ArticleMolecular and cellular biochemistry2025
Causal effect of systolic blood pressure on myocardial injury and mortality: insights from Mendelian randomization and a prospective group study.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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