2013 Ambulatory Blood Pressure Monitoring Recommendations for the Diagnosis of Adult Hypertension, Assessment of Cardiovascular and other Hypertension-associated Risk, and Attainment of Therapeutic Goals

Chronobiology International , 30(3): 355 – 410, (2013) Copyright © Informa Healthcare USA, Inc. ISSN 0742-0528 print/1525-6073 online DOI: 10.3109/07420528.2013.750490

A PB M 2 01 3 G UI DE L IN ES

2013 Ambulatory Blood Pressure Monitoring Recommendations for the Diagnosis of Adult Hypertension, Assessment of Cardiovascular and other Hypertension-associated Risk, and Attainment of Therapeutic Goals Joint Recommendations from the International Society for Chronobiology (ISC), American Association of Medical Chronobiology and Chronotherapeutics (AAMCC), Spanish Society of Applied Chronobiology, Chronotherapy, and  Vascular Risk (SECA (SECAC), C), Spanish Society of Atherosclerosis (SEA), and Romanian Society of Internal Medicine (RSIM)

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Writing Committee: Ramón C. Hermida, 1 Michael H. Smolensky, 2 Diana E. Ayala, 1 and Francesco Portaluppi3 Reviewing Committee: Juan J. Crespo, 4 Fabio Fabbian,3 Erhard Haus,5 Roberto Manfredini,3 Artemio Mojón,1 Ana Moyá,1,6 Luis Piñeiro,1,7 María T. Ríos,1,8 Alfonso Otero,9 Horia Balan10 and José R. Fernández1 1

Bioengineering and Chronobiology Laboratories, University of Vigo, Campus Universitario, Vigo, Spain, 2Cockrell School of  Engineering, Department of Biomedical Engineering, The University of Texas at Austin, Austin, Texas, USA, 3Hypertension Center, University Hospital S. Anna and Department of Medical Sciences, University of Ferrara, Ferrara, Italy, 4CS Bembrive, Gerencia de Atención Primaria de Vigo, Servicio Galego de Saúde (SERGAS), Vigo, Spain, 5Department of Pathology and  Laboratory Medicine, University of Minnesota, HealthPartners Institute for Education and Research, Regions Hospital, St. Paul, Minnesota, USA, 6CS Lérez, Gerencia Unica Integrada Pontevedra-Salnés, Servicio Galego de Saúde (SERGAS), Pontevedra, Spain, 7 Internal Medicine Department, Hospital Provincial de Pontevedra, Servicio Galego de Saúde (SERGAS), Pontevedra, Spain, 8CS A Dobl Doblada, ada, Gerencia de Atenc Atención ión Primaria de Vigo, Servicio Galego de Saúd Saúdee (SERG (SERGAS), AS), Vigo, Spai Spain, n, 9 Nephrology  Department, Complejo Hospitalario Universitario, Servicio Galego de Saúde (SERGAS), Ourense, Spain,  10 University of Medicine and Pharmacy, Bucharest, Romania.

Correlation between systolic (SBP) and diastolic (DBP) blood pressure (BP) level and target organ damage, cardiovascular disease (CVD) risk, and long-term prognosis is much greater for ambulatory BP monitoring (ABPM) than daytime office measurements. The 2013 ABPM guidelines specified herein are based on ABPM patient outcomes studies and constitute a substantial revision of current knowledge. The asleep SBP mean and sleep-time relative SBP decline are the most significant predictors of CVD events, both individually as well as jointly when combined with other ABPM-derived prognostic markers.  Thus,, they shou  Thus should ld be pre prefera ferably bly used to diag diagnose nose hyp hyperte ertension nsion and asses assesss CVD and other associated associated risks risks.. Prog Progress ressive ive decrease by therapeutic intervention of the asleep BP mean is the most significant predictor of CVD event-free interval. The 24-h BP mean is not  is  not  recommended  recommended to diagnose hypertension because it disregards the more valuable clinical information pertaining to the features of the 24-h BP pattern. Persons with the same 24-h BP mean may display radically different 24-h BP patterns, ranging from extreme-dipper to riser types, representative of markedly different risk states. Classification of  individuals by comparing office with either the 24-h or awake BP mean as masked normotens normotensives ives  (elevated clinic BP but norma nor mall ABP ABPM) M),, wh which ich sho should uld re repla place ce the ter terms ms of  isola isolated ted offic office e or white-coa white-coatt hypertensio hypertension n , an and d masked hypertensives  (normal clinic BP but elevated ABPM) is misleading and should be avoided because it disregards the clinical significa sign ificance nce of the asleep BP mean mean.. Outc Outcomeome-base based d ABPM reference reference thresholds thresholds for men, which in the absence of  compelling clinical conditions are 135/85 mmHg for the awake and 120/70 mmHg for the asleep SBP/DBP means, are lower by 10/5 mmHg for SBP/DBP in uncomplicated, low-CVD risk, women and lower by 15/10 mmHg for SBP/DBP in male and female high-risk patients, e.g., with diabetes, chronic kidney disease (CKD), and/or past CVD events. In the adult population, “

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Submitted August 23, 2012, Returned for revision September 24, 2012, Accepted October 1, 2012  Address Correspondence Correspondence to Prof. Ramón C. Hermida, Ph.D., Bioengineering and Chronobiology Chronobiology Labs, University of Vigo; Campus Universitario Vigo, 36310 Spain. Ph.: 34-986-812148; Fax: 34-986-812116; E-mail: [email protected] Prof. Francesco Portaluppi, M.D., Ph.D. Hypertension Center, S. Anna Hospital, University of Ferrara; via Savonarola 9, I-44121 Ferrara, Italy. Ph.: 39-0532-236631; Fax: 39-0532-236622; E-mail: [email protected]  Reprint Address: Same as above. 

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R. C. Hermid Hermidaa et al. the combined prevalence of masked normotension and masked hypertension is >35%. Moreover, >20% of  normotensive adults have a non-dipper BP profile and, thus, are at relatively high CVD risk. Clinic BP measurements, even if supplemented with home self-m self-measu easurem rements ents,, are unable to quan quantify tify 24-h BP pat pattern terning ing and asleep BP leve level,l, resu resultin lting g in pot potenti ential al misclassification of up to 50% of all evaluated adults. ABPM should be viewed as the new gold standard to diagnose true hyperten hype rtension sion,, acc accura urately tely asses assesss cons conseque equent nt tiss tissue/or ue/organ, gan, mat materna ernal/fet l/fetal, al, and CVD risk, and indi individu vidualiz alize e hyp hyperte ertension nsion chronotherapy. ABPM should be a priority for persons likely to have a blunted nighttime BP decline and elevated CVD risk, i.e., those who are elderly and obese, those with secondary or resistant hypertension, and those diagnosed with diabetes, CKD, metabolic syndrome, and sleep disorders. (Author Correspondence: [email protected] or [email protected] ). “

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Keywords: Clinical guidelines for the application of ambulatory blood pressure monitoring, monitoring, Ambulatory blood pressure monitoring, Cardiovascular risk, Sleep-time blood pressure, Masked normotension, Masked hypertension,  True hypertension, Hypertension chronotherapy

OUTLINE

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1. Introduction. 2. 24-h BP patterns determined by ABPM: Diagnostic implications. 3. Analyses and interpretation of ABPM data: Role of  rest-activity cycle. 4. Prognostic value of ABPM-derived characteristics. 4.1.. Pr 4.1 Progn ognost ostic ic val value ue of ABP ABPM: M: Fin Findin dings gs and lim limititations of available studies. 4.2. Comp Compara arative tive prog prognos nostic tic value of diffe different  rent   ABPM-derived characteristics. 4.3. 4. 3. Ch Chan ange gess in AB ABPM PM du duri ring ng fo follo lloww-up up as predictors of CVD risk. 5. Masked normotension and masked hypertension. 6. The “normotensive non-dipper”  paradox. 7. J-shaped relationship between BP and CVD risk. 8. Reference Reference ABPM thresholds thresholds for the diagnosis diagnosis of  hypertension. 8.1. Sex differences in ABPM reference thresholds. 8.2. Reference ABPM thresholds in high-risk patients. 8.3. Reference ABPM thresholds in pregnancy. 9. Clinical applications of ABPM. 9.1. Secondary hypertension. 9.2. 9. 2. Re Resi sist stan antt hy hype pert rten ensi sion on:: Di Diag agno nost stic ic an and d treatment issues. 9.3. Elderly patients. 9.4. Diabetes. 9.5. Obesity and metabolic syndrome. 9.6. Chronic kidney disease (CKD). 9.7. 9. 7. Ob Obsstr tru uct ctiv ivee sl slee eep p ap apn nea an and d ot oth her sleep disorders. 9.8. Pregnancy Pregnancy.. 9.9. Evaluation of treatment efficacy. 10. ABPM: Practical considerations. 10.1. Sampling rate and duration of ABPM. 10.2. 10. 2. Tim Timee int interv erval al bet betwee ween n re repea peated ted ABP ABPM M evaluations 10.3. Editing and validation of ABPM. 10.4. Requirements for healthcare personnel in charge of ABPM. 10.5. Maintenance Maintenance and utilization utilization of ABPM devices. 10.6. Patient instructions. 10.7. Sche Schedulin dulingg of pati patient entappoi appointmen ntments ts for forABPM ABPM.. 11. Conclusions. 12. ABPM: Summary of recommendations.

1. INTRODUCTION

Blood pressure (BP) exhibits 24-h variation as a consequence of both cyclic dayday-night, night, or rath rather er res rest-activ t-activity, ity, alterations in behavior (e.g., daily routine of activities and diet, mental stress, and posture), environmental phenomena (e.g., ambient temperature, noise, etc.), and endogenouss cir ou circa cadi dian an (∼24-h 24-h)) rhy rhythm thmss in neu neural ral,, end endocr ocrine ine,, endothelial, endot helial, and hemod hemodynami ynamicc variab variables les (e.g. (e.g.,, plasma nora no radr dren enali aline ne an and d ad adre rena nalin linee [au [auto tono nomi micc ne nerv rvou ouss sys yste tem] m] an and d re reni nin, n, an angi giot oten ensi sin, n, an and d al aldo dost ster eron onee [renin-angiotensin-aldosterone system]) (Baumgart, 1991; Fabbian et al., 2013; Hermida et al., 2007d; Pinotti et al., 2005;; Po 2005 Portal rtalup uppi pi & Smo Smolen lensky sky,, 200 2007; 7; Por Portalu taluppi ppi et al. al.,, 1992b, 1994b, 1996, 2012; Sica & Wilson, 2000; Smolensky  et al. al.,, 20 2007 07,, 20 2012; 12; Tr Trasf asfor orin inii et al. al.,, 19 1991 91;; Va Vara rani ni et al. al.,, 19 1999 99). ). Moreov Mor eover, er, cir circadi cadian an rhy rhythm thmss in BP and oth other er phe pheno nomen mena, a, e.g., those affec affecting ting blood blood coagula coagulation, tion, resu result lt in prom prominent  inent  24-h pat pattern ternss of ac acute ute card cardiov iovasc ascula ularr dis disease ease (CV (CVD) D) event ev ents, s, suc such h as my myoca ocardi rdial al inf infar arcti ction, on, car cardia diacc arr arrest est,, sudden cardiac cardiac death death,, plus ischemic and hemorr hemorrhagic hagic stroke str oke (Casetta et al., 2002; Cohen et al., 1997; Elliot et al., 1998;; Gal 1998 Galler lerani ani et al. al.,, 199 1997; 7; Man Manfr fredin edinii et al. al.,, 199 1996a, 6a, 1996b, 1999a, 1999b, 2004, 2013; Muller Muller et al., 1989; Portaluppi lup pi & Her Hermid mida, a, 2007 2007;; Po Porta rtalup luppi pi et al. al.,, 199 1999). 9). BP is measur mea sured ed for cli clinic nical al pur purpos poses es beca because use the dam damage age caused cau sedto to the thearte arteria riall wa walls lls is dir directl ectlyy andcontin andcontinuou uously sly pr prooportio por tional nal to the BP lev levels els mai mainta ntaine ined d ov over er tim time. e. Ther Therefo efore, re, BP must be maintained as low as possible for as long as possible, to the extent that it remains compatible with a good quality of life and does not cause undesired side effects or complications, to avert target tissue and organ damage dam age and hei height ghtene ened d CVD ris risk. k. Time awarenes awarenesss is implicit in any definition of risk, and the CVD risk due to eleva ele vated ted BP is no ex exce cepti ption on.. He Henc nce, e, to su succ ccess essfu fully  lly  prevent such risk, one needs to be aware of all significant  BP variations over time, from those occurring during the 24 h, par particu ticularl larlyy one oness rel relati ating ng to da daytim ytimee act activit ivityy and nighttime sleep, to those derived from lifestyle changes and therapeutic intervention. In spite of the knowledge on 24-h BP variability, con ventional,  ventio nal, typically daytim daytime, e, clinic BP measur measurements ements made in the physician’s office continue to be used as the basis to diagnose hypertension hypertension as well well as to evaluate evaluate treatmentt effi men efficac cacyy and clin clinical ical out outcome come (Ch (Choban obanian ian et al. al.,, Chronobiology International 

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R. C. Hermid Hermidaa et al. the combined prevalence of masked normotension and masked hypertension is >35%. Moreover, >20% of  normotensive adults have a non-dipper BP profile and, thus, are at relatively high CVD risk. Clinic BP measurements, even if supplemented with home self-m self-measu easurem rements ents,, are unable to quan quantify tify 24-h BP pat pattern terning ing and asleep BP leve level,l, resu resultin lting g in pot potenti ential al misclassification of up to 50% of all evaluated adults. ABPM should be viewed as the new gold standard to diagnose true hyperten hype rtension sion,, acc accura urately tely asses assesss cons conseque equent nt tiss tissue/or ue/organ, gan, mat materna ernal/fet l/fetal, al, and CVD risk, and indi individu vidualiz alize e hyp hyperte ertension nsion chronotherapy. ABPM should be a priority for persons likely to have a blunted nighttime BP decline and elevated CVD risk, i.e., those who are elderly and obese, those with secondary or resistant hypertension, and those diagnosed with diabetes, CKD, metabolic syndrome, and sleep disorders. (Author Correspondence: [email protected] or [email protected] ). “

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Keywords: Clinical guidelines for the application of ambulatory blood pressure monitoring, monitoring, Ambulatory blood pressure monitoring, Cardiovascular risk, Sleep-time blood pressure, Masked normotension, Masked hypertension,  True hypertension, Hypertension chronotherapy

OUTLINE

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1. Introduction. 2. 24-h BP patterns determined by ABPM: Diagnostic implications. 3. Analyses and interpretation of ABPM data: Role of  rest-activity cycle. 4. Prognostic value of ABPM-derived characteristics. 4.1.. Pr 4.1 Progn ognost ostic ic val value ue of ABP ABPM: M: Fin Findin dings gs and lim limititations of available studies. 4.2. Comp Compara arative tive prog prognos nostic tic value of diffe different  rent   ABPM-derived characteristics. 4.3. 4. 3. Ch Chan ange gess in AB ABPM PM du duri ring ng fo follo lloww-up up as predictors of CVD risk. 5. Masked normotension and masked hypertension. 6. The “normotensive non-dipper”  paradox. 7. J-shaped relationship between BP and CVD risk. 8. Reference Reference ABPM thresholds thresholds for the diagnosis diagnosis of  hypertension. 8.1. Sex differences in ABPM reference thresholds. 8.2. Reference ABPM thresholds in high-risk patients. 8.3. Reference ABPM thresholds in pregnancy. 9. Clinical applications of ABPM. 9.1. Secondary hypertension. 9.2. 9. 2. Re Resi sist stan antt hy hype pert rten ensi sion on:: Di Diag agno nost stic ic an and d treatment issues. 9.3. Elderly patients. 9.4. Diabetes. 9.5. Obesity and metabolic syndrome. 9.6. Chronic kidney disease (CKD). 9.7. 9. 7. Ob Obsstr tru uct ctiv ivee sl slee eep p ap apn nea an and d ot oth her sleep disorders. 9.8. Pregnancy Pregnancy.. 9.9. Evaluation of treatment efficacy. 10. ABPM: Practical considerations. 10.1. Sampling rate and duration of ABPM. 10.2. 10. 2. Tim Timee int interv erval al bet betwee ween n re repea peated ted ABP ABPM M evaluations 10.3. Editing and validation of ABPM. 10.4. Requirements for healthcare personnel in charge of ABPM. 10.5. Maintenance Maintenance and utilization utilization of ABPM devices. 10.6. Patient instructions. 10.7. Sche Schedulin dulingg of pati patient entappoi appointmen ntments ts for forABPM ABPM.. 11. Conclusions. 12. ABPM: Summary of recommendations.

1. INTRODUCTION

Blood pressure (BP) exhibits 24-h variation as a consequence of both cyclic dayday-night, night, or rath rather er res rest-activ t-activity, ity, alterations in behavior (e.g., daily routine of activities and diet, mental stress, and posture), environmental phenomena (e.g., ambient temperature, noise, etc.), and endogenouss cir ou circa cadi dian an (∼24-h 24-h)) rhy rhythm thmss in neu neural ral,, end endocr ocrine ine,, endothelial, endot helial, and hemod hemodynami ynamicc variab variables les (e.g. (e.g.,, plasma nora no radr dren enali aline ne an and d ad adre rena nalin linee [au [auto tono nomi micc ne nerv rvou ouss sys yste tem] m] an and d re reni nin, n, an angi giot oten ensi sin, n, an and d al aldo dost ster eron onee [renin-angiotensin-aldosterone system]) (Baumgart, 1991; Fabbian et al., 2013; Hermida et al., 2007d; Pinotti et al., 2005;; Po 2005 Portal rtalup uppi pi & Smo Smolen lensky sky,, 200 2007; 7; Por Portalu taluppi ppi et al. al.,, 1992b, 1994b, 1996, 2012; Sica & Wilson, 2000; Smolensky  et al. al.,, 20 2007 07,, 20 2012; 12; Tr Trasf asfor orin inii et al. al.,, 19 1991 91;; Va Vara rani ni et al. al.,, 19 1999 99). ). Moreov Mor eover, er, cir circadi cadian an rhy rhythm thmss in BP and oth other er phe pheno nomen mena, a, e.g., those affec affecting ting blood blood coagula coagulation, tion, resu result lt in prom prominent  inent  24-h pat pattern ternss of ac acute ute card cardiov iovasc ascula ularr dis disease ease (CV (CVD) D) event ev ents, s, suc such h as my myoca ocardi rdial al inf infar arcti ction, on, car cardia diacc arr arrest est,, sudden cardiac cardiac death death,, plus ischemic and hemorr hemorrhagic hagic stroke str oke (Casetta et al., 2002; Cohen et al., 1997; Elliot et al., 1998;; Gal 1998 Galler lerani ani et al. al.,, 199 1997; 7; Man Manfr fredin edinii et al. al.,, 199 1996a, 6a, 1996b, 1999a, 1999b, 2004, 2013; Muller Muller et al., 1989; Portaluppi lup pi & Her Hermid mida, a, 2007 2007;; Po Porta rtalup luppi pi et al. al.,, 199 1999). 9). BP is measur mea sured ed for cli clinic nical al pur purpos poses es beca because use the dam damage age caused cau sedto to the thearte arteria riall wa walls lls is dir directl ectlyy andcontin andcontinuou uously sly pr prooportio por tional nal to the BP lev levels els mai mainta ntaine ined d ov over er tim time. e. Ther Therefo efore, re, BP must be maintained as low as possible for as long as possible, to the extent that it remains compatible with a good quality of life and does not cause undesired side effects or complications, to avert target tissue and organ damage dam age and hei height ghtene ened d CVD ris risk. k. Time awarenes awarenesss is implicit in any definition of risk, and the CVD risk due to eleva ele vated ted BP is no ex exce cepti ption on.. He Henc nce, e, to su succ ccess essfu fully  lly  prevent such risk, one needs to be aware of all significant  BP variations over time, from those occurring during the 24 h, par particu ticularl larlyy one oness rel relati ating ng to da daytim ytimee act activit ivityy and nighttime sleep, to those derived from lifestyle changes and therapeutic intervention. In spite of the knowledge on 24-h BP variability, con ventional,  ventio nal, typically daytim daytime, e, clinic BP measur measurements ements made in the physician’s office continue to be used as the basis to diagnose hypertension hypertension as well well as to evaluate evaluate treatmentt effi men efficac cacyy and clin clinical ical out outcome come (Ch (Choban obanian ian et al. al.,, Chronobiology International 

Guidelines for ambulatory blood pressure monitoring

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2003; Man 2003; Mancia cia et al. al.,, 200 2007a; 7a; Pic Picker kering ing et al., al.,2005 2005). ). How Howeve ever, r, these the se conv conventi entional onal tim time-un e-unspe specifi cified ed sing single le mea measur sureements have major disadvantages. They are indicative of  the BP status of only a very brief and small fraction of  the entire 24-h BP pattern; moreover, such measurements are often affected by circumstances in the clinic that exert  significant pressor effect (“ white-co  white-coat  at ”  effect [Pick [Pickering, ering, 1995; 199 5; Pic Picker kering ing et al. al.,, 1988 1988]), ]), res result ulting ing in hig higher her than actual BP values. Additionally, clinical BP measurements can ca n be af affec fecte ted d by se seve vera rall po pote tent ntial ial sou sourc rces es of er erro rorr (Halbergg et al., 1990); these include defects in instr (Halber instrumenumentation tat ion (la (lack ck of pro proper per vali validat dation ion and peri periodi odicc cali calibra bration tion of  the measurement measurement devices plus use of inappropriate inappropriate sized BP cuffs, e.g., in slim and overweight subjects) and improper technique and procedures of measurement by inadequately quat ely train trained ed healthc healthcare are personn personnel, el, includi including ng “digit  preference” th that at lea leads ds to ob obser serve verr ro roun undd-of offf of an arb arbit itra rary  ry  last digit, usually to 0 or 5 (Pa (Patterson, tterson, 1984; Sassano Sassano et al., 1987; Wilcox, 1961). Moreover, the within-day variability  of BP, even among healthy individuals, can be so great  thatt the ide tha identif ntifica icationof tionof hyp hypert ertens ension ion and andits its pr propercateg opercateg-orization in terms of severity are highly ambiguous when based solely on unspecified single time-of-day measurements (Hermida, 1999). Finally, unusually high or low   values may occur only at certain times durin duringg the 24-h span sp an th that at ma mayy no nott be co cove vere red d by cas casua uall cli clini nicc BP sa samp mplin ling, g, as in the case of nighttim nighttimee hypertension. hypertension. The use of automatic instrumentation for non-invasivee amb siv ambula ulator toryy BP mon monito itorin ringg (AB (ABPM PM)) mak makes es it pos possib sible le toda to dayy to fo foll llow ow th thee ti time me co cour urse se of BP va vari riat atio ion n ar arou ound nd th thee clock on an individual basis. ABPM constitutes a method of BP assessment that compensates for most, if not all, of  the limita limitations tions of offic officee BP measu measuremen rements ts (Herm (Hermida, ida, 1999; 199 9; Pa Para rati ti et al. al.,, 199 1990). 0). ABP ABPM-d M-deriv erived ed da data ta all allow  ow  better characterization of BP during everyday activities and sleep and, most importantly, the findings correlate moree str mor strongly ongly than clinic BP with target organ damage, CVD ris risk, k, and lon long-te g-term rm pa patie tient nt pr progn ognosi osiss (Ay (Ayala ala & Hermida, 2013; Clement et al., 2003; Dolan et al., 2005; Eguchi Egu chi et al. al.,, 200 2008; 8; Han Hansen sen et al. al.,, 200 2007; 7; Her Hermid midaa &  Ayala, 2002, 2004, 2010; Hermida et al., 2011c, 2012a, 2012b, 2013b; Minutolo et al., 2011; Perloff et al., 1983; Salles Sal les et al. al.,, 200 2008; 8; Sta Staess essen en et al. al.,, 199 1999; 9; Ver Verdec decchi chiaa et al., 1994). Moreover, ABPM is particularly useful not  only for defining in clinical clinical trials the efficacy of hypertension medications (Coats et al., 1996), but also clinically  for evaluating individual patients (Waeber & Brunner, 1999),, espec 1999) especially ially acco according rding to the admin administr istration ation-time -time (morning versus evening) treatment regimen as a costeffe ef fect ctiv ivee me mean anss of be bette tterr pr prev even entin tingg CV CVD D ev even ents ts (Hermida, 2007; Hermida & Smolensky, 2004; Hermida et al., 2005a, 2007a, 2008a, 2010b, 2011a, 2011b, 2011d 2011d,, 2013c;; Port 2013c Portalupp aluppii & Hermi Hermida, da, 2007; Por Portalup taluppi pi & Smolensky, 2010; Portaluppi et al., 2012; Smolensky et al., 2010, 2012). However, apart from the relatively, partially  unjustified, higher cost of the currently marketed ABPM instruments than conventional cuff assessment, patient  tole to lera rabi bili lity ty to ar arou ound nd-t -the he-c -cloc lockk AB ABPM PM ha hass be been en © Informa Healthcare USA, Inc.

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discussed discus sed as a pos possib sible le lim limita itatio tion, n, mos mostly tly bec becaus ausee it  mayy ind ma induce uce mod modest est dis distur turban bance ce of nig nightt httime ime sle sleep ep (Degaute et al., 1992). Furthermore, concern has been raised by some (Mochizuki et al., 1998; Musso et al., 1997) about the low individual reproducibility of the circadian BP profile found between repeated 24-h ABPMs performed perfo rmed on the same patients. patients. Nonet Nonetheles heless, s, in terms of reproducibility ABPM is markedly superior to clinic BP measurements (Hermida et al., 2000b, 2004a; James et al., 1988). Based on the above considerations, ABPM provides the neede needed d essen essential tial time-a time-awar waree and sensi sensitive tive information matio n for sta state-ofte-of-the-ar the-artt indiv individua idualized lized diagn diagnostic ostic categorization, treatment efficacy evaluation, and CVD outcome outco me pred prediction iction.. The 2013 reco recommend mmendatio ations ns presented herein are based upon detailed analyses of the diagnostic, therapeutic, and prognostic applications of   ABPM that should be of common usage, with its intrinsic temporal information, as it is for various other clinical tests, for instance, the well established examples of glomerular merul ar filtr filtration ation rate (Nati (National onal Kidn Kidney ey Fou Foundat ndation, ion, 2002) and oral glucose tolerance test (American Diabetes  Association, 2012). 2. 24-H BP PATTERNS DETERMINED BY ABPM: DIAGNOSTIC IMPLICATIONS

Predictable changes during the 24 h in environmental and an d bi biol olog ogic ical al va vari riab able less gi give ve ri rise se to th thee ci circ rcad adia ian n patte pa ttern rn in sy systo stolic lic BP (SB (SBP), P), dia diast stoli olicc BP (DB (DBP), P), and heart rate. In many, but not all, persons with normal BP or uncomplicated essential hypertension, SBP and DBP declin dec linee to lo lowes westt lev levels els du durin ringg nig nightt httime ime slee sleep, p, ris risee  with morning awakenin awakening, g, and attain peak values during the initial hours of daytime activity. In so-called normal dippers, the asleep BP mean is lower by 10-20% relative to the daytime (awake) BP mean. In addition to this profound, sleep-related nighttime decline, the typical circadian BP pattern exhibits two daytime peaks, the first one approximately 3 h after awakening and the second one arou ar ound nd 12 h af afte terr aw awak aken enin ing, g, wi with th a sm smal alll na nadi dirr in between, in the afternoon (Hermida et al., 2002a). The extent of the nighttime BP attenuation has been mainly  quantified through the so-called “sleep-time relative BP decline”, which is defined as the percent decrease in mean BP during nighttime sleep relative to the mean BP du duri ring ng da dayt ytim imee act ctiv ivit ityy, an and d ca calc lcu ula late ted d as (100×[awa (100× [awake ke BP mean –   asleep asleep BP mean] mean]/aw /awake ake BP mean). Using this percent ratio, subjects have been arbitrarily classified as dippers or non-dippers (sleep-time relat re lativ ivee BP dec declin linee ≥ or