Association between antecedent blood pressure, hypertension-mediated organ damage and cardiovascular outcome

被引:6
|
作者
Olesen, Thomas B. [1 ,2 ]
Pareek, Manan [3 ,4 ]
Stidsen, Jacob V. [2 ]
Blicher, Marie K. [1 ]
Rasmussen, Susanne [5 ,6 ]
Vishram-Nielsen, Julie K. K. [6 ,7 ]
Maagaard, Louise [1 ]
Olsen, Michael [8 ,9 ]
机构
[1] Kolding Cty Hosp, Dept Internal Med, Kolding, Denmark
[2] Odense Univ Hosp, Steno Diabet Ctr Odense, Odense, Denmark
[3] North Zealand Hosp, Dept Cardiol, Hillerod, Denmark
[4] Yale Univ, Sch Med, Dept Internal Med, Yale New Haven Hosp, New Haven, CT 06510 USA
[5] Univ Copenhagen, Herlev Hosp, Dept Clin Physiol & Nucl Med, Copenhagen, Denmark
[6] Bispebjerg & Frederiksberg Hosp, Ctr Clin Res & Prevent, Copenhagen, Denmark
[7] Univ Hosp Copenhagen, Rigshosp, Dept Cardiol, Copenhagen, Denmark
[8] Univ Southern Denmark, Odense Univ Hosp, Ctr Individualized Med Arterial Dis CIMA, Odense, Denmark
[9] Holbaek Cent Hosp, Dept Internal Med, Cardiol Sect, Smedelundsgade 60, DK-4300 Holbaek, Denmark
关键词
Hypertension-mediated organ damage; aging; pulse wave velocity; risk stratification; atherosclerosis; left ventricular hypertrophy; RISK; TRAJECTORIES; AGE; ADULTHOOD; CHILDHOOD;
D O I
10.1080/08037051.2020.1735930
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Purpose: The objective of this study was to test if combining antecedent systolic blood pressure (SBP) with traditional risk factors and hypertension-mediated organ damage (HMOD) improves risk stratification for subsequent cardiovascular disease. Materials and methods: 1910 subjects participated in this study. Antecedent SBP was defined as the average of measurements obtained in 1982 and in 1987. Current SBP was obtained in 1993. HMOD were examined in 1993. HMOD was defined as either atherosclerotic plaque(s), increased pulse wave velocity, increased urine albumin creatinine ratio (above the 90th percentile) or left ventricular hypertrophy. Major adverse cardiovascular events (MACE) including myocardial infarction, cerebrovascular disease, heart failure and arrhythmia were obtained from national registries. Results: Subjects were divided into two age categories: a middle-aged group (aged 41 or 51) and an older group (aged 61 or 71). From 1993 to 2010, 425 events were observed. In multivariable analysis with both current and antecedent SBP adjusted for traditional risk factors, current SBP was associated with each measure of HMOD whilst antecedent SBP was not significantly associated with urine albumin creatinine ratio in the older group, LVMI in the middle-aged group, or the presence of plaque in any of the age groups (all p > 0.15). When current and antecedent SBP were evaluated together, current SBP was not associated with MACE in the middle-aged subgroup [HR = 1.09 (0.96-1.22), p = 0.18] but remained associated with MACE in the older subgroup [HR = 1.21 (1.10-1.34), p < 0.01]. Contrariwise, antecedent SBP was only associated with MACE in the middle-aged subgroup [HR = 1.24 (1.04-1.48), p = 0.02]. Adding antecedent SBP to traditional risk factors did not improve the predictive accuracy of the survival model. Conclusion: In healthy non-medicated middle-aged subjects, antecedent SBP is associated with cardiovascular outcome independently of current BP, traditional risk factors and HMOD. However, improvement in risk stratification seems to be limited.
引用
收藏
页码:232 / 240
页数:9
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