Published online before print May 2, 2005, doi: 10.1161/01.HYP.0000165673.26097.34
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Hypertension. 2005;45:1070.)
© 2005 American Heart Association, Inc.
Editorial Commentaries |
Out-of-Office Blood Pressure Measurement
A New Era
From the Hypertension Unit, Department of Medicine, Hadassah University Hospital, Mount-Scopus, Jerusalem, Israel.
Correspondence to Michael Bursztyn, MD, FAHA, Hypertension Unit, Department of Medicine, Hadassah University Hospital, Mount Scopus, PO Box 24035, Jerusalem 91240, Israel. E-mail bursz{at}cc.huji.ac.il
Twenty years ago in a seminal article, Modan et al,1 fueled the interest in metabolic abnormalities of hypertension by showing that independent of obesity but frequently associated with it, patients with hypertension are glucose intolerant and hyperinsulinemic. This is now commonly acknowledged as the metabolic syndrome (or parts of it).
An enormous volume of research had emerged that tried (somewhat in vain) to attribute hypertension to hyperinsulinemia. Despite the large progress in understanding the fascinating and expanding interrelationship between obesity, adipose tissue, sympathetic drive, renin angiotensin system, leptin, adiponectin, NO, etc, there is still much to learn about the diversity of their relationships and the heterogeneity of effector and signaling systems.
At more or less the same time period, out-of-office measurements of blood pressure evolved gradually from research to clinical tools. These are now accomplished by 24-hour ambulatory blood pressure monitoring (ABPM) and self-measured or home blood pressure (HBP), as the recent American Heart Association (AHA) scientific statement recommends.2
The advantages of ABPM is objectivity, independence of the alerting reaction, evaluation of blood pressure during sleep, and better correlation with hypertensive target organ damage and outcome than clinic blood pressure. Those of HBP are convenience, ability to repeat measurements without limitations, lower costs, and involvement of patients in their care as well as their empowerment.
The Agency for Healthcare Research and Quality (AHRQ) has issued an evidence report that has addressed many aspects of these out-of-office measurements3 and suggested future research directions. Some of the questions raised by AHRQ have been answered lately. Most important, the ability of ABPM4 and HBP5 to predict outcome has now been settled, even when clinic blood pressure is being considered. However, a point not mentioned by the AHRQ report is the reluctance of physicians to rely on measurements (in this case, blood pressure measurements), which do not conform with the large body of experience that exists for clinic blood pressure. In this issue of Hypertension, Mancia et al6 fill in the gap somewhat by showing that out-of-office blood pressure, be it ABPM or HBP, shares a relationship with metabolic parameters similar to that of clinic blood pressure. They took advantage of their population-based Pressioni Arteriose Monitorate e Loro Associazioni (PAMELA) study, in which ABPM and HBP were used, along with clinic blood pressure, and in which body mass index (BMI) and glucose and cholesterol levels were also measured. They found that as in the different stages of clinic hypertension, there is a progressive rise of BMI, glucose, cholesterol, impaired fasting glucose, diabetes mellitus, and hypercholesterolemia rates, and a decrease of HDL cholesterol in different ABPM and HBP quartiles. It should be acknowledged (as the authors did) that the HBP measurements were taken only twice and thus were not performed as recommended by AHA, 3 times twice per day, or on several days repeatedly, as recommended by the European Society of Hypertension (ESH).7 Nevertheless, the finding of similar trends for blood pressure stages or quartiles implies not only universality of the findings but also stresses their nature as a continuous variable for out-of-office measurements as well.
This could explain, in part, why some researchers found patients with "white coat hypertension" to have metabolic abnormalities relative to normotensive patients who, however, had lower HBP.8
Interestingly, in the PAMELA study,6 clinic blood pressure and HBP correlated somewhat better with BMI, glucose, and cholesterol than did 24-hour ABPM. The reason is not clear, but it is tempting to think that this may be related to the absence of blood pressure measurement during activity and sleep shared by clinic blood pressure and HBP. In that respect, at least for plasma glucose, activity and sleep markedly govern the metabolic pathway, with absorption and muscle metabolism enhanced by muscular activity to determine the fate of glucose during the day, whereas hepatic production and a much lower muscle uptake rule during the night.
In contrast to the better correlation of clinic blood pressure or HBP with metabolic parameters, ABPM is a superior tool to assess target organ damage and outcome. A major advantage of the 24-hour ABPM over clinic and HBP is its ability to measure sleep blood pressure. Such measurements were available previously only in the laboratory or for hospitalized patients. Indeed, sleep blood pressure may be one of the best predicting blood pressure variables for target organ damage as well as for prognosis.2,7 It may better represent the basic "unstimulated" blood pressure than the seated awake blood pressure measured in the clinic and by self-measurement (be it at home or elsewhere). Sleep blood pressure also introduced us to the "dipping" phenomenon, the normal blood pressure reduction during sleep. Absence of such a dip, which obviously can be assessed only by 24-hour ABPM, was repeatedly found as a strong predictor of hypertensive target organ damage and adverse clinical outcome.2,7 The 24-hour ABPM also confirmed the previously described rise of blood pressure and heart rate on awakening and the accompanying clustering of cardiovascular events in the morning hours. However, this leaves us with a yet-to-be explained paradox: how do nocturnal nondipping (that is a smaller difference between asleep and subsequent awake blood pressure) and a large morning blood pressure surge have adverse cardiovascular outcomes?
The new era of out-of-office blood pressure measurements has great promises, some of which have already been fulfilled. However, they also generate new questions, define new conditions (nondipping, white coat effect, masked hypertension, etc). Furthermore, our familiarity and extensive knowledge regarding clinic blood pressure should now be complemented and compared with data provided by these new techniques; most soaring is the inflation of normality definitions of ABPM (by day, night, 24 hours), sometimes quite different by different guidelines. For example, the 24-hour definition of normal blood pressure of AHA is <130/80 mm Hg, whereas that of ESH is <125/80 mm Hg. Furthermore, the compatibility of either 24-hour value with that common to the recommendations of both organizations (day and night values) must, at least to some extent, be limited. Even the definition of day and night may be troublesome because common behaviors such as daytime naps (also known as the siesta) will profoundly reduce daytime blood pressure if included in the daytime average;9 and getting out of bed at night to urinate, for example, raises blood pressure to daytime awake levels and may blunt an otherwise normal dipping pattern.10
However, notwithstanding these and other problems, these means for out-of-office blood pressure measurement are here to help us better serve our patients than ever before. In this new era, more studies such as the PAMELA study are needed to enhance our ability to wisely use the information gathered by these methods.
 |
Footnotes |
|---|
The opinions expressed in this editorial commentary are not necessarily those of the editors or of the American Heart Association.
|
References |
|---|
 Top References |
|---|
1. Modan M, Halkin H, Almog S, Lusky A, Eshkol A, Shefi M, Shitrit A, Fuchs Z. Hyperinsulinemia: a link between hypertension obesity and glucose intolerance. J Clin Invest. 1985; 75: 809–817.[Medline] [Order article via Infotrieve]
2. Pickering TG, Hall JE, Appel LJ, Falkner BE, Graves J, Hill MN, Jones DW, Kurtz T, Sheps SG, Roccella EJ. Recommendations for blood pressure measurement in humans and experimental animals. Part 1: blood pressure measurement in humans. Hypertension. 2005; 45: 142–161.
3. Appel L, Robinson K, Guallar E, Erlinger T, Masood SO, Jehn M, Fleisher L, Powe NR, Bass EB. Utility of blood pressure monitoring outside of the clinic setting. Evid Rep Technol Assess (Summ). 2002; Nov: 1–5.
4. Clement DL, De Buyzere ML, De Bacquer DA, de Leeuw PW, Duprez DA, Fagard RH, Gheeraert PJ, Missault LH, Braun JJ, Six RO, Van Der Niepen P, O’Brien E. Prognostic value of ambulatory blood pressure recordings in patients with treated hypertension. N Engl J Med. 2003; 348: 2407–2415.
5. Bobrie G, Chatellier G, Genes N, Clerson P, Vaur L, Vaisse B, Menard J, Mallion JM. Cardiovascular prognosis of "masked hypertension" detected by blood pressure self-measurement in elderly treated hypertensive patients. J Am Med Assoc. 2004; 291: 1342–1349.
6. Mancia G, Facchetti R, Bombelli M, Polo Friz H, Grassi G, Giannattasio C, Sega R. Relationship of office, home and ambulatory blood pressure to blood glucose, and lipid variables in the PAMELA population. Hypertension. 2005; 45: 1072–1077.
7. O’Brien E Asmar R, Beilin L, Imai Y, Mallion JM, Mancia G, Mengden T, Myers M, Padfield P, Palatini P, Parati G, Pickering T, Redon J, Staessen J, Stergiou G, Verdecchia P. European Society of Hypertension recommendations for conventional, ambulatory and home blood pressure measurement. J Hypertens. 2003; 21: 821–848.[CrossRef][Medline] [Order article via Infotrieve]
8. Julius S, Mejia A, Jones K, Krause L, Schork N, van de Ven C, Johnson E, Petrin J, Sekkarie MA, Kjeldsen SE. "White coat" versus "sustained" borderline hypertension in Tecumseh, Michigan. Hypertension. 1990; 16: 617–623.
9. Bursztyn M, Mekler J, Wachtel N, Ben-Ishay D. Siesta and blood pressure monitoring: comparability of the afternoon nap and night sleep. Am J Hypertens. 1994; 7: 217–221.[Medline] [Order article via Infotrieve]
10. Perk G, Ben-Arie L, Mekler J, Bursztyn M. Nocturnal urination may determine dipping status. Hypertension. 2001; 37: 749–752.
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||