© Europace (2017) 19, 891-911 CONSENSUS DOCUMENT doi 10.1093/europace/eux091 Hypertension and cardiac arrhythmias: a consensus document from the European Heart Rhythm Association (EHRA) and ESC Council on Hypertension, endorsed by the Heart Rhythm Society (HRS), Asia-Pacific Heart Rhythm Society (APHRS) and Sociedad Latinoamericana de Estimulaci6én Cardiaca y Electrofisiologia (SOLEACE) Gregory Y.H. Lip", Antonio Coca®, Thomas Kahan**, Giuseppe Boriani®, Antonis S. Manolis’, Michael Hecht Olsen’, Ali Oto’, Tatjana S. Potpara'®, Jan Steffel"’, Francisco Marin'?, Marcio Jansen de Oliveira Figueiredo", Giovanni de Simone", Wendy S. Tzou'®, Chern-En Chiang", and Bryan Williams'” Reviewers: Gheorghe-Andrei Dan"*, Bulent Gorenek’’, Laurent Fauchier”, Irina Savelieva", Robert Hatala”?, Isabelle van Gelder”, Jana Brguljan-Hitij”*, Serap Erdine”®, Dragan Lovic”*, Young-Hoon Kim”’, Jorge Salinas-Arce”*, Michael Field”? “tte of Crows Seces, Unies of Bimingha, UK: Aalborg Thombs Resch Unt. Department of Cn Medina, Aalborg Unversty Aalborg, Derma: Hypertension and Vac Rk Unt. Doparent of Ital Mane, Hrptal Cine (DIBAPS), Unies of Burcloa, arson, pa rola tet Depareran of Cline! Seances, Onder Hosta, Stacoln. Sade: “Deparment ef Crdlegy, Dane Unversty Hosta Cor, Stcinam, Sweden “Cardolegy Depart Univesity of Moen and Reggio Ei, Pongo di Modera Medea tal, "hed Department of Carol, Atons Unersty Schl of Medi, thers Greece Deparert of nurs Maine Hobaek Hosp snd Carr for Indwaaed Medine Arter Dees (IMA), Odense Unversty Hosta Uersty of Seuthern Denar. Denar "Osparment of Cirdolgy, Menor Ankara Hora Heit ne Heth Fndon of Turk, dara, Toray, School of Neen, Cardelogy Gin nc eng Sati ee Une Bae St "crest Crn Dever apne Carbone Cae Za Zure Saran "Our f Gr Hosta Ura es Aa Arca Urwin "croc Fede Shoot Sate roy Carin So a, rast "Depron Mase Sener Fsrc WUserty Hoya. a & PaaS Nap tor ay cava Bacon, Oven of Cd, Une ef ores cf aoe Rrra CO. USK "Dl ef Crdceg Tap Ves General Howl National Yang Ming Users, Tape Tawa. "lee of Cardo ence, University Coleg London, UK: Mcoletins Unvery Hcp Meine Facty Unversty of Medio Care Davia’-Bchiret Roars "Easehr Orang Unversity, Eker, Tork, Carte Hepa UnbestareTroustns, Tours France: George's Unverty Of London, Landon UX "NatonalCardovasuiu ste, NUSCH, Brava Sovak Repu: "Univesity of Groen Unversty Media Centar Groningen Groningen The Neth, Uieraty Medal Carr, Hypartarion sparen, Hoyptal Dr. Pte Ora bin, Stove arb Urey Geratpas Meal Scoot Hea ef Hypertension Deparment ul, Tukey. “Clive for etal dese Marri, Carly depart Hyperion canter Serbs kore Unversty Mai Cntr, Saul, Kore: "lbica Did, Mfloes, ros and *Unvarty of conan, Cnc Seance Cate, Muon USA ceed 10 Mor 2077 ecto con 10 Ma 2017 pend 19 March 2017 Hypertension is @ common cardiovascular risk factor leading to heart failure (HF), coronary artery disease, stroke, peripheral artery dis ‘ease and chronic renal insufficiency. Hypertensive heart dlsease can manifest as many cardiac archythmias, most commonly being aria fibration (AF). Both supraventricular and ventricular arrhythmias may occur in hypertensive patients, especially in those with left Corresponding autor Tek 4 121 SO7SDIC fo +4121 5075503 Eolas py np@bhamae ve Pbiste on bea ofthe Europe Saxety of Crdlogy-Al rts reve © The Author 2017. For pein pleaze ara oueralspermisinsoup com 12021090990 92 uo 189n8 Ka St EL 68/0/61/oFRHE/ecedosnojoD‘dho ajwopeDe}sdnY WON POPEOHWNOG892 GYH Lp etal ventricular hypertrophy (LVH) or HF. Also, some of the antihypertensive drugs commonly used to reduce blood presture, such as thiazide cluretcs, may result n electrolyte abnormalities (eg. hypokalaemia, hypomagnesemia), further contributing to arrhythmias, whereas effec tive control of blood pressure may prevent the development ofthe arrhythmias such as AF, In recognizing this lose relationship between hypertension and arrhythmias, the European Heart Rhythm Associaton (EHRA) and the European Society of Cardiology (ESC) Council. ‘on Hypertension convened a Task Force, with representation from the Heart Rhythm Society (HRS), Asia-Pacific Heart Rhythm Society (APHRS), and Sociedad Latinoamericana de Estimulacién Cardiaca y Electrofisiologla (SOLEACE), with the remit to comprehensively review the avalabe evidence to publish a joint consensus document on hypertension and cardiac arrhythmias, and to provide up-to-date Consensus recommendations for use in clinical practice. The ultimate judgment regarding care ofa particular patient must be made by the healthcare provider and the patient in light of al of the circumstances presented by that patent. Keywords Introduction Hypertension isa common cardiovascular risk factor and underlies ‘many cardiovascular conditions, including heart fallure (HF), coro: nary artery disease, and stroke, as well as chronic kidney disease Hypertensive hart disease can manifest 2: various eardne arryth- rmias, most commonly being arial brillation (AF). Both AF and hypertension individually contribute to an increased rsk of stroke, which is further accentuated when both are present in combina- tion. Both supraventricular arrhythmias and ventricular arthyth= rmias may occur in the hypertensive patients, especially in the presence of associated let ventricular hypertrophy (LVH) or HE. Inaddition, some of the antihypertensive drugs commonly used 10 reduce blood pressure, such as thiazide diuretics, may result in electrolyte abnormalities (eg, hypokalaemia, hypomagnesemia), further contributing to arrhythmias, whereas effective control of blood pressure may prevent the development of the arrhythmias such as AF, In recognizing thie close relationship between hypertension and arhythmias, the European Heart Rhythm Association (EHRA) and the European Society of Cardiology (ESC) Council on Hypertension corwened a Task Force, wth representation from the Heart Rhythm Society (HRS), Asia Pactie Heart Rhythm Society (APHRS) and Sociedad Latinoamericana de Estimulacin Cardaca y Electrofsiologa, (GOLEACE, withthe remit to comprehensively review the available evidence to publish a joint Consensus Document on hypertension and cardiac arhyhmias, and to provide up-to-date consensus recom- ‘mendations for use in clinical practice, The ultimate judgment regard ing care of a particular patient must be made by the healthcare provider and the patient night of all ofthe circumstances presented by that patient Evidence review Members ofthe Task Force were asked to perform a detailed titers ture review, weigh the strength of evidence for or against particular treatment or procedure, and include estimates of expected health outcomes where data exist Patient-spectic modifies, comorbidities, and issues of patient preference that might influence the choice of particular tests or therapies are considered, as are frequency of follow-up and cost effectiveness, In controversial areas, or with regard to issues without evidence other than usual clinical practice, a Hypertension + Avil fibrilation + Arrhythmias * Left ventricular hypertrophy © EHRA consensus document. consensus was achieved by agreement ofthe expert panel fer thor- cough deliberations This document was prepared by the Task Force with representa: tion from EHRA, HRS, APHRS, and SOLAECE. The document was peer-reviewed by ofcial extemal reviewers representing EHRA, HRS, APHIS, and SOLAECE, Consensus statements are evidence-based and derved primariy ‘rom published data. ln contrast to guidelines, we have oped for an ceaser and user-rendly system of ranking using ‘coloured hearts that should allow physicians to easy assess curent status of evidence and consequent guidance (Table 1). This EHRA grading of consensus statements does not have separate defnitions of Level of Evidence ‘This categoration used for consensus statements (used in conser sus documents) must not be considered as being directly smiar to that wsed for oficial society guideline recommendation, which apy a classietion (Cass Hl) and level of evidence (A,B, and C) to rec- ‘ommendations usedin offal gidaines* Thus a green heat indicates a ‘should do this’ consensus state- rent or incicated testment or procedure, that i based on a east ‘one randomized tril. oF i supported by strong observational ev dence that its beneficial and effective. yellow hear indicates tht seneral agreement andr scentife evidence favouring a may do this’ statement oF the useulnesslficacy of a treatment or proce: dure. yellow heart symbol may be supported by randomized ti als based on small number of patients or not widely applicable. “Treatment strategies for which there has been scietie evidence that they are potentially harmful and should not be used (do not do this) are indicated by aredheart. Finally, this isa consensus document that includes evidence and expert opinions from saverl countries. The pharmacologe and non pharmacologic antarrhythmic approaches discussed may, therefore, include drugs that donot have the approval of governmental regula tory agencies inal courtris Relationships with industry and other conflicts ke is EHRAESC poley to sponsor postion papers and gudeines without commercial support and all members volunteered their time, Thus all members ofthe wring group as well as reviewers have dclosed any potential confit ofinterestin deta at the end of this document 1202 1990190 92 wo 1S9n6 fq St 8E!168/9/61/0FRHe/o0edosnonOD dno oIwopeDe/'sdny LION PopEO}UNGHypertension and arrhythmias: consensus document 3893, Table | Scientific rationale of recommendations* Definitions where related toa treatment or procedure “Scintieevdence that a treatment or procedure is beneficial an elective Requires at eat ‘one randomize trial ors supported by strong observational evidence and authors’ con- seus (as ineeated by an asters) General agreement andlor sintfc evidence favour the usefuneslficacy of treatment or procedure. May be supported by randomized tras based on small numberof patients oF not widely pplable ‘Scintic evidence or general agreement not to use or recommend. treatment or procedure. ‘Consensus statement instruction Symbot ‘Should do thi "May dots ‘Do not doth eee “TWscategorzation for our consensus document shuld ot be considered a beng directs to thawed for ofc soley idee recommendations which steno (- anda eine (AB ad C) to recormendscone Pathogenesis of arrhythmias in hypertension “The occurrence of arrhythmias may have important implications on the morbidity and even mortality in hypertensive patients, ranging from supraventricular premature beats to AF, or more serious ven- ‘riculr ahythmiae and sudden cardiac death (SCD). Haemodynamic changes, neuroendocrine factors, atrial and ven- ‘wicular structural remodeling (Le. myocardial frosis) and a proar- rhythmagenic electraphysiologte phenotype of a hypertrophied let ‘ventricle all contribute to the complex pathophysiology of arhyth- rmogenessin hypertension? ‘Atrial fibrilation isthe most frequent arrhythmia in hypertensive patients and hypertension is the most prevalent co-morbidity in patients with AF. Poor BP control seems to worsen outcomes in AF via left ventricular diastole dysfunction [where associated HF is present, this is referred to as ‘heart falure with preserved lection fraction (HFPEF)], left atrial overload and remodeling. AF is also related to the circadian rhythm of BP whereby a blunted nocturnal ll, increases the occurrence of AF, perhaps due to the sustainably of high BP and the resuitant hemodynamic burden on the left atrium.” Hypertension may induce an atrial cardiomyopathy, and myocar lal changes have been described in detail! Mechanical overioad due to high BP may induce an abnormal expression ofion channels and or junctional complexes, as connexin 40 and connexin 43 which can enhance myocardium vulnerability by triggering focal ectopic and re- entry activty® Activation of the renin-anglotensn-aldosterone sys- ‘tem (RAAS) occurs in hypertension and i strongly implicated in the development of AF. AF may also induce microvascular dysfunction in the ventricles* Left ventricular hypertrophy is also the major determinant of the development of ventricular arrhythmias and SCD’ in hypertensive patients. One of the proarrhythmogenic features in LVH is the pres- ence of early after depolarizations, which may trigger sustained arhythias.” ‘Activation of the sympathetic nervous system and RAAS are Important components of the pathophysiology and development of LVH (igure 1), Sympathetic activation may tigger ventricular arrhythmias.” Prolongation and dispersion of repolarization is i another feature of the pro-arthythmogenic impact of LVH."™? Nocturnal arrhythmias have been reported in up to 50% of sleep apnoea patients and autonomic changes may be resporsible. These arrhythmias including sinus arrest, second-degree atrioventricular AY) block, ventricular premature beats (VPs), and non-sustained ventricular tachycardia. Sleep apnoea is also known to predispose to the development of AF. About 50% of sleep apnoea patients are hypertensive." and about 30% of hypertensive patients also have sleep apnoea."="* Myocardial fibrosis in the left ventricle is part of the structural remodelling process associated with LVH, and may lead to distortion ‘of myocardial structure and increased myocardial stifness, as part of the hypertensive diastolic dysfunction. At the cellular level, structural remodelling induced by hypertension ie associated with impaired cel-to-cell communication at gap junctions, and these changes are the basis of non-homogenous impulse propagation and re-entrant ventricular archythmias"” Finally, LVH isalgo-a source of myocardial Ischaemia due to the mismatch of oxygen supply and demand, Microvascular dysfunction with myocardial ischaemia has alo been reported in the erly stages of hypertension, even inthe absence of LLVH, particularly inpatients treated with thiazide diuretics" Such ‘myocardial ischemia may be a trigger of ventricular arrhythmias and Supraventricular arrhythmias ‘Supraventricular ectopics Previous studies demonstrated that supraventricular (SVPBs) and \VPBs occur frequently in hypertensive patients with LVH2 Different varabes could infuence these underbng strctrl changes. Non-pping profile (nocturnal BP reduction < 10% vs. ur- nal BP) and increased noctural BP ae markers of more advanced target organ damage; thus nor-dipping i commonly associat with amythmiss, rater than dipping pattem being causal or directly related to arrhythmia" Recovery ffom exersse may be another tiger factor for SVPBs and the subsequent occurrence of AF. Fr evap nasty of 258 patie with LVH undergoing an exercise tes, SVPBS and supraventricular tachycardia (SVT) occurring during the recovery 1202 1990190 92 wo 1S9n6 fq SP 168/9/61/0FRHe/o0edosnoOD ‘dno ojwopeDe/sdny WON POPEOHUNOG894 GYH Lp etal Perry eae Figure 1 Mechanisms of arhythmas in hypertension. LA, lft atrium: LVH, left ventricular hypertrophy; RAAS, reninangiotensinaldosterone system, phase, but not during exercise, predicted the occurence of subse quent AF? The number of SVPBscuringrecovery was correlated to the development of AF, and the incidence of AF increased from 12% ifno SVPBs occurred to 15% with 0-1 SVEB/min, and further to 37% if21SVPmin ofan SVT was sen. “Thus, patients with excessive SVPBs and LVH have a greater isk of developing AF, which is astocated with increased age systolic blood pressre and N-tsrminalpro-bran natura peptide (NT-proBNP) eves Irterestngy stroke was commonly the frst inal presenta tin, beyond manifest AF, in these study subjects. Even short rus of 20-50 SVPBS are associated with AF or some cryptogenic stroke ‘events. Smia'y, SVPBs were previously assoclated with an increased Fak of lchaemic stroke In the EMBRACE (30-chy cardiac event imonitor bet for recording AFateracerebralischami event trial among older cnyptogeni stroke oF transient ischaemic attack (TIA) patients (median CHADS, score 3), the number of SVPBs on 2 rou tine 4h Hoter was strong independent predictor of subclinical AF ‘Consensus statements References Pations wit frequent SYPB5 and LH have ahr probably of [AF and prolonged electrocardo sraphic (ECG) monitoring for AF etection may be used Utes changes may be used when managing majority of patents with SVB, including addressing recptants relevant co some patients (eg alcohol, cafene) td optimizing BP contro expe ily where LYHis present, Atrial fibrillation ve tos hgh prevalence inthe general population, hypertension i the most signfcant populaton-atrbutabe risk for AF and has been estimated tobe responsible for 14% of al AF cases™ Hypertension was present in>70% of AF ptionts in epidemiological studies”* and recent AF real-world regisvies*" and in 49-90% of patents in randomized AF trials ‘A pooled rit estimate revesled a 73% greater iklinood of AF in patents with hypertension or taking anthypertersive medication (Clas Ratio [OR] 1.73%; 95% Confidence Interval [Ci], 131-228), especially inthe presence of LVH™ Increased AF risk was also reportedin individuals with upper normal blood pressure," ‘One population-based, case-control study of patents treated {or hypertension showed a shaped relationship between blood pressure and incident AF overa 12-year follow-up, with the lowest rates of incident AF at systolic blood pressure of 120-130mmHg and diastolic blood pressure of 60-69 mmHg,” thus suggesting that optimal blood pressure control might decrease AF burden in hypertensive patients. Atria brilaton could represent a mani festation of hypertensive heart disease or hypertensive target organ damage.” In a study of patents with essential hypertension free of other cardiovascular conditions (0% 2500), the incidence of AF was 0.46% per year, and age or increase eft ventricular mass were the only independent preictors of incident AF during a 5-year follow- up. Of note, the annual incidence of stake in that study was sig- realy higher in hypertensive patients with intermittent oF chronic AF (27 and 4.6%, respectively) than in those without AF (081%, P=0.0005). Hypertension has been identifed as an independent risk factor for incident AF*-* or AF progression’ AF-related stroke and mortality”? and bleeding complications of oral antcoaguant 1202 1990190 92 wo 1S9n6 fq SP 168/9/61/0FRHe/o0edosnoOD ‘dno ojwopeDe/sdny WON POPEOHUNOGHypertension and arrhythmias: consensus document 395, therapy in AF patents anda contributor to increased risk of oor ality of treatment with vitamin K antagonists, as predicted by the SAMe-TTsRy score” (see Supplementary material onine, Tee). Importanty, AF may be asymptomatic in up to 35% of patents (including those whe also have symptomatic AF episodes) particu larly in patents with less co-morbidty (eg, with hypertension only). ‘Consensus statements References ,~ wv” AF shouldbe considered asa mai fesation of hypertensive heart seas, and optimization of hypertension management should be made Given that stroke prevention sean tralto the management of AF patients, detection of yperten slon and good blood pressure contrl shouldbe de to mi mite ther of stroke and ‘homboembolsm, as well as the bleeding ek wet on antithram bot therapy Supraventricular tachycardia Left ventricular hypertrophy is the most important predictor for developing supraventricular arhythmias. Ina recent meta analy of “1Ostudes wth 27 141 patients, the incidence of SVT (especially atria tachycardias, AF otter) in patents with LVH was 111% compared with 1.1% among patients without LVH (P< 0.001).5¢ Patients with LVH havea 3 4-fld greater odds of developing SVT (OR 339; 95% Cl, 157-731) than those without LVH, though sig nifleant heterogeneity was present (P = 98%) due to ferences in the baseline covariates such as age, male gender, hypertension, and diabetes in the individual studies:** Other arrhythmias Drugerelated bradyarrhythmias While dihydropyridine ealium channel blockers (CCBe) combine swell with blockers in the management of hypertension, caution should be exercised when combining non-dihydropyridine CCBs with beta-blockers.” There is a risk of bradycardia and AV block ‘ith non-ihyéropyriine COBs parsculary with the use of verap- rilbut alo with diazem at higher doses. A proportionality anal is of side-effects caused by drug interactions reported tothe US FDA between 1968 and 2001 indiated that the rate of conduction. related interactions between beta-blocker and verapamil leading to bradjarchythmia was approximately 10% a two-fold increase inthe rite reported for either agent taken alone’ In the Ditsizer Reinfarction study,” second-degree AV block was noted in 3.4% of patients in the treatment group receiving high-dose (360mg) ‘monly in persistent AF patients with hypertension as compared to Aecordg wth the ris ofan stop sty competing 35 hearts obtained from patients who died suddenly, and compared with 27 both age- and disease-matched and 30 age-matched control hearts from individuals who had not died suddenly sclerosis ofthe sinus node artery was seen in the cases of sudden death with hyper- tensive heart disease. Thus, AV conduction disturbances may occur in hypertensive patients with LVH, and snus node dysfunction may occur. Both elin~ «al condtions may be encountered in the subgroup of hypertersive patents suffering from sleep-disordered breathing * In these situations the electrophysiologial properties of the sinus node and AV conduction system in obstructive sleep apnoea (OSA) patients with noctummal bradyarshythmias are usualy normal wile wake, and thus primary therapy of bradyarrhythmiasin the serting of sleep apnoeas and normal AV conduction would consist of treatment ‘of OSA with continuous postive airway pressure (CPAP) which can reverse these bradyarthythmias, suggesting that OSA most likely induced the arhythmias Final, benefcil effects, abelt moderate and variable, of CPAP on blood pressure have been reported in patients with OSA: patients with more severe OSA, resistant hyper- tension, and better CPAP compliance may havea greater blood pres- sure reduction wth CPAP, Intra- and inter-atriaVinter- and intra-ventricular conduc tion delays Intra and intraatial conduction delays have been reported to be longer in patients with hypertension compared to controle ‘Arnong 9131 patients with hypertension and LVH, 564 (06%) had left bundle branch block (LBBB) Left bundle branch block was independently associated with (fold more cardiovascular death 1202 1990190 92 wo 1S9n6 fq SP 168/9/61/0FRHe/o0edosnoOD ‘dno ojwopeDe/sdny WON POPEOHUNOGGYH Lp etal (F<005), 17-old more hospitalization for HF (?<001), 35-614 ‘more SCD (P< 0.001), and 34old more eardiovascular death within 24h (?<0.001) The authors concluded that in hypertension with LVH on ECG, LBBB identifies patent at increased rskof carciovas- car mortality, SCD, and HF. Inanaraiyss ofthe losartan intervention fr endpoint reduction in hypertension (LIFE) study populton, the duration ofthe QRS com plex predicted all-cause and cardiovascular mortality in hypertensive patents with ECG-LVH in the setting of aggresive hypertensive ther- apy!” An ancilary analysis from the antihypertensive and lpid- lowering treatment to prevent heart atack trial (ALLHAT) also found that. lisinopril sgnifcanty seduced these conduction lisurbances* In a subsequent analysis of the LIFE study, among 9193 hypertensive paents with LVH treated with atenolol or losar- tan, QRS duration was independently preicve of SCD over an ppraximate mean Sear follow-up! and remained a sigifcan pre dlctor of CD even ser controling forthe presence or absence of LBBB and for changes in ECG LVH seventy over the course ofthe study Elevated resting heart rate in sinus rhythm ‘igh refnghear rate has been related to an adverse prognosis in patients with coronary artery disease (CAD) and HF.”> in hyper- tensive patients free from other overt cardiac seas, this is les clear, and an elevated resting heart rate in hypertensive subjects fee from overt cardiac disease seems to be more a risk marker than a risk ctor”? Studies assessing ambuator heart rate tend to dem onstrate that right time heat rate may bea better predictor ofcard- vascular events than daytime hear rate, Heat rate during sleep represents persistent sympathetic overactivity and appears to be a beter reflection of the mechanical stress onthe arterial wall han daytime heart rate, Nevertheles intervention tals have not demon stratedthatoweringthe hear rate with use ofbetz-bockersisbene ficial in hypertensive subjects although some beneft may be evident with Nabradine where concomitant reduced ejection fraction fs ceider." Paradoxical, the use of wabradinein Hs associated wth more AF. appropriate snus tachycardia can sometimes occur and in symptomatic patients, heart rate control with, eg, beta blockers maybe inecated”” ‘Aestngheartrate> 80—85 bpm. may be used as. guide to fur- ther investigate for occutt HF symptoms by cnical examination or determining biomarkers (such as BNF or performingan echocardio- tram, oF looking for asocated comorbiiis, such a8 arrhythmias (eg, AF and aval fuer, anaemia, hyperthyroidism and sepsis" A high resting heart rate may abo be assodated with obesity Ih addon, a high sleeping heart rate obtained via ambubtory blood pressure measurement may refect episodes of resistant hypertension with a non-dpping heart rate and blood pressure pro- fieorexpore the possibility for sleep apnoea associated wih sympa thetic overactivity by cnial story andlor by performing a polysomnography study.”*7° th AF, note that rate control should inaly am for a HR-< 110 topam, with stricter rate control symptomatic or LV function deter crates” The beneficial effects of beta-blockers on outcomes ray be less apparentin AF and reduced LY systolic function ‘Consensus Statements References e Bath snus node and AV conduction dsturban es (particulary inpatients with LYH) can ‘occur in hypertensive patients as a conse- quence of sleep apnoea and sleep dsor- ered beathingis more commen in hypertensive ptiont Thus, assessment for ‘these conditions may be performed in hyper tensive patents Conduction delays occur both atthe aril and ‘verve levelin hypertensive patients, pa ‘uly in those with LVH, exding to AF or SCD, respective. The presence of LBBB in hypertension, especialy with LVH identifies tons at increased cardiovascular risk “Thus, assessment for these condtions may be performed in hypertensive patents ‘An ieresed resting heor rate (~80-85 bpm), orends an adverse prognosis not ont in patents with CAD and HF, but in hyperten sive patints as wall Routine lowering ofthe heart rate with use of beta blockers or other agents may be comideredin hypertensive subjects uncompleated by other comorbid is (eg, paired LY function). Proposal for a standardized ‘workup’ tn most patents with hypertension and suspected arhythmias, al efforts should be made to obtain a dagnosis by documenting the archi, First, because reguar SVTS including abioventricuar nods re- ‘entrant tachycardia (AVNTR), atrioventricular re-entrant tachycardia, (AVR), arial ute and focal atrial tachycardia may lead to severe symptoms in patents with hypertension (particularly in those with advanced dastlic dysfunction, In these patients, curative treatment with eathetr ablation is avaiable 2s well as medica therapy) and can bbe associated witha high success and low complications rates Second, AF can rarely be ruled out s the undertig problem on elvical grounds alone, ad the agnosis of AF usually caves impor- tant implications atleast regarding anticoagulation." The increasing ‘evidence that silent AF is associated with a higher risk for stroke“ fas led to the recommendation of ‘opportunistic screning’ for 'AF using pulse taking or ECG in the most recent guidelines™. This recommendation is clearly also valid in hypertensive patents because they are at greater risk of stroke. However, further research is needed to define bet practice for younger patients diag- nosed, eg with hypertension (especialy those wth asymptomatic organ damage)?" as wel as new technologies suchas automated BP monitors with algorithms for AF detection, or other new technologies “Third a numberof tues suggest that ower blood pressure gous reduce the frequency of episodes with paroxysmal SVT.°* Lifestyle changes reduchg blood pressure and AF burden may ako contribute”? 1202 1990190 92 wo 1S9n6 fq SP 168/9/61/0FRHe/o0edosnoOD ‘dno ojwopeDe/sdny WON POPEOHUNOGHypertension and arrhythmias: consensus document 897 a Ca No Yes en poten [seam 4 Implantable loop recorder or jai thorapy Corvidenieentnn-ctra) Diagnosis contimod Diagnosis confmed Figure 2 Proposed ‘workup’ stndard for patients with hypertension and suspected cardiac arrhythmias. HTN, Hypertension; ECG, Becrocardiogram. “The order and type of workup of patients with arrhythmias and hypertension depends on various factors including duration and severity of symptoms, frequency of episodes and potential thera- peutic implications. A proposal for a standardized inital work up is shown in Figure 2. A personal ECG device (eg, mobile phone applications) may be another option. Implantable loop recorder (LR) may be indicated earlier in high risk’ patients with erypto- genic stroke (embolic stroke of uncertain source, ESUS) or pre symeopelsyncope where bradyarthythmias are suspected as ‘opposed to patients with palpitations, atleast in daily practice [Note that a highly symptomatic patient even with low CHA;DS>- \VASc score may still warrant a further work up with 30d event monitor or ILR. With a CHA;DS;-VASc score >? (Le. two or more stroke risk ac- ‘tors there is sufcient risk to ether consider or recommend stroke prevention in patients with AF or suspected AF on basis of (pro- ‘onged) atria high rate episodes (AHRE). ‘As a final step, 30 day event monitoring oF an implantable cardiac ‘monitor ((CM) may be used to detect rare arrhythmias. In the [EMBRACE (30-day cardlac event monitor belt for recording AF after 1 cerebral fchaemic event) trial and CRYSTAL-AF (CRYptogenic STroke and underlying Atrial. Fibrilation) study respectively, these strategies were superior to conventional folow-up (mostly 24h Holter and symptom-based diagnostics) for the detection of AF in patients post-ryptogenc stroke”? “The optimal duration cut-off forthe definition of device detected ‘AF, however, currently remains elusive: a 6min cut-off is mostly widely used, based on findings ofthe ASSERT trial (ASymptomatic ‘AF and Stroke Evaluation in Pacemaker Patients and the AF Reduction Atrial Pacing). Closely connected to ths isthe question 12021090990 92 uo 189n8 Ka St EL 68/0/61/oFRHE/ecedosnojoD‘dho ajwopeDe}sdnY WON POPEOHWNOGGYH Lp etal of the necessary AF burden to initiate anticoagulation, but >5~ ‘min burden is generally considered as ‘significant. Finally, use of new technology that can be incorporated into a smartphone may be another option to record an infrequent arrhythmic event or detect silent AF.” However, there isa disconnect between AHRE and thromboembolic events, raising the possibilty that AF is marker of increased risk fr stroke rather than a cause of stroke.”* Management approaches ‘Consensus Statements Silent AF is common, and opportu Ist screening for underying AF amongst hypertensive patents shouldbe performed. Intypertensiv patents with symp- toms suggestive ofa cardiac rhythm disorder documentation ofthe presence and type of archythmia shouldbe done for adequate management of the sch ‘The management of patients with hypertension and SVT is primar= lly deiven by the type of arrhythmia (see Figure 3). In addition, hypertension should be proactively managed, with the type of treatment determined by associated compelling indications and lor comorbidities." In general, RAS blockade with angiotensin Converting enzyme (ACE) inhibitors or ARB should be considered where LVH is present. Rate control in the presence of AF may be faciltated with a beta-blocker or non-dihydropyridine calcium blocker (verapamil, ditiazem). Supraventricular tachycardia may respond to a beta-blocker or non-dihydropytidine calcium blocker. Supraventricular tachycardia For acute management of SVT, these patients are treated as other patients with no hypertension according to published guidelines”? Vagal manoeuvres or intravenous adenosine are recommended as the inital therapy’2°* In. haemodyramically unstable patients, synchronized cardioversion is recommended” Intravenous ditia- zem, verapamil or beta-blockers are recommended for haemody- rarcaly table pavents”?™ Intravenous esmolol especialy useful for short-term control of SVT and hypertension”® For more chronic management of SVT catheter ablation isthe fst choice therapy” Similarly focal ectopic aval tachycardia can usu- ally be treated by ablation. Unlike re-entrant tachycardias focal atrial tachycardia (AT) tikely reflective ofa diseased atrium, parcuarly in patients with long-standing hypertension and more severe diastolic dysfunction and atrial remodeling For patients who refuse catheter ablation, possible options in symptomatic patients who do not have ventricular preexctation during sinus rhythm include oral beta blockers, ditazem, or verapailFecainie, propafenone, or sotalol are reasonable choices in patients without structural heart disease (eg severe LVH) who have symptomatic SYT and are not candidates, for, or prefer notto undergo, catheter ablation™ Atrial fibrillation The priory in the treatment of paints with AF is stroke pre- vertion The default ist ofr cra anticcagulation (CAAC) toa A patients ures they area low rik (deine a a CHALDS,-VASe Score in males, 1 in females)” Thus, the inital step isto idetiy “ow rik patients where no antithrombotic therapyis recommended, folowing which OAC can be consdered fr those with adetona stroke risk factors” Even a single stroke rk factor confers excess risk of stroke and mortality and the net ciical Benet is postive for treating such patients *"°° Patients with hypertension have a CHADS,-VASe score of at least and hence atleast a Class laLevel of Evidence indication for aricoaguation (which becomes a as | ngication with any addtional risk factor. Bleeding rik shouldbe assessed using wel- validated simple bleeding risk scores that draw attention to the potentally reversible bleeding rik factors such as the HAS- BLED score, but should not by itself be used to deny anticoagul tion toa patient! Indeed, patents with a clas indication for articcaguiation and a HAS-BLED score>3 may profit as much if not more from anticoagulation based on net clinical benefit than those with a lower HAS-BLED score Uncontrolled hyperten- sion (eg. SBP> 160 mmHg) and other modifiable rik factors (eg concomitant aspirin or non-steroidal an-nlanmatory drug tes iment, excessive alcohol use) should be adéressed, to minimize the risk of bleeding “The nomitamin K antagonist oral ancouguants (NOACS) are recommended asthe preferred treatment modality over vitamin K antagonists for anticoagulation: based on the resus of four inde- pendent large-scale inal tals" Subgroup analyses in patents with hypertension have mostly been consistent with the main out- come ofthe tak. ™"°7-% The use of asi for stroke prevention in AFis associated with minimal efcacy but comes with a substantia bleeding rise ths, aspirin is therefore no longer recommended (Classi)? Persistent as well as permanent AF fs common in hypertensive patients, particulary in the elderly, where rhythm control may not be an option. Elderly hypertensives often have associated HFPEF. A beta-blocker oF non-dthydropyrdie calcium Blacker may be considered fr rate controlin such patients, although RAS block- ade may help LVH regression, In the elderly, digoxin may bea 2nd lie option, Note that during rhythm control therapy, persistent {AF patients with hypertension have more morbidity and mortality 25 compared to rate control, albeit in an era before ablation fe Arial friation ablation has emerged as an efectve method for treatment of AF. n paroxysmal AF and norma sized ari, long-term freedom from symptoms can be achieved in up to BOX, but may require mute procedures"°"" in patents with perstnt AF and diseased atria, which is frequently found in patients with long- standing hypertension ong term succes rates are substan les pertia Maleh 1202 1990190 92 wo 1S9n6 fq SP 168/9/61/0FRHe/o0edosnoOD ‘dno ojwopeDe/sdny WON POPEOHUNOGHypertension and arrhythmias: consensus document 899 ‘Consensus statements (Oral amiodarone shouldbe used or ongolng management in patents wtd symptomatic SVT wha are not candidates for or prefer not to undergo catheter ablation and in whom beta blockers, itazem, flecainie, propafenone, sotalol. or verapamil are inefectve or contraindicated. “The priority nthe treatment of patients wth AF strakepreventlon nd AF patents with hypertension havea CHA;DS,-VASC score of at east thus, efecve stroke preverton may be considered with (OAC ination to good BP contro. [With addtional stroke risk factors. CHADS, VASe Score 22. OAC shouldbe used, a wel controled KA (TTR »70%) or a non-vtamin K antagonist orl anticoagulants (NOAC), with preference for ‘heater, Bledingrsk ould be assessed with focus on the modiable bleeding sk fctors, most of which can be \dantfid using the HAS-BLED score 1 The HAS-BLED score shoud be used to dency those high rik patonts (sore 23) for more care evew and follow-up, and to address the reversible bleeding risk factors (eg uncontroled hypertension) A igh HAS-BLED score alone isnot a reason to withhold OAC. ‘Aria ibelaion ablation should be used in hypertensive patients with symptomatic recurrences of AF ‘on antarhythmic dug therapy who prefer further rythm control therapy. andi first therapy in selected individuals as an aeratve to anarythmic drug therapy depending on patient choice, benef, and rise In patents with rertrant SVT and tims dependant futer, catheter ablation shouldbe used and is sociated witha high succes and low complication rate. In patents with severe structural heart diseases, such a severe LVH, history of myocardalnfrction 2nd HF, a haemodynamic significant valular seas, do nt use ecainide or propafencne. Do not se Sotalot in LVH patients, oc Ditazem and eraparl in HFEF 5 : e- ¥ WH, eft veriedarhyperropy: HFEF. Hear ture ith redved dion Faction SVT, Supraverralar weer: AF. aval iain: CHA.DS:-VASE sore, Congest Hear ure hyperanson, Age 275 souhad) Dba, Stroke Soul), Vcr Seat, Age S74, 3 Sa (emal){ OAC ol rtcongstoners sos ‘ln: VEA.viamin Kandcoagunts TTR, die In therapaie igs: NOAC, no orl neato. HAS BLED score, hyparendon, anormal ealver ncn (1 pone ‘st sre Seeing hatary or redepatan able INR. else (65 yen) plea ancomsarty (1 pant each): AVNRT, Arora nara chy x AVRT,Atiovertclarre-entan hye Ventricular arrhythmias Ventricular ectopics Ventricular arhythmas ae common among hypertensive patients, and this association may have important cial impbeations."=" Data from the Atherosceress Risk in Communities (ARIC) study of more than 15000 Acan American and white men and women showed that ‘frequent or complex ventricular ectopic beats are assocated with high blood pressure" Epidemiological data have shovin tat hypertension induced LVH is associated wth sustained ventricular archythmias *" High blood pressure isnot arhytimogenc pers but the induced ventricular overload Ventricular arrythmias are commonly observed in aortic stenosis, even when peripheral blood pressure i low the frequency ofthese arrhythmias have been demonstrated to be reduced after transcatheter artic valve implatation.™ Changes in electrophysiologcal properties can occur during. volume overload," which may be even more important under pathological condtions suchas ischaemic cas Ventricular tachycardia (VT), Ventricular fibrillation (VF), and sudden death ‘Hypertension is a risk factor for SCD, particularly in the context of increased LV mass.'™ Left ventricular hypertrophy is associated with long-term risk of CD independent of blood pressure, and the risk of SCD increases progressively with LV mas." ‘As discussed in Section Il several mechanisms have been proposed +0 explain the relationship between the presence of LVH and SCD in hypertension (Figure 4). The prolongation of repolarization 3s meas- ured by the QT interval or transmural éspersion of repolarization, present in hypertensive patients can be related tothe degree of LVH, and may be associated with an increased risk of ventricular arthyth- rmias"™" Other mechanisms, such as mismatch between oxygen supply and demand, particularly with stress, reduced coronary flow reserve and subsequent myocardial ischaemia may play arole'®” ‘There is evidence that optimal control of blood pressure and regression of LVH by antihypertensive treatment can help prevent cardiac arhythmias."*" Although an effect on the burden of ven- ‘ricularectopy has not been consistently observed even in the con- text of reversal of LVH,"®-*a reduced incidence of SCD has been demonstrated with effective BP control and regression of LVH. For example, n one study regression of electrocardographic LVH during antihypertensive therapy was associated with a 30% lower risk of SCD independently of blood pressure lowering and ether known predictors ofSCD."™ However itis als important to consider the potential influence of antinypertensive drugs on the risk of SCD. The use of thiazide 1202 1990190 92 wo 1S9n6 fq SP 168/9/61/0FRHe/o0edosnoOD ‘dno ojwopeDe/sdny WON POPEOHUNOG