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The risk of VTE is highest in the first 3 to 6 months after AF diagnosis and decreases over time. The early initiation of anticoagulation in patients with AF may reduce the risk of VTE.
Atrial fibrillation (AF) is the most common cardiac arrhythmia despite substantial efforts to understand the pathophysiology of the condition and develop improved treatments. Identifying the underlying causative mechanisms of AF in individual patients is difficult and the efficacy of current therapies is suboptimal. Consequently, the incidence of AF is steadily rising and there is a pressing need for novel therapies. Research has revealed that defects in specific molecular pathways underlie AF pathogenesis, resulting in electrical conduction disorders that drive AF. The severity of this so-called electropathology correlates with the stage of AF disease progression and determines the response to AF treatment. Therefore, unravelling the molecular mechanisms underlying electropathology is expected to fuel the development of innovative personalized diagnostic tools and mechanism-based therapies. Moreover, the co-creation of AF studies with patients to implement novel diagnostic tools and therapies is a prerequisite for successful personalized AF management. Currently, various treatment modalities targeting AF-related electropathology, including lifestyle changes, pharmaceutical and nutraceutical therapy, substrate-based ablative therapy, and neuromodulation, are available to maintain sinus rhythm and might offer a novel holistic strategy to treat AF.
KEYWORDS: Anticoagulationdirect oral anticoagulantsnon-valvular atrial fibrillationreal-world evidencestroke prevention
A surge in cortisol during acute physiological and pathophysiological stress may precipitate ventricular arrhythmia and myocardial infarction. Reduced cardiovagal baroreflex sensitivity and heart rate variability are observed during acute stress and are associated with an increased risk of acute cardiac events. In the present study, healthy young men received either a single iv bolus of saline (placebo) or hydrocortisone, 1 week apart, in accordance with a randomized, placebo-controlled, cross-over study design. Hydrocortisone acutely increased heart rate and blood pressure and reduced cardiovagal baroreflex sensitivity and heart rate variability in young men. These findings suggest that, by reducing cardiovagal baroreflex sensitivity and heart rate variability, acute surges in cortisol facilitate a pro-arrhythmic milieu and provide an important mechanistic link between stress and acute cardiac events ABSTRACT: Surges in cortisol concentration during acute stress may increase cardiovascular risk. To better understand the interactions between cortisol and the autonomic nervous system, we determined the acute effects of hydrocortisone administration on cardiovagal baroreflex sensitivity (BRS), heart rate variability (HRV) and cardiovascular reactivity. In a randomized, placebo-controlled, single-blinded cross-over study, 10 healthy males received either a single iv bolus of saline (placebo) or 200 mg of hydrocortisone, 1 week apart. Heart rate (HR), blood pressure (BP) and limb blood flow were monitored 3 h later, at rest and during the sequential infusion of sodium nitroprusside and phenylephrine (modified Oxford Technique), a cold pressor test and a mental arithmetic stress task. HRV was assessed using the square root of the mean of the sum of the squares of differences between successive R-R intervals (rMSSD). Hydrocortisone markedly increased serum cortisol 3 h following infusion and also compared to placebo. In addition, hydrocortisone elevated resting HR (+7 ± 4 beats min<sup>-1</sup> ; P < 0.001) and systolic BP (+5 ± 5 mmHg; P = 0.008); lowered cardiovagal BRS [geometric mean (95% confidence interval) 15.6 (11.1-22.1) ms/mmHg vs. 26.2 (17.4--39.5) ms/mmHg, P = 0.011] and HRV (rMSSD 59 ± 29 ms vs. 84 ± 38 ms, P = 0.004) and increased leg vasoconstrictor responses to cold pressor test (Δ leg vascular conductance -45 ± 20% vs. -23 ± 26%; P = 0.023). In young men, an acute cortisol surge is accompanied by increases in HR and BP, as well as reductions in cardiovagal BRS and HRV, potentially providing a pro-arrhythmic milieu that may precipitate ventricular arrhythmia or myocardial infarction and increase cardiovascular risk.
Objective: Hypertension accounts for more cases of atrial fibrillation (AF) than any other risk factors. AF and hypertension commonly co-exist and both are associated with endothelial dysfunction. FMD measurement using a high-resolution ultrasound has become a reliable and reproducible technique for assessment of endothelial dysfunction. To investigate whether optimising of blood pressure (BP) in patients with hypertension and AF leads to improvement in FMD. Design and method: In a longitudinal comparison, we recruited 30 participants with hypertension and permanent AF. Each participant had 3 serial BP readings and an echocardiogram. Their drug history was noted. High-resolution ultrasound was used to measure brachial artery diameter at rest and during reactive hyperaemia (endothelium-dependent FMD). Participant's BP medication was optimised according to their BP. Participants were then followed them up after 8 weeks for repeat FMD measurements. Data analysis was carried out using paired t-test on SPSS. Results: Following optimisation of BP medication, patients with permanent AF and hypertension were followed up after 8 weeks and FMD repeated. There was significant improvement in mean heart rate (77 ± 18 (baseline) vs 72 ± 17 (follow up), p = 0.01), systolic BP (140 mmHg [128 – 148] (baseline) vs 131 mmHg [122 – 146] (follow up), p = 0.03), diastolic BP (81 mmHg ± 13 (baseline) vs 77 mmHg ± 12 (follow up), p = 0.02) and mean arterial pressure (MAP) (100 mmHg ± 9 (baseline) vs 97 mmHg ± 13 (follow up), p = 0.01). Both groups had a similar baseline brachial artery diameter (p = 0.34). Endothelium-dependent FMD response was better following 8 weeks of BP optimisation but this was not significant (3.1%, 95% CI [2.3 – 4.8] (baseline) vs 5.2%, 95% CI [3.9 – 6.5] (follow up), p = 0.09). No variables were identified on univariate or multivariate analysis as independent predictors of FMD. Conclusions: Endothelial dysfunction can be improved following optimisation of BP medication suggesting modulation of endothelial function is possible in patients with permanent AF and hypertension. Longer-term improvement in FMD may have a prognostic implication.