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Associations of Hypertension and Orthostatic Hypotension with Subclinical Cardiovascular Disease
The Journals of Gerontology Series A: Biological Sciences and Medical Sciences ( IF 4.3 ) Pub Date : 2024-09-18 , DOI: 10.1093/gerona/glae234 Aldis H Petriceks 1, 2 , Lawrence J Appel 3, 4 , Edgar R Miller 3, 4 , Christine M Mitchell 4 , Jennifer A Schrack 4 , Amal A Wanigatunga 4 , Erin D Michos 3, 4 , Robert H Christenson 5 , Heather Rebuck 5 , Stephen P Juraschek 1, 2
The Journals of Gerontology Series A: Biological Sciences and Medical Sciences ( IF 4.3 ) Pub Date : 2024-09-18 , DOI: 10.1093/gerona/glae234 Aldis H Petriceks 1, 2 , Lawrence J Appel 3, 4 , Edgar R Miller 3, 4 , Christine M Mitchell 4 , Jennifer A Schrack 4 , Amal A Wanigatunga 4 , Erin D Michos 3, 4 , Robert H Christenson 5 , Heather Rebuck 5 , Stephen P Juraschek 1, 2
Affiliation
Background Orthostatic hypotension is associated with cardiovascular disease. It remains unclear if low standing blood pressure or high seated blood pressure is responsible for this association. We compared associations of orthostatic hypotension and hypertension with high-sensitivity cardiac troponin I and N-terminal pro-B-type natriuretic peptide. Methods We performed a secondary analysis of the Study to Understand Fall Reduction and Vitamin D in You (STURDY), a randomized controlled trial funded by the National Institute on Aging, between July 2015 and May 2019. Participants were community-dwelling adults, 70 years or older. Blood tests for high-sensitivity cardiac troponin I and N-terminal pro-B-type natriuretic peptide were drawn at visits concurrent with blood pressure measurements. Secondary analysis occurred in 2023. We determined associations between blood pressure phenotypes and cardiac biomarkers. Results Of 674 participants (mean age 76.5 ± 5.4 years, 43% female, 17.2% Black race), 29.1% had prior cardiovascular disease. Participants with seated hypertension had 10.1% greater high-sensitivity cardiac troponin I (95% CI = 3.8, 16.9) and 11.0% greater N-terminal pro-B-type natriuretic peptide (4.0, 18.6) than those without seated hypertension. Participants with standing hypertension had 8.6% (2.7, 14.9) greater high-sensitivity cardiac troponin I and 11.8% greater N-terminal pro-B-type natriuretic peptide (5.1, 18.9) than those without standing hypertension. Hypotensive phenotypes were not associated with either biomarker. Conclusions Both seated and standing hypertension were associated with greater high-sensitivity cardiac troponin I and N-terminal pro-B-type natriuretic peptide, but hypotensive phenotypes were not. Hypoperfusion may not be the principal mechanism behind subclinical cardiac injury among older adults with orthostatic hypotension.
中文翻译:
高血压和直立性低血压与亚临床心血管疾病的相关性
背景 直立性低血压与心血管疾病有关。目前尚不清楚是低站立血压还是高坐位血压是造成这种关联的原因。我们比较了直立性低血压和高血压与高敏心肌肌钙蛋白 I 和 N 末端 B 型利钠肽前体的关联。方法 我们在 2015 年 7 月至 2019 年 5 月期间对了解减少跌倒和体内维生素 D 的研究 (STURDY) 进行了二次分析,这是一项由美国国家老龄化研究所资助的随机对照试验。参与者是 70 岁或以上的社区居民。在测量血压的同时,在就诊时抽取高敏心肌肌钙蛋白 I 和 N 末端 B 型利钠肽前体的血液检查。二次分析发生在 2023 年。我们确定了血压表型与心脏生物标志物之间的关联。结果 在 674 名参与者 (平均年龄 76.5 ± 5.4 岁,43% 女性,17.2% 黑人)中,29.1% 既往患有心血管疾病。与无坐位高血压患者相比,坐位高血压患者的高敏心肌肌钙蛋白 I (95% CI = 3.8, 16.9) 高 10.1%,N 末端 B 型利钠肽前体 (4.0, 18.6) 高 11.0%。与没有站立期高血压的参与者相比,站立期高血压患者的高敏心肌肌钙蛋白 I 高 8.6% (2.7, 14.9),N 末端 B 型利钠肽前体 (5.1, 18.9) 高 11.8%。低血压表型与任何一种生物标志物均无关。结论 坐位和站立期高血压均与较高的高敏心肌肌钙蛋白 I 和 N 末端 B 型利钠肽前体相关,但低血压表型则不相关。 低灌注可能不是直立性低血压老年人亚临床心脏损伤的主要机制。
更新日期:2024-09-18
中文翻译:
高血压和直立性低血压与亚临床心血管疾病的相关性
背景 直立性低血压与心血管疾病有关。目前尚不清楚是低站立血压还是高坐位血压是造成这种关联的原因。我们比较了直立性低血压和高血压与高敏心肌肌钙蛋白 I 和 N 末端 B 型利钠肽前体的关联。方法 我们在 2015 年 7 月至 2019 年 5 月期间对了解减少跌倒和体内维生素 D 的研究 (STURDY) 进行了二次分析,这是一项由美国国家老龄化研究所资助的随机对照试验。参与者是 70 岁或以上的社区居民。在测量血压的同时,在就诊时抽取高敏心肌肌钙蛋白 I 和 N 末端 B 型利钠肽前体的血液检查。二次分析发生在 2023 年。我们确定了血压表型与心脏生物标志物之间的关联。结果 在 674 名参与者 (平均年龄 76.5 ± 5.4 岁,43% 女性,17.2% 黑人)中,29.1% 既往患有心血管疾病。与无坐位高血压患者相比,坐位高血压患者的高敏心肌肌钙蛋白 I (95% CI = 3.8, 16.9) 高 10.1%,N 末端 B 型利钠肽前体 (4.0, 18.6) 高 11.0%。与没有站立期高血压的参与者相比,站立期高血压患者的高敏心肌肌钙蛋白 I 高 8.6% (2.7, 14.9),N 末端 B 型利钠肽前体 (5.1, 18.9) 高 11.8%。低血压表型与任何一种生物标志物均无关。结论 坐位和站立期高血压均与较高的高敏心肌肌钙蛋白 I 和 N 末端 B 型利钠肽前体相关,但低血压表型则不相关。 低灌注可能不是直立性低血压老年人亚临床心脏损伤的主要机制。