原发性高血压非肾素依赖性醛固酮与左心室肥厚的关系

doi:10.3969/j.issn.1674-8115.2025.10.012

摘要/Abstract

摘要：

目的·通过分析原发性高血压患者左心室质量指数（left ventricular mass index，LVMI）的影响因素，探讨血醛固酮水平与左心室肥厚（left ventricular hypertrophy，LVH）的关系。方法·纳入2013年1月—2019年12月在上海交通大学医学院瑞金医院北部院区高血压科住院并经盐水负荷试验排除原发性醛固酮增多症的155例原发性高血压患者（盐水抑制后血浆醛固酮<60 pg/mL）。采集患者的一般临床资料（年龄、性别、吸烟情况、高血压病程等），体格检查结果（血压、体质量指数），血生化（肾功能、电解质、空腹血糖、血脂）、尿钠和相关激素（血浆基础及激发醛固酮、血浆基础及激发肾素、尿醛固酮、盐水抑制后血浆醛固酮等）水平，通过心脏超声评估LVMI。采用Pearson相关分析量化LVMI与各变量的线性关联，通过二元Logistic回归模型筛选LVH的独立危险因素，应用多元线性回归模型评估各变量对LVMI的影响。结果·155例原发性高血压患者平均年龄（46.85±11.08）岁，男性占51.6%。Pearson相关分析显示，LVMI与盐水抑制后血浆醛固酮（r=0.334，P<0.001）、年龄（r=0.184，P=0.032）、高血压病程（r=0.241，P=0.005）、收缩压（r=0.280，P=0.001）、脉压（r=0.339，P<0.001）具有相关性，而与舒张压、体质量指数、空腹血糖、总胆固醇、低密度脂蛋白胆固醇、甘油三酯、高密度脂蛋白胆固醇、尿钠、基础醛固酮、激发醛固酮及尿醛固酮无相关性；校正性别、吸烟史、年龄、高血压病程、体质量指数、脉压、收缩压、空腹血糖、总胆固醇等混杂因素后，二元Logistic回归表明，盐水抑制后血浆醛固酮水平每升高1 pg/mL，LVH风险增加5.1%（OR=1.051，95%CI 1.016~1.088，P=0.004）；多元线性回归显示盐水抑制后血浆醛固酮（β=0.359，P<0.001）、高血压病程（β=0.168，P=0.046）、脉压（β=0.226，P=0.008）是LVMI的独立影响因素。结论·盐水抑制后血浆醛固酮水平是原发性高血压患者LVH的独立影响因素。

关键词: 原发性高血压, 靶器官损害, 左心室肥厚, 盐水负荷试验, 醛固酮

Abstract:

Objective ·To analyze the influencing factors of left ventricular mass index (LVMI) in patients with essential hypertension, and explore the relationship between aldosterone levels and left ventricular hypertrophy (LVH). Methods ·A total of 155 patients with essential hypertension, hospitalized in the Hypertension Department of the Northern Campus of Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, from January 2013 to December 2019, and excluded from primary aldosteronism by saline load test (post-saline suppression plasma aldosterone <60 pg/mL), were enrolled. General clinical data (age, gender, smoking status, duration of hypertension, etc.), physical examination data (blood pressure and body mass index), blood biochemistry (renal function, electrolytes, fasting blood glucose, and lipids), urinary sodium, and relevant hormones (basal and activated aldosterone, basal and activated renin, urinary aldosterone, post-saline suppression aldosterone, etc.) were collected. LVMI was evaluated by echocardiography. Pearson correlation analysis was used to assess the linear association between LVMI and each variable. Binary Logistic regression models were applied to screen independent risk factors for LVH. Multiple linear regression models were used to assess the impact of variables on LVMI. Results ·The mean age of the 155 patients was (46.85±11.08) years, with 51.6% being male. Pearson correlation analysis showed that LVMI was significantly positively correlated with post-saline suppression aldosterone (r=0.334, P<0.001), age (r=0.184, P=0.032), duration of hypertension (r=0.241, P=0.005), systolic blood pressure (r=0.280, P=0.001), and pulse pressure (r=0.339, P<0.001). No significant correlations were found with diastolic blood pressure, body mass index, fasting blood glucose, total cholesterol, low-density lipoprotein cholesterol, triglyceride, high-density lipoprotein cholesterol, urinary sodium, basal aldosterone, activated aldosterone, or urinary aldosterone. After adjusting for confounders, including gender, smoking history, age, duration of hypertension, body mass index, pulse pressure, systolic blood pressure, fasting blood glucose, and total cholesterol, binary Logistic regression showed that each 1 pg/mL increase in post-saline suppression aldosterone was associated with a 5.1% increased risk of LVH (OR=1.051, 95%CI 1.016‒1.088, P=0.004). Multiple linear regression identified suppressed aldosterone (β=0.359, P<0.001), duration of hypertension (β=0.168, P=0.046), and pulse pressure (β=0.226, P=0.008) as independent influencing factors for LVMI. Conclusion ·Suppressed aldosterone is an independent influencing factor for LVH in patients with essential hypertension.

Key words: essential hypertension, target organ damage, left ventricular hypertrophy (LVH), saline load test, aldosterone

中图分类号:

R544.1

常桂丽, 刘常远, 李明春, 胡哲, 陈静, 操群安, 初少莉, 陈歆. 原发性高血压非肾素依赖性醛固酮与左心室肥厚的关系[J]. 上海交通大学学报（医学版）, 2025, 45(10): 1372-1377.

CHANG Guili, LIU Changyuan, LI Mingchun, HU Zhe, CHEN Jing, CAO Qun'an, CHU Shaoli, CHEN Xin. Relationship between non-renin-dependent aldosterone and left ventricular hypertrophy in essential hypertension[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2025, 45(10): 1372-1377.

图/表 4

参考文献 23

[1]	ĐORĐEVIĆ D B, KORAČEVIĆ G P, ĐORĐEVIĆ A D, et al. Hypertension and left ventricular hypertrophy[J]. J Hypertens, 2024, 42(9): 1505-1515.
[2]	CHUN K H, KANG S M. Blood pressure and heart failure: focused on treatment[J]. Clin Hypertens, 2024, 30(1): 15.
[3]	CUSPIDI C, FACCHETTI R, BOMBELLI M, et al. Differential value of left ventricular mass index and wall thickness in predicting cardiovascular prognosis: data from the PAMELA population[J]. Am J Hypertens, 2014, 27(8): 1079-1086.
[4]	VILLAVERDE J M F, SAAVEDRA F J M, VIDAL G A, et al. High prevalence of left ventricular hypertrophy in patients with hypertension of long course[J]. Med Clin (Barc), 2007, 129(2): 46-50.
[5]	KANNEL W B. Blood pressure as a cardiovascular risk factor: prevention and treatment[J]. JAMA, 1996, 275(20): 1571-1576.
[6]	CALÓ L A, PAGNIN E, DAVIS P A, et al. Oxidative stress and profibrotic action of aldosterone[J]. Am J Hypertens, 2005, 18(3): 441.
[7]	LASTRA-GONZALEZ G, MANRIQUE-ACEVEDO C, SOWERS J R. The role of aldosterone in cardiovascular disease in people with diabetes and hypertension: an update[J]. Curr Diab Rep, 2008, 8(3): 203-207.
[8]	FERREIRA N S, TOSTES R C, PARADIS P, et al. Aldosterone, inflammation, immune system, and hypertension[J]. Am J Hypertens, 2021, 34(1): 15-27.
[9]	CANNAVO A, ELIA A, LICCARDO D, et al. Aldosterone and myocardial pathology[J]. Vitam Horm, 2019, 109: 387-406.
[10]	AL-HASHEDI E M, ABDU F A. Aldosterone effect on cardiac structure and function[J]. Curr Cardiol Rev, 2024, 20(4): e290224227534.
[11]	OHNO Y, SONE M, INAGAKI N, et al. Nadir aldosterone levels after confirmatory tests are correlated with left ventricular hypertrophy in primary aldosteronism[J]. Hypertension, 2020, 75(6): 1475-1482.
[12]	ANANDA R A, GWINI S, BEILIN L J, et al. Relationship between renin, aldosterone, aldosterone-to-renin ratio and arterial stiffness and left ventricular mass index in young adults[J]. Circulation, 2024, 150(25): 2019-2030.
[13]	中国高血压防治指南修订委员会.中国高血压防治指南2010[J]. 中华心血管病杂志, 2011, 39(7): 579-616.
	Writing Group of 2010 Chinese Guidelines for the Management of Hypertension. 2010 Chinese guidelines for the management of hypertension[J]. Chinese Journal of Cardiology, 2011, 39(7): 579-616.
[14]	DEVEREUX R B, REICHEK N. Echocardiographic determination of left ventricular mass in man. Anatomic validation of the method[J]. Circulation, 1977, 55(4): 613-618.
[15]	European Society of Hypertension-European Society of Cardiology Guidelines Committee. 2003 European Society of Hypertension-European Society of Cardiology guidelines for the management of arterial hypertension[J]. J Hypertens, 2003, 21(6):1011-1053.
[16]	MILLS K T, BUNDY J D, KELLY T N, et al. Global disparities of hypertension prevalence and control: a systematic analysis of population-based studies from 90 countries[J]. Circulation, 2016, 134(6): 441-450.
[17]	POST W S, LARSON M G, LEVY D. Impact of left ventricular structure on the incidence of hypertension. The Framingham Heart Study[J]. Circulation, 1994, 90(1): 179-185.
[18]	LIU Y, YAN Y K, JIANG T B, et al. Impact of long-term burden of body mass index and blood pressure from childhood on adult left ventricular structure and function[J]. J Am Heart Assoc, 2020, 9(16): e016405.
[19]	DE MARCO A, FEITOSA A M, GOMES M M, et al. Pulse pressure measured by home blood pressure monitoring and its correlation to left ventricular mass index[J]. Arq Bras Cardiol, 2007, 88(1): 91-95.
[20]	CATENA C, VERHEYEN N D, URL-MICHITSCH M, et al. Association of post-saline load plasma aldosterone levels with left ventricular hypertrophy in primary hypertension[J]. Am J Hypertens, 2016, 29(3): 303-310.
[21]	SCHLAICH M P, SCHOBEL H P, HILGERS K, et al. Impact of aldosterone on left ventricular structure and function in young normotensive and mildly hypertensive subjects[J]. Am J Cardiol, 2000, 85(10): 1199-1206.
[22]	GUPTA A, SCHIROS C G, GADDAM K K, et al. Effect of spironolactone on diastolic function in hypertensive left ventricular hypertrophy[J]. J Hum Hypertens, 2015, 29(4): 241-246.
[23]	PITT B, REICHEK N, WILLENBROCK R, et al. Effects of eplerenone, enalapril, and eplerenone/enalapril in patients with essential hypertension and left ventricular hypertrophy: the 4E-left ventricular hypertrophy study[J]. Circulation, 2003, 108(15): 1831-1838.

Characteristic	Total (n＝155)	Characteristic	Total (n＝155)
Age/year	46.85±11.08	Total cholesterol/(mmol·L^-1)	4.58±0.97
Male/n(%)	80 (51.6)	High-density lipoprotein cholesterol/(mmol·L^-1)	1.11±0.25
Smoking history/n(%)	51 (32.9)	Low-density lipoprotein cholesterol/(mmol·L^-1)	3.00±0.75
Duration of hypertension/year	6.14±7.69	Fasting blood glucose/(mmol·L^-1)	5.54±1.31
Body mass index/(kg·m^-2)	25.25±3.51	Urinary sodium/mmol	155.19±74.36
Systolic blood pressure/mmHg	143.01±18.64	LVMI/(g·m^-2)	125.07±31.98
Diastolic blood pressure/mmHg	87.67±12.50	Urine aldosterone/μg	9.70±6.07
Pulse pressure/mmHg	55.34±14.78	Basal aldosterone/(pg·mL^-1)	135.10±65.24
Serum potassium/(mmol·L^-1)	3.74±0.30	Basal plasma renin activity/[ng·(mL·h)^-1]	3.69±25.91
Serum creatine/(μmol·L^-1)	74.68±12.38	Activated aldosterone/(pg·mL^-1)	165.38±81.37
Serum uric acid/(μmol·L^-1)	335.38±92.50	Activated plasma renin activity/[ng·(mL·h)^-1]	2.03±1.70
Triglyceride/(mmol·L^-1)	1.81±1.22	Suppressed aldosterone/(pg·mL^-1)	40.98±11.64

Characteristic	Total (n＝155)	Characteristic	Total (n＝155)
Age/year	46.85±11.08	Total cholesterol/(mmol·L^-1)	4.58±0.97
Male/n(%)	80 (51.6)	High-density lipoprotein cholesterol/(mmol·L^-1)	1.11±0.25
Smoking history/n(%)	51 (32.9)	Low-density lipoprotein cholesterol/(mmol·L^-1)	3.00±0.75
Duration of hypertension/year	6.14±7.69	Fasting blood glucose/(mmol·L^-1)	5.54±1.31
Body mass index/(kg·m^-2)	25.25±3.51	Urinary sodium/mmol	155.19±74.36
Systolic blood pressure/mmHg	143.01±18.64	LVMI/(g·m^-2)	125.07±31.98
Diastolic blood pressure/mmHg	87.67±12.50	Urine aldosterone/μg	9.70±6.07
Pulse pressure/mmHg	55.34±14.78	Basal aldosterone/(pg·mL^-1)	135.10±65.24
Serum potassium/(mmol·L^-1)	3.74±0.30	Basal plasma renin activity/[ng·(mL·h)^-1]	3.69±25.91
Serum creatine/(μmol·L^-1)	74.68±12.38	Activated aldosterone/(pg·mL^-1)	165.38±81.37
Serum uric acid/(μmol·L^-1)	335.38±92.50	Activated plasma renin activity/[ng·(mL·h)^-1]	2.03±1.70
Triglyceride/(mmol·L^-1)	1.81±1.22	Suppressed aldosterone/(pg·mL^-1)	40.98±11.64

Factor	r value	P value	Factor	r value	P value
Age	0.184	0.032	Low-density lipoprotein cholesterol	-0.157	0.073
Duration of hypertension	0.241	0.005	Fasting blood glucose	0.072	0.419
Systolic blood pressure	0.280	0.001	Urinary sodium	-0.032	0.712
Diastolic blood pressure	0.002	0.985	Urine aldosterone	0.101	0.251
Pulse pressure	0.339	<0.001	Basal aldosterone	0.015	0.889
Body mass index	0.159	0.064	Basal plasma renin activity	-0.097	0.359
Triglyceride	0.070	0.427	Activated aldosterone	0.046	0.596
Total cholesterol	-0.160	0.069	Activated plasma renin activity	0.073	0.404
High-density lipoprotein cholesterol	-0.125	0.158	Suppressed aldosterone	0.334	<0.001

Factor	r value	P value	Factor	r value	P value
Age	0.184	0.032	Low-density lipoprotein cholesterol	-0.157	0.073
Duration of hypertension	0.241	0.005	Fasting blood glucose	0.072	0.419
Systolic blood pressure	0.280	0.001	Urinary sodium	-0.032	0.712
Diastolic blood pressure	0.002	0.985	Urine aldosterone	0.101	0.251
Pulse pressure	0.339	<0.001	Basal aldosterone	0.015	0.889
Body mass index	0.159	0.064	Basal plasma renin activity	-0.097	0.359
Triglyceride	0.070	0.427	Activated aldosterone	0.046	0.596
Total cholesterol	-0.160	0.069	Activated plasma renin activity	0.073	0.404
High-density lipoprotein cholesterol	-0.125	0.158	Suppressed aldosterone	0.334	<0.001

Risk factor	OR (95%CI)	P value
Suppressed aldosterone	1.051 (1.016‒1.088)	0.004
Duration of hypertension	1.065 (1.001‒1.132)	0.045