collected included co-morbidity, medical history, medications, the timing of surgery, thromboembolic events, estimated risk for stroke by CHADS2 score, for significant bleeding by HAS-BLED score and mortality rate for the six-month period following surgery. RESULTS: During the period 2014-2016, 186 patients 65 years and older with atrial fibrillation underwent surgical repair of a hip fracture, 113 (60.7%) women. The mean age was 81.9±7.1 years. Eighty-nine (47.8%) did not receive any anti-coagulation, 60 (32.3%) received new oral anticoagulants (NOAC), and 37 (19.9%) warfarin. There were no differences between these groups on pre-and post-operation burden of co-morbidity, timing of surgery, surgical delay, complication rate, or mortality rate during the six months following surgery. CONCLUSIONS: Anti-coagulation for patients 65 years and older with atrial fibrillation and hip fracture did not affect the timing of surgery or the rate of complications and mortality. Based on these results the concern over emergency surgery and its complications in patients with AF is not justified.

Bolus injection of acetylcholine terminates atrial fibrillation in rats.

It is well established that a tonic increase in the availability of the atrial muscarinic K(+) channels, either by enhanced vagal tone or by steady infusion of a low-dose of cholinergic or adenosine receptor agonists, promotes the genesis of atrial fibrillation. Here, we aimed to test the hypothesis that bolus administration of a muscarinic receptor agonist would destabilize and terminate atrial arrhythmia by uniformly and transiently activating K(+) channels throughout the atria, and that if the agonist was rapidly hydrolysable, it would dissipate before the more tonic, pro-arrhythmic effects could take hold. The episodes of untreated atrial fibrillation, induced in anesthetized rats by programmed electrical stimulation via trans-esophageal bipolar catheter, lasted on average 8.6+/-2.2 min (n=32). Intravenous injection of a model hydrolysable muscarinic agonist, acetylcholine (0.2 mg/kg body weight), converted atrial fibrillation into sinus rhythm within 8.4+/-1.9 s (n=10, P<0.05). The termination of an atrial fibrillation episode was always accompanied by transient bradycardia; the sinus rhythm gradually accelerated and reached pre-atrial fibrillation values within 10-20 s of injection. In conclusion, our evidence indicates that bolus administration of rapidly hydrolysable muscarinic agonist could be an effective way to pharmacologically terminate atrial fibrillation and restore sinus rhythm.