http://informahealthcare.com/ceh ISSN: 1064-1963 (print), 1525-6006 (electronic) Clin Exp Hypertens, 2014; 36(4): 195–199 ! 2014 Informa Healthcare USA, Inc. DOI: 10.3109/10641963.2014.897717
ORIGINAL ARTICLE
Negative association between plasma aldosterone concentration/plasma renin activity and morning blood pressure surge in never-treated hypertensive patients Jung Sun Cho1, Sang Hyun Ihm2, Sung-Won Jang3, Woo-Baek Chung4, Yun-Seok Choi4, Dong-Il Shin5, Suk Min Seo5, Mahn-Won Park1, Gee Hee Kim6, Sung-ho Her1, Chan Joon Kim1, Tae-Hoon Kim7, Min Kyu Kang8, Kiyuk Chang8, and Chan Seok Park2 1
Department of Cardiology, Daejeon St. Mary’s Hospital, Daejeon, Korea, 2Department of Cardiology, Bucheon St. Mary’s Hospital, Bucheon, Korea, Department of Cardiology, St. Paul’s Hospital, Seoul, Korea, 4Department of Cardiology, Yeouido St. Mary’s Hospital, Seoul, Korea, 5Department of Cardiology, Incheon St. Mary’s Hospital, Incheon, Korea, 6Department of Cardiology, St. Vincent Hospital, Suwon, Korea, 7Department of Cardiology, Uijeongbu St. Mary’s Hospital, Uijoengbu, Korea, and 8Cardiovascular Center and Division of Cardiology, Seoul St. Mary’s Hospital, Seoul, Korea
3
Abstract
Keywords
Morning blood pressure (BP) surge (MS) has been known to be a predictor of cardiovascular events. Currently, few studies have evaluated the underlying mechanism underlying MS, which may include neurohormonal factors and the renin–angiotensin–aldosterone system (RAAS). This study aimed to examine plasma aldosterone concentration (PAC) and plasma renin activity (PRA) and BP parameters with or without MS in never-treated subjects with essential hypertension. This cross-sectional study included a total of 261 patients (mean age: 48.8 years; 60.5% male) with never-treated essential hypertension who were registered in a working group at The Catholic University of Korea. The patients were divided into the MS group, which was defined as having the highest quartile of morning BP increase from sleep (431 mmHg; n ¼ 66) and the non-MS group (31 mmHg; n ¼ 195). We collected 24-h ambulatory BP, pulse wave velocity, ankle brachial index, PAC and PRA from all patients. The measured PAC and PRA were lower in the MS group than in the non-MS group (PAC: 9.0 ± 5.4 ng/dl versus 12.2 ± 8.7 ng/dl, p50.001; PRA: 1.7 ± 1.3 ng/ml/h versus 2.6 ± 3.6 ng/ml/h, p ¼ 0.002). The MS group had greater variations in daytime, nighttime and 24-h systolic blood pressure (SBPs) than the non-MS group (24-h SBP: 15.6 ± 4.4 mm Hg for the non-MS group and 18.9 ± 4.9 mmHg for the MS group; p50.001 for each). It is generally accepted that the sympathetic nervous system plays a major role in the regulation of BP variability. Therefore, further studies on sympathetic nervous system activation in hypertensives with extreme MS are needed. MS in enrolled patients who were at relatively low risk in this study may be less affected by the RAAS.
BP variability, morning BP surge, never-treated hypertension, plasma aldosterone concentration, plasma renin activity
Introduction Morning blood pressure (BP) surge (MS) has been known to be a predictor of cardiovascular events (1–4). MS is a normal physiological phenomenon, but an extreme MS is indicative of cardiovascular risk. The association between the degree of MS and cardiovascular risk is not linear but has a threshold. However, the definition of an extreme MS varies among studies (1–5). In the International Database on Ambulatory Blood Pressure in Relation to Cardiovascular Outcome (IDACO) study, the top decile of MS (37.0 mm Hg) was independently associated with cardiovascular risk (3). However, there are currently a limited number of studies
Correspondence: Sang Hyun Ihm, MD, PhD, Division of Cardiology, Department of Internal Medicine, The Catholic University of Korea, Bucheon St. Mary’s Hospital, 2 Sosa-dong Wonmi-gu Bucheon-si Gyunggi-do 420-717, South Korea. Tel: +82-10-8724-3789. Fax: +82-21588-1511. E-mail: [email protected]
History Received 4 September 2013 Revised 1 January 2014 Accepted 7 January 2014 Published online 28 March 2014
on mechanisms underlying MS (6–12). Until now, morning pressure surge is thought to be related to the circadian rhythm. During this time, increases in cortisol enhance artery sensitivity to catecholamines and to elevate systemic vascular resistance. The activation of the renin–angiotensin–aldosterone system (RAAS) is also activated in the morning (11,12). This study aimed to examine plasma aldosterone concentration (PAC), plasma renin activity (PRA) and BP parameters with or without MS in never-treated subjects with essential hypertension.
Materials and methods This cross-sectional study included a total of 261 consecutive patients with never-treated essential hypertension who were registered in a working group at The Catholic University of Korea between March 2011 and December 2012. The patients were divided into two groups: the MS group which was defined as the highest quartile of morning BP increases from
196
J. S. Cho et al.
sleep (431 mm Hg; n ¼ 66; mean age, 48.8 ± 12.0 years) and the non-MS group (31 mm Hg; n ¼ 195; mean age, 48.4 ± 11.8 years). The enrolled patients had an systolic blood pressure (SBP) of over 135 mm Hg and a separate or simultaneous diastolic blood pressure (DBP) of over 85 mm Hg as based on 24-hour ambulatory blood pressure (13). Secondary hypertensive patients were excluded from the study. Patients with an aldosterone–renin ratio (ARR) of 30:1 underwent further examinations such as acute sodium loading tests, fludrocortisones suppression, captopril tests and computed tomography, to rule out aldosteronism (14,15). When excessive renin secretion was suspected, renal arteriography along with computed tomography or a captopril loading test angiography was performed to rule out renal artery stenosis. Office BP was measured by a physician using a mercury sphygmomanometer with subjects sitting and relaxed for 10 min. Three BP measurements were averaged for analysis, and SBP and DBP were identified by Korotkoff phases I and V. We collected 24-h ambulatory BP, PAC, PRA, pulse wave velocity (PWV) and ankle brachial index (ABI) from all patients. Ambulatory BP was monitored by using an automatic oscillometric device (validated devices, mainly spacelabs 90 207 or 90 217) at 30-min intervals during the nighttime and at 15 min intervals during the daytime. We excluded patients with 580% valid BP readings during either waking or sleeping. MS was defined as the highest quartile of the difference between the mean SBP for 2 h after waking and the average of three readings centered on the lowest SBP taken, while patients were asleep. A pre-awakening morning SBP increase was defined as the difference between the average of three readings centered on the lowest SBP taken, while patients were asleep and the average BP for 2 h before awakening (2,4). BP and heart rate were estimated as standard deviations measured at 30-min intervals during the nighttime and at 15-min intervals during the daytime by ambulatory monitoring. The patients were subdivided into four distinct categories according to the percentage of nocturnal SBP decline (100 (1-nighttime mean SBP/daytime mean SBP)): (1) extreme dippers who had a nocturnal SBP reduction is 20%; (2) dippers who had a fall of 10% but 520%; (3) non-dippers who had a fall is 0% but 510%; and (4) inverted dippers who had a fall 50% (16). PAC and PRA were measured using overnight fasting blood samples taken between 7 am and 9 am after patients rested for 30 min in a sitting position. PRA (1.3–3.95 ng/ml/h) and PAC (reference value, 4.0–31 ng/dl) values were determined by radioimmunoassay using r-counter (COBRA, PACKARD, Meriden, CT). PRA was measured using a Diasorin LiaisonÕ immunochemiluminometric analyzer (DiaSorin Ltd, Wokingham, Berkshire, UK). PAC was measured using a solid-phase radioimmunoassay kit (Siemens Ltd, Camberley, Surrey, UK). Kidney function was assessed by eGFR using a MDRD formula: GFR, in ml/min per 1.73 m2 ¼ 175 SCr (exp[1.154]) Age (exp[0.203]) (0.742 if female) (17). The registry was approved by the Institutional Review Board of The Catholic Medical Center of Korea.
Clin Exp Hypertens, 2014; 36(4): 195–199
Statistical analysis Data are expressed as mean ± SD. Non-MS and MS patient variables were analyzed by a two-sample t-test or a Wilcoxon signed-rank test as appropriate. SPSS for Windows (version 20.0; SPSS Inc., Chicago, IL) was used. Statistical analyses, such as multivariate logistic regression, were used to evaluate associations between variables, and Odds ratios are displayed with a 95% confidence interval (CI). A probability level of p50.05 was considered statistically significant.
Results The clinical characteristics of the subjects, including ABPM parameters and pulse wave velocity (PWV) according to sleep-trough morning surge, are shown in Table 1. There were no statistically significant differences between the non-MS and MS groups in 24-h SBP and DBP or daytime mean SBP and DBP (Table 1). Nighttime mean BP was lower in the MS group than in the non-MS group (nighttime SBP: 137.0 ± 15.2 mm Hg for the non-MS group, 123.7 ± 14.8 mm Hg for the MS group; p50.001) (nighttime DBP: 85.9 ± 11.8 mm Hg for the non-MS group, 80.8 ± 11.0 mm
Table 1. Patient characteristics, BP parameters and arterial stiffness according to sleep-trough morning surge. Non-MS (n ¼ 195)
MS (n ¼ 66)
p Value
Age, years 48.4 ± 11.8 48.8 ± 12.0 0.790 Men, n (%) 122 (62.6) 36 (54.5) 0.249 Body mass index, kg/m2 25.5 ± 3.3 25.1 ± 3.2 0.484 Ever-smoker, n (%) 69 (35.4) 20 (30.3) 0.548 Daily drinker, n (%) 51 (26.2) 15 (22.7) 0.627 Type 2 diabetes, n (%) 5 (3.0) 3 (5.6) 0.406 Blood pressure measurement Office SBP, mm Hg 153.7 ± 16.7 155.5 ± 16.0 0.447 Office DBP, mm Hg 93.8 ± 13.0 94.1 ± 15.1 0.873 Office PR, bpm 79.9 ± 11.7 81.4 ± 13.1 0.525 24-h SBP, mm Hg 145.6 ± 12.2 145.2 ± 11.6 0.814 24-h SBP SD 15.6 ± 4.4 18.9 ± 4.9 0.000 24-h DBP, mm Hg 92.5 ± 13.1 93.4 ± 10.2 0.594 24-h DBP SD 13.1 ± 4.2 15.2 ± 4.1 0.002 24-h PR, bpm 73.7 ± 10.4 75.2 ± 8.0 0.507 24-h PR SD 10.7 ± 4.2 16.8 ± 3.4 0.240 Day SBP, mm Hg 148.8 ± 12.6 151.4 ± 12.4 0.156 Day SBP SD 14.5 ± 4.6 16.4 ± 4.9 0.012 Day DBP, mm Hg 100.8 ± 15.2 97.2 ± 11.2 0.627 Day DBP SD 12.3 ± 4.6 13.7 ± 4.6 0.062 Day PR, bpm 76.2 ± 9.6 78.4 ± 8.2 0.340 Night SBP, mm Hg 137.0 ± 15.2 123.7 ± 14.8 50.001 Night SBP SD 12.2 ± 4.1 13.7 ± 4.4 0.025 Night DBP, mm Hg 85.9 ± 11.8 80.8 ± 11.0 0.003 Night DBP SD 9.8 ± 3.9 10.5 ± 3.9 0.058 Night PR, bpm 65.5 ± 8.4 64.8 ± 8.7 0.712 Sleep-trough morning 17.3 ± 10.5 39.9 ± 10.4 50.001 SBP increase, mm Hg Pre-awakening morning 9.9 ± 14.9 24.8 ± 13.2 50.001 SBP increase, mm Hg Arterial stiffness Pulse wave velocity, both 1555.3 ± 277.3 1539.6 ± 352.2 0.745 Ankle-brachial index, both 1.11 ± 0.10 1.12 ± 0.11 0.241 Data are expressed as the mean ± SD or median (25th to 75th percentile). MS is defined as the highest quartile of increase in sleep-trough morning SBP. SBP, systolic blood pressure; DBP, diastolic blood pressure; PR, pulse rate; bpm, beats per minute; MS, morning surge; PR, pulse rate.
PAC and PRA of morning blood pressure surges
DOI: 10.3109/10641963.2014.897717
Hg for the MS group; p ¼ 0.003). Subjects in the MS group had greater variations in daytime, nighttime and 24-h SBPs than those in the non-MS group (24-h SBP: 15.6 ± 4.4 mm Hg for the non-MS group and 18.9 ± 4.9 mm Hg for the MS Extreme dipper Dipper Nondipper Inverteddipper
The number of patients
40
30
20
10
0 >31mmHg
31-22mmHg 22-14mmHg
ORIGINAL ARTICLE
Negative association between plasma aldosterone concentration/plasma renin activity and morning blood pressure surge in never-treated hypertensive patients Jung Sun Cho1, Sang Hyun Ihm2, Sung-Won Jang3, Woo-Baek Chung4, Yun-Seok Choi4, Dong-Il Shin5, Suk Min Seo5, Mahn-Won Park1, Gee Hee Kim6, Sung-ho Her1, Chan Joon Kim1, Tae-Hoon Kim7, Min Kyu Kang8, Kiyuk Chang8, and Chan Seok Park2 1
Department of Cardiology, Daejeon St. Mary’s Hospital, Daejeon, Korea, 2Department of Cardiology, Bucheon St. Mary’s Hospital, Bucheon, Korea, Department of Cardiology, St. Paul’s Hospital, Seoul, Korea, 4Department of Cardiology, Yeouido St. Mary’s Hospital, Seoul, Korea, 5Department of Cardiology, Incheon St. Mary’s Hospital, Incheon, Korea, 6Department of Cardiology, St. Vincent Hospital, Suwon, Korea, 7Department of Cardiology, Uijeongbu St. Mary’s Hospital, Uijoengbu, Korea, and 8Cardiovascular Center and Division of Cardiology, Seoul St. Mary’s Hospital, Seoul, Korea
3
Abstract
Keywords
Morning blood pressure (BP) surge (MS) has been known to be a predictor of cardiovascular events. Currently, few studies have evaluated the underlying mechanism underlying MS, which may include neurohormonal factors and the renin–angiotensin–aldosterone system (RAAS). This study aimed to examine plasma aldosterone concentration (PAC) and plasma renin activity (PRA) and BP parameters with or without MS in never-treated subjects with essential hypertension. This cross-sectional study included a total of 261 patients (mean age: 48.8 years; 60.5% male) with never-treated essential hypertension who were registered in a working group at The Catholic University of Korea. The patients were divided into the MS group, which was defined as having the highest quartile of morning BP increase from sleep (431 mmHg; n ¼ 66) and the non-MS group (31 mmHg; n ¼ 195). We collected 24-h ambulatory BP, pulse wave velocity, ankle brachial index, PAC and PRA from all patients. The measured PAC and PRA were lower in the MS group than in the non-MS group (PAC: 9.0 ± 5.4 ng/dl versus 12.2 ± 8.7 ng/dl, p50.001; PRA: 1.7 ± 1.3 ng/ml/h versus 2.6 ± 3.6 ng/ml/h, p ¼ 0.002). The MS group had greater variations in daytime, nighttime and 24-h systolic blood pressure (SBPs) than the non-MS group (24-h SBP: 15.6 ± 4.4 mm Hg for the non-MS group and 18.9 ± 4.9 mmHg for the MS group; p50.001 for each). It is generally accepted that the sympathetic nervous system plays a major role in the regulation of BP variability. Therefore, further studies on sympathetic nervous system activation in hypertensives with extreme MS are needed. MS in enrolled patients who were at relatively low risk in this study may be less affected by the RAAS.
BP variability, morning BP surge, never-treated hypertension, plasma aldosterone concentration, plasma renin activity
Introduction Morning blood pressure (BP) surge (MS) has been known to be a predictor of cardiovascular events (1–4). MS is a normal physiological phenomenon, but an extreme MS is indicative of cardiovascular risk. The association between the degree of MS and cardiovascular risk is not linear but has a threshold. However, the definition of an extreme MS varies among studies (1–5). In the International Database on Ambulatory Blood Pressure in Relation to Cardiovascular Outcome (IDACO) study, the top decile of MS (37.0 mm Hg) was independently associated with cardiovascular risk (3). However, there are currently a limited number of studies
Correspondence: Sang Hyun Ihm, MD, PhD, Division of Cardiology, Department of Internal Medicine, The Catholic University of Korea, Bucheon St. Mary’s Hospital, 2 Sosa-dong Wonmi-gu Bucheon-si Gyunggi-do 420-717, South Korea. Tel: +82-10-8724-3789. Fax: +82-21588-1511. E-mail: [email protected]
History Received 4 September 2013 Revised 1 January 2014 Accepted 7 January 2014 Published online 28 March 2014
on mechanisms underlying MS (6–12). Until now, morning pressure surge is thought to be related to the circadian rhythm. During this time, increases in cortisol enhance artery sensitivity to catecholamines and to elevate systemic vascular resistance. The activation of the renin–angiotensin–aldosterone system (RAAS) is also activated in the morning (11,12). This study aimed to examine plasma aldosterone concentration (PAC), plasma renin activity (PRA) and BP parameters with or without MS in never-treated subjects with essential hypertension.
Materials and methods This cross-sectional study included a total of 261 consecutive patients with never-treated essential hypertension who were registered in a working group at The Catholic University of Korea between March 2011 and December 2012. The patients were divided into two groups: the MS group which was defined as the highest quartile of morning BP increases from
196
J. S. Cho et al.
sleep (431 mm Hg; n ¼ 66; mean age, 48.8 ± 12.0 years) and the non-MS group (31 mm Hg; n ¼ 195; mean age, 48.4 ± 11.8 years). The enrolled patients had an systolic blood pressure (SBP) of over 135 mm Hg and a separate or simultaneous diastolic blood pressure (DBP) of over 85 mm Hg as based on 24-hour ambulatory blood pressure (13). Secondary hypertensive patients were excluded from the study. Patients with an aldosterone–renin ratio (ARR) of 30:1 underwent further examinations such as acute sodium loading tests, fludrocortisones suppression, captopril tests and computed tomography, to rule out aldosteronism (14,15). When excessive renin secretion was suspected, renal arteriography along with computed tomography or a captopril loading test angiography was performed to rule out renal artery stenosis. Office BP was measured by a physician using a mercury sphygmomanometer with subjects sitting and relaxed for 10 min. Three BP measurements were averaged for analysis, and SBP and DBP were identified by Korotkoff phases I and V. We collected 24-h ambulatory BP, PAC, PRA, pulse wave velocity (PWV) and ankle brachial index (ABI) from all patients. Ambulatory BP was monitored by using an automatic oscillometric device (validated devices, mainly spacelabs 90 207 or 90 217) at 30-min intervals during the nighttime and at 15 min intervals during the daytime. We excluded patients with 580% valid BP readings during either waking or sleeping. MS was defined as the highest quartile of the difference between the mean SBP for 2 h after waking and the average of three readings centered on the lowest SBP taken, while patients were asleep. A pre-awakening morning SBP increase was defined as the difference between the average of three readings centered on the lowest SBP taken, while patients were asleep and the average BP for 2 h before awakening (2,4). BP and heart rate were estimated as standard deviations measured at 30-min intervals during the nighttime and at 15-min intervals during the daytime by ambulatory monitoring. The patients were subdivided into four distinct categories according to the percentage of nocturnal SBP decline (100 (1-nighttime mean SBP/daytime mean SBP)): (1) extreme dippers who had a nocturnal SBP reduction is 20%; (2) dippers who had a fall of 10% but 520%; (3) non-dippers who had a fall is 0% but 510%; and (4) inverted dippers who had a fall 50% (16). PAC and PRA were measured using overnight fasting blood samples taken between 7 am and 9 am after patients rested for 30 min in a sitting position. PRA (1.3–3.95 ng/ml/h) and PAC (reference value, 4.0–31 ng/dl) values were determined by radioimmunoassay using r-counter (COBRA, PACKARD, Meriden, CT). PRA was measured using a Diasorin LiaisonÕ immunochemiluminometric analyzer (DiaSorin Ltd, Wokingham, Berkshire, UK). PAC was measured using a solid-phase radioimmunoassay kit (Siemens Ltd, Camberley, Surrey, UK). Kidney function was assessed by eGFR using a MDRD formula: GFR, in ml/min per 1.73 m2 ¼ 175 SCr (exp[1.154]) Age (exp[0.203]) (0.742 if female) (17). The registry was approved by the Institutional Review Board of The Catholic Medical Center of Korea.
Clin Exp Hypertens, 2014; 36(4): 195–199
Statistical analysis Data are expressed as mean ± SD. Non-MS and MS patient variables were analyzed by a two-sample t-test or a Wilcoxon signed-rank test as appropriate. SPSS for Windows (version 20.0; SPSS Inc., Chicago, IL) was used. Statistical analyses, such as multivariate logistic regression, were used to evaluate associations between variables, and Odds ratios are displayed with a 95% confidence interval (CI). A probability level of p50.05 was considered statistically significant.
Results The clinical characteristics of the subjects, including ABPM parameters and pulse wave velocity (PWV) according to sleep-trough morning surge, are shown in Table 1. There were no statistically significant differences between the non-MS and MS groups in 24-h SBP and DBP or daytime mean SBP and DBP (Table 1). Nighttime mean BP was lower in the MS group than in the non-MS group (nighttime SBP: 137.0 ± 15.2 mm Hg for the non-MS group, 123.7 ± 14.8 mm Hg for the MS group; p50.001) (nighttime DBP: 85.9 ± 11.8 mm Hg for the non-MS group, 80.8 ± 11.0 mm
Table 1. Patient characteristics, BP parameters and arterial stiffness according to sleep-trough morning surge. Non-MS (n ¼ 195)
MS (n ¼ 66)
p Value
Age, years 48.4 ± 11.8 48.8 ± 12.0 0.790 Men, n (%) 122 (62.6) 36 (54.5) 0.249 Body mass index, kg/m2 25.5 ± 3.3 25.1 ± 3.2 0.484 Ever-smoker, n (%) 69 (35.4) 20 (30.3) 0.548 Daily drinker, n (%) 51 (26.2) 15 (22.7) 0.627 Type 2 diabetes, n (%) 5 (3.0) 3 (5.6) 0.406 Blood pressure measurement Office SBP, mm Hg 153.7 ± 16.7 155.5 ± 16.0 0.447 Office DBP, mm Hg 93.8 ± 13.0 94.1 ± 15.1 0.873 Office PR, bpm 79.9 ± 11.7 81.4 ± 13.1 0.525 24-h SBP, mm Hg 145.6 ± 12.2 145.2 ± 11.6 0.814 24-h SBP SD 15.6 ± 4.4 18.9 ± 4.9 0.000 24-h DBP, mm Hg 92.5 ± 13.1 93.4 ± 10.2 0.594 24-h DBP SD 13.1 ± 4.2 15.2 ± 4.1 0.002 24-h PR, bpm 73.7 ± 10.4 75.2 ± 8.0 0.507 24-h PR SD 10.7 ± 4.2 16.8 ± 3.4 0.240 Day SBP, mm Hg 148.8 ± 12.6 151.4 ± 12.4 0.156 Day SBP SD 14.5 ± 4.6 16.4 ± 4.9 0.012 Day DBP, mm Hg 100.8 ± 15.2 97.2 ± 11.2 0.627 Day DBP SD 12.3 ± 4.6 13.7 ± 4.6 0.062 Day PR, bpm 76.2 ± 9.6 78.4 ± 8.2 0.340 Night SBP, mm Hg 137.0 ± 15.2 123.7 ± 14.8 50.001 Night SBP SD 12.2 ± 4.1 13.7 ± 4.4 0.025 Night DBP, mm Hg 85.9 ± 11.8 80.8 ± 11.0 0.003 Night DBP SD 9.8 ± 3.9 10.5 ± 3.9 0.058 Night PR, bpm 65.5 ± 8.4 64.8 ± 8.7 0.712 Sleep-trough morning 17.3 ± 10.5 39.9 ± 10.4 50.001 SBP increase, mm Hg Pre-awakening morning 9.9 ± 14.9 24.8 ± 13.2 50.001 SBP increase, mm Hg Arterial stiffness Pulse wave velocity, both 1555.3 ± 277.3 1539.6 ± 352.2 0.745 Ankle-brachial index, both 1.11 ± 0.10 1.12 ± 0.11 0.241 Data are expressed as the mean ± SD or median (25th to 75th percentile). MS is defined as the highest quartile of increase in sleep-trough morning SBP. SBP, systolic blood pressure; DBP, diastolic blood pressure; PR, pulse rate; bpm, beats per minute; MS, morning surge; PR, pulse rate.
PAC and PRA of morning blood pressure surges
DOI: 10.3109/10641963.2014.897717
Hg for the MS group; p ¼ 0.003). Subjects in the MS group had greater variations in daytime, nighttime and 24-h SBPs than those in the non-MS group (24-h SBP: 15.6 ± 4.4 mm Hg for the non-MS group and 18.9 ± 4.9 mm Hg for the MS Extreme dipper Dipper Nondipper Inverteddipper
The number of patients
40
30
20
10
0 >31mmHg
31-22mmHg 22-14mmHg
