Ambulatory blood pressure, chronotherapy of hypertension and glaucoma

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Hermida, Diana E. Ayala" "autores" => array:2 [ 0 => array:4 [ "nombre" => "Ramón C." "apellidos" => "Hermida" "email" => array:1 [ 0 => "rhermida@uvigo.es" ] "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "*" "identificador" => "cor0005" ] ] ] 1 => array:2 [ "nombre" => "Diana E." "apellidos" => "Ayala" ] ] "afiliaciones" => array:1 [ 0 => array:2 [ "entidad" => "Laboratorio de Bioingeniería y Cronobiología, Atlantic Research Center for Information and Communication Technologies (AtlantTIC), Universidad de Vigo, Vigo, Pontevedra, Spain" "identificador" => "aff0005" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Presión arterial ambulatoria, cronoterapia de la hipertensión y glaucoma" ] ] "textoCompleto" => "IntroductionAlthough the diagnosis of hypertension is usually based on blood pressure (BP) values obtained conventionally in clinical practice, several independent studies have shown that the mean BP during sleep (mean at rest) is a better prognostic marker of cardiovascular risk (CV) than clinic BP and wakefulness mean or 24h ambulatory BP.<a class="elsevierStyleCrossRefs" href="#bib0270">1–4</a> In general, these studies show that when the means of activity and rest are analyzed together, only the second is a significant and independent marker of CV morbidity and mortality in both hypertensive and normotensive patients.<a class="elsevierStyleCrossRef" href="#bib0290">5</a> However, most published results are derived from studies based in a single record of ambulatory monitoring (ABPM) of each participant at the time of inclusion, which has prevented the assessment of the possible modification of CV risk associated to a reduced average sleep BP. The results of the ambulatory monitoring study for prediction of cardiovascular events (MAPEC), the first and only one published so far in which participants were randomized depending on the time of administration of the antihypertensive medication (all medication in the morning when, after getting up or the full dose of one or more antihypertensive drugs at bedtime) and periodically evaluated during the 5.6 years of follow up by 48h ABPM,<a class="elsevierStyleCrossRefs" href="#bib0275">2,6–9</a> not only corroborate that the average resting systolic BP (SBP) is a significant and independent predictor of CV events (unlike the average activity or clinic BP), but also gives evidence, for the first time, of a 17% decrease in CV risk for every 5mmHg reduction in mean resting SBP during follow-up, regardless of changes in the clinic BP or average activity calculated from the ABPM.<a class="elsevierStyleCrossRefs" href="#bib0275">2,10–12</a> In addition, patients treated at bedtime had a hazard ratio of CV episodes significantly lower than those treated when getting up (0.39, 95% CI 0.29–0.51; p<0.001). These results, taken together, indicate that the average rest BP could be a new therapeutic target for cardiovascular risk reduction, which, obviously requires an accurate assessment of patients through ABPM<a class="elsevierStyleCrossRef" href="#bib0330">13</a> and that it can be achieved more effectively by the intake of the full dose of one or more antihypertensive drugs at bedtime.<a class="elsevierStyleCrossRefs" href="#bib0295">6–9</a> Although it has been documented that administration of antihypertensives at bedtime, compared with its intake when getting up significantly improves ambulatory BP control without increasing adverse effects,<a class="elsevierStyleCrossRef" href="#bib0335">14</a> treatment at bedtime may require some caution in hypertensive patients with glaucoma due to a possible, albeit controversial, relationship between BP during sleep and progression of visual field damage and ischaemic optic nerve damage in these patients.<a class="elsevierStyleCrossRefs" href="#bib0340">15,16</a>Circadian rhythm of ambulatory blood pressure and damage progression in patients with glaucomaThe aetiology of primary open-angle glaucoma (OAG) remains uncertain, although it has been established that one of the causal mechanisms may be related to anomalies in ocular perfusion pressure (OPP).<a class="elsevierStyleCrossRef" href="#bib0350">17</a> The results of several studies suggest that a low OPP, usually measured as the difference between the BP and the intraocular pressure (IOP), may increase the risk of progression in the OAG.<a class="elsevierStyleCrossRef" href="#bib0355">18</a> By contrast, other authors have concluded that this association could be just an artefact due to the absence of the required correction for the value of the IOP,<a class="elsevierStyleCrossRef" href="#bib0360">19</a> delving, that way, into an already open dispute. The possible relationship between the OAG and the BP is even less evident.<a class="elsevierStyleCrossRef" href="#bib0365">20</a> Several epidemiological studies, limited by the use of different criteria for defining hypertension and by the excessively reduced number of evaluated subjects who developed OAG, concluded that hypertension is a possible risk factor for the development and progression of OAG.<a class="elsevierStyleCrossRef" href="#bib0365">20</a> However, more recent studies failed to document any correlation, or even an inverse relationship between hypertension and OAG.<a class="elsevierStyleCrossRef" href="#bib0370">21</a> Circadian variation of high amplitude characteristic of IOP<a class="elsevierStyleCrossRef" href="#bib0375">22</a> is an additional aspect that has scarcely been taken into account in the diagnosis, treatment and progression of glaucoma.The relationship between the circadian pattern of the BP and glaucoma is not without controversy. The results of several cross-sectional and prospective studies on the possible relationship of circadian variations in BP with damage to the visual field and progression of glaucoma patients suggest that variations in nocturnal BP could be a potential risk factor, but the results are far from conclusive.<a class="elsevierStyleCrossRef" href="#bib0380">23</a> Among other authors, Krasinska et al.,<a class="elsevierStyleCrossRef" href="#bib0385">24</a> conducted a cross sectional study in 69 hypertensive patients with OAG evaluated with 24h ABPM and, therefore, of poor reproducibility,<a class="elsevierStyleCrossRef" href="#bib0390">25</a> classified according to the dip (decline percentage in BP during sleep compared to the mean BP during the activity period) of the mean BP (MBP), concluding that patients with a non-dipper profile (dip<10%) had greater visual field defect and degeneration of the optic nerve fibres than dipper patients (dip≥10%). Apart from its transversal nature, this study has important methodological limitations, including: (i) improper use of patients for classification based on MBP dip of the same 10% threshold commonly used for PAS, as the circadian variation range of both pressures is significantly different; (ii) the use of a fixed schedule to calculate the mean of activity and rest in ABPM for all patients regardless of their individual cycle of activity and rest, and (iii) the absence of correction of results by IOP values. Meanwhile, Tokunaga et al.,<a class="elsevierStyleCrossRef" href="#bib0395">26</a> prospectively evaluated the relationship between the dip of ambulatory BP and progression of visual field defects in 15 patients with OAG and 23 with normotensive glaucoma (NTG), with 4-year follow-up after being evaluated with 48h ABPM at the time of their selection. The progression of damage was higher in non-dipper (7 of 14 patients) and extreme dipper patients (dip≥20%; 2 out of 4 patients) compared to those with a physiologically normal dipper profile (4 out of 20 patients). Among the 34 participants with dip<20% (non-dipper and dipper), those who showed progression to visual field defects had significantly lower dip than patients without progression (5.6±7.5% versus 11.2±5.2%; p=0.002), thus showing an association between the absence of adequate reduction in BP during sleep and progression of damage in patients with glaucoma. The results of the Collignon et al. study,<a class="elsevierStyleCrossRef" href="#bib0400">27</a> conducted in 51 patients with OAG and 19 with NTG, with a 2-year follow-up period after being evaluated by 24h ABPM, were similar, despite the fact that their division in non-dipper, dipper and extreme dipper categories was established based on dip thresholds of 5 and 10%, rather than 10 and 20% thresholds, common throughout medical literature. Although the sample size of these prospective studies is extremely small, the results show that the BP circadian pattern, as a whole, specifically non-dipper and extreme dipper profiles, could contribute to the progression of damage in glaucoma patients, and not only the nocturnal BP level.However, several authors have proposed the existence of a possible relationship between the level of BP during sleep and glaucoma. Specifically, it has been speculated that nocturnal hypotension may be a damage progression factor in patients with glaucoma.<a class="elsevierStyleCrossRef" href="#bib0365">20</a> Charlson et al.,<a class="elsevierStyleCrossRef" href="#bib0405">28</a> evaluated during 1-year follow-up 85 patients with TNG and previous history of progression of visual field loss, with 48h ambulatory blood pressure monitoring every 6 months. The amount of time in which the MBP during sleep was <10% of the MBP's activity average was a significant predictor (p=0.02) of damage progression, although not very specific. Apart from the small sample size and other methodological issues which limited the conclusions of the study (absence of information on the degree of association of multiple parameters evaluated with damage progression, lack of statistical significance correction due to the high number of tests performed; damage progression analyzed exclusively in binary form, i.e., as presence/absence, etc.), the definition of “hypotension” based on a predetermined decrease of MBP level (10mmHg) during sleep in relation to the MBP during activity is, at least, debatable.In this regard, it is noteworthy that international guidelines for the diagnosis and treatment of hypertension systematically have omitted, probably intentionally, any definition of “nocturnal hypotension”.<a class="elsevierStyleCrossRef" href="#bib0410">29</a> Several authors, however, have used specific thresholds of the MBP to establish the presence of nocturnal hypotension episodes. Thus, a MBP<50mmHg could be considered low as it corresponds with the lower threshold of cerebral autoregulation in healthy people. Moreover, MBP<70mmHg represents the threshold of cerebral autoregulation in hypertensive patients.<a class="elsevierStyleCrossRefs" href="#bib0415">30,31</a> Such autoregulation is the intrinsic capacity of the vessels in target organs (heart, brain, kidney) to dilate and constrict in response to changes in perfusion pressure, thereby maintaining a relatively constant blood flow.The use of a constant BP threshold to define hypertension/hypotension ignores the predictable variation of BP during 24h resulting from the interrelation of various physiological, neuroendocrine and environmental factors: (i) changes in behaviour associated with the pattern of activity-rest; (ii) divergence in relation to light-dark cycle in ambient temperature, humidity and noise; and (iii) endogen circadian variation (∼24h) in neuroendocrine, endothelial, vasoactive and haemodynamic parameters including noradrenaline and plasma adrenaline (autonomic nervous system), atrial natriuretic peptide and calcitonin, and the renin–angiotensin–aldosterone system (RAAS).<a class="elsevierStyleCrossRefs" href="#bib0425">32,33</a> Thus, it is proposed that the reference thresholds for the diagnosis of hypertension/hypotension should be established taking into account the documented factors that significantly affect BP regulation and CV risk.<a class="elsevierStyleCrossRef" href="#bib0330">13</a> An appropriate reference limit could be a tolerance range that includes a specific percentage of the reference population (normotensive) with a certain confidence level.<a class="elsevierStyleCrossRefs" href="#bib0435">34,35</a> Once the BP reference threshold has been set, given by the upper limit of the tolerance range, the so-called hyperbaric index as a measure of the load exerted by the blood on the arterial wall, it can be calculated as the total area of excess BP above the dynamic reference upper limit during 24h.<a class="elsevierStyleCrossRefs" href="#bib0445">36–38</a> The hyperbaric index, as well as the duration of the excess (percentage of 24h where the subject's BP exceeds the upper limit of the tolerance range), might be used for the diagnosis of hypertension with high reproducibility, sensitivity and specificity.<a class="elsevierStyleCrossRef" href="#bib0450">37</a> Equivalently, the hypobaric index, defined as the total area of BP deficit below the lower tolerance limit, both during 24h and for specific periods of activity and rest, can be used as a sensitive parameter to evaluate hypotension, especially in patients on antihypertensive therapy.<a class="elsevierStyleCrossRefs" href="#bib0330">13,37,38</a> Using the proposed criterion of a hypobaric index≥50mmHg/h,<a class="elsevierStyleCrossRef" href="#bib0330">13</a> the prevalence of hypertension during sleep in the last valuation with 48h ABPM of MAPEC's study participants,<a class="elsevierStyleCrossRef" href="#bib0295">6</a> randomized to ingest all the antihypertensive medication after getting up in the morning or the full dose of a drug or more at bedtime was 0.3% and 0.4%, respectively (p=0.640 between groups). Even using the more stringent criterion of a hypobaric index≥10mmHg/h, the prevalence of nocturnal hypotension was very low regardless of whether the treatment is ingested when getting up or at bedtime (2.0 and 2.3%, respectively; p=0.545).Chronotherapy of hypertension and glaucomaApart from the clear dispute between the possible relationship with glaucoma hypertension, nocturnal hypotension and/or different patterns of circadian variation in BP, there is no evidence that increased BP, especially during sleep, reduces damage progression in glaucoma.<a class="elsevierStyleCrossRef" href="#bib0350">17</a> In what seems to be the only report so far of antihypertensive chronotherapy in patients with glaucoma, Krasinska et al.,<a class="elsevierStyleCrossRef" href="#bib0460">39</a> studied the effects of the time of intake of antihypertensive medication in 88 patients with OAG, all hypertensives under treatment and supposedly controlled. Patients were divided into two treatment groups according to the results of the baseline 24h ABPM: (i) intake of the whole antihypertensive medication in the morning (at pre-set times between 0800 and 0900) on the basis that patients had a dipper profile (n=43); (ii) intake of one drug at night (always between 20.00 and 21.00 regardless of the activity/rest cycle of each patient) and the remaining medication in the morning, either because of having a non-dipper profile (n=23) or because of having an “excessive” BP increase in the morning (value not specified; n=10) or because the authors had the “conviction” that the effect of the treatment received by the patients lasted <24h (unspecified treatment; n=12). The drug administered at night in the second group was only an angiotensin converting enzyme inhibitor (ramipril, 33 cases; perindopril, 3 cases) or amlodipine (9 cases). At 6 months of this nonrandomized division, patients treated with a drug at night and the rest in the morning, compared to those treated with all medication in the morning, showed lower OPP overnight, further loss of visual fields and smaller amplitude of evoked potentials.The conclusions of Krasinska et al.,<a class="elsevierStyleCrossRef" href="#bib0460">39</a> however, should be taken with extreme caution and require proper validation due to its many and obvious limitations, including: (i) participants were not randomized to 2 treatment groups, but were classified based on pre-set and, at least, arguable criteria; (ii) the manuscript does not provide any details about which were the baseline characteristics of patients and their required similarity between treatment groups, including IOP, OPP, damage of visual fields, amplitude of evoked potentials, ischaemic damage to the optic nerve, or progression time for glaucoma; (iii) the results only provide information of the variables at the end of the study and not about their change during the 6 months of treatment, which, together with the absence of randomization, invalidates all findings; (iv) the classification criteria for administering a drug at night are not only arbitrary but contradictory; thus, a greater increase in morning BP is associated with a higher dip towards a dipper profile and therefore, with lower, not higher, CV risk<a class="elsevierStyleCrossRef" href="#bib0275">2</a>; therefore, both from the standpoint of the BP circadian pattern as well as the CV risk, patients with an elevated morning increase in BP are closer to dipper subjects rather than non-dipper, with whom, however, they were included in the same treatment group (a drug at bedtime); (v) the choice of drugs and doses to be administered at night is not justified nor does it respond to objective clinical or therapeutic criteria, as dihydropyridines are characterized by not modifying the ABP dip<a class="elsevierStyleCrossRefs" href="#bib0465">40,41</a>; (vi) as in other works by the same authors<a class="elsevierStyleCrossRef" href="#bib0385">24</a> the use of a fixed schedule to calculate the mean waking and sleep BP for all patients, regardless of their individual cycle of activity and rest, is inappropriate, which, together with poor reproducibility of 24h<a class="elsevierStyleCrossRef" href="#bib0390">25</a> ABPM leads to great uncertainty when it comes to a proper classification of patients regarding dipper or non-dipper<a class="elsevierStyleCrossRef" href="#bib0330">13</a> and (vii) the use of clinical or home BP to establish that all participants were “hypertension controlled” regardless of the results of the ABPM is inadequate<a class="elsevierStyleCrossRef" href="#bib0330">13</a>; when ABPM is available, clinical BP is irrelevant to assess the degree of control, given the high CV risk of masked hypertension and, more specifically, of nocturnal hypertension.<a class="elsevierStyleCrossRef" href="#bib0330">13</a> For those reasons, unfortunately, the study of Krasinska et al.,<a class="elsevierStyleCrossRef" href="#bib0460">39</a> does not provide evidence for or against treatment at bedtime in hypertensive patients with glaucoma.DiscussionThe morbidity and mortality associated with hypertension and glaucoma is obviously different. Glaucoma, with a prevalence of around 2% of the population over 40 years is, after cataracts and followed by diabetic retinopathy, the leading risk factor for visual impairment and blindness. Hypertension, meanwhile, is a chronic process with a prevalence over 40% of the Western adult population. In our area, more than 45% of total mortality is related to hypertension, mainly through stroke, coronary heart disease and heart failure. Current knowledge of several clinically relevant aspects of diagnosis and treatment of hypertension indicates that<a class="elsevierStyleCrossRef" href="#bib0475">42</a>: (i) between the various parameters that can be calculated from the measurement of clinic, home and ambulatory BP, only the mean ambulatory BP during sleep is a significant and independent marker of CV morbidity and mortality<a class="elsevierStyleCrossRefs" href="#bib0275">2,4</a>; (ii) reducing cardiovascular risk in hypertensive patients is associated significantly and independently only with the progressive decrease due to the treatment of mean ambulatory BP during sleep and not to changes in mean clinical activity or BP<a class="elsevierStyleCrossRefs" href="#bib0275">2,10–12</a>; and (iii) the intake of antihypertensive drugs in one dose at bedtime, rather than on getting up, especially those that modulate or block the RAAS,<a class="elsevierStyleCrossRefs" href="#bib0480">43,44</a> improves control of ambulatory BP during sleep<a class="elsevierStyleCrossRefs" href="#bib0465">40,41,43,44</a> and significantly increases survival without CV events.<a class="elsevierStyleCrossRefs" href="#bib0295">6,45,46</a> In the MAPEC study,<a class="elsevierStyleCrossRef" href="#bib0295">6</a> intake of at least one antihypertensive drug at full dose at bedtime, compared with intake of all medications when getting up, reduced the risk of total events after 5.6 years of follow-up by 61%, and major events (CV death, heart attack and stroke) by 67%, which was significantly associated with better BP control during sleep. Moreover, with treatment at bedtime the risk of retinal artery occlusion was reduced by 79%<a class="elsevierStyleCrossRef" href="#bib0295">6</a> and diabetic retinopathy by 92%.<a class="elsevierStyleCrossRef" href="#bib0300">7</a> Pending a possible confirmation by other ongoing prospective studies,<a class="elsevierStyleCrossRefs" href="#bib0500">47–49</a> besides those recently published,<a class="elsevierStyleCrossRefs" href="#bib0490">45,46</a> these results document the benefits of proper use of ABPM in assessing cardiovascular risk and chronotherapy (timing of treatment with the aim of improving the efficiency and/or reduce adverse effects) in reducing the said risk.In patients with glaucoma, beyond the controversies summarized in this document and the uncertainty derived from them, the possible influence of BP during sleep on the progression of damage makes ABPM use advisable as a clinical assessment tool. If the patient with glaucoma is also hypertensive, regular use of the ABPM should be essential, both for assessing the degree of ABP control as well as to objectively determine the absence of nocturnal hypotension, especially if, based on the current recommendations of a growing number of international scientific societies,<a class="elsevierStyleCrossRefs" href="#bib0330">13,50–53</a> the option of bedtime administration of antihypertensives is chosen as a more favourable regimen for reducing CV risk.Conflict of interestsThe authors report no conflicts of interest." 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Ambulatory blood pressure, chronotherapy of hypertension and glaucoma

Presión arterial ambulatoria, cronoterapia de la hipertensión y glaucoma

Ramón C. Hermida

Corresponding author

rhermida@uvigo.es

Corresponding author.

, Diana E. Ayala

Laboratorio de Bioingeniería y Cronobiología, Atlantic Research Center for Information and Communication Technologies (AtlantTIC), Universidad de Vigo, Vigo, Pontevedra, Spain

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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Although the diagnosis of hypertension is usually based on blood pressure &#40;BP&#41; values obtained conventionally in clinical practice&#44; several independent studies have shown that the mean BP during sleep &#40;mean at rest&#41; is a better prognostic marker of cardiovascular risk &#40;CV&#41; than clinic BP and wakefulness mean or 24<span class="elsevierStyleHsp" style=""></span>h ambulatory BP&#46;<a class="elsevierStyleCrossRefs" href="#bib0270"><span class="elsevierStyleSup">1&#8211;4</span></a> In general&#44; these studies show that when the means of activity and rest are analyzed together&#44; only the second is a significant and independent marker of CV morbidity and mortality in both hypertensive and normotensive patients&#46;<a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">5</span></a> However&#44; most published results are derived from studies based in a single record of ambulatory monitoring &#40;ABPM&#41; of each participant at the time of inclusion&#44; which has prevented the assessment of the possible modification of CV risk associated to a reduced average sleep BP&#46; The results of the ambulatory monitoring study for prediction of cardiovascular events &#40;MAPEC&#41;&#44; the first and only one published so far in which participants were randomized depending on the time of administration of the antihypertensive medication &#40;all medication in the morning when&#44; after getting up or the full dose of one or more antihypertensive drugs at bedtime&#41; and periodically evaluated during the 5&#46;6 years of follow up by 48<span class="elsevierStyleHsp" style=""></span>h ABPM&#44;<a class="elsevierStyleCrossRefs" href="#bib0275"><span class="elsevierStyleSup">2&#44;6&#8211;9</span></a> not only corroborate that the average resting systolic BP &#40;SBP&#41; is a significant and independent predictor of CV events &#40;unlike the average activity or clinic BP&#41;&#44; but also gives evidence&#44; for the first time&#44; of a 17&#37; decrease in CV risk for every 5<span class="elsevierStyleHsp" style=""></span>mmHg reduction in mean resting SBP during follow-up&#44; regardless of changes in the clinic BP or average activity calculated from the ABPM&#46;<a class="elsevierStyleCrossRefs" href="#bib0275"><span class="elsevierStyleSup">2&#44;10&#8211;12</span></a> In addition&#44; patients treated at bedtime had a <span class="elsevierStyleItalic">hazard ratio</span> of CV episodes significantly lower than those treated when getting up &#40;0&#46;39&#44; 95&#37; CI 0&#46;29&#8211;0&#46;51&#59; <span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;001&#41;&#46; These results&#44; taken together&#44; indicate that the average rest BP could be a new therapeutic target for cardiovascular risk reduction&#44; which&#44; obviously requires an accurate assessment of patients through ABPM<a class="elsevierStyleCrossRef" href="#bib0330"><span class="elsevierStyleSup">13</span></a> and that it can be achieved more effectively by the intake of the full dose of one or more antihypertensive drugs at bedtime&#46;<a class="elsevierStyleCrossRefs" href="#bib0295"><span class="elsevierStyleSup">6&#8211;9</span></a> Although it has been documented that administration of antihypertensives at bedtime&#44; compared with its intake when getting up significantly improves ambulatory BP control without increasing adverse effects&#44;<a class="elsevierStyleCrossRef" href="#bib0335"><span class="elsevierStyleSup">14</span></a> treatment at bedtime may require some caution in hypertensive patients with glaucoma due to a possible&#44; albeit controversial&#44; relationship between BP during sleep and progression of visual field damage and ischaemic optic nerve damage in these patients&#46;<a class="elsevierStyleCrossRefs" href="#bib0340"><span class="elsevierStyleSup">15&#44;16</span></a></p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Circadian rhythm of ambulatory blood pressure and damage progression in patients with glaucoma</span><p id="par0010" class="elsevierStylePara elsevierViewall">The aetiology of primary open-angle glaucoma &#40;OAG&#41; remains uncertain&#44; although it has been established that one of the causal mechanisms may be related to anomalies in ocular perfusion pressure &#40;OPP&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0350"><span class="elsevierStyleSup">17</span></a> The results of several studies suggest that a low OPP&#44; usually measured as the difference between the BP and the intraocular pressure &#40;IOP&#41;&#44; may increase the risk of progression in the OAG&#46;<a class="elsevierStyleCrossRef" href="#bib0355"><span class="elsevierStyleSup">18</span></a> By contrast&#44; other authors have concluded that this association could be just an artefact due to the absence of the required correction for the value of the IOP&#44;<a class="elsevierStyleCrossRef" href="#bib0360"><span class="elsevierStyleSup">19</span></a> delving&#44; that way&#44; into an already open dispute&#46; The possible relationship between the OAG and the BP is even less evident&#46;<a class="elsevierStyleCrossRef" href="#bib0365"><span class="elsevierStyleSup">20</span></a> Several epidemiological studies&#44; limited by the use of different criteria for defining hypertension and by the excessively reduced number of evaluated subjects who developed OAG&#44; concluded that hypertension is a possible risk factor for the development and progression of OAG&#46;<a class="elsevierStyleCrossRef" href="#bib0365"><span class="elsevierStyleSup">20</span></a> However&#44; more recent studies failed to document any correlation&#44; or even an inverse relationship between hypertension and OAG&#46;<a class="elsevierStyleCrossRef" href="#bib0370"><span class="elsevierStyleSup">21</span></a> Circadian variation of high amplitude characteristic of IOP<a class="elsevierStyleCrossRef" href="#bib0375"><span class="elsevierStyleSup">22</span></a> is an additional aspect that has scarcely been taken into account in the diagnosis&#44; treatment and progression of glaucoma&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">The relationship between the circadian pattern of the BP and glaucoma is not without controversy&#46; The results of several cross-sectional and prospective studies on the possible relationship of circadian variations in BP with damage to the visual field and progression of glaucoma patients suggest that variations in nocturnal BP could be a potential risk factor&#44; but the results are far from conclusive&#46;<a class="elsevierStyleCrossRef" href="#bib0380"><span class="elsevierStyleSup">23</span></a> Among other authors&#44; Krasinska et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0385"><span class="elsevierStyleSup">24</span></a> conducted a cross sectional study in 69 hypertensive patients with OAG evaluated with 24<span class="elsevierStyleHsp" style=""></span>h ABPM and&#44; therefore&#44; of poor reproducibility&#44;<a class="elsevierStyleCrossRef" href="#bib0390"><span class="elsevierStyleSup">25</span></a> classified according to the dip &#40;decline percentage in BP during sleep compared to the mean BP during the activity period&#41; of the mean BP &#40;MBP&#41;&#44; concluding that patients with a <span class="elsevierStyleItalic">non-dipper</span> profile &#40;dip<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>10&#37;&#41; had greater visual field defect and degeneration of the optic nerve fibres than <span class="elsevierStyleItalic">dipper</span> patients &#40;dip<span class="elsevierStyleHsp" style=""></span>&#8805;<span class="elsevierStyleHsp" style=""></span>10&#37;&#41;&#46; Apart from its transversal nature&#44; this study has important methodological limitations&#44; including&#58; &#40;i&#41; improper use of patients for classification based on MBP dip of the same 10&#37; threshold commonly used for PAS&#44; as the circadian variation range of both pressures is significantly different&#59; &#40;ii&#41; the use of a fixed schedule to calculate the mean of activity and rest in ABPM for all patients regardless of their individual cycle of activity and rest&#44; and &#40;iii&#41; the absence of correction of results by IOP values&#46; Meanwhile&#44; Tokunaga et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0395"><span class="elsevierStyleSup">26</span></a> prospectively evaluated the relationship between the dip of ambulatory BP and progression of visual field defects in 15 patients with OAG and 23 with normotensive glaucoma &#40;NTG&#41;&#44; with 4-year follow-up after being evaluated with 48<span class="elsevierStyleHsp" style=""></span>h ABPM at the time of their selection&#46; The progression of damage was higher in <span class="elsevierStyleItalic">non-dipper</span> &#40;7 of 14 patients&#41; and extreme <span class="elsevierStyleItalic">dipper</span> patients &#40;dip<span class="elsevierStyleHsp" style=""></span>&#8805;<span class="elsevierStyleHsp" style=""></span>20&#37;&#59; 2 out of 4 patients&#41; compared to those with a physiologically normal <span class="elsevierStyleItalic">dipper</span> profile &#40;4 out of 20 patients&#41;&#46; Among the 34 participants with dip<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>20&#37; &#40;<span class="elsevierStyleItalic">non-dipper</span> and <span class="elsevierStyleItalic">dipper</span>&#41;&#44; those who showed progression to visual field defects had significantly lower dip than patients without progression &#40;5&#46;6<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>7&#46;5&#37; versus 11&#46;2<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>5&#46;2&#37;&#59; <span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#46;002&#41;&#44; thus showing an association between the absence of adequate reduction in BP during sleep and progression of damage in patients with glaucoma&#46; The results of the Collignon et al&#46; study&#44;<a class="elsevierStyleCrossRef" href="#bib0400"><span class="elsevierStyleSup">27</span></a> conducted in 51 patients with OAG and 19 with NTG&#44; with a 2-year follow-up period after being evaluated by 24<span class="elsevierStyleHsp" style=""></span>h ABPM&#44; were similar&#44; despite the fact that their division in <span class="elsevierStyleItalic">non-dipper</span>&#44; <span class="elsevierStyleItalic">dipper</span> and extreme <span class="elsevierStyleItalic">dipper</span> categories was established based on dip thresholds of 5 and 10&#37;&#44; rather than 10 and 20&#37; thresholds&#44; common throughout medical literature&#46; Although the sample size of these prospective studies is extremely small&#44; the results show that the BP circadian pattern&#44; as a whole&#44; specifically <span class="elsevierStyleItalic">non-dipper</span> and extreme <span class="elsevierStyleItalic">dipper</span> profiles&#44; could contribute to the progression of damage in glaucoma patients&#44; and not only the nocturnal BP level&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">However&#44; several authors have proposed the existence of a possible relationship between the level of BP during sleep and glaucoma&#46; Specifically&#44; it has been speculated that nocturnal hypotension may be a damage progression factor in patients with glaucoma&#46;<a class="elsevierStyleCrossRef" href="#bib0365"><span class="elsevierStyleSup">20</span></a> Charlson et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0405"><span class="elsevierStyleSup">28</span></a> evaluated during 1-year follow-up 85 patients with TNG and previous history of progression of visual field loss&#44; with 48<span class="elsevierStyleHsp" style=""></span>h ambulatory blood pressure monitoring every 6 months&#46; The amount of time in which the MBP during sleep was &#60;10&#37; of the MBP&#39;s activity average was a significant predictor &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#46;02&#41; of damage progression&#44; although not very specific&#46; Apart from the small sample size and other methodological issues which limited the conclusions of the study &#40;absence of information on the degree of association of multiple parameters evaluated with damage progression&#44; lack of statistical significance correction due to the high number of tests performed&#59; damage progression analyzed exclusively in binary form&#44; i&#46;e&#46;&#44; as presence&#47;absence&#44; etc&#46;&#41;&#44; the definition of &#8220;hypotension&#8221; based on a predetermined decrease of MBP level &#40;10<span class="elsevierStyleHsp" style=""></span>mmHg&#41; during sleep in relation to the MBP during activity is&#44; at least&#44; debatable&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">In this regard&#44; it is noteworthy that international guidelines for the diagnosis and treatment of hypertension systematically have omitted&#44; probably intentionally&#44; any definition of &#8220;nocturnal hypotension&#8221;&#46;<a class="elsevierStyleCrossRef" href="#bib0410"><span class="elsevierStyleSup">29</span></a> Several authors&#44; however&#44; have used specific thresholds of the MBP to establish the presence of nocturnal hypotension episodes&#46; Thus&#44; a MBP<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>50<span class="elsevierStyleHsp" style=""></span>mmHg could be considered low as it corresponds with the lower threshold of cerebral autoregulation in healthy people&#46; Moreover&#44; MBP<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>70<span class="elsevierStyleHsp" style=""></span>mmHg represents the threshold of cerebral autoregulation in hypertensive patients&#46;<a class="elsevierStyleCrossRefs" href="#bib0415"><span class="elsevierStyleSup">30&#44;31</span></a> Such autoregulation is the intrinsic capacity of the vessels in target organs &#40;heart&#44; brain&#44; kidney&#41; to dilate and constrict in response to changes in perfusion pressure&#44; thereby maintaining a relatively constant blood flow&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">The use of a constant BP threshold to define hypertension&#47;hypotension ignores the predictable variation of BP during 24<span class="elsevierStyleHsp" style=""></span>h resulting from the interrelation of various physiological&#44; neuroendocrine and environmental factors&#58; &#40;i&#41; changes in behaviour associated with the pattern of activity-rest&#59; &#40;ii&#41; divergence in relation to light-dark cycle in ambient temperature&#44; humidity and noise&#59; and &#40;iii&#41; endogen circadian variation &#40;&#8764;24<span class="elsevierStyleHsp" style=""></span>h&#41; in neuroendocrine&#44; endothelial&#44; vasoactive and haemodynamic parameters including noradrenaline and plasma adrenaline &#40;autonomic nervous system&#41;&#44; atrial natriuretic peptide and calcitonin&#44; and the <span class="elsevierStyleItalic">renin&#8211;angiotensin&#8211;aldosterone system</span> &#40;RAAS&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0425"><span class="elsevierStyleSup">32&#44;33</span></a> Thus&#44; it is proposed that the reference thresholds for the diagnosis of hypertension&#47;hypotension should be established taking into account the documented factors that significantly affect BP regulation and CV risk&#46;<a class="elsevierStyleCrossRef" href="#bib0330"><span class="elsevierStyleSup">13</span></a> An appropriate reference limit could be a tolerance range that includes a specific percentage of the reference population &#40;normotensive&#41; with a certain confidence level&#46;<a class="elsevierStyleCrossRefs" href="#bib0435"><span class="elsevierStyleSup">34&#44;35</span></a> Once the BP reference threshold has been set&#44; given by the upper limit of the tolerance range&#44; the so-called hyperbaric index as a measure of the load exerted by the blood on the arterial wall&#44; it can be calculated as the total area of excess BP above the dynamic reference upper limit during 24<span class="elsevierStyleHsp" style=""></span>h&#46;<a class="elsevierStyleCrossRefs" href="#bib0445"><span class="elsevierStyleSup">36&#8211;38</span></a> The hyperbaric index&#44; as well as the duration of the excess &#40;percentage of 24<span class="elsevierStyleHsp" style=""></span>h where the subject&#39;s BP exceeds the upper limit of the tolerance range&#41;&#44; might be used for the diagnosis of hypertension with high reproducibility&#44; sensitivity and specificity&#46;<a class="elsevierStyleCrossRef" href="#bib0450"><span class="elsevierStyleSup">37</span></a> Equivalently&#44; the hypobaric index&#44; defined as the total area of BP deficit below the lower tolerance limit&#44; both during 24<span class="elsevierStyleHsp" style=""></span>h and for specific periods of activity and rest&#44; can be used as a sensitive parameter to evaluate hypotension&#44; especially in patients on antihypertensive therapy&#46;<a class="elsevierStyleCrossRefs" href="#bib0330"><span class="elsevierStyleSup">13&#44;37&#44;38</span></a> Using the proposed criterion of a hypobaric index<span class="elsevierStyleHsp" style=""></span>&#8805;<span class="elsevierStyleHsp" style=""></span>50<span class="elsevierStyleHsp" style=""></span>mmHg&#47;h&#44;<a class="elsevierStyleCrossRef" href="#bib0330"><span class="elsevierStyleSup">13</span></a> the prevalence of hypertension during sleep in the last valuation with 48<span class="elsevierStyleHsp" style=""></span>h ABPM of MAPEC&#39;s study participants&#44;<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">6</span></a> randomized to ingest all the antihypertensive medication after getting up in the morning or the full dose of a drug or more at bedtime was 0&#46;3&#37; and 0&#46;4&#37;&#44; respectively &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#46;640 between groups&#41;&#46; Even using the more stringent criterion of a hypobaric index<span class="elsevierStyleHsp" style=""></span>&#8805;<span class="elsevierStyleHsp" style=""></span>10<span class="elsevierStyleHsp" style=""></span>mmHg&#47;h&#44; the prevalence of nocturnal hypotension was very low regardless of whether the treatment is ingested when getting up or at bedtime &#40;2&#46;0 and 2&#46;3&#37;&#44; respectively&#59; <span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#46;545&#41;&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Chronotherapy of hypertension and glaucoma</span><p id="par0035" class="elsevierStylePara elsevierViewall">Apart from the clear dispute between the possible relationship with glaucoma hypertension&#44; nocturnal hypotension and&#47;or different patterns of circadian variation in BP&#44; there is no evidence that increased BP&#44; especially during sleep&#44; reduces damage progression in glaucoma&#46;<a class="elsevierStyleCrossRef" href="#bib0350"><span class="elsevierStyleSup">17</span></a> In what seems to be the only report so far of antihypertensive chronotherapy in patients with glaucoma&#44; Krasinska et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0460"><span class="elsevierStyleSup">39</span></a> studied the effects of the time of intake of antihypertensive medication in 88 patients with OAG&#44; all hypertensives under treatment and supposedly controlled&#46; Patients were divided into two treatment groups according to the results of the baseline 24<span class="elsevierStyleHsp" style=""></span>h ABPM&#58; &#40;i&#41; intake of the whole antihypertensive medication in the morning &#40;at pre-set times between 0800 and 0900&#41; on the basis that patients had a <span class="elsevierStyleItalic">dipper</span> profile &#40;n<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>43&#41;&#59; &#40;ii&#41; intake of one drug at night &#40;always between 20&#46;00 and 21&#46;00 regardless of the activity&#47;rest cycle of each patient&#41; and the remaining medication in the morning&#44; either because of having a <span class="elsevierStyleItalic">non-dipper</span> profile &#40;n<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>23&#41; or because of having an &#8220;excessive&#8221; BP increase in the morning &#40;value not specified&#59; n<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>10&#41; or because the authors had the &#8220;conviction&#8221; that the effect of the treatment received by the patients lasted &#60;24<span class="elsevierStyleHsp" style=""></span>h &#40;unspecified treatment&#59; n<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>12&#41;&#46; The drug administered at night in the second group was only an angiotensin converting enzyme inhibitor &#40;ramipril&#44; 33 cases&#59; perindopril&#44; 3 cases&#41; or amlodipine &#40;9 cases&#41;&#46; At 6 months of this nonrandomized division&#44; patients treated with a drug at night and the rest in the morning&#44; compared to those treated with all medication in the morning&#44; showed lower OPP overnight&#44; further loss of visual fields and smaller amplitude of evoked potentials&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">The conclusions of Krasinska et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0460"><span class="elsevierStyleSup">39</span></a> however&#44; should be taken with extreme caution and require proper validation due to its many and obvious limitations&#44; including&#58; &#40;i&#41; participants were not randomized to 2 treatment groups&#44; but were classified based on pre-set and&#44; at least&#44; arguable criteria&#59; &#40;ii&#41; the manuscript does not provide any details about which were the baseline characteristics of patients and their required similarity between treatment groups&#44; including IOP&#44; OPP&#44; damage of visual fields&#44; amplitude of evoked potentials&#44; ischaemic damage to the optic nerve&#44; or progression time for glaucoma&#59; &#40;iii&#41; the results only provide information of the variables at the end of the study and not about their change during the 6 months of treatment&#44; which&#44; together with the absence of randomization&#44; invalidates all findings&#59; &#40;iv&#41; the classification criteria for administering a drug at night are not only arbitrary but contradictory&#59; thus&#44; a greater increase in morning BP is associated with a higher dip towards a <span class="elsevierStyleItalic">dipper</span> profile and therefore&#44; with lower&#44; not higher&#44; CV risk<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">2</span></a>&#59; therefore&#44; both from the standpoint of the BP circadian pattern as well as the CV risk&#44; patients with an elevated morning increase in BP are closer to <span class="elsevierStyleItalic">dipper</span> subjects rather than <span class="elsevierStyleItalic">non-dipper</span>&#44; with whom&#44; however&#44; they were included in the same treatment group &#40;a drug at bedtime&#41;&#59; &#40;v&#41; the choice of drugs and doses to be administered at night is not justified nor does it respond to objective clinical or therapeutic criteria&#44; as dihydropyridines are characterized by not modifying the ABP dip<a class="elsevierStyleCrossRefs" href="#bib0465"><span class="elsevierStyleSup">40&#44;41</span></a>&#59; &#40;vi&#41; as in other works by the same authors<a class="elsevierStyleCrossRef" href="#bib0385"><span class="elsevierStyleSup">24</span></a> the use of a fixed schedule to calculate the mean waking and sleep BP for all patients&#44; regardless of their individual cycle of activity and rest&#44; is inappropriate&#44; which&#44; together with poor reproducibility of 24<span class="elsevierStyleHsp" style=""></span>h<a class="elsevierStyleCrossRef" href="#bib0390"><span class="elsevierStyleSup">25</span></a> ABPM leads to great uncertainty when it comes to a proper classification of patients regarding <span class="elsevierStyleItalic">dipper</span> or <span class="elsevierStyleItalic">non-dipper</span><a class="elsevierStyleCrossRef" href="#bib0330"><span class="elsevierStyleSup">13</span></a> and &#40;vii&#41; the use of clinical or home BP to establish that all participants were &#8220;hypertension controlled&#8221; regardless of the results of the ABPM is inadequate<a class="elsevierStyleCrossRef" href="#bib0330"><span class="elsevierStyleSup">13</span></a>&#59; when ABPM is available&#44; clinical BP is irrelevant to assess the degree of control&#44; given the high CV risk of masked hypertension and&#44; more specifically&#44; of nocturnal hypertension&#46;<a class="elsevierStyleCrossRef" href="#bib0330"><span class="elsevierStyleSup">13</span></a> For those reasons&#44; unfortunately&#44; the study of Krasinska et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0460"><span class="elsevierStyleSup">39</span></a> does not provide evidence for or against treatment at bedtime in hypertensive patients with glaucoma&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0020">Discussion</span><p id="par0045" class="elsevierStylePara elsevierViewall">The morbidity and mortality associated with hypertension and glaucoma is obviously different&#46; Glaucoma&#44; with a prevalence of around 2&#37; of the population over 40 years is&#44; after cataracts and followed by diabetic retinopathy&#44; the leading risk factor for visual impairment and blindness&#46; Hypertension&#44; meanwhile&#44; is a chronic process with a prevalence over 40&#37; of the Western adult population&#46; In our area&#44; more than 45&#37; of total mortality is related to hypertension&#44; mainly through stroke&#44; coronary heart disease and heart failure&#46; Current knowledge of several clinically relevant aspects of diagnosis and treatment of hypertension indicates that<a class="elsevierStyleCrossRef" href="#bib0475"><span class="elsevierStyleSup">42</span></a>&#58; &#40;i&#41; between the various parameters that can be calculated from the measurement of clinic&#44; home and ambulatory BP&#44; <span class="elsevierStyleItalic">only</span> the mean ambulatory BP during sleep is a significant and independent marker of CV morbidity and mortality<a class="elsevierStyleCrossRefs" href="#bib0275"><span class="elsevierStyleSup">2&#44;4</span></a>&#59; &#40;ii&#41; reducing cardiovascular risk in hypertensive patients is associated significantly and independently <span class="elsevierStyleItalic">only</span> with the progressive decrease due to the treatment of mean ambulatory BP during sleep and not to changes in mean clinical activity or BP<a class="elsevierStyleCrossRefs" href="#bib0275"><span class="elsevierStyleSup">2&#44;10&#8211;12</span></a>&#59; and &#40;iii&#41; the intake of antihypertensive drugs in one dose at bedtime&#44; rather than on getting up&#44; especially those that modulate or block the RAAS&#44;<a class="elsevierStyleCrossRefs" href="#bib0480"><span class="elsevierStyleSup">43&#44;44</span></a> improves control of ambulatory BP during sleep<a class="elsevierStyleCrossRefs" href="#bib0465"><span class="elsevierStyleSup">40&#44;41&#44;43&#44;44</span></a> and significantly increases survival without CV events&#46;<a class="elsevierStyleCrossRefs" href="#bib0295"><span class="elsevierStyleSup">6&#44;45&#44;46</span></a> In the MAPEC study&#44;<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">6</span></a> intake of at least one antihypertensive drug at full dose at bedtime&#44; compared with intake of all medications when getting up&#44; reduced the risk of total events after 5&#46;6 years of follow-up by 61&#37;&#44; and major events &#40;CV death&#44; heart attack and stroke&#41; by 67&#37;&#44; which was significantly associated with better BP control during sleep&#46; Moreover&#44; with treatment at bedtime the risk of retinal artery occlusion was reduced by 79&#37;<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">6</span></a> and diabetic retinopathy by 92&#37;&#46;<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">7</span></a> Pending a possible confirmation by other ongoing prospective studies&#44;<a class="elsevierStyleCrossRefs" href="#bib0500"><span class="elsevierStyleSup">47&#8211;49</span></a> besides those recently published&#44;<a class="elsevierStyleCrossRefs" href="#bib0490"><span class="elsevierStyleSup">45&#44;46</span></a> these results document the benefits of proper use of ABPM in assessing cardiovascular risk and chronotherapy &#40;timing of treatment with the aim of improving the efficiency and&#47;or reduce adverse effects&#41; in reducing the said risk&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">In patients with glaucoma&#44; beyond the controversies summarized in this document and the uncertainty derived from them&#44; the possible influence of BP during sleep on the progression of damage makes ABPM use advisable as a clinical assessment tool&#46; If the patient with glaucoma is also hypertensive&#44; regular use of the ABPM should be essential&#44; both for assessing the degree of ABP control as well as to objectively determine the absence of nocturnal hypotension&#44; especially if&#44; based on the current recommendations of a growing number of international scientific societies&#44;<a class="elsevierStyleCrossRefs" href="#bib0330"><span class="elsevierStyleSup">13&#44;50&#8211;53</span></a> the option of bedtime administration of antihypertensives is chosen as a more favourable regimen for reducing CV risk&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Conflict of interests</span><p id="par0055" class="elsevierStylePara elsevierViewall">The authors report no conflicts of interest&#46;</p></span></span>"
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          "titulo" => "Introduction"
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          "titulo" => "Circadian rhythm of ambulatory blood pressure and damage progression in patients with glaucoma"
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          "titulo" => "Chronotherapy of hypertension and glaucoma"
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    "fechaRecibido" => "2015-04-22"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; Hermida RC&#44; Ayala DE&#46; Presi&#243;n arterial ambulatoria&#44; cronoterapia de la hipertensi&#243;n y glaucoma&#46; Med Clin &#40;Barc&#41;&#46; 2016&#59;146&#58;30&#8211;34&#46;</p>"
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