The prevalence data for atrial fibrillation (AF) are dated. The present retrospective study estimated the current and projected prevalence of AF and atrial flutter (AFL) in the United States using a ...large national database. Claims data drawn from July 2004 to December 2005 from the MarketScan research databases from Thomson Reuters were used to identify patients aged ≥20 years with nontransient AF and/or AFL and age- and gender-matched controls without these conditions. Of the 21,648,681 patients in the databases, 242,903 (1.12%) had nontransient AF and/or AFL (222,605 AF only, 5,376 AFL only, and 14,922 AF and AFL). Patients with AF only, AFL only, and AF and AFL had a greater (p <0.001) prevalence of co-morbidities, including hypertension (62.0%, 61.3%, and 57.0%, respectively) and coronary artery disease (43.0%, 44.7%, and 44.5%, respectively), than matched controls (45.1% hypertension and 19.4% coronary artery disease). Applying the US Census Bureau population estimates to the prevalence rates for AF and/or AFL in the databases, it was estimated that 3.03 million persons in the United States had AF only, 0.07 million had AFL only, and 0.19 million had AF and AFL in 2005. The projected prevalence for 2050 was 7.56 million for AF only, 0.15 million for AFL only, and 0.44 million for AF and AFL. In conclusion, the current prevalence of AF and AFL is high and is projected to increase considerably by 2050. The current and projected increases in the prevalence of AF are greater than predicted by a previous sentinel study and might reflect more than the aging of the population.
The most important factor in treating hypertension is assessing an individual patient's true blood pressure load, the cornerstone being research-grade office determination. Office blood pressure ...should be supplemented with out-of-office measurement, including home and ambulatory monitoring (if available), which we consider complementary and not interchangeable. Controversy remains for initiation of treatment of white coat hypertension, where cardiovascular risk lies between normotension and sustained hypertension; antihypertensive therapy should be considered unless low cardiovascular risk, wherein pressures should be followed for progression to sustained hypertension. Available data do not support intensification of therapy for the white coat effect due to the similar cardiovascular risk to controlled hypertension. Given the higher cardiovascular risk of the masked effect, initiation of therapy for masked hypertension and intensification for masked uncontrolled hypertension are indicated, acknowledging the dearth of supporting data. Optimally, randomized controlled trials are needed to determine the benefit of treating the 4 incongruous phenotypes between office and out-of-office measurements, that is, those with white coat or masked effects. We make no recommendations regarding chronotherapy pending results of ongoing trials.
Apparent resistant hypertension, defined as uncontrolled office blood pressure despite ≥ 3 antihypertensive medications including a diuretic or use of ≥ 4 medications regardless of blood pressure, ...occurs in ≤ 15% of treated hypertensives. Apparent refractory hypertension, defined as uncontrolled office pressure despite use of 5 or more medications including a diuretic, occurs in ≤ 10% of resistant cases. Both are associated with increased comorbidity and enhanced cardiovascular risk. To rule out pseudo-resistant or pseudo-refractory hypertension, employ guideline-based methodology for obtaining pressure, maximize the regimen, rule out white-coat effect, and assess adherence. True resistant hypertension is characterized by volume overload and aldosterone excess, refractory by enhanced sympathetic tone. Spironolactone is the preferred agent for resistance, with lower doses. Spironolactone, potassium binders, or both, are preferred if the estimated glomerular filtration rate is below 45. If significant albuminuria, finerenone is indicated. The optimal treatment of refractory hypertension is unclear, but sympathetic inhibition (α-β blockade, centrally acting sympathoinhibitors, or both) seems reasonable. Renal denervation has shown minimal benefit for resistance, but its role in refractory hypertension remains to be defined.
Abstract
Aims
This post hoc analysis of the ATHENA trial (NCT00174785) assessed the effect of dronedarone on the estimated burden of atrial fibrillation (AF)/atrial flutter (AFL) progression to ...presumed permanent AF/AFL, and regression to sinus rhythm (SR), compared with placebo.
Methods and results
The burden of AF/AFL was estimated by a modified Rosendaal method using available electrocardiograms (ECG). Cumulative incidence of permanent AF/AFL (defined as ≥6 months of AF/AFL until end of study) or permanent SR (defined as ≥6 months of SR until end of study) were calculated using Kaplan–Meier estimates. A log-rank test was used to assess statistical significance. Hazard ratios (HRs) with corresponding 95% confidence intervals (CIs) were estimated using a Cox model, adjusted for treatment group. Of the 4439 patients included in this analysis, 2208 received dronedarone, and 2231 placebo. Baseline and clinical characteristics were well balanced between groups. Overall, 304 (13.8%) dronedarone-treated patients progressed to permanent AF/AFL compared with 455 (20.4%) treated with placebo (P < 0.0001). Compared with those receiving placebo, patients receiving dronedarone had a lower cumulative incidence of permanent AF/AFL (log-rank P < 0.001; HR: 0.65; 95% CI: 0.56–0.75), a higher cumulative incidence of permanent SR (log-rank P < 0.001; HR: 1.19; 95% CI: 1.09–1.29), and a lower estimated AF/AFL burden over time (P < 0.01 from Day 14 to Month 21).
Conclusion
These results suggest that dronedarone could be a useful antiarrhythmic drug for early rhythm control due to less AF/AFL progression and more regression to SR vs. placebo, potentially reflecting reverse remodeling.
Clinical trial registration
NCT00174785
Graphical Abstract
Graphical Abstract
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