Effects of Statin Therapy on Clinical Outcomes of Survivors of Acute Myocardial Infarction with Severe Systolic Heart Failure.

OBJECTIVE: Large randomized trials have failed to show a beneficial effect of statin treatment in chronic HF. The investigators tried to evaluate the long-term effects of statin therapy in patients with new onset heart failure (HF) following acute myocardial infarction (AMI). METHODS: Between January 2008 and December 2011, a total of 13,616 AMI patients were enrolled in the Korea Acute Myocardial Infarction Registry (KAMIR) which was a prospective, multi-center, nationwide, web-based database of AMI in Korea. From this database, we studied 1,055 patients with AMI who had newly developed severe acute HF [left ventricular ejection fraction ≤ 40%] and were discharged alive. The patients were divided into two groups, a statin group (n = 756) and a no-statin group (n = 299). We investigated the one-year major adverse cardiovascular events (MACEs), including all-cause mortality, MI, and any revascularization of each group. We then performed a propensity-score matched analysis. RESULTS: In the original cohort, one-year MACEs were similar between the two groups (16.5% vs. 14.7% in the statin or no-statin groups; p = 0.47). Propensity-score matching yielded 256 pairs, and in that population we observed comparable results in terms of MACEs (18.0% vs. 12.5% in the statin or no-statin groups, p = 0.11) and mortality (5.1% vs. 3.5% in the statin or no-statin groups, p = 0.51). Cox-regression analysis revealed that statin therapy was not an independent predictor for occurrence of a MACE [Hazard ratio (HR) 1.11, 95% CI 0.79-1.57, p = 0.54] or all-cause mortality (HR 1.42, 95% CI 0.75-2.70, p = 0.28). CONCLUSION: Statin therapy was not associated with a reduction in the long-term occurrence of MACEs or mortality in survivors of AMI with severe acute HF in this retrospective cohort study.

Anatomical Popliteal Artery Entrapment Syndrome Caused by an Aberrant Plantaris Muscle.

PURPOSE: We report on cases of anatomical popliteal artery entrapment syndrome (PAES) caused by an aberrant plantaris muscle and highlight the involvement of this muscle in PAES. MATERIALS AND METHODS: Seven symptomatic PAES legs in six patients treated at The Division of Vascular Surgery, Asan Medical Center, Seoul, Korea, between 1995 and 2011 were included in this study. We retrospectively analyzed patient records, magnetic resonance imaging (MRI) and/or computed tomography (CT) scans of the knee joint, Doppler pressure studies, CT angiographies, and conventional femoral arteriographies. RESULTS: Five males and one female patient with a median age of 32 (18-53) years old were enrolled in the study. All patients complained of intermittent claudication of the affected leg. All aberrant plantaris muscles were higher and more medially located than normal plantaris muscles, causing occlusion of the popliteal artery upon forced plantar flexion of the ankle. For arterial lesions, five occlusions of the popliteal artery and two patent popliteal arteries with positive provocation were noted. As for treatment, myotomy of the aberrant plantaris muscle was done for two non-occlusive PAES legs. For occlusive PAES legs, one thrombectomy, one saphenous vein graft interposition of the popliteal artery followed by myotomy, and two below-knee femoro-popliteal bypasses were performed. The median follow-up period was 88 (7-148) months. CONCLUSION: An aberrant plantaris muscle can cause anatomical PAES. Classification or diagnosis of PAES should be based on axial studies using CT scans or MRI using various reconstruction methods. Treatment, including myotomy of the plantaris muscle, should be individualized.

Mycophenolate Mofetil Ameliorates Diabetic Nephropathy in db/db Mice.

Chronic low-grade inflammation is an important factor in the pathogenesis of diabetic complication. Mycophenolate mofetil (MMF) has an anti-inflammatory effect, inhibiting lymphocyte proliferation. Previous studies showed attenuation of diabetic nephropathy with MMF, but the underlying mechanisms were unclear. This study aimed to identify the effect of MMF on diabetic nephropathy and investigate its action mechanisms in type 2 diabetic mice model. Eight-week-old db/db and control mice (db/m mice) received vehicle or MMF at a dose of 30 mg/kg/day for 12 weeks. MMF-treated diabetic mice showed decreased albuminuria, attenuated mesangial expansion, and profibrotic mRNA expressions despite the high glucose level. The number of infiltrated CD4(+) and CD8(+) T cells in the kidney was significantly decreased in MMF-treated db/db mice and it resulted in attenuating elevated intrarenal TNF-α and IL-17. The renal chemokines expression and macrophages infiltration were also attenuated by MMF treatment. The decreased expression of glomerular nephrin and WT1 was recovered with MMF treatment. MMF prevented the progression of diabetic nephropathy in db/db mice independent of glycemic control. These results suggest that the effects of MMF in diabetic nephropathy are mediated by CD4(+) T cell regulation and related cytokines.

Effect of onion peel extract on endothelial function and endothelial progenitor cells in overweight and obese individuals.

OBJECTIVES: Acute or chronic intake of polyphenol-rich foods has been reported to improve endothelial function. Quercetin, found abundantly in onion, is a potent antioxidant flavonoid. The aim of this study was to investigate whether consumption of onion peel extract (OPE) improves endothelial function in healthy overweight and obese individuals. METHODS: This was a randomized double-blind, placebo-controlled study. Seventy-two healthy overweight and obese participants were randomly assigned to receive a red, soft capsule of OPE (100 mg quercetin/d, 50 mg quercetin twice daily; n = 36 participants) or an identical placebo capsule (n = 36) for 12 wk. Endothelial function, defined by flow-mediated dilation (FMD), circulating endothelial progenitor cells (EPCs) by flow cytometry, and laboratory test were determined at baseline and after treatment. RESULTS: Baseline characteristics and laboratory findings did not significantly differ between the two groups. Compared with baseline values, the OPE group showed significantly improved FMD at 12 wk (from 12.5 ± 5.2 to 15.2 ± 6.1; P = 0.002), whereas the placebo group showed no difference. Nitroglycerin-mediated dilation did not change in either group. EPC counts (44.2 ± 25.6 versus 52.3 ± 18.6; P = 0.005) and the percentage of EPCs were significantly increased in the OPE group. When FMD was divided into quartiles, rate of patients with endothelial dysfunction defined as lowest quartile (cutoff value, 8.6%) of FMD improved from 26% to 9% by OPE. CONCLUSION: Medium-term administration of OPE an improvement in FMD and circulating EPCs.

Biochemical and clinical correlation of intraplaque neovascularization using contrast-enhanced ultrasound of the carotid artery.

OBJECTIVE: Several biomarkers reflecting inflammatory or proteolytic activity have been known to represent plaque vulnerability. Moreover, a recent study confirmed that contrast-enhanced ultrasound (CEUS) can visualize intraplaque neovascularization (IPN) and demonstrate plaque vulnerability. In this study, we tried to demonstrate that IPN detected by CEUS was correlated with several well-known biomarkers and clinical outcome in patients with coronary artery disease (CAD). METHODS: Patients with stable CAD were screened by conventional carotid ultrasound and patients with carotid plaque thickness more than 2 mm were performed by CEUS for the presence of IPN. Plasma levels of biomarkers and clinical outcomes were evaluated. RESULTS: Among consecutive 89 patients fulfilled the inclusion criteria, 30 patients without IPN (group 1) and 59 patients with IPN (group 2) were analyzed. There were no significant difference in baseline characteristics except for mean age (62.9±10.1 yrs versus 68.4±9.6 yrs, p=0.015). On multivariate analysis, only MMP-9 (p=0.021, 95% CI 1.002-1.027) showed a significant association with IPN. But patients with IPN showed only trend for a history of cardiovascular disease (CVD) (44% versus 30%, p=0.19) and one-year cardiovascular events (CVE) (6.8% versus 3.3%, p=0.50) compared to group 1. Maximum plaque thickness (p=0.04, 95% CI 1.230-6.322) showed a significant correlation with the clinical outcome including CVD or CVE. CONCLUSION: MMP-9 correlated with IPN on CEUS. For clinical implication, however, large prospective studies are needed.

Mitochondrial dynamics in the heart as a novel therapeutic target for cardioprotection.

Traditionally, mitochondria have been regarded solely as energy generators for cells; however, accumulating data have demonstrated that these complex organelles play a variety of roles within the cardiomyocyte that extend beyond this classic function. Mitochondrial dynamics involves mitochondrial movements and morphologic alterations by tethering, fusion, and fission, which depend on cellular energy requirements and metabolic status. Many studies have indicated that mitochondrial dynamics may be a fundamental component of the maintenance of normal cellular homeostasis and cardiac function. Mitochondrial dynamics is controlled by the protein machinery responsible for mitochondrial fusion and fission, but cardiomyocytes are densely packed as part of an intricate cytoarchitecture for efficient and imbalanced contraction; thus, mitochondrial dynamics in the adult heart are restricted and occur more slowly than in other organs. Cardiac mitochondrial dynamics is important for cardiac physiology in diseased conditions such as ischemia-reperfusion (IR) injury. Changes in mitochondrial morphology through modulation of the expression of proteins regulating mitochondrial dynamics demonstrates the beneficial effects on cardiac performance after IR injury. Thus, accurately defining the roles of mitochondrial dynamics in the adult heart can guide the identification and development of novel therapeutic targets for cardioprotection. Further studies should be performed to establish the exact mechanisms of mitochondrial dynamics.

A case of systemic amyloidosis following ankylosing spondylitis associated with congestive heart failure.

Secondary (amyloid A [AA]) amyloidosis is a systemic disease characterized by amyloid deposition in many organs, leading to impaired function. Although cardiac involvement may occur with AA amyloidosis, significant deposition of amyloid in the heart is considered an infrequent observation and is rarely the cause of death. It occurs in 5% of patients with poorly controlled chronic inflammatory disease, mainly rheumatoid arthritis, ankylosing spondylitis, and familial Mediterranean fever. The authors report a case of AA amyloidosis diagnosed by rectal and skin biopsies, with cardiac involvement demonstrated by typical echocardiographic features in the presence of low voltage on electrocardiography.