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Purpose Plasma lipoprotein-associated phospholipase A₂ (Lp-PLA₂) binds to low-density lipoprotein. The levels of Lp-PLA₂ reflect the plaque burden, and are upregulated in acute coronary syndrome (ACS). We investigated the diagnostic value of Lp-PLA2 levels and found that it might be a potential biomarker for ACS. Materials and methods We classified 226 study participants into three groups: patients without significant stenosis (control group), patients with significant stenosis with stable angina (SA group), and patients with ACS (ACS group). Results Lp-PLA₂ and high-sensitivity C-reactive protein (hs-CRP) levels were significantly greater in the ACS group than in the SA group (p=0.044 and p=0.029, respectively). Multivariate logistic regression analysis revealed that Lp-PLA₂ levels are significantly associated with ACS (odds ratio=1.047, p=0.013). The addition of Lp-PLA₂ to the ACS model significantly increased the global χ² value over traditional risk factors (28.14 to 35.602, p=0.006). The area under the receiver operating characteristic curve for Lp-PLA₂ was 0.624 (p=0.004). The addition of Lp-PLA₂ level to serum hs-CRP concentration yielded an integrated discrimination improvement of 0.0368 (p=0.0093, standard error: 0.0142) and improved the ability to diagnose ACS. Conclusion Lp-PLA₂ levels are related to plaque stability and might be a diagnostic biomarker for ACS.

Procoagulant or impaired fibrinolytic states as well as inflammatory reactions mediated by cytokines are likely involved in the pathogenesis of acute ischemic stroke. We examined the potential relationship between interleukin 6 (IL-6) and hemostatic markers. The procoagulant and fibrinolytic states were assessed in 46 patients with acute stroke by measuring plasma levels of plasminogen activator inhibitor-1 (PAI-1), thrombin-antithrombin complex (TAT), and plasminogen-antiplasmin complex (PAP). Circulating IL-6 levels were measured using ELISA (Quantikine, R and D systems, MN, USA). Circulating IL-6 (mean, 26.5 pg/mL) and PAI-1 (mean, 19.9 ng/mL) levels were higher in patients with acute stroke than in healthy subjects (mean, 3.0 pg/mL, 10.4 ng/mL, respectively). TAT levels were statistically different according to the etiologic subtypes of stroke (atherogenic, 2.5 ng/mL; lacunar 3.2 ng/mL; cardiogenic 9.9 ng/mL, p = 0.021). Neither procoagulant levels nor fibrinolytic markers significantly correlated with circulating IL-6 levels. Our findings suggest that elevated proinflammatory cytokines during the initial hours of ischemic stroke may be an independent pathogenic factor or a consequence of the thrombotic event with no relationship to the procoagulant or fibrinolytic states.

Here, we evaluate the efficacy of the Clo-Sur PAD nonwoven hydrophilic wound dressing (HWD) on hemostasis in an arterial-access site after transradial percutaneous coronary angiography compared with the RadiStop compression device (CD). Eighty patients who had undergone transradial coronary angiography with or without intravascular ultrasound were randomly assigned to the HWD or CD group. The time required to achieve hemostasis was measured, and the incidence of vascular complications was assessed. No significant differences in clinical and procedural characteristics were observed between the HWD group (n = 40) and the CD group (n = 40). A significant reduction in the time required to achieve hemostasis (58.7 +/- 32.6 minutes versus 131.3 +/- 59.1 minutes; p0.001) was associated with the use of HWD. The incidence of vascular complications was similar in both groups (5% for HWD versus 2.5% for CD; p = 0.500). No major complications, such as large hematoma or acute radial occlusion, occurred in the HWD group. In conclusion, HWD represents a safe alternative to the compression method. Hemostasis can be achieved more quickly using HWD, with no increase in access site complications, as compared to CD.

Small dense LDL (sd-LDL) has recently emerged as an important coronary artery disease (CAD) risk factor. This study was performed to investigate how LDL particle size is related to CAD and acute coronary syndrome (ACS). Blood samples were collected from 504 patients that underwent coronary angiography to evaluate chest pain. The LDL particle size of these samples was measured. The mean LDL particle size was smaller in patients with angiographically proven CAD than in the controls (26.41 ± 0.95 vs 26.73 ± 0.64 nm, p < 0.001), and was negatively correlated with the Framingham risk score (r = -0.121, p = 0.007). Patients with more extensive CAD had smaller LDL particles. LDL particle size was also smaller in patients with acute coronary syndrome as compared to non-ACS patients (26.09 ± 1.42 vs 26.54 ± 0.63 nm, p = 0.011). These results suggest that sd-LDL is independently associated with the incidence and extent of CAD, and can be a risk factor for the development of ACS in the Korean population.

The hepatopulmonary syndrome (HPS) is defined as the triad of liver disease, pulmonary gas exchange abnormalities leading to arterial deoxygenation, and widespread pulmonary vascular dilatation. Although both acute and chronic liver diseases have been associated with HPS, most commonly it is associated with cirrhosis. Portal hypertension seems to be the predominant factor related to this syndrome. The hallmark of pulmonary vascular changes in HPS is dilated vessels at the precapillary and capillary level and direct arteriovenous communications. This causes right-to-left shunting of blood flow, mismatch between ventilation and perfusion, and diffusion limitation. Contrast transthoracic echocardiography may be the only diagnostic test to demonstrate right-to-left shunt in these patients. It is performed by intravenous injection of agitated saline as an echocardiographic contrast, while visualizing the atria. In the case of HPS, contrast appears in the left atrium 2 to 5 s after it is seen in the right atrium. Case Report