This retrospective, single-center, cross-sectional analysis consecutively enrolled adult patients aged 21–90 years with suspected CAD who underwent coronary angiography (CAG)-based examination and PCI at the Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, between September 8, 2019, and February 27, 2022. The exclusion criteria were as follows: ① Patients who did not undergo CAG; ② Patients with no significant CAD on CAG; and, ③ Patients who did not undergo PCI. Ultimately, 1,159 patients were included in the analysis (Figure 1).

Random blood sugar samples were collected within 24 h of admission from all subjects. The serum was separated by centrifugation at 3,000 rpm for 10 min and stored at −80 °C for the subsequent analysis. Triglyceride concentrations were quantified using the glycerophosphate oxidase-peroxidase (GPOPAP) method with a commercial kit (Catalog No.: CH0101151) from Beijing Jiuqiang Biotechnology Co., Ltd. (Roche Diagnostics, Basel, Switzerland). The intra- and inter-assay coefficients of variation (CV) for the internal quality control materials in this laboratory were both less than 5%, meeting the quality control standards. And AMI categories, with the latter identified by typical symptoms, ST-segment changes on electrocardiogram (13), and elevated cardiac enzymes (14). Hypertension was defined as systolic blood pressure ≥140 mmHg and/or diastolic blood pressure ≥90 mmHg, or current use of antihypertensive medication (15). Left ventricular ejection fraction (EF) was assessed using transthoracic echocardiography during the index hospitalization. The measurement was performed by experienced sonographers in accordance with the current guidelines of the American Society of Echocardiography, and the biplane Simpson's method of discs was the preferred technique for calculation.

Demographic characteristics, clinical history (including diabetes, stroke, smoking, and alcohol consumption), ancillary test results, and laboratory parameters were collected. These included EF and levels of creatinine (Cr), random blood sugar (RBS), C-reactive protein (CRP), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), LDL-C, glycated hemoglobin (HbA1c), etc.

Precise 95% confidence intervals (CI) were calculated for all the diagnostic performance metrics. Continuous variables were presented as mean ± standard deviation, whereas categorical variables were described as frequency (percentage, %). Group comparisons employed t-tests or χ² tests. Univariate and multivariate logistic regression analyses were performed to assess the association between TG levels and hypertension. The odds ratios (OR) and 95% CIs were calculated. Trend tests were performed by TG level quartile grouping. Restricted cubic spline (RCS) models were used to fit the nonlinear relationship between TG and hypertension using an inflection point analysis. Subgroup analyses were stratified by age, sex, HbA1c level, and EF, and interactions were tested. All analyses were performed using the statistical software package R (http://www.R-project.org; R Foundation) and Free Statistics software version 1.9.1. Statistical significance was set at P < 0.05.

Patients with CAD undergoing PCI were divided into two groups based on their hypertension status: the hypertension group (56.9%, 660/1,159) and the non-hypertension group (43.1%, 499/1,159). In the hypertensive group, the proportion of patients with angina was significantly higher than that of patients with AMI (P < 0.05), and the proportions of patients without diabetes and stroke were also significantly higher than those of patients with diabetes and stroke (P < 0.001). Additionally, the proportion of female patients in the hypertensive group was significantly higher than that in the non-hypertensive group (P < 0.05), suggesting that sex may be an important factor influencing the development of TG-induced hypertension. Compared with the non-hypertensive group, patients in the hypertensive group had significantly higher TG levels (2.0 ± 1.3 mmol/L vs. 1.8 ± 1.3  mmol/L; P < 0.01) and were older (60.2 ± 9.7 years vs. 57.6 ± 10.0 years; P < 0.001), indicating that dyslipidemia and advancing age are closely associated with hypertension development. Additionally, significant differences in Cr, HDL-C, and HbA1c levels were observed between the two groups, suggesting that renal function, lipid metabolism, and glycemic control may play synergistic roles in the pathogenesis of hypertension (Table 1).

Univariate analysis revealed significant positive correlations between AMI; age; sex; diabetes; stroke; serum Cr, TG, HDL-C, and HbA1c levels; and, hypertension risk (P < 0.05). Significant differences in age, sex, diabetes, and stroke were observed between the two groups. These factors are not only associated with hypertension onset but may also influence CAD progression and post-intervention outcomes through multiple pathophysiological pathways. This analysis provides a foundation for subsequent multivariate adjustments (Table 2).

Multivariate logistic regression analysis (n = 1,159) examined the association between the TG level quartiles and hypertension (Table 3). In the unadjusted model, TG levels showed a significant positive correlation with hypertension (OR = 1.18, 95% CI: 1.06–1.31). After adjusting for age and sex in Model I, the association strengthened (OR = 1.22, 95% CI: 1.10–1.36), indicating that demographic factors are important confounders. Model II, further adjusted for diabetes, alcohol consumption, smoking, and stroke history, yielded results similar to Model I (OR = 1.22, 95% CI: 1.09–1.35), suggesting these clinical and behavioral factors had limited impact on the association. Model III, which further adjusted for Cr, RBS, CRP,TC, HDL-C, LDL-C, and HbA1c levels based on Model II, still showed a significant association between TG level and hypertension (OR = 1.23, 95% CI: 1.03–1.47), indicating that TG level is an independent risk factor for hypertension. To further validate the robustness of the results, a sensitivity analysis was conducted by grouping TG levels into quartiles. The results showed a positive correlation between TG levels and the risk of hypertension. Compared with the lowest quartile (Q1), the highest quartile (Q4) showed a significantly increased risk of hypertension (OR = 2.61, 95% CI: 1.68–4.05), further supporting the important role of TG in the development of hypertension.

Restricted cubic spline analysis (Figure 2) revealed a nonlinear relationship between the TG level and hypertension after adjusting for sex, age, diabetes, alcohol consumption, smoking, stroke, AMI, and Cr, RBS, CRP, TC, HDL-C, LDL-C, and HbA1c levels (P = 0.024). This manifested as a gradually decreasing curved slope with increasing TG levels, indicating a saturation effect. Breakpoint analysis further validated this phenomenon: when TG levels were below 3.863 mmol/L, the risk of hypertension increased with increasing TG levels. However, when TG levels exceeded 3.863 mmol/L, the hypertension risk no longer showed a significant increase (Table 4), suggesting that above this threshold, other factors may become more dominant, or the effect of TG may reach a plateau. This finding may have important implications for setting clinical intervention targets.

To further explore the influence of other risk factors on the association between TG level and hypertension, subgroup analyses were conducted based on sex (male/female), age (<60/≥60 years), HbA1c (<6.0%/≥6.0%), and EF (<50%/≥50%). The results showed the strongest association between TG level and hypertension in the <50% EF subgroup (interaction, P < 0.05), suggesting that cardiac dysfunction may amplify the effect of TG on hypertension. No significant interactions were observed in the sex, HbA1c, or age subgroups, indicating that although these factors independently influence hypertension, they do not substantially alter the relationship between TG level and hypertension. These findings highlight the importance of strict TG level control in patients with heart failure. (Table 4 and Figure 3).

The nonlinear relationship observed in our study offers a fresh perspective on the complex role of TG in cardiovascular disease. Below the inflection point of 3.86 mmol/L, TG levels exhibited a positive correlation with the risk of hypertension, which aligns with the conclusions of numerous previous studies. The increased risk in this range is likely driven by several mechanisms: elevated TG levels induce systemic inflammatory responses and oxidative stress, impair nitric oxide-mediated endothelium-dependent vasodilation, and promote vascular remodeling; This pathophysiological cascade, encompassing systemic inflammation, oxidative stress, and impaired vasodilation, provides a mechanistic foundation for the observed association (16), these processes collectively contribute to increased peripheral vascular resistance and blood pressure (11, 17). However, when the TG concentration exceeded this threshold of 3.86 mmol/L, the association with hypertension risk demonstrated a saturation effect, wherein the risk no longer increased significantly with further rises in concentration. This J-shaped pattern contrasts with the linear associations often reported in general populations, underscoring the unique pathophysiological state of post-PCI patients (18),The non-linear, J-shaped relationship we identified between triglyceride levels and hypertension is consistent with the complex dynamics observed for other established cardiovascular risk factors. Notably, a dose-response meta-analysis has revealed a similar non-linear association between resting heart rate and the incidence of hypertension, suggesting that such threshold effects may be a fundamental characteristic in the pathophysiology of cardiovascular disease (19). A plausible explanation for this phenomenon is that at very high TG concentrations, the physical size of lipoprotein particles increases substantially (20), thereby reducing their ability to penetrate the arterial intima and cause direct damage to endothelial cells. This leads to a plateau in their direct atherogenic effects.

This leads to a plateau in their direct atherogenic effects. Notably, the inflection point identified in our study (3.86 mmol/L or ∼340 mg/dL) is substantially higher than the levels associated with increased cardiovascular risk in general populations (e.g., >89 mg/dL, as reported in recent studies). This discrepancy may be explained by the distinct clinical profile of our cohort, which comprised patients undergoing elective PCI, predominantly without acute myocardial infarction.Thus, our findings underscore the limitations of applying the traditional cardiovascular risk stratification system to this specific patient population (21). In this high-risk setting, it is highly probable that most patients were receiving guideline-directed medical therapy, including statins. Therefore, the measured TG levels represent on-treatment or residual concentrations (22). We hypothesize that in such a pharmacologically managed population, the threshold at which TG exerts a discernible effect on hypertension risk is shifted upward, possibly because its pathophysiological impact must be substantial enough to manifest against the backdrop of intensive secondary prevention. This observation highlights the context-dependent nature of TG-associated risk and underscores the need for population-specific risk stratification thresholds rather than a uniform approach. The non-linear, J-shaped relationship we identified between triglyceride levels and hypertension is consistent with the complex dynamics observed for other established cardiovascular risk factors (23).

One of the most instructive findings of our study is the clarification of the significant amplifying effect of cardiac dysfunction (EF < 50%) on the association between TG and hypertension. This phenomenon may stem from multifaceted pathophysiological interactions. In the setting of heart failure, pre-existing neurohormonal activation and metabolic dysfunction likely create a milieu that potentiates the pressor effects of triglycerides (24). Firstly, patients with reduced EF often exhibit overactivation of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system (25), which in itself creates a potent background for elevated blood pressure. Against this backdrop, abnormal TG metabolism may synergize with this neuroendocrine axis, exacerbating vasoconstriction and sodium-water retention. Secondly, the insulin resistance state prevalent in heart failure patients can further exacerbate hypertriglyceridemia by increasing hepatic very-low-density lipoprotein synthesis and reducing peripheral tissue clearance of TG (18). Insulin resistance itself can also activate RAAS and promote oxidative stress, creating a vicious cycle that amplifies the adverse impact of TG on blood pressure. The clinical significance of managing TG in this high-risk population extends beyond its association with hypertension.

Beyond our specific findings regarding hypertension, the broader clinical relevance of TG in high-risk CAD populations is further substantiated by recent evidence. Specifically,our findings resonate strongly with and are powerfully corroborated by a seminal 2025 study (26), which identified triglycerides as a key predictor of extreme cardiovascular risk and event recurrence in CAD patients. This convergence of evidence solidifies the position of TG as a critical residual risk factor in the statin era. Our work extends this paradigm by delineating a specific, independent J-shaped association between TG and the prevalence of hypertension—the most common comorbidity in this population. Thus, while links TG to hard clinical endpoints, our study elucidates its profound impact on a major, pervasive risk factor. Together, these findings compellingly argue that targeted TG management could yield dual benefits: mitigating the risk of major adverse events while simultaneously improving control of pivotal modifiable risk factors like hypertension, especially in high-risk subgroups such as patients with impaired cardiac function (27).

Our results have potential implications for clinical practice. Current guidelines generally recommend maintaining TG levels below 1.7 mmol/L (150 mg/dL) for cardiovascular risk management (28). Our study found that TG levels remain associated with hypertension risk even at higher concentrations (up to 3.86 mmol/L). Therefore, for CAD patients post-PCI, especially those with preserved EF, maintaining TG levels below 3.86 mmol/L might represent a more targeted preliminary management goal. This implies that targeting TG levels below this inflection point, particularly in high-risk subgroups, could represent a tailored therapeutic strategy (29, 30). For patients with EF < 50%, our data strongly suggest that strict control of TG may yield additional benefits for blood pressure management. This approach addresses the unmet need for adjunctive lipid management in high-risk patients, such as those with heart failure, beyond conventional statin therapy (31). This hypothesis urgently needs validation in future prospective interventional studies.

The strengths of our study include its focus on a well-defined and clinically highly relevant population (CAD undergoing PCI) and being the first to describe the J-shaped relationship between TG and hypertension and the modifying role of EF in this population. However, several limitations must be considered cautiously. First, the retrospective cross-sectional design precludes any causal inference, and the observed associations could be influenced by residual confounding or reverse causality. Second, we could not incorporate data on body mass index or the use of lipid-lowering medications (particularly fibrates and fish oil preparations), which may confound both TG levels and their association with hypertension. Finally, the single-center design and relatively limited sample size may restrict the generalizability of our findings and introduce some instability in subgroup analyses (e.g., the EF < 50% group). Future large-scale, multicenter prospective cohort studies that meticulously collect data on medication use and anthropometric measurements are essential to confirm our observations.