Faculty of Nursing and Health Sciences, Nord University, Levanger, Høgskoleveien 27, 7601 Levanger, Norway.
Department of Circulation and Medical Imaging, Medicine and health sciences, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
BMC Cardiovasc Disord. 2022 Nov 8;22(1):472. doi: 10.1186/s12872-022-02921-1.
Studies suggest increased risk for an outcome in people with joint exposures that share common causal pathways. The objective of this study was to determine the risk of incident acute myocardial infarction (AMI) following exposure to both albuminuria and/or anxiety and depression symptoms.
Participants who provided urine samples to the HUNT2 (1995-97) or HUNT3 (2007-2009) surveys were followed until the end of 2016. Albuminuria was measured by Albumin Creatine Ratio (ACR) and participants self-reported mood and anxiety symptoms on the Hospital Anxiety and Depression scale. We used Cox regression to estimate hazard ratios (HRs) for first incident AMI considering interaction between exposures and additive models to calculate the proportion of AMI that were attributable to the synergy of both exposures, adjusted for the Framingham variables.
Eleven thousand fourteen participants free of previous AMI were eligible for participation, with 1234 incident AMIs occurred during a mean 13.7 years of follow-up. For participants who had a healthier CVD risk profile, the HR for AMI of having both albuminuria (3-30 mg/mmol) and depression (≥8) was 2.62 (95% 1.12-6.05) compared with a HR 1.34 (95% CI 1.04-1.74) with raised ACR only (Likelihood Ratio-test 0.03). Adding anxiety (≥8) to albuminuria (3-30) tripled the risk (HR 3.32 95% CI 1.43-7.17). The additive models suggest that these risks are not higher than expected based on each risk factor alone.
This study indicate that the risk of AMI in persons with elevated albuminuria but with an otherwise healthy CVD profile might be amplified by anxiety and depression symptoms. The increased risk with joint risk factors is not higher than expected based on each risk factor alone, which indicate that the risk factors do not share causal pathways.
研究表明，具有共同因果途径的联合暴露人群发生某一结局的风险增加。本研究的目的是确定暴露于蛋白尿和/或焦虑抑郁症状后新发急性心肌梗死（AMI）的风险。
参加 HUNT2（1995-1997 年）或 HUNT3（2007-2009 年）调查并提供尿液样本的参与者随访至 2016 年底。白蛋白尿通过白蛋白肌酐比（ACR）测量，参与者在医院焦虑抑郁量表上自我报告情绪和焦虑症状。我们使用 Cox 回归估计首次发生 AMI 的风险比（HR），考虑暴露因素之间的相互作用，并使用加性模型计算归因于两种暴露协同作用的 AMI 比例，调整 Framingham 变量。
11014 名无既往 AMI 的参与者符合参与条件，在平均 13.7 年的随访中发生了 1234 例新发 AMI。对于 CVD 风险谱更健康的参与者，同时存在蛋白尿（3-30mg/mmol）和抑郁（≥8）的 AMI 风险比为 2.62（95%CI 1.12-6.05），而仅 ACR 升高（HR 1.34，95%CI 1.04-1.74）的 HR 为 1.34（95%CI 1.04-1.74）（似然比检验 0.03）。将焦虑（≥8）添加到白蛋白尿（3-30）中，风险增加三倍（HR 3.32，95%CI 1.43-7.17）。加性模型表明，这些风险并不高于仅基于每个危险因素的预期风险。
本研究表明，在具有升高的白蛋白尿但 CVD 特征健康的个体中，焦虑和抑郁症状可能会放大 AMI 的风险。联合危险因素的风险增加并不高于仅基于每个危险因素的预期风险，这表明危险因素不具有因果关系。
