Background: F-fluorodeoxyglucose (FDG) positron emission tomography (PET) is a promising modality for detecting active lesions of cardiac sarcoidosis (CS). However, determining whether ¹⁸F-FDG uptake in the myocardium is physiological is challenging due to metabolic shift in myocardial cells. Although methods for inhibiting physiological myocardial ¹⁸F-FDG uptake have been proposed, no standard methods exist. This study therefore aimed to compare the effect of an 18-h fast (long fasting (LF)) with heparin loading plus a 12-h fast (HEP) before ¹⁸F-FDG PET scan. Methods: We analyzed the effects of LF and HEP on the inhibition of physiological myocardial ¹⁸F-FDG uptake in healthy subjects (18 in HEP and 19 in LF) and in patients with known or suspected CS (96 in HEP and 69 in LF). In CS, the lower uptake of ¹⁸F-FDG in the myocardium was evaluated. A visual four-point scale was used to assess myocardial ¹⁸F-FDG uptake in comparison with hepatic uptake (1 lower, 2 similar, 3 somewhat higher, 4 noticeably higher). Results: Myocardial ¹⁸F-FDG uptake was 1.68 ± 1.06 in LF and 3.17 ± 1.16 in HEP in healthy subjects (p < 0.0001), whereas it was 1.48 ± 0.99 in LF and 2.48 ± 1.33 in HEP in CS patients (p < 0.0001). Logistic regression and regression trees revealed the LF was the most effective in inhibiting myocardial ¹⁸F-FDG uptake. In addition, serum free fatty acid levels on intravenous ¹⁸F-FDG injection were a possible biomarker. Conclusions: LF is effective in inhibiting myocardial ¹⁸F-FDG uptake, and consequently, it could be useful for evaluating active lesions of CS in ¹⁸F-FDG PET images.

Background— Insulin resistance is associated with atherosclerosis, but its mechanism is unknown. It has been reported that insulin receptor substrate (IRS)-1 deficient ( IRS-1 ^−/− ) mice showed insulin resistance without type 2 diabetes, whereas the IRS-2 deficient ( IRS-2 ^−/− ) mice showed insulin resistance with type 2 diabetes. Methods and Results— We investigated neointima formation in the IRS-1 ^−/− and IRS-2 ^−/− mice at 8 and 20 weeks. The IRS-2 ^−/− mice showed much greater neointima formation than the IRS-1 ^−/− and wild-type mice at 8 weeks. At 20 weeks, the IRS-2 ^−/− mice had greater neointima formation than the IRS-1 ^−/− mice, which showed more enhanced neointima formation than the wild-type mice. The IRS-1 ^−/− and IRS-2 ^−/− mice had dyslipidemia, hypertension, and insulin resistance. The IRS-2 ^−/− mice had more metabolic abnormalities than the IRS-1 ^−/− mice at 8 and 20 weeks. IRS-2 expression was detected, but IRS-1 expression was not detected in the vessels. Conclusions— The neointima formation in the IRS-1 ^−/− and IRS-2 ^−/− mice appears to be related to abnormalities induced by the altered metabolic milieu in insulin-resistant states. Moreover, because neointima formation was much greater in the IRS-2 ^−/− mice than in the IRS-1 ^−/− mice at 8 and 20 weeks, it is suggested that a lack of IRS-2 renders the vasculature more susceptible to injury in the abnormal metabolic milieu, and IRS-2 may have a protective effect on neointima formation. We conclude that IRS-2 is protective and retards the development of neointima formation in insulin-resistant states.

There has been no report about outcome of pitavastatin versus atorvastatin therapy in high-risk patients with hypercholesterolemia. Hypercholesterolemic patients with one or more risk factors for atherosclerotic diseases (n = 664, age = 65, male = 54%, diabetes = 76%, primary prevention = 74%) were randomized to receive pitavastatin 2 mg/day (n = 332) or atorvastatin 10 mg/day (n = 332). Follow-up period was 240 weeks. The primary end point was a composite of cardiovascular death, sudden death of unknown origin, nonfatal myocardial infarction, nonfatal stroke, transient ischemic attack, or heart failure requiring hospitalization. The secondary end point was a composite of the primary end point plus clinically indicated coronary revascularization for stable angina. The mean low-density lipoprotein cholesterol (LDL-C) level at baseline was 149 mg/dL. The mean LDL-C levels at 1 year were 95 mg/dL in the pitavastatin group and 94 mg/dL in the atorvastatin group. There were no differences in LDL-C levels between both groups, however, pitavastatin significantly reduced the risk of the primary end point, compared to atorvastatin (pitavastatin = 2.9% and atorvastatin = 8.1%, HR, 0.366; 95% CI 0.170-0.787; P = 0.01 by multivariate Cox regression) as well as the risk of the secondary end point (pitavastatin = 4.5% and atorvastatin = 12.9%, HR = 0.350; 95%CI = 0.189-0.645, P = 0.001). The results for the primary and secondary end points were consistent across several prespecified subgroups. There were no differences in incidence of adverse events between the statins. Pitavastatin therapy compared with atorvastatin more may prevent cardiovascular events in hypercholesterolemic patients with one or more risk factors for atherosclerotic diseases despite similar effects on LDL-C levels.