How Low Can a Person's Blood Pressure Go Before Death
Ambulatory claret pressure (ABP) monitoring (ABPM) has go increasingly important for the management of patients with hypertension.1–3 Well-nigh studies have shown that mean 24-hour ABP is a improve predictor of morbidity and bloodshed than part BP (OBP).4 However, in that location is still debate on the relative importance of daytime and nighttime ABP and on the prognostic significance of the night–day BP ratio. Studies that reported on daytime and nighttime ABP separately found that both BPs carried significant prognostic information in patients with hypertension.4–9 Whereas the prognostic value of daytime and dark ABP was about similar in ii studies,5,7 others directly compared the prognostic value of the two BPs and constitute that nighttime ABP was a significantly better predictor than daytime ABP.vi,viii,ix Also results on the nighttime–day BP ratio are non consequent in hypertension. Some studies observed a significantly meliorate prognosis in patients with a greater decline in nighttime ABPvi,10 but this was non confirmed by others.vii,11
Divergent results amongst studies may be attributable to differences in methodology, written report population, sample size, and stop points. To better appreciate the prognostic significance of daytime and nighttime ABP and the night–day BP ratio in hypertension, and to assess whether the results would differ for mortality and various types of cardiovascular (CV) events, we pooled the individual data of hypertensive patients from 4 prospective studies, performed in Europe and coordinated in Belgium.6,vii,12,13 Common features of the 4 studies were that both fatal and nonfatal events were registered during prospective follow-upward and that terminate betoken committees used the same criteria for validation of the events. Nosotros report on the prognostic value of daytime and nighttime ABP and their ratio for all-crusade, noncardiovascular (NCV), and CV mortality, and for fatal and nonfatal coronary centre illness (CHD), stroke, and an amass of major CV events.
Methods
Nosotros used individual information of hypertensive patients from four studies performed in Europe and coordinated at the universities of Ghent7 or Leuven.13–15 Three of the studies were performed in close collaboration of the 2 groups.7,14,15 The studies were approved past the advisable institutional review committees and all subjects gave informed consent. Inclusion and exclusion criteria and results on the prognostic significance of various aspects of ABP in these studies have been reported previously.6,seven,12–16 Patients with severe coexisting disease, debilitating illness, dementia, and impairment of renal function were usually excluded from these studies, and for the current meta-assay nosotros also excluded patients with a history of major CV disease at baseline, namely myocardial infarction, stroke, and congestive heart failure.
The Convalescent blood pressure level Monitoring and Handling of Hypertension (APTH) trial12,xv included 419 patients who were ≥18 years former and whose diastolic OBP measured off agile treatment and on placebo was 95 through 114 mm Hg. During the six-calendar month trial, patients were randomized to antihypertensive therapy on the footing of ABP or OBP, whereafter follow-up was continued for v more years.12 The Role versus Convalescent claret force per unit area (OvA) written report7 included patients who had been treated with antihypertensive drugs for ≥3 months by the time of the inclusion visit. Prerequisite for inclusion was documented hypertension, defined as diastolic BP >ninety mm Hg under handling or >95 mm Hg without treatment, at two split up visits before the enrollment visit. The total number of recruited patients amounted to 1963. Subsequently exclusion of 41 patients from the APTH trial who were also included in the OvA study and 115 patients with a history of CV disease at inclusion, 1807 patients remained for the electric current analyses. Follow-up amounted to 6.v years afterward the end of the study inclusion period. The Systolic Hypertension in Europe (Syst-Eur) trial randomized 4695 patients who were ≥lx years old and had a systolic BP of 160 to 219 mm Hg with a diastolic BP <95 mm Hg during the placebo run-in period.6,fourteen,16 ABPM was performed in 1108 patients, that is during the run-in menses in 695 patients, and, presently afterward randomisation, during placebo in 187 patients and during agile treatment in 226 patients. Later on the finish of the double-blind phase of the trial, all patients received agile study drugs and follow-upward was extended past five years.17 After exclusion of 27 patients whose OBP was normal when ABPM was performed later randomization into the placebo grouping, and 61 patients with a history of CV illness, 1020 patients remained for the current meta-analysis. The fourth study was performed in ≥threescore-twelvemonth-old patients, registered in ane principal care (I Care) practice in Flanders, Belgium, irrespective of blood force per unit area.13 The study included 462 patients of whom 12 were crippled, demented, or admitted in a dwelling for sick elderly people. ABPM was performed in 383 of the remaining patients, of whom 251 were hypertensive based on clinic systolic BP ≥140 mm Hg or diastolic BP ≥xc mm Hg or taking antihypertensive therapy. Subsequently exclusion of 29 patients with prior CV illness, 222 hypertensive patients remained for the assay. Follow-up amounted to 10 years afterward the finish of the baseline test period.
Blood Force per unit area
Office BP was the boilerplate of 26 or three7,12,13 BPs measured in the sitting position past the auscultatory technique using the 5th Korotkoff sound for diastolic BP, during the baseline visit, closest to ABPM. ABP was monitored during 24 hours, by utilise of validated devices. BP was measured every xv minutes12,xiii or at intervals of not more than than 30 minutes6,seven during daytime and every 30 minutes,12,thirteen or at intervals of not more than hour6,7 during the dark. In the current assay daytime ABP was the average BP from 10 am to viii pm and nighttime ABP was the average BP from midnight to 6 am, which corresponds well with the bodily awake and asleep ABP.18 The nighttime–day BP ratio was calculated from these values.
Outcomes
Outcome variables were: (1) all-cause bloodshed; (2) CV mortality, including all fatal CV events; (3) NCV mortality; (iv) Coronary heart affliction (CHD) including sudden death and fatal and nonfatal myocardial infarction. Sudden death included any decease of unknown origin occurring immediately or within 24 hours of the onset of acute symptoms, also equally unattended expiry for which no likely crusade could be established. Myocardial infarction was divers as 2 of the post-obit 3 disorders: typical breast pain, electrocardiographic changes and increased cardiac enzymes; cardiac enzymes included creatine kinase (CK), CK-MB or aspartate aminotransferase (AST), which had to exist college than 2 times the upper limit of normality; (v) Fatal and nonfatal stroke, defined equally a neurological deficit with symptoms continuing for >24 hours or leading to death with no apparent cause other than vascular; transient ischemic attack was non an finish point; (six) Major CV disease (CVD) including CV bloodshed and nonfatal myocardial infarction and stroke. All events that occurred during follow-upwards were corroborated by the report terminate bespeak committees, using the same diagnostic criteria. One of the authors took part in the 4 committees.
Statistical Assay
Database management and statistical analyses were performed using SAS software, version 8.2 (SAS Institute Inc). Private patient data from the 4 studies were pooled for the meta-assay. Data are reported equally mean±SD or as percentages. Nosotros used Cox proportional hazards regression analysis to assess the prognostic significance of the various BPs, later testing the proportional hazards assumption. All analyses were stratified by study. For patients who experienced multiple events, analysis was restricted to the first result under study. The hazard ratio (HR) represents the risk associated with a 1 SD increase in BP. In multivariable Cox regression analysis, we adapted for age, gender, smoking, serum full cholesterol, diabetes, and antihypertensive treatment at the time of ABPM. To appraise whether the consequence was contained from other BP measurements, nosotros performed additional adjustments for other BPs. We tested whether the effect of BP on outcome differed (one) among the studies, and (2) by handling status, by inclusion of the appropriate interaction terms in the Cox models. Sensitivity analyses were performed for the models which included both daytime and nighttime ABP; analyses were done (ane) with consecutive exclusion of each written report, and (2) separately in men and women, older and younger patients, and treated and untreated patients, with tests of heterogeneity by utilise of advisable interaction terms. A ii-tailed probability value ≤0.05 was considered meaning.
Results
Patient Characteristics at Baseline
Age of the 3468 included participants averaged 60.8±thirteen.1 years (range: eighteen to 96; median: 62.8); 44.eight% were men, 13.vii% were electric current smokers, 8.four% had diabetes and 61.4% were nether antihypertensive treatment at the time of ABPM. BMI averaged 27.vii±4.5 kg/mii. OBP averaged 159.0±19.9/91.0±11.7 mm Hg, daytime ABP 143.v±17.0/87.1±eleven.7 mm Hg, nighttime ABP 129.eight±17.6/75.4±12.three mm Hg, and the nighttime–twenty-four hours BP ratio 0.907±0.085/0.866±0.095. Delight come across Table S1 at http://hyper.ahajournals. org for split up data of the 4 studies.
Follow-Upwards
Median follow-upward fourth dimension was half-dozen.57 years (range: 0.08 to 13.one), and total follow-up time amounted to 23 164 patient-years. The total number of events during follow-up, including first and subsequent events, consisted of 324 deaths (145 from a CV crusade: CHD: 68; CHF: 29; stroke: 31; other: 17) and 72 nonfatal myocardial infarctions and 93 nonfatal strokes. Delight see Table S2 for split up information of the four studies.
Prognostic Significance of Daytime and Dark Blood Pressure
Table 1 gives the HRs of the relationships of daytime, nighttime, and 24-hour ABP with the study end points, with adjustment for OBP and the other covariates. Systolic daytime and nighttime ABP significantly and independently predicted all outcomes, except NCV bloodshed which was only predicted past night ABP. Diastolic daytime and nighttime ABP predicted CVD, CHD, and stroke, but mortality was but significantly predicted by nighttime ABP. Amid the other covariates age, male gender, smoking, total cholesterol, and diabetes at baseline predicted outcome to diverse extents in the different models. However, antihypertensive treatment at the time of ABPM was never a significant predictor of events. The interaction terms of the diverse ABPs with studies and with treatment were never significant.
Blood Pressure | Death | NCV Death | CV Death | CVD | CHD | Stroke |
---|---|---|---|---|---|---|
Data are hazard ratios (95% confidence intervals) for each 1 standard divergence higher blood force per unit area, stratified for report and adapted for age, gender, smoking, total cholesterol, diabetes, antihypertensive treatment, and office blood pressure. | ||||||
Significance of chance ratios: | ||||||
*P≤0.05; | ||||||
†P≤0.01; | ||||||
‡P≤0.001. | ||||||
BP indicates blood pressure; CHD, coronary heart disease; CV, cardiovascular; CVD, cardiovascular disease; NCV, noncardiovascular. | ||||||
No. of events | 324 | 179 | 145 | 272 | 129 | 113 |
Systolic BP | ||||||
Daytime | one.21† (1.06–i.37) | i.11 (0.94–ane.32) | 1.33† (1.11–1.61) | 1.40‡ (one.22–1.60) | 1.39‡ (1.xv–i.69) | i.56‡ (1.28–1.92) |
Nighttime | one.34‡ (1.20–i.49) | 1.26† (i.08–1.48) | 1.42‡ (1.21–i.66) | i.47‡ (1.30–1.65) | 1.fifty‡ (1.26–1.78) | 1.57‡ (1.31–1.87) |
24-hour | i.32‡ (1.16–1.49) | 1.23* (one.04–1.46) | one.43‡ (1.19–i.71) | i.50‡ (one.31–1.71) | 1.49‡ (1.23–1.80) | one.69‡ (i.38–two.07) |
Diastolic BP | ||||||
Daytime | one.xi (0.97–1.28) | ane.13 (0.94–1.37) | 1.09 (0.88–1.34) | one.24† (1.07–1.44) | 1.25* (one.01–1.54) | i.32* (1.05–1.64) |
Night | ane.27‡ (1.11–1.45) | 1.20* (1.00–1.44) | 1.34† (i.11–one.62) | 1.32‡ (1.15–i.51) | i.30† (1.06–one.60) | one.34† (1.09–1.66) |
24-60 minutes | 1.xix† (1.04–ane.36) | one.xx* (1.00–1.43) | one.17 (0.96–i.43) | 1.28‡ (1.11–ane.47) | i.26* (one.02–1.55) | 1.35† (ane.09–one.67) |
Table ii summarizes the HRs when both daytime and nighttime ABP were included in the models, together with the other covariates. Systolic night ABP significantly predicted death, CVD, CHD, and stroke, and diastolic night ABP predicted all-cause and CV mortality and CVD. Daytime ABP did not add prognostic precision to nighttime ABP (P>0.05). Figures 1 and two summarize the adapted HRs according to gender, age beneath or to a higher place median age and treatment status, with inclusion of systolic daytime and nighttime ABP in the same models. Whereas the HR was not significant for daytime ABP (except for stroke in the older patients), night ABP was a pregnant predictor of all-cause bloodshed and CVD (largest number of events) in all subgroups, and for near subgroups for the other end points. None of the interaction terms of BP with, respectively, gender, age, and treatment status, reached statistical significance. In addition, the interaction terms were not significant for diastolic ABP, except for dark ABP, age, and CVD (P=0.04; data non shown).
Claret Pressure | Death | NCV Death | CV Death | CVD | CHD | Stroke |
---|---|---|---|---|---|---|
Data are adventure ratios (95% conviction intervals) for each i standard deviation higher blood force per unit area, stratified for study and adjusted for age, gender, smoking, total cholesterol, diabetes and antihypertensive treatment, and the other blood pressure. | ||||||
Significance of hazard ratios: | ||||||
*P≤0.05; | ||||||
†P≤0.01; | ||||||
‡P≤0.001. | ||||||
BP indicates claret force per unit area; CHD, coronary heart disease; CV, cardiovascular; CVD, cardiovascular disease; NCV, noncardiovascular. | ||||||
Systolic BP | ||||||
Daytime | 1.04 (0.88–1.21) | 0.97 (0.78–1.20) | 1.13 (0.90–ane.43) | i.16 (0.98–i.37) | 1.08 (0.84–1.39) | 1.28 (0.99–1.66) |
Nighttime | 1.34‡ (i.17–1.54) | 1.33† (1.10–ane.61) | one.34† (one.10–1.63) | ane.36‡ (1.17–1.59) | ane.39† (1.11–i.75) | 1.38† (one.x–1.74) |
Diastolic BP | ||||||
Daytime | 0.93 (0.79–one.11) | 1.03 (0.82–one.29) | 0.83 (0.64–ane.07) | one.04 (0.86–1.25) | 1.03 (0.78–ane.36) | i.14 (0.86–i.51) |
Nighttime | ane.28† (one.08–1.51) | one.19 (0.94–ane.49) | 1.40† (1.09–i.78) | 1.21* (i.01–ane.46) | 1.17 (0.89–1.54) | 1.21 (0.92–i.59) |

- Download figure
- Download PowerPoint
Figure 1. Gamble ratios and 95% confidence limits for all-cause, noncardiovascular, and cardiovascular mortality in subgroups according to gender, median historic period, and treatment status, for daytime and nighttime systolic blood pressure (SBP), with stratification for study, simultaneous inclusion of both blood pressures in the models and adjustment for age, gender, smoking, total cholesterol, diabetes, and antihypertensive treatment (except in the specific subgroup analysis). *P≤0.05; †P≤0.01; ‡P≤0.001. None of the between-subgroup interaction terms was statistically pregnant. Ne/Np indicates number of events/number of patients.

- Download figure
- Download PowerPoint
Figure 2. Take chances ratios and 95% confidence limits for major cardiovascular disease, coronary center affliction, and stroke in subgroups co-ordinate to gender, median age, and treatment condition, for daytime and nighttime systolic blood pressure level (SBP), with stratification for study, simultaneous inclusion of both claret pressures in the models and aligning for age, gender, smoking, total cholesterol, diabetes, and antihypertensive treatment (except in the specific subgroup analysis). *P≤0.05; †P≤0.01; ‡P≤0.001. None of the between-subgroup interaction terms was statistically meaning. Ne/Np indicates number of events/number of patients.
The analyses on all-crusade mortality and major CVD were too repeated with consecutive exclusion of each study. Whereas the HR was never meaning for daytime ABP, systolic and diastolic nighttime ABP remained pregnant predictors of consequence in all analyses, except for diastolic ABP and all-cause mortality when the Syst-Eur trial was excluded (P=0.09).
Prognostic Significance of the Night–Day Blood Pressure Ratio
Table 3 gives the adjusted HRs of the relationships of the night–day BP ratio with result. Earlier adjustment for 24-hour ABP, the systolic dark–day BP predicted all finish points, simply the relationship persisted just for all-crusade mortality afterwards additional aligning for 24-hour ABP. The diastolic dark–day ratio predicted all-cause and CV decease before and after adjustment for 24-hour ABP.
Death | NCV Death | CV Death | CVD | CHD | Stroke | |
---|---|---|---|---|---|---|
Data are take chances ratios (95% confidence intervals) for each one standard departure higher night-24-hour interval blood force per unit area ratio, stratified for study and adapted for age, gender, smoking, total cholesterol, diabetes, and antihypertensive treatment, and, in addition, for 24-hour ABP. | ||||||
Significance of hazard ratios: | ||||||
*P≤0.05; | ||||||
†P≤0.01; | ||||||
‡P≤0.001. | ||||||
BP indicates claret pressure; CHD, coronary heart disease; CV, cardiovascular; CVD, cardiovascular disease; NCV, noncardiovascular. | ||||||
Unadjusted for 24-hour BP | ||||||
Blood force per unit area | ||||||
Systolic BP | 1.18‡ (one.07–1.30) | i.18* (1.03–1.35) | 1.eighteen* (one.03–ane.37) | 1.20‡ (one.07–1.34) | ane.21* (1.03–1.43) | i.21* (1.02–1.43) |
Diastolic BP | ane.15† (1.04–ane.28) | 1.xi (0.96–one.28) | 1.21† (1.04–1.40) | 1.12 (0.99–ane.25) | 1.09 (0.91–1.30) | 1.11 (0.93–i.32) |
Adjusted for 24-hour BP | ||||||
Blood pressure level | ||||||
Systolic BP | 1.13* (1.02–1.24) | 1.fourteen (0.99–i.30) | 1.xi (0.96–ane.28) | 1.11 (0.99–1.25) | i.14 (0.96–1.35) | 1.10 (0.93–1.thirty) |
Diastolic BP | 1.14* (1.02–one.26) | 1.09 (0.94–1.26) | 1.20* (1.03–i.39) | i.09 (0.97–1.23) | 1.07 (0.89–i.28) | 1.07 (0.89–1.28) |
Word
The main findings of the present meta-analysis of individual patient data on the prognostic significance of ABP in hypertensive patients without major cardiovascular disease at baseline are as follows for systolic BP. (one) Daytime and nighttime ABP significantly predict all-cause and CV bloodshed, CHD, stroke and an aggregate of major CVD, independently from OBP and misreckoning factors. Only dark ABP predicts NCV mortality. (two) Nighttime ABP adds to the prognostic significance of daytime ABP for all end points; daytime ABP does non add prognostic precision to dark ABP. (3)The prognostic significance of the night–day BP ratio for death, CVD, CHD, and stroke only persists for all-cause mortality later adjustment for 24-60 minutes ABP. Like but less consequent results were observed for diastolic ABP.
Autonomously from studies included in the current meta-assay,6,7,13 few other studies investigated the prognostic significance of daytime and nighttime ABP in hypertensive patients, with adjustment for OBP and other covariates. Daytime ABP significantly and independently predicted all-crusade mortality,8,9,19 CV, and stroke mortality8 in patients referred for ABPM, all strokes in older hypertensive patients,20 and an aggregate of CV events in refractory hypertension.21 Nighttime ABP independently predicted all-crusade,8,ix CV, and stroke mortality8 but not total stroke.20 When daytime and dark ABP were included in the same model for the prediction of death, nighttime ABP was superior to daytime ABP for all-crusade,8,ix CV, cardiac, and stroke mortality.8 Our results ostend these observations for all-cause and CV mortality for both systolic and diastolic ABP. In addition, we observed that systolic nighttime ABP was the better predictor for NCV death and fatal and nonfatal CVD, CHD, and stroke. These results were consistent in men and women, in young and old, and in treated and untreated patients for most of the outcomes. In that location is currently no clear explanation why nighttime ABP would exist a better predictor of outcome than daytime ABP, but several factors could exist involved. BP is more than variable during the day than during the night because of physical and mental activity so that it is possible that intermittent BP measurements may not completely capture the true average daytime ABP. It is of notation that Khattar et al,five who used continuous intraarterial ABP recordings, reported that the prognostic value of daytime and nighttime ABP for CV events was about similar, only the 2 BPs were not included in the aforementioned model. Nighttime BP is likely to exist more than stable so that intermittent BP measurements may be more than representative of the truthful night boilerplate BP. Moreover, BP during slumber is more than closely related to basal BP which has been shown to predict life expectancy better than casual BP.22 Finally, nighttime ABP may be influenced past slumber apnoea in some patients, which is associated with a worse prognosis.23
The relative importance of daytime and nighttime ABP has besides been assessed in population-based studies but the results accept not been quite consequent. Nighttime ABP appeared to exist superior to daytime ABP for mortality,24,25 but others found that nighttime and daytime ABP were of similar importance.26 In add-on, Hansen et al27 observed that daytime and nighttime ABP both predicted an amass of CV events for diastolic BP but that only daytime ABP, rather than dark ABP, was significant for systolic BP.
Nosotros assessed the effect of the nocturnal decline of BP on prognosis past using the nighttime–twenty-four hours BP ratio as a continuous variable. We observed that the systolic nighttime–solar day BP ratio was significantly associated with bloodshed, which persisted for all-cause mortality subsequently adjustment for 24-hour ABP. The pregnant associations of CVD, CHD, and stroke with the systolic night–mean solar day BP ratio did not persist after adjustment for 24-hour BP. The diastolic nighttime–day BP ratio predicted all-cause and cardiovascular mortality, both before and after adjustment for 24-hour ABP. Few other studies reported on the prognostic significance of the night–day BP ratio in hypertension. Khattar et al5,11 institute that this ratio did not carry whatsoever prognostic data for CV events, and this was also observed in a population-based written report of elderly men.28
The electric current meta-analysis has strengths and limitations. To achieve our aim to appraise the prognostic significance of daytime and nighttime ABP for bloodshed and cause-specific CV events in a large sample of patients with hypertension and no history of major CV affliction at baseline, we pooled the individual patient data of 4 European studies which were performed or coordinated in Belgium.half-dozen,7,12–17 Common features of these studies are: the prospective design; follow-up for fatal and nonfatal events; and evaluation of events by blinded finish indicate committees, which used the same definitions of events. The different pick criteria of the various studies are a potential limitation of the current meta-analysis. On the other hand, the database represents a broad and comprehensive spectrum of hypertensive patients with regard to age, gender, type of hypertension, antihypertensive handling, and blazon of intendance (primary care and specialist care). In addition, use of appropriate interaction terms and sensitivity analyses indicates that the predictive power of daytime and nighttime ABP did not differ among the iv studies and that the results were roughly like in men and women, in younger and older patients, and in treated and untreated patients. However, because the studies included only Causasians, our findings cannot be extrapolated to hypertensive patients of other ethnic origin.
In conclusion, we observed that both daytime and night ABP carry prognostic information for mortality and fatal and nonfatal CHD and stroke in hypertensive patients, which is contained from OBP and a number of confounders; that nighttime ABP is in general a better predictor of upshot than daytime ABP, and that the night–day BP ratio predicts mortality, fifty-fifty after adjustment for 24-hour ABP.
Perspectives
ABPM is an important adjunct in the direction of hypertension, because information technology is, in general, a ameliorate predictor of upshot than OBP. Daytime ABP carries independent prognostic information and this could be an statement to limit ABPM to the daytime flow. Information technology appears all the same that dark ABP is a improve predictor than daytime ABP, so that ABPM over the full 24 hours with separate analyses of daytime and nighttime ABP is warranted. Nocturnal BP may be a target to reduce CV morbidity and mortality in hypertensive patients.
Continuing medical education (CME) credit is bachelor for this article. Go to http://cme.ahajournals.org to take the quiz.
The authors gratefully admit the help of Nicole Ausseloos and Véronique Cornelissen for the preparation of the manuscript.
Disclosures
None.
Footnotes
References
- 1 Chobanian AV, Bakris GL, Black Hour, Cushman WC, Green LA, Izzo JL, Jones DW, Materson BJ, Oparil South, Wright JT, Roccella EJ. and the National High Blood Pressure level Education Program Coordinating Committee. Seventh report of the Joint National Committee on prevention, detection, evaluation and treatment of high claret pressure. Hypertension . 2003; 42: 1206–1252.LinkGoogle Scholar
- ii The Job Force for the Management of Arterial Hypertension of the European Society of Hypertension and of the European Society of Cardiology. 2007 Guidelines for the Management of Arterial Hypertension. J Hypertens . 2007; 25: 1105–1187.CrossrefMedlineGoogle Scholar
- 3 O'Brien East, Asmar R, Beilin L, Imai Y, Mallion JM, Mancia G, Mengden T, Myers 1000, Padfield P, Palatini P, Parati Grand, Pickering T, Redon J, Staessen J, Stergiou G, Verdecchia P. European Society of Hypertension recommendations for conventional, convalescent and home blood pressure measurement. J Hypertens . 2003; 21: 821–848.CrossrefMedlineGoogle Scholar
- 4 Fagard RH, Celis H. Prognostic significance of diverse characteristics of out-of-the-office blood force per unit area. J Hypertens . 2004; 22: 1663–1666.CrossrefMedlineGoogle Scholar
- v Khattar RS, Swales JD, Baufield A, Dore C, Senior R, Lahiri A. Prediction of coronary and cerebrovascular morbidity and bloodshed by directly continuous ambulatory blood pressure monitoring in essential hypertension. Circulation . 1999; 100: 1071–1976.CrossrefMedlineGoogle Scholar
- 6 Staessen JA, Thijs 50, Fagard R, O'Brien ET, Clement D, de Leeuw Pw, Mancia G, Nachev C, Palatini P, Parati G, Tuomilehto J, Webster J. Predicting cardiovascular take chances using conventional vs ambulatory claret force per unit area in older patients with systolic hypertension. JAMA . 1999; 282: 539–546.CrossrefMedlineGoogle Scholar
- 7 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 Due east. Prognostic value of ambulatory claret pressure recordings in patients with treated hypertension. N Engl J Med . 2003; 348: 2407–2415.CrossrefMedlineGoogle Scholar
- eight Dolan Due east, Stanton A, Thijs L, Hinedi Thou, Atkins Northward, McClory Due south, Den Hond Due east, McCormack P, Staessen JA, O'Brien E. Superiority of ambulatory over clinic blood pressure measurement in predicting mortality. Hypertension . 2005; 46: 156–161.LinkGoogle Scholar
- 9 Ben-Dov IZ, Kark JD, Ben-Ishay D, Mekler J, Ben-Arie L, Bursztyn M. Predictors of all-cause mortality in clinical ambulatory monitoring. Hypertension . 2007; 49: 1235–1241.LinkGoogle Scholar
- 10 Verdecchia P, Porcellati C, Schillaci G, Borgioni C, Ciucci A, Battistelli M, Guerrieri M, Gatteschi C, Zampi I, Santucci A, Santucci C, Reboldi One thousand. Convalescent claret pressure. An independent predictor of prognosis in essential hypertension. Hypertension . 1994; 24: 793–801.LinkGoogle Scholar
- eleven Khattar RS, Swales JD, Dore C, Senior R, Lahiri A. Effect of aging in the prognostic significance of ambulatory, systolic, diastolic and pulse pressure in essential hypertension. Circulation . 2001; 104: 783–789.CrossrefMedlineGoogle Scholar
- 12 Celis H, Staessen JA, Thijs Fifty, Buntinx F, De Buyzere M, Den Hond East, Fagard RH, O'Brien ET. Cardiovascular risk in white-glaze and sustained hypertensive patients. Blood Pressure level . 2002; xi: 352–356.CrossrefMedlineGoogle Scholar
- 13 Fagard RH, Van Den Broeke C, Decort P. Prognostic significance of claret pressure level measured in the role, at dwelling and during ambulatory monitoring in older patients in general practise. J Hum Hypertens . 2005; 19: 801–807.CrossrefMedlineGoogle Scholar
- 14 Staessen JA, Fagard R, Thijs L, Celis H, Arabidze GG, Birkenhäger WH, Bulpitt CJ, de Leeuw Pow, Dollery CT, Fletcher AE, Forette F, Leonetti G, Nachev C, O'Brien ET, Rosenfeld J, Rodicio JL, Tuomilehto J, Zanchett A. Randomised double-blind comparing of placebo and active treatment for older patients with isolated systolic hypertension. Lancet . 1997; 350: 757–764.CrossrefMedlineGoogle Scholar
- fifteen Staessen JA, Byttebier G, Buntinx F, Celis H, O'Brien ET, Fagard R. Antihypertensive handling based on conventional or ambulatory blood pressure level measurement. JAMA . 1997; 278: 1065–1072.CrossrefMedlineGoogle Scholar
- 16 Fagard RH, Staessen JA, Thijs Fifty, Gasowski J, Bulpitt CJ, Clement D, de Leeuw Prisoner of war, Dobovisek J, Jääskivi M, Leonetti Grand, O'Brien E, Palatini P, Parati G, Rodicio JL, Vanhanen H, Webster J. Response to antihypertensive therapy in older patients with sustained and nonsustained systolic hypertension. Circulation . 2000; 102: 1139–1144.CrossrefMedlineGoogle Scholar
- 17 Staessen JA, Thijs L, Fagard R, Celis H, Birkenhäger WH, Bulpitt CJ, de Leeuw Pow, Fletcher AE, Forette F, Leonetti G, McCormack P, Nachev C, O'Brien Due east, Rodicio JL, Rosenfeld J, Sarti C, Tuomilehto J, Webster J, Yodfat Y, Zanchetti A. Effects of immediate versus delayed antihypertensive therapy on outcome in the Systolic Hypertension in Europe Trial. J Hypertens . 2004; 22: 847–857.CrossrefMedlineGoogle Scholar
- 18 Fagard R, Brguljan J, Thijs L, Staessen J. Prediction of the bodily awake and asleep blood pressures by various methods of 24-h pressure analysis. J Hypertens . 1996; xiv: 557–563.CrossrefMedlineGoogle Scholar
- 19 Dawes MG, Coats AJ, Juszczak E. Daytime ambulatory systolic claret pressure is more than constructive at predicting bloodshed than clinic blood pressure. Blood Printing Monit . 2006; xi: 111–118.CrossrefMedlineGoogle Scholar
- 20 Kario Yard, Ishikawa J, Egushi K, Morinari M, Hoshide S, Ishikawa S, Shimada K. Sleep pulse pressure and awake mean pressure as independent predictors for stroke in older hypertensive patients. Am J Hypertens . 2004; 17: 439–445.CrossrefMedlineGoogle Scholar
- 21 Redon J, Campos C, Narciso ML, Rodicio JL, Pascual JM, Ruilope LM. Prognostic value of ambulatory claret force per unit area monitoring in refractory hypertension. A prospective study. Hypertension . 1998; 31: 712–718.CrossrefMedlineGoogle Scholar
- 22 Smirk FH, Veale AM, Alstad KS. Basal and supplemental blood pressures in human relationship to life expectancy and hypertension symptomatology. N Z Med J . 1959; 58: 711–735.MedlineGoogle Scholar
- 23 Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V. Obstructive sleep apnea as a risk gene for stroke and death. NEJM . 2005; 353: 2034–2041.CrossrefMedlineGoogle Scholar
- 24 Kikuya Yard, Ohkubo T, Asayama K, Metoki H, Obara T, Saito S, Hashimoto J, Totsune K, Hoshi H, Satoh H, Imai Y. Ambulatory blood pressure and 10-year risk of cardiovascular and noncardiovascular mortality. The Ohasama Study. Hypertension . 2005; 45: 240–245.LinkGoogle Scholar
- 25 Sega R, Facchetti R, Bombelli M, Cesana K, Corrao Chiliad, Grassi M, Mancia G. Prognostic value of convalescent and dwelling blood pressures compared with part blood pressure in the general population: follow-upwards results from the PAMELA report. Circulation . 2005; 111: 1777–1783.LinkGoogle Scholar
- 26 Hansen TW, Jeppesen J, Rasmussen Due south, Ibsen H, Torp-Pedersen C. Ambulatory blood pressure and mortality. A population-based study. Hypertension . 2005; 45: 499–504.LinkGoogle Scholar
- 27 Hansen TW, Jeppesen J, Rasmussen S, Ibsen H, Torp-Pedersen C. Ambulatory blood pressure monitoring and risk of cardiovascular disease: a population based written report. Am J Hypertens . 2006; 19: 243–250.CrossrefMedlineGoogle Scholar
- 28 Björklund Thou, Lind L, Zethelius B, Berglund Fifty, Lithell H. Prognostic significance of 24-h ambulatory claret pressure level characteristics for cardiovascular morbidity in a population of elderly men. J Hypertens . 2004; 22: 1691–1697.CrossrefMedlineGoogle Scholar
Source: https://www.ahajournals.org/doi/10.1161/hypertensionaha.107.100727
0 Response to "How Low Can a Person's Blood Pressure Go Before Death"
Enregistrer un commentaire