Hypertension remains a major contributor to the global disease burden and mortality, representing a critical public health challenge. While the cumulative lipid accumulation product (LAP), a marker of abdominal and visceral fat deposition, has shown cross-sectional associations with hypertension, existing studies inadequately address the impact of long-term cumulative LAP exposure on hypertension risk. Furthermore, causal relationships between cumulative LAP and incident hypertension remain underexplored.

To evaluate the association between cumulative LAP and hypertension risk and assess its predictive capacity for incident hypertension.

Data were derived from the Guizhou Natural Population Cohort Study database. Participants were enrolled from November 20, 2010, to December 19, 2012, and followed up from April 2016 to October 2020. A total of 3 548 subjects were ultimately included in the analysis. Participants were divided into four quartiles based on cumulative LAP (Q1-Q4 groups) : Q1 (cumulative LAP ≤14.54, n=887), Q2 (14.54<cumulative LAP≤24.35, n=887), Q3 (24.35<cumulative LAP≤39.21, n=887), and Q4 (cumulative LAP >39.21, n=887). Subjects were further categorized into non-hypertension group (n=2 696) and hypertension group (n=852) based on the development of new-onset hypertension. The relationship between cumulative LAP and hypertension was evaluated using the Cox proportional hazards regression model. The dose-response relationship between cumulative LAP and hypertension risk was assessed using restricted cubic splines. Time-dependent receiver operating characteristic (ROC) curves were constructed to evaluate the predictive ability of cumulative LAP for hypertension. Participants with follow-up duration <3 years and those with pre-hypertension were excluded.

Among the 3 548 adults included, 1 607 (45.3%) were men and 1 941 (54.7%) were women, with a mean age of (42.5±14.1) years. During the follow-up period, 852 (11.2%) subjects were newly diagnosed with hypertension. Significant differences were observed between the non-hypertension and hypertension groups in terms of gender, age, education level, family history of hypertension, excessive intake of oil, excessive intake of salt, insufficient intake of fresh fruits, proportion of inadequate sleep, BMI, diastolic blood pressure, fasting plasma glucose (FPG), and cumulative LAP (P<0.05). The results of the Cox proportional hazards regression model showed that, compared with the Q1 group, the risk of hypertension increased progressively in the Q2 group (aHR=1.330, 95%CI=1.053-1.681), Q3 group (aHR=1.706, 95%CI=1.364-2.134), and Q4 group (aHR=2.339, 95%CI=1.869-2.928) after adjusting for potential confounders (P<0.05). The restricted cubic spline analysis revealed a non-linear dose-response relationship between cumulative LAP and hypertension risk (P_{non-linearity}<0.01), with the risk of new-onset hypertension increasing with cumulative LAP but stabilizing after cumulative LAP >65. The time-dependent ROC curves for predicting hypertension incidence showed that the area under the ROC curve (AUC) for the overall population was 0.617, 0.590, 0.603, and 0.634 for continuous average exposure of 6, 7, 8, and 9 years, respectively. The AUC for men was 0.600, 0.561, 0.571, and 0.558, and for women, it was 0.638, 0.629, 0.647, and 0.711. For urban populations, the AUC was 0.596, 0.565, 0.602, and 0.621, while for rural populations, it was 0.629, 0.592, 0.594, and 0.635.

Cumulative LAP is an independent risk factor for the onset of hypertension, but it is not an ideal indicator for predicting the onset of hypertension, and its predictive value for the onset of hypertension is relatively limited.

高血压是造成全球疾病负担和死亡的主要因素，已成为当今社会普遍的公共卫生问题之一。累积脂质蓄积指数（LAP）可反映腹部和内脏脂肪蓄积程度，多项横断面研究表明，LAP与高血压有显著相关性，但这些研究并没有充分考虑长期暴露下LAP对高血压发病风险的影响，LAP与高血压发病因果关系的研究仍较为少见。

评估累积LAP与高血压发病风险的相关性，探讨该指标对高血压发病的预测能力。

采用贵州省自然人群队列研究数据库，于2010-11-20—2012-12-19纳入研究对象，收集基线资料，并于2016年4月—2020年10月进行随访，最终纳入3 548例研究对象。将患者按累积LAP分为4个水平（Q1~Q4组），Q1组（累积LAP≤14.54，n=887），Q2组（14.54<累积LAP≤24.35，n=887），Q3组（24.35<累积LAP≤39.21，n=887），Q4组（累积LAP >39.21，n=887）。并依据是否有新发高血压将患者分为非高血压组（n=2 696）和高血压组（n=852）。采用Cox比例回归模型评估累积LAP与高血压的关系。采用限制性立方样条评估累积LAP与高血压发病风险的量效关系。绘制累积LAP预测高血压的时间依赖性受试者工作特征（ROC）曲线。排除随访时间<3年、高血压前期人群。

纳入的3 548例成年人中男1 607例（45.3%），女1 941例（54.7%），平均年龄（42.5±14.1）岁，随访期间有852例（11.2%）新诊断为高血压。非高血压组和高血压组研究对象性别、年龄、受教育程度、高血压家族史、油摄入过量、盐摄入过量、新鲜水果摄入不足、缺乏睡眠占比、BMI、舒张压、空腹血糖（FPG）、累积LAP比较，差异有统计学意义（P<0.05）。Cox比例回归模型结果显示，与Q1组比较，在调整了潜在协变量后，Q2组（aHR=1.330，95%CI=1.053~1.681）、Q3组（aHR=1.706，95%CI=1.364~2.134）、Q4组（aHR=2.339，95%CI=1.869~2.928）高血压发病风险均逐渐升高（P<0.05）。限制性立方样条结果显示，累积LAP与高血压风险呈非线性量效关系（P_非线性<0.01），新发高血压风险随着累积LAP的升高而升高，但累积LAP >65后趋于稳定。绘制累积LAP预测新发高血压的时间依赖性ROC曲线，结果提示累积LAP预测连续平均暴露6、7、8、9年后，总人群高血压发病的ROC曲线下面积（AUC）分别为0.617、0.590、0.603、0.634，男性高血压发病的AUC分别为0.600、0.561、0.571、0.558，女性高血压发病的AUC分别为0.638、0.629、0.647、0.711，城市人群高血压发病的AUC分别为0.596、0.565、0.602、0.621，农村人群高血压发病的AUC分别为0.629、0.592、0.594、0.635。

累积LAP升高是高血压发病的独立危险因素，但不是预测高血压发病的理想指标，对于高血压发病的预测价值较为有限。