BackgroundFibroblast growth factor 23 (FGF23), with its co-receptor Klotho, plays a crucial role in phosphate metabolism. Several recent studies suggested that circulating FGF23 and α-Klotho concentrations might be related to cardiovascular abnormalities in patients with advanced renal failure.PurposeUsing data from 100 cardiology inpatients who were not undergoing chronic hemodialysis, the association of circulating levels of FGF23, α-Klotho, and other calcium-phosphate metabolism-related parameters with the left ventricular ejection fraction (LVEF) and left ventricular mass (LVM) was analyzed.Methods and ResultsLVEF was measured using the modified Simpson method for apical 4-chamber LV images and the LVM index (LVMI) was calculated by dividing the LVM by body surface area. Univariate analysis showed that log transformed FGF23, but not that of α-Klotho, was significantly associated with LVEF and LVMI with a standardized beta of −0.35 (P<0.001) and 0.26 (P<0.05), respectively. After adjusting for age, sex, estimated glomerular filtration rate, and serum concentrations of intact parathyroid hormone, and 25-hydroxyvitamin D as covariates into the statistical model, log-transformed FGF23 was found to be a statistically positive predictor for decreased left ventricular function and left ventricular hypertrophy.ConclusionsIn cardiology department inpatients, circulating FGF23 concentrations were found to be associated with the left ventricular mass and LVEF independent of renal function and other calcium-phosphate metabolism-related parameters. Whether modulation of circulating FGF23 levels would improve cardiac outcome in such a high risk population awaits further investigation.

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BackgroundSeveral studies have shown that serum uric acid (UA) is associated with left ventricular (LV) hypertrophy. Serum levels of parathyroid hormone (PTH), which has bbe shown to be correlated with UA, is also known to be associated with cardiac hypertrophy; however, whether the association between UA and cardiac hypertrophy is independent of PTH remains unknown.PurposeWe investigated whether the relationship between serum uric acid (UA) and LV hypertrophy is independent of intact PTH and other calcium-phosphate metabolism-related factors in cardiac patients.Methods and ResultsIn a retrospective study, the association between UA and left ventricular mass index was assessed among 116 male cardiac patients (mean age 65±12 years) who were not taking UA lowering drugs. The median UA value was 5.9 mg/dL. Neither age nor body mass index differed significantly among the UA quartile groups. Patients with higher UA levels were more likely to be taking loop diuretics. UA showed a significant correlation with intact PTH (R = 0.34, P<0.001) but not with other calcium-phosphate metabolism-related factors. Linear regression analysis showed that log-transformed UA showed a significant association with left ventricular mass index, and this relationship was found to be significant exclusively in patients who were not taking loop and/or thiazide diuretics. Multivariate logistic regression analysis showed that log-transformed UA was independently associated with LV hypertrophy with an odds ratio of 2.79 (95% confidence interval 1.48–5.28, P = 0.002 per one standard deviation increase).ConclusionsAmong cardiac patients, serum UA was associated with LV hypertrophy, and this relationship was, at least in part, independent of intact PTH levels, which showed a significant correlation with UA in the same population.

A 52-year-old man was admitted to our hospital due to shortness of breath that developed one week after the diagnosis of influenza infection. He had a past history of myocarditis associated with influenza B infection 16 years before the current admission. The patient's left ventricular function showed diffuse hypokinesis with a left ventricular ejection fraction of 28%. Due to the progression of heart failure, the infusion of catecholamines and insertion of an intra-aortic balloon pump were required. The patient was discharged uneventfully on the 23rd hospital day. A significant increase in the serum antibody titer against influenza A virus subtype H3N2 led to a diagnosis of recurrent fulminant influenza myocarditis.

SummaryThe role of pentraxin 3 (PTX3) has been implicated in the process of plaque vulnerability. However, few studies have addressed the direct relationship between plaque morphology and plasma PTX3. We evaluated the relationship between coronary vulnerable plaque, assessed by optical coherence tomography (OCT), and plasma PTX3 in patients with coronary artery disease (CAD).OCT was used to determine plaque vulnerability in 51 patients with non-ST segment elevation acute coronary syndrome (NSTE-ACS; n = 17) and stable angina (SA; n = 34). Both highly-sensitive C-reactive protein and systemic plasma PTX3 were measured.Based on the OCT findings, patients were divided into 3 groups; a fibrous plaque (n = 18), thick-cap fibroatheroma (ThCFA) (n = 19), and thin-cap fibroatheroma (TCFA) (n = 14) groups. ThCFA was defined as a lipid-rich plaque (lipid content in ≥ 2 quadrant) covered with ≥ 65 μm thick fibrous cap, and TCFA was that with < 65 μm. There were no differences in patient characteristics between the 3 groups except for the presence of ACS and eicosapentaenoic acid levels. TCFA was more frequently observed with plaque rupture and intraluminal thrombus compared with the other 2 groups. Plasma PTX3 levels were higher in the TCFA group compared with the fibrous plaque and ThCFA groups, and showed weak correlation with cap thickness.Plasma PTX3 level was associated with plaque vulnerability assessed by OCT in patients with CAD. (Int Heart J 2016; 57: 18-24)