Arteriosclerosis, particularly aortosclerosis, is the most critical risk factor associated with cardiovascular, cerebrovascular, and renal diseases. The pulsatile hemodynamics in the central aorta consists of blood pressure, flow, and stiffness and substantially differs from the peripheral hemodynamics in muscular arteries. Arteriosclerotic changes with age appear earlier in the elastic aorta, and age-dependent increases in central pulse pressure are more marked than those apparent from brachial pressure measurement. Central pressure can be affected by lifestyle habits, metabolic disorders, and endocrine and inflammatory diseases in a manner different from brachial pressure. Central pulse pressure widening due to aortic stiffening increases left ventricular afterload in systole and reduces coronary artery flow in diastole, predisposing aortosclerotic patients to myocardial hypertrophy and ischemia. The widened pulse pressure is also transmitted deep into low-impedance organs such as the brain and kidney, causing microvascular damage responsible for lacunar stroke and albuminuria. In addition, aortic stiffening increases aortic blood flow reversal, which can lead to retrograde embolic stroke and renal function deterioration. Central pressure has been shown to predict cardiovascular events in most previous studies and potentially serves as a surrogate marker for intervention. Quantitative and comprehensive evaluation of central hemodynamics is now available through various noninvasive pressure/flow measurement modalities. This review will focus on the clinical usefulness and mechanistic rationale of central hemodynamic measurements for cardiovascular risk management.

Endothelial dysfunction is one of the hallmarks of atherogenesis, and correlates with many cardiovascular risk factors. One of the features of endothelial dysfunction is the loss of nitric oxide (NO) bioavailability, resulting in derangements in the vasodilatory response of the vessel wall. Flow mediated dilatation (FMD) of the brachial artery is an accepted method for non-invasive assessment of systemic endothelial function. FMD is examined extensively in the context of cardiovascular research, and has been utilised as a routine assessment in large cohorts such as the Framingham Heart Study, Young Finns Study, and Gutenberg Heart Study. However, FMD is less known in the context of vascular surgery research, despite the similarities between the underpinning disease mechanisms. This review will provide a summary of FMD in terms of its history of development and the conduct of the test in research settings. It will further highlight the key literature of FMD as a biomarker for vascular surgeons, particularly in the context of abdominal aortic aneurysms and lower limb peripheral arterial disease.

Aims: Adiponectin, an adipocyte-specific secretory protein, abundantly exists in the blood stream while its concentration paradoxically decreases in obesity. Hypoadiponectinemia is one of risks of cardiovascular diseases. However, impact of serum adiponectin concentration on acute ischemic myocardial damages has not been fully clarified. The present study investigated the association of serum adiponectin and creatine kinase (CK)-MB levels in subjects with ST-segment elevation myocardial infarction (STEMI).

Methods: This study is a physician-initiated observational study and is also registered with the University Hospital Medical Information Network (Number: UMIN 000014418). Patients were admitted to Senri Critical Care Medical Center, given a diagnosis of STEMI, and treated by primary percutaneous coronary intervention (PCI). Finally, 49 patients were enrolled and the association of serum adiponectin, CK-MB, and clinical features were mainly analyzed.

Results: Serum adiponectin levels decreased rapidly and reached the bottom at 24 hours after recanalization. Such reduction of serum adiponectin was inversely correlated with the area under the curve (AUC) of serum CK-MB (p=0.013). Serum adiponectin concentrations were inversely correlated with AUC of serum CK-MB. In multivariate analysis, serum adiponectin concentration on admission (p=0.002) and collateral (p=0.037) were significantly and independently correlated with serum AUC of CK-MB.

Conclusion: Serum AUC of CK-MB in STEMI subjects was significantly associated with serum adiponectin concentration on admission and reduction of serum adiponectin levels from baseline to bottom. The present study may provide a possibility that serum adiponectin levels at acute phase are useful in the prediction for prognosis after PCI-treated STEMI subjects.

Aim: Soluble cell adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1, E-selectin, and P-selectin, have been suggested to be associated with cardiovascular disease (CVD) risk; however, the nature and magnitude of the association between VCAM-1 and CVD risk is uncertain. We aimed to assess the association of VCAM-1 with CVD risk and determine its potential utility for CVD risk prediction.

Methods: VCAM-1 concentrations were measured at baseline in the PREVEND prospective study of 2,638 participants. Hazard ratios (95% confidence intervals [CI]) and measures of risk discrimination for CVD (e.g., C-index) and reclassification (i.e., net reclassification improvement) of participants were assessed.

Results: During a median follow-up of 9.9 years, 614 CVD events occurred. Plasma VCAM-1 was weakly associated with several cardiovascular risk markers. In analyses adjusted for established cardiovascular risk factors, the hazard ratio (95% CI) for CVD per 1 standard deviation increase in log_e VCAM-1 was 0.91 (0.84–0.99; P =0.020), which remained consistent after additional adjustment for body mass index, alcohol consumption, triglycerides, renal function, and C-reactive protein; hazard ratio (95% CI) 0.89 (0.82–0.97; P =0.006). Comparing the top versus bottom quintiles of VCAM-1 levels, the corresponding adjusted hazard ratios were 0.74 (0.57–0.96; P =0.023) and 0.70 (0.54–0.91; P =0.007) respectively. Adding VCAM-1 to a CVD risk prediction model containing conventional risk factors did not improve the C-index or net reclassification.

Conclusions: Plasma VCAM-1 is inversely and independently associated with CVD. However, VCAM-1 provides no significant improvement in CVD risk assessment beyond conventional CVD risk factors.

Aim: Poor sleep has been shown to be associated with the development of cardiovascular risk factors, such as obesity, in both adults and children. This study aimed to investigate the relationship between sleep duration and arterial stiffness indices in Japanese children and early adolescents.

Methods: The data on 102 students (56 males, 46 females; mean age, 11.9±1.8 years) were analyzed. As non-invasive arterial stiffness parameters, the cardio-ankle vascular index (CAVI) and heart-ankle pulse wave velocity (haPWV) were evaluated. Their students' sleep habits (bedtime and wake times on a usual weekday) were investigated using questionnaires, and based on these, their sleep durations were calculated.

Results: The CAVI values in the males and females were 4.8±0.9 and 4.7±0.9 (arbitrary unit), respectively. haPWV values in the males and females were 5.5±0.6 and 5.4±0.6 m/s, respectively. Sleep duration in the males, but not in the females, was negatively correlated with CAVI (r=－0.356) and haPWV (r=－0.356), suggesting that students with short sleep duration could have increased arterial stiffness. After adjusting for confounders, such as age, sex, systolic blood pressure, heart rate, adiposity, and physical fitness, the correlation of sleep duration with CAVI, but not with haPWV, was still significant (partial r=－0.253, p＜0.05).

Conclusion: Our findings suggest that shorter sleep duration influences arterial stiffening even in childhood.

Aim: Leukocyte profile has been related to clinical outcome in patients with ST-segment elevation (STE) myocardial infarction (MI). However, whether eosinophil to leukocyte ratio (ELR) predicts clinical outcome in patients who have undergone primary percutaneous coronary intervention (PCI) remains unclear. Therefore, we examined the prognostic value of ELR in this patient population.

Methods: We retrospectively analyzed the data of 331 consecutive patients who underwent primary PCI for STEMI between January 2009 and March 2015. All leukocyte types were counted and ELR was calculated for all patients 24 h after hospital admission. The primary study endpoint was major adverse cardiac events (MACEs) within up to one year of follow-up duration.

Results: MACEs including cardiac deaths in 9.4% of the patients, MI in 1.5%, and target lesion or vessel revascularization in 10.3%, occurred within one year in 68 patients (20.5%). The mean ELR was significantly lower in patients with MACEs than in patients without MACEs (0.20±0.51 vs.0.49±0.66, respectively; p＜0.001). An ELR ＜0.1 at 24 h was identified as the best cut-off value for mortality prediction. Multivariate analysis identified that an ELR ＜0.1 (odds ratio [OR]=0.38; 95% confidence interval [CI]=0.22–0.67; p＜0.001) and chronic kidney disease (OR=2.38; CI=1.33–4.24; p=0.003) are independent predictors of MACEs.

Conclusion: In primary PCI patients with STEMI, ELR at 24 h was an independent predictor of MACEs in addition to the usual coronary risk factors and commonly used biomarkers.

Aims: In chronic diseases, keeping adherence to medication is very difficult. The objective of this study was to evaluate the impact of administration timing simplification protocol (ATSP) on medication adherence and clinical parameters of cardiovascular diseases.

Methods: 210 out-patients with cardiovascular disease, who were taking two or more pills of any type of medication per day for more than one year, were enrolled and randomized. The intervention group followed the simplified administration schedule of ATSP with two main strategies: 1) moving medication from “pc” (30 minute after meal) to “stat. pc” (immediately after meal); and 2) moving medication time from “at evening” to “at morning.” In contrast, the control group maintained the same medication schedule. Both patient groups were equally educated about the names and effects of the medication.

Results: The intervention group had more pills than the control group with marginal statistical significance (5.1±2.3 vs 4.6±1.8, p=0.05). The total frequency of administration was significantly higher in the intervention group than that of the control group (2.9±1.0 vs 2.6±0.9, p=0.03) at the baseline. In the intervention group, the frequency was significantly decreased to 1.5±0.6 times per day after following ATSP application (p＜0.01). In both patient groups, knowledge about the medication was significantly improved by education. However, medication adherence was only improved in the intervention group. Interestingly, total cholesterol was significantly decreased in the intervention group (p＜0.01). The decrease in serum cholesterol concentration was significantly correlated with the improvement in medication adherence evaluated with Morisky Medication Adherence Scale (MMAS)-8 items (r=0.507, p＜0.01).

Conclusion: ATSP was shown to be an effective strategy to improve medication adherence in chronic cardiovascular disease patients.

Aim: Circulating levels of high-density lipoprotein cholesterol (HDL-C) are decreased in patients with heart failure (HF). We tested whether HDL-C serum levels are associated with cardiac contractile dysfunction in a minipig HF model.

Methods: Blood samples were collected from 13 adult male minipigs: 1) before pacemaker implantation, 2) 10 days after surgery, and 3) 3 weeks after high-rate LV pacing. Serum cholesterol efflux capacity (CEC), an index of HDL functionality, was assessed through four mechanisms: ATP Binding Cassette transporter A1 (ABCA1), ATP Binding Cassette transporter G1 (ABCG1), Scavenger Receptor-Class B Type I (SR-BI) and Passive Diffusion (PD).

Results: HDL-C serum levels significantly decrease in minipigs with HF compared with baseline (p＜0.0001). Serum CEC mediated by PD and SR-BI, but not ABCA1 or ABCG1, significantly decrease in animals with HF (p＜0.05 and p＜0.005, respectively).

Discussion: HDL-C serum levels and partial serum CEC reduction may play a pathophysiological role in the cardiac function decay sustained by high-rate LV pacing, opening new avenues to understand of the pathogenesis of nonischemic myocardial remodeling.

Aim: Early intervention before the progression of chronic kidney disease (CKD) is essential to prevent end-stage renal disease (ESRD) and cardiovascular complications. This study evaluated the correlation between metabolic and lifestyle-related factors and the decline of estimated glomerular filtration rate (eGFR) over 1 year in a Japanese population without CKD.

Methods: Subjects who received two consecutive annual health checkups from 2013 to 2015 were involved. Factors associated with eGFR decline were identified using multiple regression models.

Results: A total of 2531 subjects aged 58.9±11.7 years old were included in this study. Baseline levels of HDL-C and ApoA1 correlated with the eGFR decline over 1 year defined as eGFR reduction rate of 15% or more and/or eGFR at the next year ＜60 ml/min/m² (odds ratio (OR) 0.87 (per 10 mg/dl); 95% CI, 0.80–0.94; p=0.0012, 0.90 (per 10 mg/dl); 0.86–0.96; p=0.0004, respectively). A U-shaped relationship between the eGFR decline and HDL-C or ApoA1 levels was not observed in non-CKD population of this study. Metabolic syndrome was significantly associated with eGFR decline (OR 1.32; 1.04–1.67; p=0.0205), although obesity-related factors did not show a significant correlation with eGFR decline over 1 year.

Conclusion: Low HDL-C and ApoA1 levels significantly correlated with eGFR decline in a short period of 1 year. Metabolic syndrome also showed a significant association with eGFR decline. This study suggests the importance of hypertension and low HDL-C in the metabolic syndrome effect on eGFR decline rather than obesity in non-CKD population.