Abstract

Atrial fibrillation (AF) is the most common sustained arrhythmia encountered in clinical practice. It is associated with a significant increase in thromboembolic complications, for example, stroke and thromboembolism. Loss of synchrony between atria and ventricles leads to continuous atrial and ventricular mechanical dysfunction followed by the development of heart failure and decreased functional capacity. Patients with AF also report impaired quality of life as well as decline in cognitive function, and increased mortality when compared to patients in sinus rhythm.¹

Lone AF, defined as AF in younger adults (age below 60 years) with no clinical history or echocardiographic evidence of concomitant cardiovascular or pulmonary conditions or an acute trigger, represents only a minority of cases of arrhythmia. Also given that more and more emerging risk factors for AF development have been recognized (e.g., obesity, obstructive sleep apnea, strenuous physical activity, inflammation, and so on), “lone AF” has essentially become a diagnosis of exclusion.^2,3 Even in such cases, the risk of adverse outcomes appeared to be higher compared to patients without AF.⁴

The vast majority of AF cases develop as a consequence of pre-existing cardiovascular diseases as well as noncardiac conditions, which are associated with structural and electrical changes that precipitate the development and persistence of AF. Arterial hypertension is highly prevalent within the general population and is therefore often present concomitantly with AF, as well as sharing a range of risk factors.^5,6

Despite the availability of diagnostic methods and the availability of various antihypertensive drugs, further improved awareness of high blood pressure, adherence to treatment, and hypertension control is highly relevant for many patients.⁷ Hypertension almost inevitably leads to cardiovascular diseases (as is the case for coronary artery disease and heart failure), which strengthens the link between hypertension and AF even more.⁸

In the current review article, we provide an overview of the epidemiological parallels between hypertension and AF, common pathophysiological pathways, and the implications of high blood pressure on outcomes in AF patients in various clinical scenarios.

EPIDEMIOLOGY OF HYPERTENSION AND AF: A 1-WAY PATH?

A retrospective analysis of 80 million adults in the United States found that the prevalence of hypertension was estimated to be 32.6% between 2009 and 2012.⁷ There were more males suffering from hypertension aged <45 years whilst for those ≥65 of age, the opposite gender relationship was observed. between age 45 and 64 years, prevalence hypertension in males females remains approximately similar.⁷

The National Health and Nutrition Examination Survey in 2011–2012 found that 17.2% of adults in the United States are unaware they have high blood pressure; also, over 10% of hypertensive patients failed to reach target blood pressure despite use of ≥4 drugs from 3 different drug classes, i.e., resistant hypertension.⁷ The prevalence of hypertension demonstrates an increasing trend over past decades, and projections showed further anticipated increases up to 41.4%.⁷ In the elderly, its prevalence is even higher (65.0% among US adults 60 years of age or older) with a higher percentage receiving treatment (86.1%) but a lower proportion of patients achieve blood pressure control (50.5%).⁷

The rising prevalence of hypertension is associated with increases in overall mortality. Life expectancy of normotensive individuals is approximately 5 years higher than in their hypertensive counterparts. Indeed, there were over 70,000 deaths attributable to hypertension that equated to a death rate of 19.9 in 2013. Amongst cardiovascular risk factors hypertension is the leading cause of death in females and only second after smoking as the cause of death in males. Of note, cardiovascular diseases are likely to occur 7 years later on a background of normal blood pressure.⁷

Unfortunately, reliable data from the developing as well as low- and middle-income countries are more scarce compared to developed high-income countries, and variability in studies design, population selection, methodology, and so on make direct comparison of the data hard to interpret.⁹ Overall, there have been global disparities in hypertension prevalence and control.^9,10 Reported prevalence is higher in low- and middle-income countries than in high-income countries, while hypertension awareness, treatment, and control were much lower in low- and middle-income than in high-income countries.¹⁰ Furthermore, the larger growing populations in developing countries make a greater impact upon the global burden of hypertension.⁹ One of reasons for the increasing hypertension prevalence is major achievements in prevention and treatment of cardiovascular diseases leading to improved survival, increased life expectancy, and therefore an ageing population.¹¹

Such trends are evident for AF epidemiology. In the Framingham Heart Study of over 200 thousand person-years, age-adjusted AF prevalence increased 4-fold from 20.4 to 96.2 cases and 13.7 to 49.4 cases per 1,000 person-years in males and females, respectively.¹² A similar trend was apparent for the age-adjusted AF incidence that increased from 3.7 to 13.4 cases per 1,000 person-years and 2.5 to 8.6 cases in males and females, respectively.¹² Furthermore, AF prevalence and incidence also show age-dependency. In the Rotterdam Study, for example, the prevalence of AF was 1.3% in men and 1.7% in women in patients aged of 55 to 59 years, but reached 24.2% and 16.1%, respectively, in those who were older than 85 years of age.¹³ Lifetime risks for development of AF were approximately 1 in 4 in both the Framingham Heart Study (age of 40 years and older) and Rotterdam Study (age of 55 years and older).^14,15

According to the global burden of disease study published in 2014, over 20 million males and 12 million females were estimated to suffer from AF worldwide, and close to 5 million new AF cases were added to AF burden annually.¹⁶ During the 2 past decades AF-associated health burden evaluated with the disability adjusted life-years, increased by approximately 19%.¹⁶ The estimated age-adjusted AF prevalence and incidence rates increased by 26.7 and 16.8 per 100,000 person-years in males as well as 13.2 and 15.7 per 100,000 person-years in females, respectively.¹⁶ Western developed countries, i.e., United States and European Union, are major contributor to the global burden of AF, with approximately 8 and 9 million AF cases estimated.^13,16 The prevalence and incidence of AF in developing countries is likely to be lower, and also varies between developed countries.^17,18

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When current trends in the incidence and prevalence of AF (derived in the Olmsted County cohort) were applied, the projected number of AF cases by the year of 2050 is likely to increase 2–3 fold with 35% of new patients with AF attributed to growing AF incidence while another 65%—due to increase in population size, largely explained by increased survival accompanied by shift in age distribution (less due to population expansion itself).^19,20 In European countries, if the trends from the Rotterdam study remain, the numbers of individuals with AF is projected to double by 2060.¹³

Accurate assessment of AF epidemiology is subject to bias because of the absence of population-based data in many countries and peculiarities with regards to the clinical course of AF, for example, asymptomatic (silent) AF or those presenting with very short intermittent episodes.

Single time-point screening for AF via pulse palpation or short-term electrocardiogram recording was capable of identifying AF in as much as 1% of the screened population with previously unknown AF. This increased when subgroup of elder patients (e.g., 65 years of age or older) was chosen.^21,22 The probability of catching the episode of paroxysmal AF correlates with the duration of electrocardiogram monitoring. This was shown in patients with cryptogenic stroke who underwent electrocardiogram monitoring with implantable cardiac monitors. Cumulative detection rates of AF increased with continued monitoring, increasing from 3.7% at 1 month, to 12.4% at 1 year and reaching 30% at 3 years.²³

Thus, the burden of AF reaching epidemic levels in the 21^st century is an ever increasing reality.²⁴ Given that population ageing is at least in part attributable to improved survival due to implications of evidence-based treatment into routine clinical practice, the prevalence of comorbidities such as hypertension, coronary artery disease, diabetes mellitus, chronic kidney disease, heart failure, is also increasing alongside with aging, contributing to the growing AF burden. These conditions are intimately linked to each other, and the rate of their coexistence is high.

Hypertension is now the leading cardiovascular risk factor to predispose to AF globally. Mechanisms by which hypertension predisposes to AF development are summarized in the Figure 1. The evidence from multiple cohorts has confirmed a strong association between 2 conditions (see Table 1) leading to the inclusion of blood pressure indices into clinical risk scores for AF prediction (Table 2).

MECHANISMS OF AF: FROM HYPERTENSION TO ARRHYTHMIA?

Risk factors and pathophysiology of AF have been studied extensively but definite mechanisms have not yet been fully elucidated and those that have are poorly understood. AF has a complex origin with multiple pathways of excitation. Notwithstanding epidemiological parallels between hypertension and AF, their coexistence is a common clinical scenario, but other cardiovascular and noncardiovascular conditions can also be causative of arrhythmia.⁶ Irrespective of the underlying condition, a combination of diverse (but often interplaying) pathways lead to structural and functional changes followed by electrophysiological, contractile, and architectural disturbances within the left atrium, commonly defined as atrial cardiomyopathy and serve together as an arrhythmogenic substrate for AF initiation and persistence.²⁵

To be responsible for arrhythmia development, there needs to be focal ectopic firing occurring from the triggered activity (early or, more frequently, delayed after depolarizations) and re-entry cycles formation, maintained by shortened atrial refractoriness, slowed conduction, and unidirectional blocks. These include structural remodeling, particularly left atrial fibrosis; dysfunction of autonomic nervous system; ion channel dysfunction; and calcium handling abnormalities.⁶

Structural remodeling

Structural remodeling is essential for arrhythmia initiation and perpetuation in the majority of AF cases. The mechanisms of structural remodeling both in the left atrium and left ventricles have been reviewed recently.²⁶ Diffuse accumulation of fibrotic tissue, e.g., collagen fibers and fibroblasts, in the extracellular matrix of atrial myocardium, is the hallmark of structural remodeling. Moreover cardiac fibroblasts and other cellular populations (e.g., progenitor cells, endothelial cells, etc.) via epithelial to mesenchymal transitions, can switch to a more profibrotic phenotype, the myofibroblast, with a higher capacity to proliferate and synthesize components of extracellular matrix.²⁶

Apart from being the major source of collagen synthesis in the heart, the myofibroblasts also play roles in the release of a range of signalling molecules (including the upregulation of proinflammatory cytokines). Furthermore, there is direct involvement of cardiac fibroblasts/myofibroblasts in atrial arrhythmogenesis due to electrical coupling with cardiomyocytes, by interference with impulse propagation and slow conduction. Subsequently, myofibroblasts may cause reduction in cardiomyocytes resting membrane potential due to leakage of cardiomyocyte electrical current, fluctuations in action potential duration, appearance of delayed after depolarisations, leading to ectopic activity.^6,27

Overall, turnover of extracellular matrix (like collagen synthesis) and degradation, as well as cardiac fibroblast proliferation and dedifferentiation are subject to multiple external influences, for example, inflammatory cytokines, reactive oxygen species, and hemodynamic load (Figure 2). However, the main effector for structural remodeling is the rennin–angiotensin axis activation, specifically angiotensin II.^5,26 Profibrotic effects of angiotensin II are largely mediated by the transforming growth factor beta 1 that via Smad pathway upregulates expression of particular genes, as well as increased aldosterone production, activation of nicotinamide adenine dinucleotide phosphate oxidase, increased inflammatory responses, and apoptosis.^26,28 Interestingly, transforming growth factor beta 1 is associated with a minor but significant increase in the risk of incident AF (standard mean difference 0.67; 95% confidence interval [CI] 0.29–1.05 when assessed as continuous variable; odds ratio 1.01, 95% CI 1.01–1.02, when assessed as categorical variable).²⁹

Recently, thrombin via protease-activated receptors promotes fibrotic, hypertrophic, and inflammatory responses in atrial fibroblasts, for example, the expression of transforming growth factor beta 1 and monocyte chemoattractant protein-1 expression are upregulated as well as incorporation of 3-hydroxyproline was increased suggesting enhanced collagen synthesis by fibroblasts.³⁰ The latter changes translate into higher AF inducibility and complexity of the AF substrate. Of note, thrombin inhibition with dabigatran resulted in reduced alpha-smooth muscle actin expression (marker of transition of cardiac fibroblasts to myofibroblasts) and endomysial fibrosis.³⁰ Given that AF is associated with activation of coagulation and represents hypercoagulable state, these experimental findings are intriguing.

Finally, the atrial myocardium is more prone to develop fibrosis compared to ventricles.^31,32 Also, AF itself augments structural remodeling in the left atrium closing the vicious cycle and promoting arrhythmia progression to persistent and chronic presentation.^5,33

Autonomic dysregulation

Dysregulation in the autonomic nervous system also contributes to the development of substrate for AF, the onset of arrhythmia and its maintenance. The left atrium has an extensive neural network of sympathetic and parasympathetic fibers, which form nerves, ganglia, and plexi, accumulating data from the baroreceptors, chemoreceptors, and mechanical stress receptors, located in the kidneys, major arteries (e.g., aorta, carotid bodies), and heart itself.³⁴ Indeed, arrhythmia onset was shown to be triggered by the synchronous increased sympathovagal discharge or fluctuations in autonomic tone^35,36; when driven by strenuous physical activity or in patients with structural heart disease sympathetic flow contributes,³⁷ while vagal influences may be amenable for AF in patients with no evidence of structural heart disease, i.e., lone AF.³⁴

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What are the effects of sympathetic and parasympathetic system on atrial electrophysiology? Sympathetic activation via β1-adrenergic receptors leads to cellular calcium overload due to increased calcium influx vial-type calcium channels as well as release of calcium from the sarcoplasmic reticulum via ryanodine receptors during diastole. Excess of calcium is removed via sodium–calcium exchanger with a 3 (Na⁺) to 1 (Ca²⁺) ratio, generating electrical current sufficient for occurrence of delayed after depolarisations. With respect to action potential, the influence of sympathetic flow may vary with the plateau phase remaining unchanged or reduced. This is due to synergistic effect of increased l-type calcium current and potassium currents (ultra-rapid delayed rectified current, slow delayed rectified current, and acetylcholine-dependent current).³⁴

Effects of parasympathetic system are mediated via muscarinic receptors and in contrast to effects of sympathetic system are associated with definite shortening of action potential duration and hence, decreased refractoriness due to inhibition of l-type calcium current and activation of acetylcholine-dependent potassium current.^34,38 With the onset of arrhythmia further shortening of action potential occurs because of autoprotective limitation of calcium entry to cells, that is activated as a result of calcium overload due to the high atrial activation rate. Ectopic activation is further supported with the spontaneous calcium release from the sarcoplasmic reticulum.³⁴

Effect of hypertension on AF substrate

Are there similarities between the pathogenesis of AF and hypertension? A close relationship is apparent with respect to atrial fibrosis, given that hypertension may cause substantial structural changes in the left atrium.²⁵ Persistent hyperactivation of the rennin–angiotensin–aldosterone axis is one of the key mechanisms in the development of arterial hypertension with changes observed both in vascular beds and myocardium as well as other target organs, including vasoconstriction, cellular proliferation and hypertrophy, cells uncoupling, apoptosis, and fibrosis.³⁹ Moreover, renin–angiotensin–aldosterone system activation is associated with increased sympathetic flow and vice versa, sympathetic activation enhances renin synthesis in the juxtaglomerular cells.⁴⁰

Substantial data linking electrical, structural, and autonomic remodeling in hypertension and AF have been derived from studies on renal sympathetic denervation in animal experiments (Table 3) and human studies (Table 4). Early data obtained in the first human studies and animal experiments show an overall favorable effect of renal sympathetic denervation on electrophysiological parameters, which might affect AF inducibility and sustainability that translated into decreased recurrence rate in AF patients (Tables 3 and 4). However, there is still inconsistency between studies and criticisms due to study design and small number of patients involved. Thus, clinical trials that address renal sympathetic denervation as an complementary procedure to pulmonary vein isolation have started.⁴¹

When switching from the systemic effects of sympathetic and rennin–angiotensin–aldosterone system activation to simple hemodynamic fluctuations as a link between hypertension and AF, it is apparent that left ventricular diastolic dysfunction (associated with myocardial hypertrophy caused by hypertension) as well as arterial stiffening due to aging, hypertension, and other risk factors all lead to increased left ventricular filling pressures, and retrograde mechanical overload and stretching of left atrium (Figure 1). This is supported with both experimental and clinical data. In various hypertension models, Lau et al. observed progressive biatrial hypertrophy, left atrial dysfunction, and greater AF inducibility along with significant conduction slowing. This coupled with inflammatory cell infiltration and increased interstitial fibrosis resulted in longer and more fractionated AF episodes. Some electrical and structural changes became apparent as early as in 5 weeks after the onset of hypertension, some appeared later, but progressive atrial remodeling at a background of hypertension is indisputable.^42,43

Examination of large cohort data from the Framingham Heart Study show higher augmentation index (hazard ratio [HR] 1.16; 95% CI 1.02–1.32), central pulse pressure (HR 1.14; 95% CI 1.02–1.28), and lower flow-mediated dilation (HR 1.27; 95% CI 0.63–0.99) to be associated with increased risk of incident AF.⁴⁴ Echocardiographic Doppler indices of left ventricular diastolic dysfunction are predictive of AF onset too.^45,46

PROGNOSTIC IMPACT OF HYPERTENSION IN AF

AF may have a variety of implications with respect to patient prognosis. Participants from the Cardiovascular Health Study had poorer outcomes when AF was present at baseline or developed during follow-up, for example, ischemic stroke (HR 1.98, 95% CI 1.63–2.39), coronary heart disease (HR 1.76, 95% CI 1.54–2.03), myocardial infarction (HR 1.40, 95% CI 1.14–1.71), heart failure (HR 3.18, 95% CI 2.78–3.64).⁴⁷ Similar evidence comes from a large primary care database in the United Kingdom that included over 4 million adults aged 30–90 years, where AF was associated with ischemic heart disease (HR 2.52, 95% CI 2.23–2.84), heart failure (HR 3.80, 95% CI 3.50–4.12), ischemic stroke (HR 2.72, 95% CI 2.19–3.38), hemorrhagic stroke (HR 2.22, 95% CI 1.60–3.08), chronic kidney disease (HR 1.42, 95% CI 1.31–1.54), peripheral arterial disease (HR 2.09, 95% CI 1.73–2.53), and vascular dementia (HR 1.57, 95% CI 1.14–2.17).⁴⁸

Despite advances in diagnosis and treatment mortality from causes associated with AF remains high and has been shown to increase over past decades with age-standardized mortality rates rising from 70.6 to 107.1 per 100,000 of population; also, there was a 2.0% annual percent increase in 1999–2009, and to 4.5% up to 2014 in the United States.⁴⁹ This rise in AF-associated mortality particularly affected younger subjects compared to the whole AF population that is represented by elderly people, e.g., 3.7% and 7.3% before and after year 2010, respectively.⁴⁹

How we best manage AF patients co-presenting with hypertension to improve patient outcomes is subject to much discussion. Hypertension is known to be an independent risk factor for range of cardiovascular complications while blood pressure reduction is associated with lower risk of adverse events.^50–52 It is beyond the scope of current review to analyse all possible reciprocal relationships between AF, hypertension, and their respective complications. However, we focus on the impact of hypertension on stroke and systemic thromboembolism in AF and rhythm control management in AF.

Stroke prevention in AF

Prevention of stroke and other thromboembolic events is the principal component of AF management given that AF is associated with 5-fold elevated risk of stroke overall. Albeit AF confers procoagulant state itself stroke risk is largely determined by co-presenting stroke risk factors.⁵³ Oral anticoagulation with either vitamin K antagonists or nonvitamin K antagonists oral anticoagulant should therefore be considered in patients with at least 1 additional stroke risk factor^1,54 given that even a single stroke risk factor is associated with significantly increased risk.^55,56

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Hypertension is a well-established stroke risk factor not only in AF patients but also in patients with sinus rhythm.⁵⁷ In the large Swedish nation-wide AF cohort study presence of hypertension was shown to be associated with 19%; 95% CI 12–25% greater risk of ischemic stroke and 17%; 95% CI 11–22% greater risk of combination of ischemic stroke, transient ischemic attack, and systemic embolism.⁵⁸ Hypertension has been therefore incorporated into various stroke risk assessment schemes in line with other risk factors, including the guideline recommended CHA₂DS₂-VASc score (Table 5).^1,59

Bleeding risk, along with AF-related stroke risk, must be evaluated in patients suitable for oral anticoagulant.⁶⁰ There are a range of factors which put patients at high risk of bleeding. Importantly, many risk factors confer both increased stroke and bleeding risk,⁶¹ but many of them are also modifiable factors, hence a high bleeding risk score is not to rule out the use of oral anticoagulation but to highlight the importance of risk factor management. Indeed, uncontrolled hypertension is one of the independent risk factors for development of intracranial hemorrhage (HR 1.32, 95% CI 1.15–1.52) and major bleeding (HR 1.25, 95% CI 1.16–1.33).⁵⁸ Bleeding risk assessment using the HAS-BLED score (Table 5), includes uncontrolled hypertension (defined as blood pressure above 160 mm Hg) as one of the risk factors for bleeding.^1,53,59

In the latest guidelines, nonvitamin K antagonists oral anticoagulants are recommended as first-line treatment in patients with AF requiring OAC.⁶² Preference to nonvitamin K antagonists oral anticoagulants has been given in anticoagulation-naïve patient given their overall advantages over warfarin therapy as evidenced from trials and real-world data together with favorable pharmacokinetics and pharmacodynamics^63–67; however, warfarin is a reasonable alternative, particularly when well managed and time in therapeutic range is high.^1,54,62,68 Many factors may interfere with the quality of anticoagulation control, including comorbidity and requirement to take many drugs.^69,70

To avoid a trial period of vitamin K antagonists in the anticoagulation-naïve patients and aid decision making with respect to choice of oral anticoagulation the SAMe-TT₂R₂ score (Table 5) was developed and validated to distinguish patients who are capable of reaching the required time in therapeutic range with warfarin.^69,71

Thus, AF and hypertension, stroke and bleeding risks, and even anticoagulation management are closely interlaced. Blood pressure control is an essential component of AF management. A schematic pathway for stroke prevention in the hypertensive patients with diagnosed or clinically suspected AF is shown in the Figure 3.

Rhythm control therapy in AF and hypertension

Rhythm and rate control strategies appeared to have similar effect in term of patients outcomes. The main advantage of a rhythm control strategy would be in symptomatic patients with AF where they are treated with the antiarrhythmic drugs or referred to either direct current cardioversion, catheter ablation of AF or both at different stages of the clinical course of this arrhythmia.¹ Given that hypertension contributes to structural and electrical remodeling in AF, it appeared to be predictive of AF recurrence after sinus rhythm restoration by either means. Recent studies on effect of hypertension on AF ablation outcome arrhythmia recurrence are summarized in Table 6.

However, approximately 30% of AF patients are asymptomatic and how best to treat this cohort of patients is of growing concern. A proportion of patients are fortunate enough to have AF detected by chance, often due to routine medical examinations for other reasons. The absence of symptoms does not remove or reduce the risk of associated stroke, with this cohort of patients often found to have a higher CHA₂DS₂VASc score than symptomatic patients.²² Unfortunately, for the vast majority of patients with asymptomatic AF the first opportunity to detect this arrhythmia is in the context of an acute stroke.⁷² One in 5 ischemic strokes are attributable to AF, of which greater than 20% AF are diagnosed after the stroke event.⁷³

Overall the meta-analysis of Lin et al. that included 17 studies revealed a greater risk of postablation AF recurrence in hypertensive patients compared to those with normal blood pressure (relative risk 1.31, 95%CI 1.13–1.51); however, there was significant heterogeneity acknowledged.⁷⁴ An earlier meta-analysis did not demonstrate a significant association between hypertension presence and AF recurrence.⁷⁵

Effectiveness of blood pressure management including control of other factors associated with blood pressure elevation has to be considered. Indeed, aggressive risk factor management that included blood pressure control along with weight reduction, blood lipids and glucose control, sleep-disordered breathing management, smoking and alcohol cessation resulted in greater reduction of LA volume index and LV hypertrophy compared to control subjects. This translates into a higher AF-free survival rate compared to conventional treatment.⁷⁶ Importance of early blood pressure control in slowing the rate of adverse remodeling seen in the myocardium of hypertensive patients is illustrated in the study by Fredersdorf et al.⁷⁷ They found lone AF to be a predictor of LA volume reduction after successful pulmonary vein isolation, while hypertension and LV hypertrophy interfered with the reverse remodeling.⁷⁷ Hypertension is one of independent predictors of overall procedural safety as evidenced from large real-world observational studies.⁷⁸

Target organ damage in hypertension is also associated with AF recurrence. In the cohort of patients from the Atrial Fibrillation Follow up Investigation of Rhythm Management (AFFIRM) trial those with normal left ventricular geometry experienced a 2-fold longer AF-free period while concentric left ventricular hypertrophy was associated with AF recurrence in the rhythm control arm (HR 1.49, 95% CI 1.10–2.01).⁷⁹ Significant left ventricular diastolic dysfunction that is commonly related to myocardial hypertrophy also places patients at higher risk of AF recurrence after catheter ablation.⁸⁰

Subsequently, hypertension has been incorporated into several decision-making tools to aid rhythm control management (Table 7). Hypertension was found to be predictive of arrhythmia progression from paroxysmal to more sustained types (i.e., persistent or permanent). Among patients with paroxysmal AF participating in European Heart Survey hypertension was more common in those who developed persistent or permanent AF during 1-year follow-up (71% vs. 60%, HR 1.52, 95% CI 1.05–2.20).⁸¹ This was further confirmed in a prospective survey on AF management, the RECORD-AF study (odds ratio 1.5, 95% CI 1.1–2.0).⁸²

CONCLUSION

Hypertension has a significant role as cardiovascular risk factor and has been shown to promote AF. Due to the growing prevalence of both conditions their co-presentation will be even more common in the future. Targeting blood pressure and optimizing its control should therefore be one of the major components of AF management to improve patient outcomes. The use of nonvitamin K antagonists oral anticoagulants where appropriate should be used in parallel in such patients as part of risk factor management as the prognosis of AF-related stroke is by far worse than that for non-AF related stroke.⁷²

DISCLOSURES

G.Y.H.L.: Consultant for Bayer/Janssen, BMS/Pfizer, Biotronik, Medtronic, Boehringer Ingelheim, Microlife, and Daiichi-Sankyo. Speaker for Bayer, BMS/Pfizer, Medtronic, Boehringer Ingelheim, Microlife, Roche, and Daiichi-Sankyo.

Other authors declared no conflict of interest.

REFERENCES