Abstract 15505: Elevated Plasma Levels of Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 and Myeloperoxidase in Patients With Takotsubo Cardiomyopathy
Background: Takotsubo cardiomyopathy (TC) is characterized by left ventricular apical ballooning and intact coronary arteries. The pathogenesis of this disorder is likely to be catecholamine-mediated myocyte damage, microvascular dysfunction and subsequent oxidative stress; however, a number of possible alternative theories have been suggested. Circulating levels of soluble lectin-like oxidized low-density lipoprotein receptor-1 (sLOX-1) are recognized as a useful biomarker for acute coronary syndrome. In addition, myeloperoxidase (MPO), a member of the heme peroxidase superfamily, may play a key role in plaque instability. The aim of this study was to compare plasma sLOX-1 and MPO levels between TC patients and patients with coronary artery disease.
Methods: Plasma sLOX-1 and MPO levels were measured in patients with TC (n=30), stable angina pectoris (SAP, n=66) and unstable angina pectoris (UAP, n=72) using a sandwich ELISA method.
Results: Plasma sLOX-1 levels and MPO levels were significantly higher in TC patients compared with SAP patients (P<0.0001) or UAP patients (P<0.01). In TC patients, plasma sLOX-1 levels were positively correlated with neutrophil count and NT-BNP levels (neutrophil count, R=0.49, P<0.01; NT-BNP, R=0.69, P<0.0002). Moreover plasma sLOX-1 levels were positively correlated with plasma MPO levels (R=0.53, P=0.0053). However they were not correlated with serum C-reactive protein levels. Additionally, there was a tendency for plasma sLOX-1 levels to be negatively correlated with left ventricular ejection fraction (R=0.38, P=0.052).
Conclusions: This study demonstrates for the first time that plasma sLOX-1 levels and MPO levels, two markers of oxidative stress, are elevated in TC patients compared with SAP and UAP patients. These findings strongly suggest that oxidative stress plays an important role in the pathophysiology of Takotsubo cardiomyopathy.
Author Disclosures: T. Matsushita: None. Y. Matsumura: None. T. Yoshiyama: None. K. Shimeno: None. R. Matsumoto: None. Y. Abe: None. K. Kamimori: None. T. Naruko: None. K. Sugioka: None. M. Nakagawa: None. M. Yoshiyama: None. M. Ueda: None.
- © 2016 by American Heart Association, Inc.