Krishnan Balaji, Patarroyo-Aponte Margarita, Duprez Daniel, Pritzker Marc, Missov Emil, Benditt David G
Cardiac Arrhythmia Center (Syncope Clinic) and Cardiovascular Division, University of Minnesota Medical School, Minneapolis, Minnesota.
Cardiac Arrhythmia Center (Syncope Clinic) and Cardiovascular Division, University of Minnesota Medical School, Minneapolis, Minnesota.
Heart Rhythm. 2015 Jun;12(6):1287-94. doi: 10.1016/j.hrthm.2015.02.015. Epub 2015 Feb 12.
The pathophysiology of orthostatic hypotension (OH) is multifactorial, with the most frequent causes being adverse effects of cardioactive drugs. In 20%-40% of cases, the etiology is unknown. In recent reports, altered levels of endogenous neuropeptides have been observed in noncardiac syncope, but B-type natriuretic peptide (BNP) and its amino-terminal cleavage fragment (NT-proBNP) have not been studied.
The purpose of this study was to assess the possibility that BNP with its diuretic and vasorelaxant properties could contribute to OH.
This prospective observational study comprised 85 consecutive OH subjects (58 women, age 49 ± 23 years) referred to a tertiary-care syncope clinic. All patients had normal left ventricular systolic and diastolic function, and clinical and laboratory findings consistent with euvolemia or modest hypovolemia. In 45 of 85 individuals (53%), an OH cause was determined.
Among the remaining 40 patients (21 women, age 57 ± 16 years) with OH of unknown cause, 6 of 40 (15%) exhibited unexpectedly elevated plasma NT-proBNP levels (14000, 5210, 2570, 7990, 3480, and 6680 pg/mL). In contrast, NT-proBNP values were normal (ie, <300 pg/mL) in the remaining 34 patients with OH of unknown cause and 45 patients with OH of known etiology. At 8 to 12 months of follow-up, volume repletion therapy requirements in patients with initial increased NT-proBNP diminished in conjunction with gradual fall of NT-proBNP concentrations.
In select patients, markedly elevated levels of BNP or NT-proBNP may be associated with and possibly contribute to symptomatic OH.
体位性低血压（OH）的病理生理机制是多因素的，最常见的原因是心血管活性药物的不良反应。在20%-40%的病例中，病因不明。最近的报告显示，非心源性晕厥患者体内内源性神经肽水平发生了变化，但B型利钠肽（BNP）及其氨基末端裂解片段（NT-proBNP）尚未得到研究。
本研究旨在评估具有利尿和血管舒张特性的BNP可能导致OH的可能性。
这项前瞻性观察性研究纳入了85例连续转诊至三级医疗晕厥诊所的OH患者（58名女性，年龄49±23岁）。所有患者左心室收缩和舒张功能正常，临床和实验室检查结果与血容量正常或轻度血容量不足一致。85例患者中有45例（53%）确定了OH病因。
在其余40例病因不明的OH患者（21名女性，年龄57±16岁）中，40例中有6例（15%）血浆NT-proBNP水平意外升高（分别为14000、5210、2570、7990、3480和6680 pg/mL）。相比之下，其余34例病因不明的OH患者和45例病因明确的OH患者的NT-proBNP值均正常（即<300 pg/mL）。在随访8至12个月时，初始NT-proBNP升高的患者对容量补充治疗的需求随着NT-proBNP浓度的逐渐下降而减少。
在部分患者中，BNP或NT-proBNP水平显著升高可能与症状性OH相关，并可能导致症状性OH。
