Simultaneous evaluation of fatty acid and triglycerides after percutaneous coronary intervention.

BACKGROUND: Clinical studies have shown that the ratio of eicosapentaenoic acid to arachidonic acid (EPA/AA ratio) as well as the triglyceride (TG) levels can be considered as independent risk factors for cardiovascular diseases. The aim of this study was to investigate whether simultaneous evaluation of the EPA/AA ratio and TG level can affect the incidence of cardiovascular events after percutaneous coronary intervention (PCI). METHODS AND RESULTS: We retrospectively examined the clinical records of 1585 patients who underwent successful PCI for acute coronary syndrome or stable angina. They were divided into four categories based on an EPA/AA ratio of 0.4 and a TG level of 150 mg/dl (a method termed the "Fatty Acid Window"). Among the four categories, the incidence of major adverse cardiac events (MACE) was measured for a maximum of five years after PCI. MACE was defined as cardiac death, non-fatal myocardial infarction, or revascularization due to new coronary stenosis or restenosis. The Kaplan-Meier method and the Cox proportional hazards regression analysis demonstrated that patients with both lower EPA/AA ratios and higher TG levels had a significantly higher incidence of MACE. In addition, patients with either lower EPA/AA ratios or higher TG levels also had a higher incidence of MACE compared to patients with both higher EPA/AA ratios and lower TG levels. CONCLUSION: Evaluating both EPA/AA ratios and TG levels, a method termed the "Fatty Acid Window", can be useful in predicting the occurrence of cardiovascular events after PCI.

Relationship between serum uric acid levels and the incidence of cardiovascular events after percutaneous coronary intervention.

BACKGROUND: The role of serum uric acid (SUA) as an independent risk factor for coronary artery disease remains unclear. The aim of this study was to investigate whether the SUA levels could affect the incidence of major adverse cardiac events (MACE) after percutaneous coronary intervention (PCI). METHODS AND RESULTS: We retrospectively examined the clinical records of 1,949 patients who underwent successful PCI. First, they were divided into two groups based on an SUA level of 7.0mg/dl. Among the two groups, the incidence of MACE was measured for a maximum of 5 years after PCI. Next, we divided them into 6 groups at SUA intervals of 1.0mg/dl and estimated the hazard ratios of each group. The Kaplan-Meier curve demonstrated that patients with SUA levels of >7.0mg/dl had a higher incidence of MACE than those with 7.0mg/dl or less. However, according to the multivariate analysis, the SUA level was not significantly correlated with the incidence of MACE because other factors could strongly affect it. Meanwhile, the group with SUA levels between 4.1-5.0mg/dl had a lower hazard ratio compared to groups with SUA levels of more than 5.1mg/dl. However, the hazard ratio of the group with SUA levels of 4.0mg or less was not lower than that of the group with SUA levels of 4.1-5.0mg/dl. Even after adjustment for several parameters, nearly the same results before adjustment were obtained for the hazard ratios of each group. CONCLUSION: The present study demonstrated that the SUA level was one of the most valuable predictors of cardiovascular events after PCI, with elevated SUA levels adversely affecting secondary prevention.

Rab10-Positive Tubular Structures Represent a Novel Endocytic Pathway That Diverges From Canonical Macropinocytosis in RAW264 Macrophages.

Using the optogenetic photo-manipulation of photoactivatable (PA)-Rac1, remarkable cell surface ruffling and the formation of a macropinocytic cup (premacropinosome) could be induced in the region of RAW264 macrophages irradiated with blue light due to the activation of PA-Rac1. However, the completion of macropinosome formation did not occur until Rac1 was deactivated by the removal of the light stimulus. Following PA-Rac1 deactivation, some premacropinosomes closed into intracellular macropinosomes, whereas many others transformed into long Rab10-positive tubules without forming typical macropinosomes. These Rab10-positive tubules moved centripetally towards the perinuclear Golgi region along microtubules. Surprisingly, these Rab10-positive tubules did not contain any endosome/lysosome compartment markers, such as Rab5, Rab7, or LAMP1, suggesting that the Rab10-positive tubules were not part of the degradation pathway for lysosomes. These Rab10-positive tubules were distinct from recycling endosomal compartments, which are labeled with Rab4, Rab11, or SNX1. These findings suggested that these Rab10-positive tubules may be a part of non-degradative endocytic pathway that has never been known. The formation of Rab10-positive tubules from premacropinosomes was also observed in control and phorbol myristate acetate (PMA)-stimulated macrophages, although their frequencies were low. Interestingly, the formation of Rab10-positive premacropinosomes and tubules was not inhibited by phosphoinositide 3-kinase (PI3K) inhibitors, while the classical macropinosome formation requires PI3K activity. Thus, this study provides evidence to support the existence of Rab10-positive tubules as a novel endocytic pathway that diverges from canonical macropinocytosis.