Metabolic syndrome and diabetes are associated with increased risk of cardiac dysfunction independently of underlying coronary artery disease. The underlying pathogenesis is partially understood but accumulating evidence suggests that alterations of cardiac energy metabolism might contribute to the development of contractile dysfunction. Recent findings suggest that myocardial mitochondrial dysfunction may play an important role in the pathogenesis of cardiac contractile dysfunction in type 2 diabetes. This review is focused on evaluating mechanisms for the mitochondrial abnormalities that may be involved in the development and progression of cardiac dysfunction in diabetes.
Coronary Artery Disease ; Diabetic Cardiomyopathies ; Energy Metabolism ; Mitochondria

The concept that atherosclerosis is an inflammation has been increasingly recognized, and subsequently resulted in great interest in revealing the inflammatory nature of the atherosclerotic process. More recently, a large body of evidence has supported the idea that inflammatory mechanisms play a pivotal role throughout all phases of atherogenesis, from endothelial dysfunction and the formation of fatty streaks to plaque destabilization and the acute coronary events due to vulnerable plaque rupture. Indeed, although triggers and pathways of inflammation are probably multiple and vary in different clinical entities of atherosclerotic disorders, an imbalance between anti-inflammatory mechanisms and pro-inflammatory factors will result in an atherosclerotic progression. Vascular endothelial dysfunction and lipoprotein retention into the arterial intima have been reported as the earliest events in atherogenesis with which inflammation is linked. Inflammatory has also been extended to the disorders of coronary microvasculature, and associated with special subsets of coronary artery disease such as silent myocardial ischemia, myocardial ischemia-reperfusion, cardiac syndrome X, variant angina, coronary artery ectasia, coronary calcification and in-stent restenosis. Inflammatory biomarkers, originally studied to better understand the pathophysiology of atherosclerosis, have generated increasing interest among researches and clinicians. The identification of inflammatory biomarkers and cellular/molecular pathways in atherosclerotic disease represent important goals in cardiovascular disease research, in particular with respect of the development of therapeutic strategies to prevent or reverse atherosclerotic diseases.
Atherosclerosis ; immunology ; metabolism ; Coronary Artery Disease ; immunology ; metabolism ; Humans ; Inflammation ; metabolism ; physiopathology

OBJECTIVE: To observe the expression of phosphatase and tensin homology deleted on chromosome ten (PTEN) in myocardial tissue in patients with coronary heart disease, and explore the relevance between the expression of PTEN and the occurrence and development of coronary heart disease. METHODS: A total of 16 death cases with pathological diagnosis of coronary heart disease were collected as experimental group, and 19 cases without myocardial lesions were selected as control group. The expression of PTEN protein and its mRNA were detected by immunohistochemistry and real-time fluorescence quantitative PCR respectively. The correlation between the expression of PTEN and the pathogenesis of coronary heart disease was analyzed. RESULTS: The expression of PTEN protein in myocardium in cases with coronary heart disease was significantly lower compared with the control group (P < 0.05). There was no statistical difference of the expression of PTEN mRNA between experimental and control group (P > 0.05). CONCLUSION PTEN may be involved in the occurrence and development of coronary heart disease.
Coronary Artery Disease/pathology* ; Humans ; Myocardium/metabolism* ; PTEN Phosphohydrolase/metabolism* ; RNA, Messenger/metabolism*

OBJECTIVETo evaluate the quality of the radial artery for coronary artery bypass grafting (CABG) from patients with diabetes by observing the morphology of the radial artery and detecting the expression of vascular endothelial growth factor (VEGF) which may attribute to the long-term patency rate of the coronary artery bypass grafting.

METHODSSamples from 20 cases of diabetic and non-diabetic patients were prospective collected from June 2009 to December 2010. HE staining technique was used to test the morphology of radial artery through the observation of 20 cases of diabetic and 20 cases of non-diabetic patients who undergone CABG. The intimal thicken of the radial artery in the two groups of patients was compared. Western blot and immunofluorescence were then used to test the expression and location of VEGF in the two groups of patients.

RESULTSThe radial artery endothelial thickening index and intima/media ratio were significantly higher in the diabetic patients when compared with non-diabetic patients (0.90 ± 0.28 vs. 0.29 ± 0.25, t = 7.27, P < 0.01; 0.90 ± 0.21 vs. 0.37 ± 0.18, t = 8.57, P < 0.01). The expression of VEGF in diabetic patients was significantly higher than non-diabetic patients as revealed by Western blot (1.20 ± 0.21 vs. 0.67 ± 0.15, t = 6.49, P < 0.01). Immunofluorescence showed that VEGF distributed in the cytoplasm of the endothelial cells of diabetic patients radial artery.

CONCLUSIONSDiabetic patient's radial artery intimal thickness is significantly higher than non-diabetic patient's. VEGF may be an important inflammatory cytokine which is leading the radial artery intima thickening in the diabetic patients. The choice of the radial artery grafts in diabetic patients for CABG should be careful.

Aged ; Coronary Artery Bypass ; Coronary Artery Disease ; metabolism ; surgery ; Diabetes Mellitus ; pathology ; Female ; Humans ; Male ; Middle Aged ; Prospective Studies ; Radial Artery ; metabolism ; pathology ; Vascular Endothelial Growth Factor A ; metabolism

OBJECTIVETo review the functional mechanism of apolipoprotein J (apoJ) in the process of atherosclerosis and the feasibility of apoJ as a therapeutic endpoint.

DATA SOURCESRelevant articles published in English from 1983 to present were selected from PubMed. The terms of "atherosclerosis, apolipoprotein J, clusterin (CLU), oxidative stress, and inflammation" were used for searching.

STUDY SELECTIONArticles studying the role of apoJ with atherosclerosis and restenosis after injury were reviewed. Articles focusing on the intrinsic determinants of atherosclerosis were selected. The exclusion criteria of articles were that the studies on immunologic vasculitis.

RESULTSApoJ, involved in numerous physiological process important for lipid transportation and vascular smooth muscle cell differentiation, including apoptotic cell death, cell-cycle regulation, cell adhesion, tissue remodeling, immune system regulation, and oxidative stress, plays a role in the development of clinical atherosclerosis. In the process of relieving atherosclerosis, apoJ can promote cholesterol and phospholipid export from macrophage-foam cells, and exhibit cytoprotective and anti-inflammatory actions by interacting with lots of known inflammatory proteins which may predict the onset of clinical cardiovascular events and may actually play a causal role in mediating atherosclerotic disease such as C-reactive protein, paraoxonase, and leptin. As known as CLU, apoJ has been identified to play central roles in the process of vascular smooth cells migration, adhesion, and proliferation, which can contribute significantly to restenosis after vascular injury.

CONCLUSIONSIntense effort and substantial progress have been made to identify the apoJ that relieves atherosclerosis and vascular restenosis after percutaneous coronary intervention. More work is needed to elucidate the exact mechanisms of and the interrelationship between the actions of apoJ and to successfully achieve regression of atherosclerosis by regarding it as a therapeutic endpoint.

Cardiovascular Diseases ; genetics ; mortality ; Clusterin ; genetics ; metabolism ; Coronary Artery Disease ; genetics ; metabolism ; Coronary Restenosis ; genetics ; metabolism ; Humans

PURPOSE: Abnormality in the composition of lipid metabolism is well known to be a main cause of atherosclerosis. Accordingly the abnormality in lipid metabolism after suffering from Kawasaki disease may lead to premature coronary atherosclerosis. The aim of this study is to investigate the abnormalities of lipid metabolism in patients with Kawasaki disease. We studied 67 patients with Kawasaki disease. METHODS: We serially measured total cholesterol, HDL-cholesterol, and triglyceride(period 1 : at admission, period 2 : 24-48 hours after the defervescence, period 3 : 2-3 weeks after the onset of disease, period 4 : 2-3 months after the onset of disease, period 5 : 6 months after the onset of disease, period 6 : 1 year after the onset of disease, period 7 : 2 years after the onset of disease). RESULTS: In patients with Kawasaki disease, HDL was relatively low(P=0.07) in the acute stage (period 2) compared with control group, but recovered in the subacute stage(period 3) and stayed the same level. Total cholesterol was low(P=0.02) in the acute stage(period 1) compared with control group, but recovered in the subacute stage(period 3) and stayed at the same level. CONCLUSION: Kawasaki disease, a systemic vasculitis of unknown etiology, may cause abnormalities in lipid metabolism, especially at the acute stage by affecting endothelial metabolism. To understand the long-term effect of this metabolic abnormalities, we have to study more patients for a longer period of time.
Atherosclerosis ; Cholesterol ; Coronary Artery Disease ; Humans ; Lipid Metabolism ; Metabolism ; Mucocutaneous Lymph Node Syndrome* ; Systemic Vasculitis

OBJECTIVE: To investigate the expression of monocyte chemotactic protein-1 (MCP-1) and its receptor CC chemokine receptor-2 (CCR-2) in coronary atherosclerosis plaques between sidden coronary death (SCD) and non-SCD. Methods The expression levels of MCP-1 and CCR-2 in SCD group, coronary atherosclerosis group (non-SCD), control group (normal coronary artery) were detected by immunohistochemistry. RESULTS: Positive rates of MCP-1 among the three groups were 78%, 47%, and 0%, respectively, with significant expressing differences between each two groups (P<0.05). Positive rates of CCR-2 among three groups were 72%, 47%, and 0%, respectively, with significant expressing differences between the SCD group and coronary atherosclerosis group as well as between the SCD group and control group (P<0.05), but with no significant expressing difference between coronary atherosclerosis group and control group (P>0.05). CONCLUSION Overexpression of MCP-1 and CCR-2 in coronary atherosclerotic plaques is closely correlated with SCD.
Chemokine CCL2/metabolism* ; Coronary Artery Disease/pathology* ; Death, Sudden, Cardiac/pathology* ; Humans ; Immunohistochemistry ; Receptors, CCR2/metabolism*

OBJECTIVETo compare the morphometry and endothelial nitric oxide synthase (eNOS) expression of radial artery (RA) between young and elderly patients with coronary atherosclerotic heart disease.

METHODSFrom February 2008 to June 2009, 219 patients underwent coronary artery bypass grafting (CABG) with autologous RA, 57 patients aged beyond 70 years and 64 patients aged under 60 years. Before RA was harvested, a modified Allen test was routinely performed. If positive, RA would be further evaluated with Doppler ultrasound examination. In both groups RA was collected for HE staining to evaluate percentage of luminal narrowing (LN) and relationship between intima and media width at maximum intimal thickness (IMR). Immunofluorescence and Western blot were used to investigate the location and expression level of eNOS within the wall of RA.

RESULTSMorphometry of RA in both young and elderly patients represented mild or moderate intimal hyperplasia, and medial calcification was not found. LN in elderly patients was (22 ± 6)%, while in young patients, it was (23 ± 6)%. IMR in elderly patients was 0.36 ± 0.21, while in young patients, it was 0.42 ± 0.19. There was no significant difference in both LN and IMR between two groups (P > 0.05). Immunofluorescence indicated RA in both groups revealed a high expression of eNOS in intima and media, particularly in the smooth muscle of media. The values of relative integrated optical density in elderly patients was 1.21 ± 0.13, while in young patients, it was 1.25 ± 0.12. Also there was no significant difference in the expression level of eNOS within the wall of RA (P > 0.05).

CONCLUSIONAfter preoperative assessment with modified Allen's test and Doppler analysis, RA used as graft in the elderly has similar quality and function with young patients, and it may lead to a high patency in long term.

Aged ; Coronary Artery Bypass ; Coronary Artery Disease ; enzymology ; pathology ; surgery ; Female ; Humans ; Male ; Middle Aged ; Nitric Oxide Synthase Type III ; metabolism ; Radial Artery ; enzymology ; pathology

BACKGROUNDThe relationship between chronic obstructive pulmonary disease (COPD) and coronary artery disease (CAD) remains largely unknown. This study aimed to explore the association of COPD with CAD, especially with multi-vessel disease (VD).

METHODSThe data of 354 patients who underwent multi-detector computed tomography (MDCT) for suspected CAD were analyzed. Luminal narrowing was defined as at least one lesion 50% or greater stenosis. The analysis of serum biochemistry profile and spirometry were performed on all eligible patients, and the diagnosis of COPD was defined as the criteria of Global Initiative for Chronic Obstructive Lung Disease.

RESULTSPatients with CAD had a significantly higher complication of COPD than those without CAD (11.8% vs. 3.7%, P < 0.001). Comparing with patients without COPD, those with COPD were more likely to have multi-VD, proportion of smoking and high C-reactive protein (CRP) (P < 0.001). Multivariate Logistic regression analysis revealed that the multi-VD was significantly correlated with COPD (P=0.012) and CRP (P=0.015).

CONCLUSIONSThere was a high complication of COPD in patients with CAD, and COPD may be a critical risk factor for CAD, especially for multi-VD. CAD and COPD were closely associated and the interplay of systemic inflammation might in part explain the relationship between them.

Coronary Artery Disease ; complications ; diagnostic imaging ; metabolism ; Humans ; Pulmonary Disease, Chronic Obstructive ; complications ; diagnostic imaging ; metabolism ; Radiography ; Risk Factors

BACKGROUND AND OBJECTIVES: The recently discovered myokine irisin has a proposed role in adipose tissue metabolism. The aim of this study was to evaluate the relationship between serum irisin level and the coronary artery severity in patients with stable coronary artery disease (CAD). SUBJECTS AND METHODS: Sixty-three patients who underwent coronary angiography (CA) diagnosed with stable CAD and twenty-six patients with normal coronary artery (NCA) were enrolled in the study. Stable CAD patients were divided into two groups as high synergy between percutaneous coronary intervention with taxus and cardiac surgery (SYNTAX) score (≥23) and lower SYNTAX score (<23). Serum irisin level measurement was carried out using human irisin colorimetric enzyme-linked immunosorbent assay (ELISA) commercial kit (AG-45A-0046EK-KI01, Adipogen, San Diego, CA, USA) as recommended by the manufacturer's protocol. RESULTS: The patients with stable CAD with a higher SYNTAX score (score ≥23) had significantly lower serum irisin levels (127.91±55.38 ng/mL), as compared the patients with a low SYNTAX score (score <23) (224.69±92.99 ng/mL) and control group (299.54±123.20 ng/mL). Irisin levels showed significant differences between all groups (p<0.001). CONCLUSION: Serum irisin level is an independent predictor of coronary artery severity in patients with stable CAD.
Adipose Tissue ; Angina, Stable* ; Atherosclerosis ; Coronary Angiography ; Coronary Artery Disease* ; Coronary Vessels* ; Enzyme-Linked Immunosorbent Assay ; Humans ; Metabolism ; Percutaneous Coronary Intervention ; Taxus ; Thoracic Surgery