Mean platelet volume: An important predictor of coronary collateral development

Collaterals, which develop in response to ischemic stimuli derived from coronary artery disease (CAD), contribute to reduction of infarct size, left ventricular dysfunction, and mortality. However, there is considerable variation among patients with coronary heart disease regarding the extent of coronary collateral development (CCD). In this study, we aimed to investigate the association of the degree of platelet activation via mean platelet volume (MPV) with coronary collateral circulation. Therefore, 210 patients who underwent coronary angiography and had coronary stenosis ≥50 % in at least one coronary artery were included in the study. Clinical information and analyses of blood samples were obtained from a review of the patients’ chart. Blood samples for MPV were analyzed by K3 EDTA and collateral vessels were graded according to the Rentrop classification. In the study group, 150 of the 210 patients were found to have inadequate CCD. Although there was no difference between the two groups with regard to platelet count, MPV levels were significantly higher in the patients who had inadequate CCD (11.3?±?1.0 fl vs. 9.5?±?1.5 fl, p?<?0.001). Furthermore, the Gensini score was significantly lower in patients who had inadequate CCD (45?±?46 vs. 91?±?35, p?<?0.001). MPV, Gensini score, age, female gender, total cholesterol, red cell distribution width, triglyceride, and fasting glucose levels were found to have univariate association with poor CCD. In multivariate logistic regression model, MPV (OR?=?2.45, p?<?0.001) and Gensini score (OR?=?0.98, p?<?0.001) were found to be the independent predictors of impaired CCD. In receiver operator characteristic curve analysis, optimal cut-off value of MPV to predict inadequate CCD was found as >9.6 fl, with 96% sensitivity and 84.7% positive predictive value. In conclusion, we can say that MPV is an important, simple, effortless, and cost effective tool and can be useful in predicting the CCD in patients with significant CAD.     

Delayed Haematological recovery after autologous stem cell transplantation is associated with favourable outcome in acute myeloid leukaemia

Autologous stem cell transplantation (ASCT) is applied to consolidate first remission in patients with acute myeloid leukaemia (AML). However, outcome after ASCT widely varies among AML patients. We analyzed the prognostic significance of haematological recovery for neutrophils [absolute neutrophil count (ANC) >1·0 × 10⁹/l] and platelets (platelet count >20·0 × 10⁹/l), stratifying at day 20 after ASCT in 88 consecutive and homogeneously treated AML patients in first remission. We observed that patients with delayed recovery had better overall survival (OS; ANC: P < 0·0001 and platelets: P = 0·0062) and time to progression (TTP; ANC: P = 0·0003 and platelets: P = 0·0125). Delayed recovery was an independent marker for better OS and TTP in a multivariate analysis including age, gender, number of transfused CD34+ cells, cytogenetics, FLT3‐internal tandem duplication and NPM1 mutation. Our results suggest that delayed neutrophil and platelet recovery is associated with longer OS and TTP in AML patients consolidated with ASCT in first remission.     

The relation between mean platelet volume and coronary collateral vessels in patients with acute coronary syndromes

ObjectiveElevated mean platelet volume (MPV) has been proposed as a risk factor for coronary artery disease (CAD) and is associated with poor clinical outcome in acute coronary syndrome (ACS). We aimed to evaluate the association of MPV with presence of coronary collateral vessel (CCV) in patients with ACS.MethodsA total of 417 patients with ACS were included in the study. All patients underwent coronary angiography on the first day after admission and patients with a greater than or equal to 80% obstruction in at least one epicardial coronary artery were included in the study. The CCVs are graded according to the Rentrop scoring system and a Rentrop grade 0 was accepted as no CCV development (Group 1), Rentrop Grade 1–2–3 were accepted as presence of CCV development (Group 2).ResultsThe median of MPV was 9.1 ± 1.4 fl. Mean age was 60 ± 12 year. Group 1 consisted of 233 (55.9%) patients and Group 2 consisted of 184 (44.1%) patients. Presence of CCV was significantly associated with high levels of MPV (p = 0.005). Presence of CCV was also associated with presence of diabetes and systolic blood pressure.ConclusionHigh MPV on admission was associated with presence of CCV in patients with ACS.     

血管内皮生长因子与冠状动脉粥样硬化及侧枝循环形成的关系

探讨血管内皮生长因子与冠状动脉粥样硬化狭窄程度及冠状动脉侧枝循环形成的关系 ,应用酶联免疫吸附法检测 10 2例经冠状动脉造影确诊的冠心病患者和 43例冠状动脉造影正常者的冠状动脉血浆血管内皮生长因子浓度 ,作冠状动脉病变Leaman记分和侧枝循环Rentrop分级 ,并分析血管内皮生长因子与其的关系。结果发现 ,冠心病患者冠状动脉血浆血管内皮生长因子平均浓度明显高于正常对照组 ( 2 2 5± 147ng L比 74± 5 2ng L ,P <0 .0 1) ,而且冠心病患者中侧枝循环形成者血管内皮生长因子平均浓度明显高于无侧枝循环形成者 ( 2 99± 15 2ng L比 2 0 2± 12 2ng L ,P <0 .0 5 ) ;血浆血管内皮生长因子浓度与Leaman记分呈显著正相关 (r=0 .693 ,P <0 .0 0 1)。结果提示 ,血管内皮生长因子与冠状动脉粥样硬化狭窄程度及冠状动脉侧枝循环形成具有一定的关系 ,血管内皮生长因子可能既有促进冠状动脉侧枝循环形成的作用 ,又在动脉粥样硬化发展中起到一定的双重调节作用     

Renal impairment and coronary collaterals in patients with acute coronary syndrome

Objective

We aimed to elucidate the relationship between mild-to-moderate renal impairment and the development of coronary collateral vessels (CCV) in patients with acute coronary syndrome (ACS).

Methods

We enrolled 461 patients with ACS who underwent coronary angiography for the first time. The development of CCV was assessed with the Rentrop score. Kidney function was classified according to the estimated glomerular filtration rate (eGFR). The Gensini score was used to show the extent of atherosclerosis.

Results

The mean eGFR value was 89.9?±?24.3 U/l for patients with no development of collaterals and 82.7?±?20.5 for patients who had CCV. The mean age was 59?±?11 years and 349 patients (75.7?%) were male. Rentrop classifications 1-2-3 (presence of CCV) were determined in 222 (48.1?%) patients. The presence of CCV was significantly associated with low levels of eGFR (p?=?0.001), increased serum creatinine levels (p?=?0.034), high levels of serum albumin (0.036), and the Gensini score (p?<?0.001). Multivariate analysis showed that the Gensini score was an independent predictor of the presence of CCV (OR?=?1.090, 95?% CI: 1.032–1.151, p?=?0.002).

Conclusion

We suggest that the association between mild-to-moderate renal impairment and the presence of CCV may be explained by increased myocardial ischemia and severe CAD.     

The association between circulating endothelial progenitor cells and coronary collateral formation

Aim

We investigated the relationship between coronary collateral formation and circulating endothelial progenitor cells (EPC) in patients undergoing coronary angiography.

Methods and results

Circulating CD133⁺/34⁺ and CD34⁺/KDR⁺ EPCs were determined in 68 patients (normal coronary vessels in 24 patients and coronary artery disease (CAD) in 44 patients) (age: 58.7 ± 10.1, 64.7% male). Circulating EPCs were higher among patients with normal coronary vessels compared to patients with CAD for CD133⁺/34⁺ (p < 0.05) and CD34⁺/KDR⁺ cells (p < 0.05). The number of EPCs were significantly greater in patients with good coronary collateral formation (p < 0.05). EPC count was independent predictor for coronary collateral formation after adjustment for other cardiovascular risk factors and extent of CAD (p = 0.037).

Conclusion

In patients with severe coronary stenosis, those with increased circulating EPCs had better collateral formation compared to those with lower EPC counts. Our findings implicate that in addition to presence of critical stenosis, intact response of bone marrow is necessary for collateral formation in CAD.     

Prognostic value of paroxysmal nocturnal haemoglobinuria clone presence in aplastic anaemia patients treated with combined immunosuppression: results of two‐centre prospective study

Paroxysmal nocturnal haemoglobinuria (PNH) clones are frequently detected in patients with aplastic anaemia (AA). To evaluate the prognostic role of PNH clone presence we conducted a prospective study in 125 AA patients treated with combined immunosuppressive therapy (IST). Seventy‐four patients (59%) had a PNH clone (PNH+ patients) at diagnosis, with a median clone size of 0·60% in granulocytes and 0·15% in red blood cells. The response rate at 6 months was higher in PNH+ patients than that in PNH‐ patients, both after first‐ and second‐line IST: 68% vs. 45%, P = 0·0164 and 53% vs. 13%, P = 0·0502 respectively. Moreover, 42% of PNH+ patients achieved complete remission compared with only 16% of PNH‐ patients (P = 0·0029). In multivariate logistic regression analysis, PNH clone presence (odds ratio 2·56, P = 0·0180) and baseline absolute reticulocyte count (ARC) ≥30 × 10⁹/l (odds ratio 5·19, P = 0·0011) were independent predictors of response to treatment. Stratification according to PNH positivity and ARC ≥30 × 10⁹/l showed significant distinctions for cumulative incidence of response, overall and failure‐free survival. The results of this prospective study confirmed the favourable prognostic value of PNH clone presence in the setting of IST for AA.     

An unbalanced monocyte macrophage polarization in the bone marrow microenvironment of patients with poor graft function after allogeneic haematopoietic stem cell transplantation

Poor graft function (PGF) is a severe complication of allogeneic haematopoietic stem cell transplantation (allo‐HSCT). Murine studies have demonstrated that effective haematopoiesis depends on the specific bone marrow (BM) microenvironment. Increasing evidence shows that BM macrophages (MФs), which constitute an important component of BM immune microenvironment, are indispensable for the regulation of haematopoietic stem cells (HSCs) in the BM. However, little is known about the number and function of BM MФs or whether they directly interact with HSCs in PGF patients. In the current prospective case‐control study, PGF patients showed a significant increase in classically activated inflammatory MФs (M1; 2·18 ± 0·11% vs. 0·82 ± 0·06%, P < 0·0001), a striking reduction in alternatively activated anti‐inflammatory MФs (M2; 3·02 ± 0·31% vs. 21·89 ± 0·90%, P < 0·0001), resulting in a markedly increased M1/M2 ratio (0·82 ± 0·06 vs. 0·06 ± 0·002; P < 0·0001) in the BM compared with good graft function patients. Meanwhile, standard monocyte subsets were altered in PGF patients. Dysfunctional BM MФs, which were characterized by reduced proliferation, migration and phagocytosis, were evident in PGF patients. Furthermore, BM MФs from PGF patients with high tumour necrosis factor‐α and interleukin 12 levels and low transforming growth factor‐β levels, led to impaired BM CD34⁺ cell function. In summary, our data indicate that an unbalanced BM M1/M2 ratio and dysfunctional MФs may contribute to the occurrence of PGF following allo‐HSCT.     

The S447X variant of lipoprotein lipase gene is inversely associated with severity of coronary artery disease

Hyperlipidemia is a major risk factor for coronary artery disease (CAD). Lipoprotein lipase (LPL) is an important enzyme in lipoprotein metabolism. S447X polymorphism of the LPL gene has been implicated in the pathogenesis of CAD. Carriers of X447 allele were reported to have lower triglyceride and higher high-density lipoprotein cholesterol levels as well as a reduced risk of CAD. We hypothesized that S447X gene polymorphism might have a protective effect for CAD. A total of 178 subjects (mean age 42.97 ± 6.5 years) who underwent coronary angiography for clinical indications were included in the study. The patients had been referred for evaluation of chest pain and/or abnormal stress tests, and were selected consecutively. Gensini scores were used to assess the severity of CAD; 97 patients were diagnosed with angiographically proven CAD, and 81 subjects did not display significant CAD (≥70%) angiographically. Genotyping of LPL S447X polymorphism was performed by real-time polymerase chain reaction amplification and fluorescent probe melting point analysis on the light cycler. The minor allele frequencies of LPL 447X allele were 11.1% and 6.2% among subjects without CAD compared with CAD subjects (P = 0.081) and 447X allele had favorable effects on lipid levels among CAD patients; 447X homozygotes and heterozygotes displayed lower total cholesterol (171 ± 37 vs 208 ± 48 mg/dl, P = 0.02), lower triglycerides (121 ± 72 vs 184 ± 86 mg/dl, P = 0.02), lower low-density lipoprotein cholesterol (102 ± 27 vs 129 ± 39 mg/dl, P = 0.03). Gensini scores were significantly lower among the heterozygotes and homozygotes of LPL 447X allele than in the LPL S447 homozygotes (15 ± 23 vs 25 ± 30, P = 0.048). S447X polymorphism of LPL gene may have a protective role for the severity of CAD. The beneficial effects of S447X polymorphism of the LPL gene may be through its favorable effects on lipid levels.     

Impact of obstructive sleep apnea in recruitment of coronary collaterality during inaugural acute myocardial infarction

BackgroundObstructive sleep apnea (OSA) may lead to myocardial preconditioning by increasing coronary collateral vessel recruitment in patients with acute coronary occlusion.AimTo determine the relationship between the severity of obstructive sleep apnea and coronary collaterality during acute myocardial infarction.MethodsThis study prospectively included 71 patients with an inaugural myocardial infarction who had undergone a coronary angiography within 24 h of onset. All patients underwent an overnight polygraph before discharge and were classified according to the apnea–hypopnea index (AHI). Coronary collaterals were scored by visual analyses and according to the Rentrop grading system.ResultsMean age was 59 ± 11 years and 83% of patients were men. All patients had complete or subtotal occlusion of the infarct-related artery. After the sleep study, patients were divided into two groups: 25 were suffering from OSA (AHI > 15/h). Patients with OSA showed better collateral vessel development (Rentrop score ≥ 1) compared to non-OSA patients (68 vs. 41%, P = 0.032). AHI was significantly higher in patients with developed coronary collaterals (Rentrop ≥ 1) compared to those without collaterality (17.74 ± 13.2 vs. 12.24 ± 10.9, P = 0.025).ConclusionCoronary collateral development may be increased in OSA patients who are presenting with a first myocardial infarction.     

Abnormal Levels of Circulating Endothelial Progenitor Cells During Exacerbations of COPD

Cardiovascular morbidity and mortality is increased in patients with chronic obstructive pulmonary disease (COPD). Reduced levels of circulating endothelial progenitor cells (EPCs) are associated with increased risk of death in patients with stable coronary artery disease (CAD). Likewise, during acute events of CAD, the number of circulating EPCs increases under the influence of vascular endothelial growth factor (VEGF) and systemic inflammation. Abnormal levels of circulating EPCs have been reported in patients with COPD. However, the response of EPCs to episodes of exacerbation of the disease (ECOPD) has not been investigated yet. We hypothesized that similar to what occurs during acute events of CAD, levels of circulating EPCs would increase during ECOPD. We compared levels of circulating EPCs (assessed by the % of CD34⁺KDR⁺ cells determined by flow cytometry) in patients hospitalized because of ECOPD (n = 35; 65 ± 9 years [mean ± SD]; FEV₁ = 46 ± 15% predicted), patients with stable COPD (n = 44; 68 ± 8 years; FEV₁ = 49 ± 17% predicted), smokers with normal lung function (n = 10; 60 ± 9 years), and healthy never smokers (n = 10; 62 ± 4 years). To investigate potential mechanisms of EPC regulation, we assessed both VEGF and high-sensitivity C-reactive protein (hsC-RP) in plasma. Our results show that EPC levels were higher (p < 0.05) in patients with ECOPD (1.46 ± 1.63%) than in those with stable disease (0.68 ± 0.83%), healthy smokers (0.65 ± 1.11%), and healthy never smokers (1.05 ± 1.36%). The percentage of circulating EPCs was positively related to VEGF plasma levels during ECOPD (r = 0.51, p = 0.003). In a subset of 12 patients who could be studied during both ECOPD and clinical stability, the EPCs levels increased during ECOPD. We conclude that EPC levels are increased during ECOPD, likely in relation to VEGF upregulation.     

Melatonin ameliorates low‐grade inflammation and oxidative stress in young Zucker diabetic fatty rats

The aim of this study was to investigate the effects of melatonin on low‐grade inflammation and oxidative stress in young male Zucker diabetic fatty (ZDF) rats, an experimental model of metabolic syndrome and type 2 diabetes mellitus (T2DM). ZDF rats (n = 30) and lean littermates (ZL) (n = 30) were used. At 6 wk of age, both lean and fatty animals were subdivided into three groups, each composed of 10 rats: naive (N), vehicle treated (V), and melatonin treated (M) (10 mg/kg/day) for 6 wk. Vehicle and melatonin were added to the drinking water. Pro‐inflammatory state was evaluated by plasma levels of interleukin‐6 (IL‐6), tumor necrosis factor‐α (TNF‐α), and C‐reactive protein (CRP). Also, oxidative stress was assessed by plasma lipid peroxidation (LPO), both basal and after Fe²⁺/H₂O₂ inducement. ZDF rats exhibited higher levels of IL‐6 (112.4 ± 1.5 pg/mL), TNF‐α (11.0 ± 0.1 pg/mL) and CRP (828 ± 16.0 µg/mL) compared with lean rats (IL‐6, 89.9 ± 1.0, P < 0.01; TNF‐α, 9.7 ± 0.4, P < 0.01; CRP, 508 ± 21.5, P < 0.001). Melatonin lowered IL‐6 (10%, P < 0.05), TNF‐α (10%, P < 0.05), and CRP (21%, P < 0.01). Basal and Fe²⁺/H₂O₂‐induced LPO, expressed as malondialdehyde equivalents (µmol/L), were higher in ZDF rats (basal, 3.2 ± 0.1 versus 2.5 ± 0.1 in ZL, P < 0.01; Fe²⁺/H₂O₂‐induced, 8.7 ± 0.2 versus 5.5 ± 0.3 in ZL; P < 0.001). Melatonin improved basal LPO (15%, P < 0.05) in ZDF rats, and Fe²⁺/H₂O₂‐ induced LPO in both ZL (15.2%, P < 0.01) and ZDF rats (39%, P < 0.001). These results demonstrated that oral melatonin administration ameliorates the pro‐inflammatory state and oxidative stress, which underlie the development of insulin resistance and their consequences, metabolic syndrome, diabetes, and cardiovascular disease.     

Presence of endothelial colony-forming cells is associated with reduced microvascular obstruction limiting infarct size and left ventricular remodelling in patients with acute myocardial infarction

Endothelial colony-forming cells (ECFCs) are known to increase after acute myocardial infarction (AMI). We examined whether the presence of ECFCs is associated with preserved microvascular integrity in the myocardium at risk by reducing microvascular obstruction (MVO). We enrolled 88 patients with a first ST elevation AMI. ECFC colonies and circulating progenitor cells were characterized at admission. MVO was evaluated at 5 days and infarct size at 5 days and at 6-month follow-up by magnetic resonance imaging. ECFC colonies were detected in 40 patients (ECFC^pos patients). At 5 days, MVO was of greater magnitude in ECFC^neg versus ECFC^pos patients (7.7 ± 5.3 vs. 3.2 ± 5%, p = 0.0002). At 6 months, in ECFC^pos patients, there was a greater reduction in infarct size (−32.4 ± 33 vs. −12.8 ± 24%; p = 0.003) and a significant improvement in left ventricular (LV) volumes and ejection fraction. Level of circulating CD34+/VEGF-R2+ cells was correlated with the number of ECFC colonies (r = 0.54, p < 0.001) and relative change in infarct size (r = 0.71, p < 0.0001). The results showed that the presence of ECFC colonies is associated with reduced MVO after AMI, leading to reduced infarct size and less LV remodelling and can be considered a marker of preserved microvascular integrity in AMI patients.     

Increased platelet activation in patients with slow coronary flow

We tested the hypothesis that increased platelet activation may be present in patients with slow coronary flow (SCF) and may contribute to the pathogenesis of slow coronary flow phenomenon (SCFP). Fifty patients angiographically proven normal coronary flow (control group; mean age = 61.3 ± 7.0 years, 43 male) and 50 patients with angiographically proven SCF in all coronary arteries (patient group; man age = 62.7 ± 6.7 years, 38 male) were included in the present study. Coronary flow rates of all subjects were documented by Thrombolysis In Myocardial Infarction frame count (TIMI frame count). Patients with a corrected TIMI frame count greater than two standard deviations from normal published range for the particular vessel were considered as having SCF. Complete blood count and mean platelet volume (MPV) was measured from whole blood sample with Abbott Cell-Dyne 4000 cell counter. Plasma sP-selectin concentrations were analyzed with sP-Selectin ELISA kit. There were no statistically significant differences between the two groups with respect to baseline demographic, clinical and lipid parameters. Not only MPV values but also plasma sP-selectin levels were significantly higher in patients with the patients with SCF compared to those of controls (for MPV; 8.2 ± 0.7 vs. 7.2 ± 0.6 fl, P < 0.001, for sP-Selectin; 1.5 ± 0.3 vs. 1.0 ± 0.2 ng/ml, P < 0.001). Interestingly, significant positive correlations were detected between mean TIMI frame counts and MPV and sP-selectin levels (for MPV; r = 0.56, P < 0.001, for sP-selectin r = 0.67, P < 0.001). The current study demonstrates that platelet activity is increased in the patients with SCF compared to that of the patients with normal coronary flow.     

Relationship between brachial‐ankle pulse wave velocity and invasively measured aortic pulse pressure

Although brachial‐ankle pulse wave velocity (baPWV) has been widely used as an index of arterial stiffness, no consensus exists about whether baPWV can reflect central aortic stiffness. The authors investigated the association between baPWV and invasively measured aortic pulse pressure (APP) in a total of 109 consecutive patients (mean age, 62.3 ± 11.3 years; 67.9% men). Most patients (91%) had obstructive coronary artery disease, and mean baPWV and APP values were 1535 ± 303 cm/s and 66.8 ± 22.5 mm Hg, respectively. In univariate analysis, there was a significant linear correlation between baPWV and APP (r = .635, P < .001). The correlation between baPWV and APP remained significant even after controlling for potential confounders (β = 0.574, P < .001; R² = .469). Arterial stiffness measured by baPWV showed a strong positive correlation with invasively measured APP, independent of clinical confounders. Therefore, baPWV can be a good marker of central aortic stiffness.     

Intra-abdominal fat estimation by bio-electrical impedance analysis in patients with fibrocalculous pancreatic diabetes compared with BMI matched type 2 diabetic subjects and healthy controls

Background and aimsIntra-abdominal adipose tissue (IAAT) is a major contributor to insulin resistance (IR) in type 2 diabetes mellitus (T2D). Prior studies have demonstrated evidence of IR in fibrocalculous pancreatic diabetes (FCPD). However, no data exists on IAAT estimation in FCPD. Hence, we compared IAAT area among FCPD patients and an equal number of body mass index (BMI) matched T2D patients and healthy controls.MethodsWe recruited 60 patients with FCPD between January 2019 and February 2020. Body composition analysis was performed via bio-electrical impedance analysis.ResultsThe mean ages were 37.82 ± 10.07, 51.02 ± 9.9, and 30.7 ± 11.51 years for patients in the FCPD, T2D, and control groups, respectively. The mean BMI of patients in the three groups was 20.65 ± 2.01, 20.83 ± 1.49, and 20.91 ± 1.59 kg/m², respectively (P = 0.684). The mean IAAT area of patients in the FCPD, T2D, and control groups was 67.93 ± 43.38, 117.78 ± 48.03, and 100.52 ± 42.31 cm², respectively. IAAT was significantly lower in patients with FCPD compared with those in the other two groups (P < 0.0001). In the entire cohort, IAAT showed significant positive correlation with age (r = 0.20), abdominal circumference (r = 0.80), waist hip ratio (r = 0.75), and LDL level (r = 0.25) (P < 0.05).ConclusionsPatients with FCPD have significantly lower IAAT compared to BMI matched T2D subjects and healthy controls. IAAT does not appear to be a major contributor to insulin resistance observed in patients with FCPD.     

Association between carbonyl stress markers and the risk of acute coronary syndrome in patients with type 2 diabetes mellitus–A pilot study

Background and aimsCarbonyl stress is one of the mechanisms responsible for diabetes and its complications. The study was planned to examine the relationship between carbonyl stress markers and the risk of acute coronary syndrome (ACS) in patients with type 2 diabetes mellitus (T2DM).MethodsForty T2DM patients with ACS and forty T2DM patients without ACS participated in this cross-sectional pilot study. Routine biochemical investigations, creatine kinase-total (CK-T), and creatine kinase-MB (CK-MB) levels were estimated. Serum carbonyl stress markers were analysed by enzyme-linked immunosorbent assay. Binary logistics regression was done to determine the predictive value of carbonyl stress markers for ACS.ResultsFasting plasma glucose, serum total methylglyoxal (MG), methylglyoxal derived hydroimidazolones-1 (MG-H1), and N^ε-carboxymethyl-lysine (CML) levels were significantly higher in T2DM patients with ACS than in those without ACS. Serum glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and glyoxalase-1 (GLO1) levels were significantly lower in T2DM patients with ACS than in those without ACS. Fasting plasma glucose level was significantly positively correlated with serum MG (r = 0.441, P < 0.001), CML (r = 0.649, P < 0.001), MG-H1 (r = 0.725, P < 0.001), and negatively correlated with serum GAPDH (r = – 0.268, P = 0.012) and GLO1 (r = – 0.634, P = 0.016). Receiver operating characteristic curve analysis showed that serum GAPDH and GLO1 could predict the risk of ACS in T2DM patients.ConclusionThese findings revealed that high carbonyl stress due to lower levels of GAPDH and GLO1 may predispose patients with T2DM for more risk of ACS.     

冠心病合并糖尿病患者血浆SDF-1水平及与冠状动脉侧支循环的相关性研究

目的 探讨冠心病合并糖尿病（DM）患者血浆基质细胞衍生因子-1（SDF-1）水平及与冠状动脉侧支循环的关系。方法纳入79例拟诊冠心病并行冠状动脉造影（CAG）的患者。根据CAG结果分为：正常对照组（n=26）及冠心病组（n=53）。冠心病组又根据患者是否合并DM分为：合并DM亚组（n=21）与未合并DM亚组（n=32）。采用ELISA法检测患者血浆中SDF-1的水平;用Rentrop分级系统对冠状动脉侧支血管形成进行评级。比较各组患者血浆SDF-1的水平,并对冠心病患者SDF-1的水平与Rentrop分级进行直线相关分析。结果冠心病组患者血浆SDF-1水平低于对照组,两组差异有统计学意义（P〈0.05）;冠心病合并DM亚组SDF-1水平低于未合并DM亚组,两亚组间差异亦有统计学意义（P〈0.05）。合并DM亚组冠脉侧支循环形成率为33.3%,低于未合并DM亚组冠脉侧支循环的形成率（75.0%）,两亚组侧支循环形成率有统计学差异（P〈0.05）。冠心病组患者SDF-1水平与Rentrop的分级呈正相关（r=0.508,P〈0.01）。结论冠心病合并DM患者血浆中SDF-1水平及侧支循环形成的能力降低,SDF-1水平与冠状动脉侧支循环形成的能力呈正相关。     

Risk factors for avascular necrosis among Filipino patients with systemic lupus erythematosus

Aim: To describe the clinical features and risk factors for avascular necrosis (AVN) in a cohort of Filipino patients with systemic lupus erythematosus (SLE). Methods: We reviewed the medical records of SLE patients with a diagnosis of AVN, seen at the University of Santo Tomas (Manila, Philippines) Section of Rheumatology, from 1995 to 2005. The diagnosis of AVN was based on clinical symptoms and confirmed by plain radiographs or magnetic resonance imaging. Possible risk factors for the development of AVN were identified. The clinical data of SLE patients without AVN were also obtained and served as controls. Results: Of the 540 patient charts reviewed, 43 (8.0%) patients (41 female, 2 male) with AVN were included. Out of a total of 66 joints involved, the hip was the most frequently involved. We included 93 SLE patients without AVN who were matched for age, sex and disease duration as the control group. Mean daily prednisone dose (11.9 ± 7.2 vs 9.3 ± 6.6 mg, P = 0.023), mean cumulative prednisone‐equivalent dose in first month of SLE diagnosis (1.5 ± 0.8 vs 1.3 ± 0.8 g, P = 0.011), and total cumulative prednisone‐equivalent dose (30.0 ± 2.7 vs 20.3 ± 1.9 g, P = 0.023) were higher in the AVN group than in the controls. Clinical variables significantly associated with AVN included the presence of vasculitis (OR = 4.45, 95% CI 1.65–12.18, P = 0.0007), the use of intravenous pulse steroids (OR = 2.92, 95% CI 1.21–7.08, P = 0.008), and the mean total cumulative prednisone‐equivalent dose ≥ 23.4 g (OR = 2.92, 95% CI 1.3–6.6, P = 0.007). Conclusion: Corticosteroid use and vasculitis were consistent risk factors seen among Filipino SLE patients who developed AVN during the course of their disease.     

Increased circulating monocyte count is related to good collateral development in coronary artery disease

Monocytes have been shown to take an important role in collateral growth in animal studies. The aim of the study was to investigate the relation of circulating monocyte count with collateral development in patients with severely stenotic CAD. Patients who had > or =95% stenosis in at least one major coronary artery were included in the study. Coronary angiograms of 210 eligible patients from our database were analyzed again and 103 of them had good and 107 had poor collateral development according to Cohen-Rentrop method. Only the monocyte count was found to be significantly different between two groups (671+/-218 mm(-3) versus 522+/-195 mm(-3), p<0.001) when multivariate analysis was performed and an increased monocyte count was observed in the good collateral group (Odds ration [OR], 2.918; 95% confidence interval [CI], 1.281-6.648, p=0.011). This study in which the relationship between monocyte count in blood and collateral development was disclosed has a potential importance in clinical and basic cardiovascular medicine.