Lipoprotein(a) stimulates the proliferation of cultured human arterial smooth muscle cells through two pathways

AbstractWe investigated the effect of lipoprotein(a) (Lp(a)) on proliferation of human arterial smooth muscle cells (SMCs) and its mechanisms of action. Low density lipoprotein (LDL), Lp(a) and apolipoprotein(a) (apo(a)) significantly stimulated the proliferation of SMCs. Lp(a) and apo(a) reduced the amount of active transforming growth factor-β (TGF-β) with the mink lung epithelial cell bioassay, however LDL had no effect. Lp(a), but not apo(a), significantly stimulated the proliferation of SMCs even in the presence of a neutralizing antibody for TGF-β. Our results suggest that Lp(a) stimulates the proliferation of SMCs via apo(a)-induced inhibition of TGF-β activation and stimulation of SMCs by the LDL-particle of Lp(a)

Papillary Muscle Dysfunction Attenuates Ischemic Mitral Regurgitation in Patients With Localized Basal Inferior Left Ventricular Remodeling Insights From Tissue Doppler Strain Imaging

ObjectivesThe purpose of this research was to test whether papillary muscle (PM) dysfunction attenuates ischemic mitral regurgitation (MR) in patients with left ventricular (LV) remodeling of a similar location and extent.BackgroundPapillary muscle dysfunction could attenuate tethering and MR because of PM elongation. However, variability in the associated LV remodeling, which exaggerates tethering, can influence the relationship between PM dysfunction and MR.MethodsIn 40 patients with a previous inferior myocardial infarction but without other lesions, the LV volume, sphericity, PM tethering distance, PM longitudinal systolic strain, and MR fraction were quantified by echocardiography. The patients were divided into two groups: group 1 with significant basal inferoposterior LV bulging but without advanced LV bulging involving other territories, therefore with a similar location and extent of LV remodeling, and group 2 without significant LV bulging.ResultsThe medial PM tethering distance was significantly correlated with the %MR fraction (r2= 0.64, p < 0.01), and multiple regression analysis identified an increase in the tethering distance as the only independent determinant of the MR fraction in all subjects and also in group 1. The PM longitudinal systolic strain had no significant relationships with MR fraction in all subjects with variable degrees of LV remodeling, but it had a significant inverse correlation with the MR fraction (r2= 0.33, p < 0.01) in group 1 with LV remodeling of a similar location and extent, indicating that PM dysfunction is associated with less MR.ConclusionsPapillary muscle dysfunction, reducing its longitudinal contraction to induce leaflet tethering, attenuates ischemic MR in patients with basal inferior LV remodeling