高血压和直立性低血压与亚临床心血管疾病的关系

Aldis H Petriceks, Lawrence J Appel, Edgar R Miller, Christine M Mitchell, Jennifer A Schrack, Amal A Wanigatunga, Erin D Michos, Robert H Christenson, Heather Rebuck, Stephen P Juraschek
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引用次数: 0

摘要

背景 直立性低血压与心血管疾病有关。目前仍不清楚是站立时血压低还是坐位时血压高导致了这种关联。我们比较了正性低血压和高血压与高敏心肌肌钙蛋白 I 和 N 端前 B 型利钠肽的关系。方法 我们在 2015 年 7 月至 2019 年 5 月期间对美国国家老龄化研究所资助的随机对照试验 "减少跌倒和您体内的维生素 D 研究"(STURDY)进行了二次分析。参与者为 70 岁或以上居住在社区的成年人。在就诊时抽血检测高敏心肌肌钙蛋白 I 和 N 端前 B 型钠尿肽,同时测量血压。二次分析于 2023 年进行。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% 为女性,17.2% 为黑人)中,29.1% 曾患有心血管疾病。与非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)和 N 端前 B 型钠尿肽(4.0,18.6)分别高出 10.1%和 11.0%。与没有站立性高血压的人相比,站立性高血压患者的高敏心肌肌钙蛋白 I 高出 8.6% (2.7, 14.9),N-末端前 B 型钠尿肽高出 11.8% (5.1, 18.9)。低血压表型与这两种生物标志物均无关联。结论 坐位高血压和站立高血压都与高敏心肌肌钙蛋白 I 和 N 端前-B 型钠尿肽增加有关,但低血压表型与之无关。低灌注可能不是患有正性低血压的老年人亚临床心脏损伤的主要机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Associations of Hypertension and Orthostatic Hypotension with Subclinical Cardiovascular Disease
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.
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