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Background: The purpose of this study was to investigate axial load resistance of the tibia depending on the thickness of tibial tuberosity osteotomy in medial open-wedge distal tuberosity proximal tibial osteotomy (OWDTO). The hypothesis is that a thin tibial tuberosity osteotomy shows high axial load resistance of the tibia., Methods: The OWDTO model was constructed from imitation bones of the tibia. Distal tibial tuberosity osteotomy was performed with thicknesses of 7, 14, and 21 mm (n = 5 for each group). Cyclic axial-load fatigue tests were performed to investigate the strain at five measurement points on the OWDTO model. An axial-load failure test was also performed to investigate the maximum strain for failure., Results: The 7-mm OWDTO model showed a significantly lower stain range than the 14-mm model at the middle part of the lateral hinge (P = 0.0263, mean difference: -852.6 με), posterior part (P = 0.0465, mean difference: -1040.0 με), posterior tibial cortex (P < 0.0001, mean difference: -583.4 με), and plate (P = 0.0029, mean difference: -121.6 με). There were no significant differences in the strain at the tibial tuberosity between the groups. The axial load for complete failure was significantly higher in the 7-mm model than in the 21-mm model (P = 0.0010, mean difference: 2577.0 N). The failure points were at the lateral hinges., Conclusions: Thinner distal tibial tuberosity osteotomy is more resistant to axial load and may be recommended for the prevention of tibial and lateral hinge fractures after OWDTO., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Background: B-type natriuretic peptide (BNP) has been widely used for the diagnosis of heart failure, its severity, and prognosis. However, little is known about factors related to disproportionately low BNP levels even during acute heart failure conditions., Methods and Results: Among 424 patients hospitalized for acute heart failure, we categorized the patients into the HFpEF (LVEF > 50%) or HFrEF (LVEF ≤ 50%) group and subdivided them into disproportionately low BNP (LB) group and high BNP (HB) group using a cut-off BNP level of 200 pg/mL at admission. The proportion of patients with LB was higher in the HFpEF group (22.2%) than in the HFrEF group (10.9%, p = 0.002). Patients with LB had a high BMI, lower blood pressure, and history of previous cardiovascular surgery in the HFpEF group, while patients in the HFrEF group had a high BMI and smaller left ventricular end-diastolic volume index. Furthermore, presence of LB in the HFrEF group was related to good prognosis, but LB in the HFpEF group was an indicator of poor prognosis as HB group., Conclusions: The factors associated with LB were different between the HFpEF and HFrEF groups. LB was related to good prognosis in HFrEF, but not in HFpEF., Competing Interests: Declaration of Competing Interest The authors declare that they have no conflicts of interest., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Several studies have shown that subjects with higher serum bilirubin may have a lower risk of cardiovascular disorders. We herein investigated whether serum bilirubin concentration is associated with lower extremity ischemia among cardiology patients. In total, 935 patients without a history of angioplasty or bypass surgery of the lower limb arteries and who had bilateral ankle-brachial index measurements were included in the study. Peripheral arterial disease (PAD) was defined to be present when ABI of either or both sides was <0.9. Overall, the serum total bilirubin concentration ranged between 0.1 and 2.7mg/dL (normal range, 0.1-1.0mg/dL). Across the bilirubin tertiles, age did not differ significantly. On the other hand, male patients (median 0.6mg/dL, interquartile range (IQR) 0.4-0.7mg/dL) had significantly higher bilirubin levels than female patients (median 0.5mg/dL, IQR 0.4-0.7mg/dL, P=0.014). Logistic regression analysis showed that, as compared with the lowest bilirubin tertile (0.1-0.4mg/dL), the highest tertile (0.7-2.7mg/dL) was significantly negatively associated with prevalent PAD after adjusting for sex, age, eGFR, white blood cell count, inorganic phosphate, HbA1C, total and HDL cholesterol, triglycerides, current smoking, diabetic medication, and statin use. This association remained significant when only those with serum bilirubin in the normal range were included in the analysis. Among cardiology patients, serum bilirubin concentration was significantly negatively associated with prevalence of PAD. The underlying mechanism and therapeutic indications should be investigated in further investigations., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Infected aortic aneurysm and inflammatory aortic aneurysm each account for a minor fraction of the total incidence of aortic aneurysm and are associated with periaortic inflammation. Despite the similarity, infected aortic aneurysm generally shows a more rapid change in clinical condition, leading to a fatal outcome; in addition, delayed diagnosis and misuse of corticosteroid or immunosuppressing drugs may lead to uncontrolled growth of microorganisms. Therefore, it is mandatory that detection of aortic aneurysm is followed by accurate differential diagnosis. In general, infected aortic aneurysm appears usually as a saccular form aneurysm with nodularity, irregular configuration; however, the differential diagnosis may not be easy sometimes for the following reasons: (1) symptoms, such as abdominal and/or back pain and fever, and blood test abnormalities, such as elevated C-reactive protein and enhanced erythrocyte sedimentation rate, are common in infected aortic aneurysm, but they are not found infrequently in inflammatory aortic aneurysm; (2) some inflammatory aortic aneurysms are immunoglobulin (Ig) G4-related, but not all of them; (3) the prevalence of IgG4 positivity in infected aortic aneurysm has not been well investigated; (4) enhanced uptake of 18F-fluorodeoxyglucose (FDG) by 18F-FDG-positron emission tomography may not distinguish between inflammation mediated by autoimmunity and that mediated by microorganism infection. Here we discuss the characteristics of these two forms of aortic aneurysm and the points of which we have to be aware before reaching a final diagnosis., (Copyright © 2011 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.)

Aims: Recurrent hypoxia due to sleep apnea syndrome is implicated in cardiovascular events, especially in diabetic patients, but the underlying mechanisms remain controversial. We previously reported that angiotensin II receptor blockers can improve hypoxia-induced left ventricular remodeling. The aim of this study was to examine the effect on left ventricular remodeling of adding a calcium channel blocker to angiotensin II receptor blocker therapy in diabetic mice exposed to recurrent hypoxia., Main Methods: Male db/db mice (8-week-old) and age-matched control db/+ mice were fed a Western diet and subjected to recurrent hypoxia (oxygen at 10+/-0.5% for 8h daily during the daytime) or normoxia for 3weeks. Hypoxic db/db mice were treated with the vehicle, olmesartan (3mg/kg/day), nifedipine (10mg/kg/day), or both drugs., Key Findings: Recurrent hypoxia caused hypertrophy of cardiomyocytes, interstitial fibrosis, and a significant increase in expression of the oxidative stress marker 4-hydroxy-2-nonenal (4-HNE) in the left ventricular myocardium. Treatment with olmesartan, nifedipine, or both drugs had no effect on systolic blood pressure, and each treatment achieved similar suppression of 4-HNE expression. Olmesartan and the combination with olmesartan and nifedipine significantly prevented cardiomyocyte hypertrophy more than treatment with nifedipine alone. On the other hand, olmesartan combined with nifedipine significantly reduced cytokine expression, superoxide production and matrix metalloproteinase (MMP)-9 activity, and significantly suppressed interstitial fibrosis in the left ventricular myocardium., Significance: The combination with olmesartan and nifedipine, as well as a monotherapy with olmesartan, exerts preferable cardioprotection in diabetic mice exposed to recurrent hypoxia., (Copyright 2010 Elsevier Inc. All rights reserved.)

Because of the importance of long-chain fatty acids (LCFAs) as a myocardial energy substrate, myocardial LCFA metabolism has been of particular interest for the understanding of cardiac pathophysiology. Recently, by using radiolabeled LCFA analogues, myocardial LCFA metabolism has been clinically evaluated, which revealed a total defect of myocardial LCFA accumulation in a small number of subjects. The mechanism for the cellular LCFA uptake process is still disputable, but recent results suggest that fatty acid translocase (FAT)/CD36 is a transporter in the heart. In the present study, we analyzed mutations and protein expression of the FAT/CD36 gene in 47 patients who showed total lack of the accumulation of a radiolabeled LCFA analogue in the heart. All the patients carried two mutations in the FAT/CD36 gene, and expression of the FAT/CD36 protein was not detected on either platelet or monocyte membranes. Our results showed the link between mutations of the FAT/CD36 gene and a defect in the accumulation of LCFAs in the human heart.

We have previously reported that serum and/or urinary human heart-type cytoplasmic fatty acid-binding protein (HH-FABPc) can be used as an early indicator of myocardial injury (Clin Biochem 1991; 24: 195-201). To confirm the usefulness of HH-FABPc as an early diagnostic indicator of acute myocardial infarction (AMI), its serum and urinary levels were measured in samples obtained within 6 h after the onset of acute coronary syndrome related symptoms. Samples were collected from 97 patients, who were composed of 63 with AMI, 24 with unstable angina and 10 with chest pain syndrome. The positivity of serum and urinary HH-FABPc and cardiac creatine kinase isozyme MB (CK-MB) was analyzed in these samples. Serum HH-FABPc levels in AMI were above normal in 91.4% (64/70) of the samples tested within 3 h of the onset of symptoms and in 100% (111/111) of those tested at 3-6 h. Elevated urinary HH-FABPc levels in AMI were obtained in 88.9% (8/9) of samples at 0-3 h and in 75% (6/8) at 3-6 h. CK-MB activity in AMI was positive in 20% (8/40) and 66.3% (53/80) of serum samples at 0-3 h and 3-6 h, respectively. HH-FABPc was always positive when a serum sample was positive for CK-MB. Serum HH-FABPc at 0-6 h in chest pain syndrome and in unstable angina were positive in 17.8% (5/28) and 56.7% (34/60), respectively. The elevated HH-FABPc in serum and urine was noted much earlier than that of CK-MB during the hyperacute phase of AMI. HH-FABPc showed high positive value in unstable angina, but it was low in normal coronary patients having chest pain. However, HH-FABPc level in unstable angina and chest pain syndrome was lower than that of AMI. Thus, HH-FABPc may be a valuable indicator for the diagnosis of hyperacute myocardial infarction.