Obesity paradox in pulmonary hypertension due to left ventricular systolic dysfunction.

OBJECTIVE: Pulmonary hypertension (PH) due to left ventricular systolic dysfunction (PH-HFrEF) is a common heart disease with poor prognosis. In this study, we explored the risk factors for PH-HFrEF and investigated the related factors affecting the prognosis of PH-HFrEF patients. METHODS: The study recruited consecutive patients with PH-HFrEF and systolic pulmonary artery pressure (sPAP) of more than 40 mm Hg with left ventricular ejection fraction (LVEF) of less than 45% on echocardiography. Patients with left ventricular systolic dysfunction (HFrEF) but without PH (sPAP < 30 mmHg and LVEF < 45%) were chosen as the control group. Patients were followed up for 18 months, and major adverse cardiac events (MACE) were recorded. RESULTS: In total, 93 patients with PH-HFrEF formed the study group and 93 LVEF-matched patients with HFrEF were enrolled as controls. Body mass index (BMI) in PH-HFrEF patients was significantly lower compared with the control group (p < 0.05). Multivariate logistic regression analysis revealed that low BMI was an independent predictor of the presence of PH in patients with HFrEF (p < 0.05). There were 23 (24.7%) MACE in the PH-HFrEF group and 18 (19.4%) MACE in the control group. Cox regression analysis showed that low BMI was an independent predictor of MACE occurrence in the PH-HFrEF group (p < 0.05). CONCLUSION: Low BMI appear to be significantly associated with PH occurrence in patients with HFrEF, and is an independent predictor of MACE in patients with PH-HFrEF.

Relationship between soluble Semaphorin4D and cognitive impairment in patients with obstructive sleep apnea-hypopnea syndrome.

To investigate the relationship between plasma soluble semaphorin4D (sSema4D) and obstructive sleep apnea-hypopnea syndrome (OSAHS), and to ascertain the effect of sSema4D on cognitive dysfunction in patients with OSAHS. We prospectively recruited 30 men with moderate-severe OSAHS diagnosed by polysomnography, and 30 healthy controls with matched gender, age and education level. Montreal Cognitive Assessment (MoCA) was administered to determine cognitive impairment. Plasma sSema4D levels were measured. Among the total of 60 study patients, the overall plasma sSema4D level was 7.81 ± 1.91 ng/ml. Plasma sSema4D level in OSAHS group was significantly higher than that in controls (8.92 ± 1.79 vs 6.70 ± 1.28 ng/ml, p < 0.001). In OSAHS subgroup, patients with cognition impairment (CI) had higher plasma sSema4D level (10.50 ± 1.16 vs 8.00 ± 1.41 ng/ml, p < 0.001) and apnea-hypopnea index (AHI) (48.1 ± 14.0 vs 30.3 ± 9.2, p < 0.001) than those in non-CI group. Multiple logistic regression revealed that plasma sSema4D level (AOR 2.824, 95 % CI 1.562-5.103; p = 0.001) and BMI (AOR 2.237, 95 % CI 1.345-3.722; p = 0.002) were significantly associated with OSAHS, and plasma sSema4D was a significant predictor of CI after adjustment for other confounders (AOR 4.956, 95 % CI 1.581-15.538; p = 0.006). OSAHS patients, especially those with cognition impairment, are featured by elevated plasma sSema4D level, and sSema4D is significantly associated with cognition impairment induced by OSAHS.

Relationship between severity of obstructive sleep apnea and adverse cardiac outcomes in non-diabetic patients presenting with myocardial infarction.

Previous studies that have reported an association between obstructive sleep apnea and adverse cardiac events were confounded by a high prevalence of diabetes mellitus. We investigated the relationship between obstructive sleep apnea and the occurrence of major adverse cardiac events in non-diabetic patients who presented with ST-segment elevation myocardial infarction. A total of 41 patients who underwent overnight sleep screening within 5 days after admission for myocardial infarction from January 2007 to December 2008 were identified. Major adverse cardiac events-defined as a composite of cardiac death, non-fatal myocardial infarction, hospitalization for angina and congestive heart failure at 5-year follow-up-were determined. The patients were divided into two groups: those who experienced major adverse cardiac events and those who did not. In the overall cohort, the prevalence of obesity was 4.9 %. A total of 13 (31.7 %) patients had major adverse cardiac events. The mean apnea-hypopnea index was 25.4 ± 20.3. The group that experienced major adverse cardiac events had a higher apnea-hypopnea index than the group that did not (36.1 ± 21.0 vs 20.4 ± 18.2; P = 0.016). After adjusting for the resolution of ST-segment elevation and the use of a glycoprotein IIb/IIIa inhibitor, logistic regression analysis revealed that the apnea-hypopnea index remained an independent predictor of major adverse cardiac events (odds ratio 1.044; 95 % confidence interval 1.003-1.086; P = 0.033). In non-diabetic patients, the severity of obstructive sleep apnea was associated with the occurrence of major adverse cardiac events at 5-year follow-up after ST-segment elevation myocardial infarction.

Serum adropin level in patients with stable coronary artery disease.

OBJECTIVES: Adropin is a newly identified secreted protein implicated in the regulation of insulin sensitivity and vascular endothelial function. Recent studies have shown that lower serum adropin level is related to acute myocardial infarction and coronary atherosclerosis. The primary objective of this study was to ascertain the association of serum adropin level with stable coronary artery disease (SCAD). METHODS: We prospectively recruited a cohort of patients with SCAD and similar sample size subjects without coronary artery disease as controls. Their serum adropin levels were measured, and the severity of coronary atherosclerosis in SCAD patients was quantified with the syntax score. RESULTS: A total of 116 patients with SCAD and 116 control subjects without coronary artery disease were recruited. Patients with SCAD had lower serum adropin levels when compared with the controls (59.2±19.3 versus 70.0±18.2 pg/mL, P<0.001). The multiple logistic regression revealed that low serum adropin level was a significant predictor of SCAD (AOR 0.976, 95% CI 0.960-0.992; p=0.003). Through the gamma regression model, it was further revealed that serum adropin level is significantly associated with syntax score (coefficient: -0.134, 95% CI: -0.212- -0.056; p=0.001). CONCLUSIONS: Low serum adropin level is a significant predictor of SCAD. It is also associated with syntax score, thus indicating the close relationship between adropin and coronary atherosclerosis.

Association of cystatin C with coronary artery calcification in patients undergoing multidetector computed tomography.

ABSTRACT: Cystatin C is associated with atherosclerosis, but the relationship between cystatin C and coronary artery calcification (CAC) is uncertain. The purpose of this study was to evaluate the predictive value of cystatin C on the occurrence and severity of CAC.A total of 1447 hospitalized patients with coronary computed tomography angiography were selected in this study. According to the CAC score (CACS), patients were divided into calcification group (with CAC, n = 749) and control group (without CAC, n = 698). The calcification group was further divided into low calcification group (CACS < 100, n = 407), medium calcification group (CACS 100-400, n = 203), and high calcification group (CACS≥400, n = 139).Patients with CAC had higher cystatin C level than those in control group (P < .05). With the increase of calcification score, the cystatin C level showed an upward trend. The cystatin C level in the high calcification group was significantly higher than those in the low and medium calcification group (P < .05). ROC curve analysis showed that cystatin C had a high predictive value for the occurrence of CAC [area under the curve 0.640, 95% confidence interval (95% CI) 0.591-0.690, cut-off value 0.945 mg/L, sensitivity 0.683, specificity 0.558, P < .05] and severe CAC (area under the curve 0.638, 95% CI 0.550-0.762, cut-off value 0.965 mg/L, sensitivity 0.865, specificity 0.398, P < .05). Multivariate logistic regression analysis showed that cystatin C was an independent predictor of severe CAC (AOR 3.748, 95% CI 1.138-10.044, P < .05).Cystatin C was significantly associated with the occurrence and severity of CAC, suggesting that cystatin C had the potential as a predictor of CAC.

Adropin inhibits the phenotypic modulation and proliferation of vascular smooth muscle cells during neointimal hyperplasia by activating the AMPK/ACC signaling pathway.

In-stent restenosis (ISR) remains an inevitable problem for some patients receiving drug-eluting stent (DES) implantation. Intimal hyperplasia is an important biological cause of ISR. It has been previously reported that adropin is a potentially protective factor in cardiovascular disease. Therefore, the present study investigated the function of adropin in inhibiting smooth muscle cell (SMC) phenotype modulation and proliferation, causing intimal hyperplasia. A total of 56 patients who visited the hospital consecutively (25 with ISR and 31 without ISR), who were followed up between April 2016 and March 2019, 1 year following DES, were analyzed to evaluate the association between in-stent neointimal volume and adropin serum levels. Rat aorta smooth muscle cells (RASMCs) were used to determine the effects of adropin on their phenotypic modulation and proliferation using western blot, MTT, PCR and immunofluorescence analyses. Adropin serum levels in the ISR group were significantly lower than those in the non-ISR group. Furthermore, linear regression analysis revealed that only adropin levels were negatively associated with neointimal volume in both groups. The overall adropin levels of the 56 patients and the percentages of neointimal volume revealed a strong negative association. In vitro, adropin suppressed angiotensin II (Ang II)-induced phenotypic modulation in RASMCs by restoring variations of osteopontin and α-smooth muscle actin. Furthermore, compared with the Ang II group, adropin markedly decreased the percentage of G2/M-phase cells. Finally, adropin negatively regulated the phenotypic modulation and proliferation of RASMCs via the AMP-activated protein kinase/acetyl-CoA carboxylase (AMPK/ACC) signaling pathway. In conclusion, an independent, negative association was revealed between adropin and intimal hyperplasia; specifically, adropin inhibited the phenotypic modulation and proliferation of RASMCs by activating the AMPK/ACC signaling pathway. Therefore, adropin may be used as a potential predictor and therapeutic target for intimal hyperplasia and ISR.

Effect of beraprost on pulmonary hypertension due to left ventricular systolic dysfunction.

Beraprost is used to treat peripheral chronic arterial occlusive disease. However, the efficacy and safety of beraprost in patients with pulmonary hypertension (PH) due to left ventricular systolic dysfunction (PH-HFrEF) remains unknown. The primary objective of this study was to determine the effects of beraprost on PH-HFrEF.We prospectively recruited patients with PH-HFrEF as determined by echocardiography and right cardiac catheterization. Beraprost sodium was given orally (1 µg/kg/d) added to the usual treatment, and patients were evaluated at 1-year follow-up.Twenty-five patients were recruited with baseline systolic pulmonary artery pressure (PAP) of 49.5 ±â€Š10.8 mm Hg. Systolic PAP results at 3, 6, 9, and 12 months were 39.1 ±â€Š8.1, 30.4 ±â€Š5.2, 27.7 ±â€Š3.0, and 27.0 ±â€Š4.7 mm Hg, respectively, which were all significantly lower than systolic PAP at baseline (P < .05). Left ventricular ejection fraction results at 6 months (43.5 ±â€Š7.0%), 9 months (47.0 ±â€Š5.5%), and 12 months (48.2 ±â€Š4.8%) were significantly higher than at baseline (34.7 ±â€Š9.2%) (P < .05). Six-minute walking distance at 3 months (282.8 ±â€Š80.6 m), 6 months (367.1 ±â€Š81.2 m), 9 months (389.8 ±â€Š87.1 m), and 12 months (395.7 ±â€Š83.4 m) increased with time, and all were significantly higher than baseline (190.1 ±â€Š75.5 m) (P < .05). One patient developed atrial fibrillation and recovered to sinus rhythm after intravenous administration of amiodarone. There were no instances of cardiac-related death, severe bleeding, or severe impairment of liver function.Routine oral administration of beraprost sodium added to the usual treatment may improve cardiopulmonary hemodynamics and exercise capacityin patients with PH-HFrEF.

Adropin is associated with hyperhomocysteine and coronary atherosclerosis.

Homocysteine has been recognized as a risk factor for atherosclerosis and cardiovascular diseases. Adropin is a newly-identified energy homeostasis protein with a potential protective effect against coronary artery disease (CAD). This study attempted to measure the correlation between serum homocysteine and adropin levels in patients with CAD, and to ascertain how the two hormones could affect the severity of coronary atherosclerosis. A cohort of CAD patients who had undergone coronary angiography was prospectively recruited. The serum homocysteine and adropin levels of the patients were measured and the severity of coronary atherosclerosis was quantified with the SYNTAX score. The data were analyzed with a generalized structural equation model. In total, 170 consecutive patients were recruited with a mean serum homocysteine level of 15.9±8.3 µmol/l, and 76 (44.7%) patients were identified as hyperhomocysteinemic with a serum homocysteine level >15 µmol/l. Serum homocysteine level was found to be significantly negatively correlated with serum adropin level (r=-0.169, P=0.028). Patients with hyperhomocysteinemia had lower serum adropin levels and higher SYNTAX scores than patients without hyperhomocysteinemia. Further analysis with a generalized structural equation model showed that adropin was significantly associated with hyperhomocysteinemia (adjusted odds ratio: 0.95, 95% confidence interval: 0.93 to 0.98; P=0.002), which in turn was significantly associated with the SYNTAX score (coefficient: 4.71, 95% confidence interval: 1.39 to 8.03; P=0.005). In conclusion, the serum homocysteine level was inversely correlated with the serum adropin level in patients with CAD. A low serum adropin level was associated with hyperhomocysteinemia and more severe coronary atherosclerosis, as reflected by a higher SYNTAX score.

Knockdown of ezrin suppresses the migration and angiogenesis of human umbilical vein endothelial cells in vitro.

Progressive tumor growth is dependent on angiogenesis. The mechanisms by which endothelial cells (ECs) are incorporated to develop new blood vessels are not well understood. Recent studies reveal that the ezrin radixin moesin (ERM) family members are key regulators of cellular activities such as adhesion, morphogenetic change, and migration. We hypothesized that ezrin, one of the ERM family members, may play important roles in ECs organization during angiogenesis, and new vessels formation in preexisting tissues. To test this hypothesis, in this study, we investigated the effects of ezrin gene silencing on the migration and angiogenesis of human umbilical vein endothelial cells (HUVECs) in vitro. HUVECs were transfected with plasmids with ezrin-targeting short hairpin RNA by using the lipofectamine-2000 system. Wound assay in vitro and three-dimensional culture were used to detect the migration and angiogenesis capacity of HUVECs. The morphological changes of transfected cells were observed by confocal and phase contrast microscopy. Our results demonstrated that the decreased expression of ezrin in HUVECs significantly induced the morphogenetic changes and cytoskeletal reorganization of the transfected cells, and also reduced cell migration and angiogenesis capacity in vitro, suggesting that ezrin play an important role in the process of HUVECs migration and angiogenesis.

Sleep apnoea is a risk factor for acute kidney injury after coronary artery bypass grafting.

OBJECTIVES: Acute kidney injury (AKI) is a common complication in patients who undergo coronary artery bypass grafting (CABG). Sleep apnoea is associated with sympathetic activation, inflammatory reaction and plaque burden. The possible status of sleep apnoea as a risk factor for AKI after CABG has not been studied. METHODS: We recruited 169 patients for an overnight sleep study using a Food and Drug Administration-approved portable device before they underwent elective CABG. AKI after CABG was defined as a relative increase of greater than 25% or an absolute increase of greater than 0.5 mg/dl in the serum creatinine level from baseline within 5 days after CABG. A generalized structural equation model (gSEM) was then applied to ascertain whether sleep apnoea, defined as an Apnoea-Hypopnoea index (AHI) of 15 or higher, was associated with AKI after CABG after adjusting for the effects of confounding variables. RESULTS: Of the 150 patients (88.8%) who completed the study, the incidence of AKI after CABG was 22.7%. The mean AHI was higher in the AKI group (27.4 ± 19.8) than that in the non-AKI group (18.3 ± 16.5; P < 0.01). The prevalence of sleep apnoea was higher in the AKI group (64.7%) than that in the non-AKI group (45.7%; P = 0.05). The patients in the AKI group were older (P < 0.01) and shorter (P = 0.03) and had higher systolic blood pressures (P = 0.01), greater waist circumferences (P = 0.04) and larger left atrial diameters (P < 0.01) than those in the non-AKI group. The patients in the AKI group had higher serum haemoglobin levels (P = 0.04) and lower glucose levels (P < 0.01) than those in the non-AKI group. A gSEM based on binomial distributions showed that sleep apnoea was an independent predictor of AKI after CABG (adjusted odds ratio, 2.89; confidence interval, 1.09-7.09; P = 0.03) after adjustment for the effects of haemoglobin, glucose levels, the left atrial diameter and systolic blood pressure. CONCLUSIONS: Sleep apnoea is prevalent and is associated with AKI after CABG. The data presented here provide the first insights into the potential of treating sleep apnoea to attenuate the risk of AKI after CABG.

Influence of insulin resistance on in-stent restenosis in patients undergoing coronary drug-eluting stent implantation after long-term angiographic follow-up.

OBJECTIVE: Previous studies have reported that insulin resistance is related to early in-stent restenosis (ISR) after coronary stenting. This study aimed to evaluate the influence of insulin resistance on the long-term angiographic outcome in patients undergoing coronary drug-eluting stent (DES) implantation. MATERIALS AND METHODS: Within a single hospital-based cohort of patients (n=529) who underwent coronary DES implantation, angiographic follow-up was performed successfully for 417 study patients at 12-48 months after coronary stenting. ISR was defined as stenosis of at least 50% of the luminal diameter. Fasting plasma glucose and fasting plasma insulin were measured. Insulin resistance was expressed by the homeostasis model assessment index (HOMA-IRI). RESULTS: Among the 417 patients who completed angiographic follow-up (mean 17.5±10.2 months), 58 patients (13.9%) had ISR whereas the remaining 359 patients (86.1%) did not have ISR. Patients with ISR had higher insulin resistance index (IRI) than nonrestenosis patients (P=0.004). Multiple logistic regression analysis (logit) showed that IRI was associated significantly with ISR (adjusted odds ratio 1.476, 95% confidence interval 1.227-1.776; P<0.001). In the nondiabetes subgroup of 309 patients, IRI was higher in patients with ISR than in nonrestenosis patients, as confirmed in a separate logit analysis (adjusted odds ratio 1.456, 95% confidence interval 1.152-1.839; P=0.002). Multiple linear regression analysis showed that IRI was associated significantly with in-stent diameter stenosis degree (P=0.043). CONCLUSION: Insulin resistance was associated with ISR in patients undergoing coronary DES implantation at long-term angiographic follow-up.

Sleep apnea is associated with new-onset atrial fibrillation after coronary artery bypass grafting.

PURPOSE: New-onset atrial fibrillation (AF) after coronary artery bypass grafting (CABG) remains a prevalent problem. We investigated the relationship between sleep apnea and new-onset post-CABG AF during inhospital stay. MATERIALS AND METHODS: We prospectively recruited 171 patients listed for an elective CABG for an overnight sleep study. Sleep apnea was defined as apnea-hypopnea index greater than or equal to 5. RESULTS: Among the 160 patients who completed the study, those in the sleep apnea group (n=128; 80%) had larger left atrial diameter (40.4±5.4 vs 38.4±6.0 mm; P=.03) and left ventricular end-diastolic dimension (52.6±7.9 vs 49.2±6.8 mm; P=.03) than those in the non-sleep apnea group. The incidence of new-onset post-CABG AF was higher for the sleep apnea than non-sleep apnea groups (24.8% vs 9.7%; P=.07). There was 1 inhospital death and 2 patients with acute renal failure requiring dialysis after CABG in the sleep apnea group. None of the patients developed inhospital stroke. Multiple logistic regression analysis showed that sleep apnea was an independent predictor of post-CABG AF (odds ratio, 4.4; 95% confidence interval, 1.1-18.1; P=.04). CONCLUSION: Sleep apnea is prevalent in patients undergoing CABG. It increases the susceptibility to new-onset AF after CABG, probably related to atrial and ventricular remodeling.

Sleep apnoea and unscheduled re-admission in patients undergoing coronary artery bypass surgery.

INTRODUCTION: Although it has been recognised as a cardiovascular risk factor, data on sleep apnoea screening before coronary artery bypass grafting (CABG) are scarce. This study sought to determine the prevalence, predictors and effects of sleep apnoea on re-admission in patients undergoing CABG. METHOD: We prospectively recruited 152 patients to undergo an overnight sleep study before CABG. Sleep apnoea was defined as an apnoea-hypopnoea index of ≥15 events per hour. Data on unscheduled re-admission due to cardiovascular events were collected. RESULTS: Among the 138 patients who completed the sleep study, sleep apnoea was diagnosed in 69 (50%). The patients who had sleep apnoea had a lower left ventricular ejection fraction (p = 0.029), a larger left atrial diameter (p = 0.014) and a larger left ventricular end-systolic dimension (p = 0.019) than those who did not. Angiographic SYNTAX and Gensini scores were similar in patients with and without sleep apnoea. The generalised structural equation model revealed that hypertension, a high body mass index and chronic renal failure were independent predictors of sleep apnoea (p < 0.05). After an average follow-up of 6 ± 3 months, 12 patients with sleep apnoea (17.3%) and three patients without sleep apnoea (4.3%) were involved in unscheduled re-admission. Patients with sleep apnoea were almost five times more likely to have an unscheduled re-admission due to cardiovascular events (adjusted odds ratio: 4.63, 95% CI: 1.24-17.31, p = 0.023) than those without sleep apnoea. CONCLUSIONS: Sleep apnoea was prevalent and predictive of unscheduled re-admissions in patients scheduled for CABG.

Effects of gender on the prevalence of obstructive sleep apnea in patients with coronary artery disease.

STUDY OBJECTIVE: Male predominance has been observed in obstructive sleep apnea (OSA) studies conducted in the community and sleep clinics. Due to the different demographic and patient risk profiles of the studies involved, we investigated the effects of gender on OSA prevalence among patients with coronary artery disease (CAD). METHODS: We prospectively recruited a cohort of CAD patients for an overnight sleep study using a home testing portable diagnostic device. OSA was defined as apnea-hypopnea index (AHI) ≥ 15. RESULTS: One hundred sixty-two consecutive patients (male, n = 81; female, n = 81) were recruited, and most (60%) presented with acute coronary syndrome. The female patients were older (61 ± 10 versus 56 ± 10 years, p < 0.001), less likely to be smokers (8.6% versus 34.6%, p < 0.001), and more likely to have diabetes mellitus (70.4% versus 46.9%, p = 0.002) and chronic renal failure (17.3% versus 4.9%, p = 0.012) than the male patients. The sleep study's success rate was higher in female than male patients (88.9% versus 74.1%, p = 0.047). No significant differences were observed between them in the AHI, oxygen desaturation index, baseline SpO2, lowest SpO2, or total time SpO2 < 90%. The prevalence of OSA for the female and male patients was 40.3% and 35.0%, respectively (p = 0.323). CONCLUSION: Prevalence of OSA is high in CAD patients with no evidence of sex predilection. The lack of male predominance could be due to females being older and with more comorbidities.

Beneficial effects of intracoronary tirofiban bolus administration following upstream intravenous treatment in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention: the ICT-AMI study.

BACKGROUND: We investigated whether an additional intracoronary tirofiban bolus administration following upstream intravenous treatment could further improve myocardial reperfusion and clinical outcome in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). METHODS: A total of 453 eligible STEMI patients were randomly allocated to intracoronary bolus administration of tirofiban (10 µg/kg; n=229) or saline (10 mL; n=224) during primary PCI, followed by intravenous tirofiban infusion (0.15 µg/kg/min) for 24-36 h. Serum levels of P-selectin, vWF, CD40L and serum amyloid A (SAA) in the coronary sinus were measured before and after intracoronary bolus administration. The primary endpoint was ST-segment resolution (STR) at 90 min after the procedure. Second endpoints included corrected TIMI frame count (cTFC), left ventricular volumes and ejection fraction (EF), and major adverse cardiac events (MACE) at 30-day and 6-month follow-up. RESULTS: Intracoronary tirofiban administration resulted in a higher rate of completed STR (59.0% vs. 44.6%, P=0.002), lower cTFC (21.6±5.4 vs. 23.7±7.8, P=0.048), and significantly reduced coronary sinus levels of P-selectin, vWF, CD40L and SAA. Patients treated with intracoronary tirofiban had a trend toward less MACE at 30 days (3.1% vs. 6.7%, P=0.072). At 6 months, left ventricular end-systolic volume was smaller, EF was higher and MACE-free survival was improved (96.1% vs. 90.6%, P=0.020) in the intracoronary tirofiban group. CONCLUSIONS: An additional intracoronary tirofiban bolus administration following upstream intravenous treatment reduces coronary circulatory platelet activation and inflammatory process, and significantly improves myocardial reperfusion and left ventricular function as well as 6-month MACE-free survival for STEMI patients undergoing primary PCI.

Influence of insulin resistance on long-term outcomes in patients.

BACKGROUND: Insulin resistance (IR) is significantly associated with coronary artery disease and cardiovascular events in patients with or without type 2 diabetes mellitus. This study aimed to evaluate the influence of IR on long-term outcomes of patients undergoing percutaneous coronary intervention (PCI) with sirolimus-eluting stent (SES) implantation. METHODS: A total of 467 consecutive patients undergoing SES-based PCI were divided into IR group (n = 104) and non-IR group (n = 363). The patients were followed up for one year. The rate of major adverse cardiac events (MACEs) including death, non-fatal myocardial infarction and recurrent angina pectoris was compared by the log-rank test, and the independent risk factors were identified by the Cox regression analysis. RESULTS: MACEs occurred more frequently, and cumulative survival rate was lower in the IR group than in the non-IR group during the follow-up (all P < 0.05). IR was an independent risk factor for the occurrence of cardiac death and non-fatal myocardial infarction (OR = 2.76, 95%CI = 1.35 - 5.47, P = 0.034). Old age, diabetes, and multi-vessel disease were determinants for recurrent angina pectoris after PCI (P < 0.05). Subgroup analysis revealed that IR (OR = 3.35, 95%CI = 1.07 - 13.59, P = 0.013) and multi-vessel disease (OR = 2.19, 95%CI = 1.01 - 5.14, P = 0.044) were independent risk predictors for recurrent angina pectoris in patients with diabetes after PCI. CONCLUSIONS: IR is associated with reduced MACE-free survival and remains an independent predictor for recurrent angina pectoris after PCI with SES implantation.

[Effects of vimentin on invasion and metastasis of prostate cancer cell lines PC-3M-1E8 and PC-3M-2B4].

BACKGROUND & OBJECTIVE: Vimentin, a cytoskeleton protein, is involved in regulating the migration and proliferation of cells. This study was to detect the expression of vimentin in prostate cancer cell lines PC-3M-1E8 and PC-3M-2B4, and evaluate the effects of vimentin on invasion and metastasis of prostate cancer cells. METHODS: Two-dimensional gel electrophoresis (2-DE) followed by matrix-assisted laser desorption/time of flight mass spectrometry (MALDI TOF-MS) were used to detect the expression of vimentin in prostate cancer cell lines PC-3M-1E8 and PC-3M-2B4. Genetic intervention of vimentin gene and in vitro invasion assay were used to investigate the effects of vimentin on the invasion and metastasis of prostate cancer cells. RESULTS: The protein level of vimentin was higher in PC-3M-1E8 cells with high metastatic potential than in PC-3M-2B4 cells with low metastatic potential. Eukaryotic vectors expressing antisense-and sense-vimentin were constructed successfully and transfected into PC-3M-1E8 and PC-3M-2B4 cells separately. The number of invasive cells was significantly lower in PC-3M-1E8/vas cells with antisense-vimentin than in control PC-3M-1E8/3.1(-) cells (99.3+/-4.8 vs. 319.4+/-6.5, P<0.01), and significantly higher in PC-3M-2B4/vs cells with sense-vimentin than in control PC-3M-2B4/3.1(+) cells (330.5+/-5.8 vs. 98.6+/-7.5, P<0.01). CONCLUSION: Vimentin is a promising marker for predicting the invasion and metastasis of prostate cancer cells.