Causal effect of systolic blood pressure on myocardial injury and mortality: insights from Mendelian randomization and a prospective group study.

IF 3.7 2区 生物学 Q3 CELL BIOLOGY
Chuting Wang, Huadong Tang, Qiuxiang Yang, Yagui Lu, Zhijian Lin, Yuekui Zhang
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Abstract

This study aimed to examine the causal relationship between systolic blood pressure (SBP) and myocardial injury (MI), and to evaluate its prognostic implications for all-cause and cardiovascular mortality. A two-stage analytical approach was used. First, Mendelian randomization (MR) was conducted to assess the independent causal effects of SBP on six MI-related phenotypes, with adjustment for potential confounders, including lipid profiles, glycemic indices, and anthropometric traits. Second, data from 4459 participants in the National Health and Nutrition Examination Survey, with a follow-up period of up to 15 years, were analyzed. The dose-response relationship between SBP and MI was assessed using restricted cubic spline analysis. Thresholds based on sex-, age-, and comorbidities were identified using the Johnson-Neyman interaction model. MR analysis demonstrated a causal association between elevated SBP and increased risks of acute heart failure (odds ratio [OR] = 1.523), MI (OR = 1.014), and ischemic stroke (OR = 33.339). In the prospective group analysis, SBP ≥ 180 mmHg was associated with a 213.4% increased risk of MI (OR = 3.134, p = 0.003), and a graded increase in mortality was observed (hazard ratio [HR] = 2.783 for all-cause death; HR = 1.888 for cardiovascular death). Sex-stratified analysis demonstrated that the lowest MI risk occurred at SBP levels of 120-150 mmHg in men and extended to 162 mmHg in women. Among individuals aged ≥ 43 years, the risk of all-cause mortality significantly increased when SBP exceeded 135 mmHg (p < 0.001). A U-shaped relationship between SBP and mortality was observed in individuals aged ≥ 58 years with MI, with the lowest risk at 113 mmHg. Genetic and observational evidence support a causal role of elevated SBP in the development of MI. The findings demonstrate sex- and age-specific thresholds, along with a U-shaped mortality curve, providing a nuanced framework for individualized blood pressure management strategies.

收缩压对心肌损伤和死亡率的因果影响:孟德尔随机化和前瞻性组研究的见解。
本研究旨在探讨收缩压(SBP)与心肌损伤(MI)之间的因果关系,并评估其对全因死亡率和心血管死亡率的预后意义。采用了两阶段分析方法。首先,通过孟德尔随机化(MR)来评估收缩压对六种心肌梗死相关表型的独立因果影响,并对潜在的混杂因素进行调整,包括脂质谱、血糖指数和人体测量特征。其次,研究人员分析了4459名全国健康与营养调查参与者的数据,随访时间长达15年。收缩压和心肌梗死之间的剂量-反应关系采用限制三次样条分析进行评估。使用Johnson-Neyman相互作用模型确定基于性别、年龄和合并症的阈值。MR分析显示收缩压升高与急性心力衰竭(优势比[OR] = 1.523)、心肌梗死(OR = 1.014)和缺血性卒中(OR = 33.339)风险增加之间存在因果关系。在前瞻性组分析中,收缩压≥180 mmHg与心肌梗死风险增加213.4%相关(OR = 3.134, p = 0.003),死亡率呈分级增加(全因死亡的风险比[HR] = 2.783;心血管死亡的风险比[HR] = 1.888)。性别分层分析表明,男性收缩压120-150 mmHg时心肌梗死风险最低,女性收缩压为162 mmHg。在年龄≥43岁的个体中,当收缩压超过135 mmHg时,全因死亡风险显著增加(p
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来源期刊
Molecular and Cellular Biochemistry
Molecular and Cellular Biochemistry 生物-细胞生物学
CiteScore
8.30
自引率
2.30%
发文量
293
审稿时长
1.7 months
期刊介绍: Molecular and Cellular Biochemistry: An International Journal for Chemical Biology in Health and Disease publishes original research papers and short communications in all areas of the biochemical sciences, emphasizing novel findings relevant to the biochemical basis of cellular function and disease processes, as well as the mechanics of action of hormones and chemical agents. Coverage includes membrane transport, receptor mechanism, immune response, secretory processes, and cytoskeletal function, as well as biochemical structure-function relationships in the cell. In addition to the reports of original research, the journal publishes state of the art reviews. Specific subjects covered by Molecular and Cellular Biochemistry include cellular metabolism, cellular pathophysiology, enzymology, ion transport, lipid biochemistry, membrane biochemistry, molecular biology, nuclear structure and function, and protein chemistry.
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