Background:Aldosterone production and mineralocorticoid receptor activation are implicated in myocardial fibrosis and cardiovascular events.Methods:Cardiac structure and function were assessed in 4547 participants without prevalent heart failure (HF) in the ARIC study (Atherosclerosis Risk in Communities), with echocardiography, aldosterone, and plasma renin activity measurement (2011–2013). Subjects were characterized by plasma renin activity as suppressed (≤0.5 ng/mL per hour) or unsuppressed (>0.5 ng/mL per hour). Cross-sectional relationships with cardiac structure and function, and longitudinal relationships with outcomes (HF hospitalization; HF and all-cause death; HF, death, myocardial infarction, and stroke; and incident atrial fibrillation) were assessed. Models were adjusted for demographic and anthropometric characteristics and additively, for blood pressure and antihypertensives.Results:Evidence of primary aldosteronism physiology was prevalent (11.6% with positive screen) and associated with echocardiographic parameters. Renin suppression was associated with greater left ventricular mass, left ventricular volumes, and left atrial volume index, and a lower E/A ratio (adjusted P<0.001 for all). Higher aldosterone was associated with greater left ventricular mass and lower global longitudinal strain and lateral E′. The highest tertile of aldosterone was associated with a hazard ratio of 1.37 (95% CI, 1.06–1.77; 5.5-year follow-up) for incident atrial fibrillation relative to the lowest. Renin suppression was associated with HF (hazard ratio, 1.34 [95% CI, 1.05–1.72]; 7.3-year follow-up), although these relationships did not remain statistically significant after additional adjustment for hypertension.Conclusions:Renin suppression and aldosterone excess, consistent with primary aldosteronism pathophysiology, were associated with cardiac structural and functional alterations and may represent an early target for mitigation of fibrosis with mineralocorticoid receptor antagonists.

中文翻译：

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醛固酮增多症范围内的心脏结构和功能：社区研究中的动脉粥样硬化风险


背景：醛固酮的产生和盐皮质激素受体的激活与心肌纤维化和心血管事件有关。方法：ARIC 研究（社区动脉粥样硬化风险）中，对 4547 名没有普遍心力衰竭 (HF) 的参与者的心脏结构和功能进行了评估，包括超声心动图、醛固酮，和血浆肾素活性测量（2011-2013）。受试者的血浆肾素活性被表征为抑制（≤0.5 ng/mL/小时）或未抑制（>0.5 ng/mL/小时）。评估了与心脏结构和功能的横截面关系，以及与结果（心力衰竭住院；心力衰竭和全因死亡；心力衰竭、死亡、心肌梗塞和中风；以及心房颤动事件）的纵向关系。根据人口统计和人体测量特征以及血压和抗高血压药物对模型进行调整。结果：原发性醛固酮增多症生理学的证据很普遍（筛查结果为阳性，占 11.6%），并且与超声心动图参数相关。肾素抑制与较大的左心室质量、左心室容积和左心房容积指数以及较低的 E/A 比值相关（全部调整后的P <0.001）。较高的醛固酮与较大的左心室质量和较低的整体纵向应变和横向 E' 相关。相对于最低的醛固酮三分位数，最高三分位数的房颤发生风险比为 1.37（95% CI，1.06-1.77；5.5 年随访）。肾素抑制与心力衰竭相关（风险比，1.34 [95% CI，1.05-1.72]；7.3 年随访），尽管在对高血压进行额外调整后，这些关系并未保持统计学显着性。结论：肾素抑制和醛固酮过量与原发性醛固酮增多症病理生理学一致，与心脏结构和功能改变相关，可能代表盐皮质激素受体拮抗剂减轻纤维化的早期目标。