Background Arterial stiffness with aging predicts cardiovascular diseases (CVDs) and target organ damage. While sarcopenia has been linked to arterial stiffness, the association of myosteatosis and visceral adiposity with arterial stiffness remains underexplored. As age-related fat redistribution, including myosteatosis and visceral obesity, often precedes overt sarcopenia, their early evaluation may be beneficial in preventing arterial stiffness. Therefore, this cross-sectional study aimed to assess whether myosteatosis and visceral obesity are associated with increased arterial stiffness.
Methods A total of 6,004 subjects without CVD who underwent abdominal computed tomography and brachial-ankle pulse wave velocity (baPWV) between 2012 and 2013 during health examinations were included. Visceral fat area and total abdominal muscle area (TAMA) were measured at the L3 vertebral level. Muscle quality was assessed using the normal attenuation muscle area (NAMA)/TAMA index, where a lower value indicates a reduced proportion of healthy muscle (NAMA) and a higher presence of myosteatosis.
Results After adjusting for multiple cardiovascular risk factors, including myosteatosis, visceral obesity was significantly associated with elevated baPWV in men (odds ratio [OR]=1.32; 95% confidence interval [CI]=1.10 to 1.60; P=0.004). In contrast, in women, myosteatosis was significantly associated with elevated baPWV in a fully adjusted model that included visceral obesity (OR=3.26; 95% CI=1.13 to 9.44; P=0.029).
Conclusion Ectopic fat infiltration, including visceral obesity and myosteatosis, was significantly associated with increased arterial stiffness. Notably, visceral obesity was significantly associated with elevated baPWV in men, while myosteatosis was significantly associated with elevated baPWV in women after adjustment.
Background The role of aspirin in primary cardiovascular disease prevention in patients with diabetes remains controversial. However, some studies have suggested beneficial effects of cilostazol on cardiovascular disease in patients with diabetes. We prospectively investigated the antiplatelet effects of cilostazol compared with aspirin in patients with diabetes and cardiovascular risk factors.
Methods We randomly assigned 116 patients with type 2 diabetes and cardiovascular risk factors but no evident cardiovascular disease to receive aspirin at a dose of 100 mg or cilostazol at a dose of 200 mg daily for 14 days. The primary efficacy outcome was antiplatelet effects of aspirin and cilostazol assessed with the VerifyNow system (aspirin response units [ARU]) and PFA-100 (closure time [CT]). Secondary outcomes were changes of clinical laboratory data (ClinicalTrials.gov Identifier: NCT02933788).
Results After 14 days, there was greater decrease in ARU in aspirin (–28.9%±9.9%) compared cilostazol (–0.4%±7.1%, P<0.001) and was greater increase in CT in aspirin (99.6%±63.5%) compared cilostazol (25.7%±54.1%, P<0.001). The prevalence of aspirin resistance was 7.5% according to VerifyNow (defined by ARU ≥550) and 18.9% according to PFA-100 (CT <192 seconds). Compared with aspirin, cilostazol treatment was associated with increased high density lipoprotein cholesterol (7.1%±12.7% vs. 4.2%±18.0%, P=0.006) and decreased triglycerides (–9.4%±33.7% vs. 4.4%±17.57%, P=0.016). However, there were no significant changes in total and low density lipoprotein cholesterol, C-reactive protein level, and cluster of differentiation 40 ligand between cilostazol and aspirin groups.
Conclusion Aspirin showed better antiplatelet effects assessed with VerifyNow and PFA-100 compared with cilostazol. However, there were favorable changes in atherogenic dyslipidemia only in the cilostazol.
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Methods The study included 39,418 Koreans without T2D at baseline. The risk of T2D was evaluated based on four different definitions of metabolic health and obesity status and according to the baseline TyG index within each metabolic health and obesity group.
Results During the median follow-up at 38.1 months, 726 individuals developed T2D. Compared with the metabolically healthy non-obese (MHNO) group with low TyG index, the MHO group with high TyG index showed increased risk of T2D in all four definitions of metabolic health with multivariate-adjusted hazard ratios of 2.57 (95% confidence interval [CI], 1.76 to 3.75), 3.72 (95% CI, 2.15 to 6.43), 4.13 (95% CI, 2.67 to 6.38), and 3.05 (95% CI, 2.24 to 4.15), when defined by Adult Treatment Panel III, Wildman, Karelis, and homeostasis model assessment (HOMA) criteria, respectively.
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Clozapine, an atypical antipsychotic agent, has been linked to several cases of acute pancreatitis and hypertriglyceridemia. However, neither acute pancreatitis nor hypertriglyceridemia associated with clozapine has yet been reported in the Republic of Korea. Based on recent experience, we report on a case of severe hypertriglyceridemia and acute pancreatitis associated with clozapine. A 37-year-old schizophrenic woman in good physical condition presented with abdominal pain of acute onset. She had been taking clozapine for 20 months to control her schizophrenia. On admission, her serum triglyceride level was 6,670 mg/dL. Elevated serum amylase and lipase levels, as well as abdominal computed tomography findings, were compatible with acute pancreatitis. After discontinuing the use of clozapine, the serum triglyceride level was normalized and acute pancreatitis resolved.
Two of the common causes of hypercalcemia are malignancy and primary hyperparathyroidism. These disorders are easily diagnosed by the clinical manifestations and measurement of the serum intact parathyroid hormone (PTH) level. On the other hand, hyperthyroidism is an uncommon cause of hypercalcemia. The diagnosis of hypercalcemia associated with hyperthyroidism can only be made by excluding the common causes of hypercalcemia and by observing the improvement of the hypercalcemia and its associated symptoms with normalizing the thyroid function. Herein we reported our experience with a 67 year-old woman who presented with nausea and vomiting. She showed elevated serum calcium and phosphorus levels. Serum intact PTH level was 1.1 pg/mL (normal range; 10~65). The results of the thyroid function test were compatible with hyperthyroidism. After resolution of the thyrotoxicosis with combination treatment of methimazol and Lugol's solution, the patient's serum calcium and phosphorus levels were normalized and the symptoms were improved.