Christa Martin, Weng Andreas M, Geier Bettina, Wörmann Caroline, Scheffler Anne, Lehmann Leane, Oberberger Johannes, Kraus Bettina J, Hahner Stefanie, Störk Stefan, Klink Thorsten, Bauer Wolfgang R, Hammer Fabian, Köstler Herbert
Comprehensive Heart Failure Center, University of Würzburg, Würzburg, Germany.
Department of Internal Medicine I, University Hospital Würzburg, Würzburg, Germany.
Eur Heart J Cardiovasc Imaging. 2019 Mar 1;20(3):263-270. doi: 10.1093/ehjci/jey134.
Sodium intake has been linked to left ventricular hypertrophy independently of blood pressure, but the underlying mechanisms remain unclear. Primary hyperaldosteronism (PHA), a condition characterized by tissue sodium overload due to aldosterone excess, causes accelerated left ventricular hypertrophy compared to blood pressure matched patients with essential hypertension. We therefore hypothesized that the myocardium constitutes a novel site capable of sodium storage explaining the missing link between sodium and left ventricular hypertrophy.
Using 23Na magnetic resonance imaging, we investigated relative sodium signal intensities (rSSI) in the heart, calf muscle, and skin in 8 PHA patients (6 male, median age 55 years) and 12 normotensive healthy controls (HC) (8 male, median age 61 years). PHA patients had a higher mean systolic 24 h ambulatory blood pressure [152 (140; 163) vs. 125 (122; 130) mmHg, P < 0.001] and higher left ventricular mass index [71.0 (63.5; 106.8) vs. 55.0 (50.3; 66.8) g/m2, P = 0.037] than HC. Compared to HC, PHA patients exhibited significantly higher rSSI in the myocardium [0.31 (0.26; 0.34) vs. 0.24 (0.20; 0.27); P = 0.007], calf muscle [0.19 (0.16; 0.22) vs. 0.14 (0.13; 0.15); P = 0.001] and skin [0.28 (0.25; 0.33) vs. 0.19 (0.17; 0.26); P = 0.014], reflecting a difference of +27%, +38%, and +39%, respectively. Treatment of PHA resulted in significant reductions of the rSSI in the myocardium, calf muscle and skin by -13%, -27%, and -29%, respectively.
Myocardial tissue rSSI is increased in PHA patients and treatment of aldosterone excess effectively reduces rSSI, thus establishing the myocardium as a novel site of sodium storage in addition to skeletal muscle and skin.
钠摄入已被证明与左心室肥厚有关，且独立于血压，但潜在机制仍不清楚。原发性醛固酮增多症（PHA）是一种由于醛固酮过量导致组织钠过载的疾病，与血压匹配的原发性高血压患者相比，会导致左心室肥厚加速。因此，我们推测心肌构成了一个能够储存钠的新部位，这解释了钠与左心室肥厚之间缺失的联系。
我们使用23Na磁共振成像技术，研究了8例PHA患者（6例男性，中位年龄55岁）和12例血压正常的健康对照者（HC）（8例男性，中位年龄61岁）心脏、小腿肌肉和皮肤中的相对钠信号强度（rSSI）。PHA患者的24小时动态收缩压平均值更高[152（140；163）vs. 125（122；130）mmHg，P < 0.001]，左心室质量指数也更高[71.0（63.5；106.8）vs. 55.0（50.3；66.8）g/m2，P = 0.037]。与HC相比，PHA患者心肌中的rSSI显著更高[0.31（0.26；0.34）vs. 0.24（0.20；0.27）；P = 0.007]，小腿肌肉[0.19（0.16；0.22）vs. 0.14（0.13；0.15）；P = 0.001]和皮肤[0.28（0.25；0.33）vs. 0.19（0.17；0.26）；P = 0.014]中的rSSI也更高，分别反映出差异为+27%、+38%和+39%。PHA的治疗导致心肌、小腿肌肉和皮肤中的rSSI分别显著降低-13%、-27%和-29%。
PHA患者的心肌组织rSSI增加，醛固酮过量的治疗有效降低了rSSI，从而确立了心肌作为除骨骼肌和皮肤之外的一个新的钠储存部位。
