RESUMEN

Circulating microRNA has recently emerged as a promising biomarker for cardiovascular disease. This study sought to evaluate the diagnostic and prognostic value of circulating miR-133a as a marker of acute myocardial infarction in acute chest pain patients undergoing coronary angiography.Plasma was collected from 312 patients with chest pain on admission in the emergency department and 67 healthy controls. MiR-133a was detected using real-time quantitative PCR and enhanced accu-TnI, creatinine kinase-MB mass, and myoglobin were measured by immunoassay. End-point events (serious adverse cardiovascular events which require hospitalization or cardiovascular death) were examined in the AMI (acute myocardical infarction) group within 1, 6, 12, and 24 months.The miR-133a level was higher in AMI patients than in non-AMI patients (P < 0.001). In the ROC analysis, the sensitivity of miR-133a in diagnosis of AMI is 0.61 and the specificity is 0.68. In the prognostic analysis, only 1 endpoint event was observed in the non-AMI group; the amount of cases with end-point events in the AMI group at 1,6,12, and 24 months were 8, 19, 28, and 35, respectively. The cutoff value of miR-133a was determined using the median value of the AMI group and separated the patients into a positive group and a negative group. The Kaplan-Meier survival curve showed no significant difference in survival was detected in AMI patients between the miR-133a positive group and negative group after follow-up (12-month: x2 = 1.353, P = 0.245; 24-month: x2 = 3.722, P = 0.054). After adjusting for age, gender, Killip classes, prior myocardiac infarction history, myoglobin, LVEF (left ventricular ejection fraction), diabetes, hypertension, smoking and systolic blood pressure, miR133a had a significant association with the risk of events at 12 months (HR = 2.869, P = 0.024) and 24 months (HR = 3.936, P = 0.001).In patients undergoing coronary angiography, circulating miR-133a is upregulated in AMI patients, but it does not provide enough accuracy for clinical AMI diagnosis because it also rises in unstable angina patients. Its prognostic value in AMI is uncertain mainly for the number of cases with end-point event was small and may be further validated in a larger, better designed study.

Asunto(s)

Síndrome Coronario Agudo/sangre , Síndrome Coronario Agudo/genética , Dolor en el Pecho/sangre , Dolor en el Pecho/genética , Angiografía Coronaria , Insuficiencia Cardíaca/sangre , Insuficiencia Cardíaca/genética , MicroARNs/sangre , MicroARNs/genética , Infarto del Miocardio/sangre , Infarto del Miocardio/genética , Síndrome Coronario Agudo/diagnóstico por imagen , Adulto , Anciano , Anciano de 80 o más Años , Dolor en el Pecho/diagnóstico por imagen , Femenino , Insuficiencia Cardíaca/diagnóstico por imagen , Humanos , Masculino , Persona de Mediana Edad , Infarto del Miocardio/diagnóstico por imagen , Pronóstico , Sensibilidad y Especificidad , Regulación hacia Arriba/genética , Adulto Joven

RESUMEN

Curcumin, as a main pharmacological component in the traditional Chinese medicine-turmeric, has shown anti-inflammatory, anti-oxidation, anti-tumor and anti-fibrotic effects. This study aimed to investigate the possible underlying signaling pathway which was involved in the inhibition of LDL-induced proliferation of mesangial cells and matrix by curcumin. Rat mesangial cells in vitro were incubated with low-density lipoprotein (LDL) and different concentrations of curcumin (0, 6.25, 12.5, 25.0 μmol/L) or p38 MAPK inhibitor, SB203580 (10 μmol/L). Under LDL incubation, mesangial cells proliferated, the expression of MMP-2 mRNA and protein was decreased, the expression of COX-2 mRNA and protein was increased, reactive oxygen species (ROS) generation was increased and p38 MAPK was activated significantly (P<0.05). When LDL-induced cells were treated with curcumin in the concentration of 12.5 or 25.0 μmol/L, LDL-induced proliferation of mesangial cells was suppressed, the expression of MMP-2 mRNA and protein increased, the expression of COX-2 mRNA and protein downregulated, the production of ROS inhibited and p38 MAPK inactivated (P<0.05). In conclusion, curcumin can inhibit the LDL-induced proliferation of mesangial cells and up-regulate the expression of MMP-2, which may be related with the inhibitory effect of curcumin on COX-2 expression, ROS production and p38 MAPK.

RESUMEN

Curcumin, as a main pharmacological component in the traditional Chinese medicine-turmeric, has shown anti-inflammatory, anti-oxidation, anti-tumor and anti-fibrotic effects. This study aimed to investigate the possible underlying signaling pathway which was involved in the inhibition of LDL-induced proliferation of mesangial cells and matrix by curcumin. Rat mesangial cells in vitro were incubated with low-density lipoprotein (LDL) and different concentrations of curcumin (0, 6.25, 12.5, 25.0 μmol/L) or p38 MAPK inhibitor, SB203580 (10 μmol/L). Under LDL incubation, mesangial cells proliferated, the expression of MMP-2 mRNA and protein was decreased, the expression of COX-2 mRNA and protein was increased, reactive oxygen species (ROS) generation was increased and p38 MAPK was activated significantly (P<0.05). When LDL-induced cells were treated with curcumin in the concentration of 12.5 or 25.0 μmol/L, LDL-induced proliferation of mesangial cells was suppressed, the expression of MMP-2 mRNA and protein increased, the expression of COX-2 mRNA and protein downregulated, the production of ROS inhibited and p38 MAPK inactivated (P<0.05). In conclusion, curcumin can inhibit the LDL-induced proliferation of mesangial cells and up-regulate the expression of MMP-2, which may be related with the inhibitory effect of curcumin on COX-2 expression, ROS production and p38 MAPK.

Asunto(s)

Animales , Ratas , Antiinflamatorios no Esteroideos , Farmacología , Western Blotting , Proliferación Celular , Células Cultivadas , Curcumina , Farmacología , Ciclooxigenasa 2 , Genética , Metabolismo , Relación Dosis-Respuesta a Droga , Regulación hacia Abajo , Inhibidores Enzimáticos , Farmacología , Matriz Extracelular , Metabolismo , Expresión Génica , Imidazoles , Farmacología , Lipoproteínas LDL , Farmacología , Metaloproteinasa 2 de la Matriz , Genética , Metabolismo , Células Mesangiales , Metabolismo , Piridinas , Farmacología , Ratas Sprague-Dawley , Especies Reactivas de Oxígeno , Metabolismo , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Proteínas Quinasas p38 Activadas por Mitógenos , Metabolismo

RESUMEN

<p><b>OBJECTIVE</b>To compare the differences in nitric oxide (NO) release and endothelium-derived hyperpolarizing factor (EDHF)-mediated hyperpolarization between human radial artery (RA) and saphenous vein (SV) through direct measurement of NO and membrane potential.</p><p><b>METHODS</b>RA (n = 8), SV (n = 23), and surgical prepared SV (PV, n = 9, dilatation with normal saline solution at a pressure of 100 - 600 mmHg, 1 mmHg = 0.133 kPa) segments (5 mm long) taken from patients undergoing coronary artery bypass grafting were placed in an organ chamber. The NO-sensitive electrode and intracellular glass microelectrode was used to directly measure the NO release and the membrane potential changes in response to acetylcholine (ACh) and bradykinin (BK) before and after incubation with NG-nitro-L-arginine, indomethacin, and oxyhemoglobin.</p><p><b>RESULTS</b>The basal release of NO in RA [(11.9 ± 1.8) nmol/L] was significantly greater than that in SV [(9.9 ± 2.8) nmol/L, P = 0.041]. BK-induced NO release in RA was lower than that in SV [for BK 10(-7) mol/L: (25.8 ± 3.6) nmol/L vs. (43.7 ± 8.2) nmol/L, P = 0.006]. Both basal and ACh- or BK-induced NO release in PV were significantly reduced [basal release: PV (3.4 ± 1.4) nmol/L; P = 0.006 vs. RA; P = 0.002 vs. SV; stimulated release: for ACh 10(-5) mol/L: PV (4.8 ± 3.2) nmol/L; vs. RA (28.6 ± 7.9) nmol/L, P = 0.005; vs. SV (27.4 ± 3.7) nmol/L, P = 0.003; for BK 10(-7) mol/L: PV (7.0 ± 3.6) nmol/L; vs. RA (25.8 ± 3.6) nmol/L, P = 0.016; vs. SV (43.7 ± 8.2) nmol/L, P = 0.004]. EDHF-mediated hyperpolarization was greater in RA than that in SV [ACh 10(-5) mol/L: (-9.7 ± 1.9) mV vs. (-4.5 ± 1.1) mV, n = 17, P = 0.002].</p><p><b>CONCLUSIONS</b>RA is superior to SV in terms of NO basal release and EDHF-mediated endothelial function. Surgical preparation and pressure dilatation may severely impair the NO-mediated endothelial function of SV, which may contribute to the poor long-term patency of SV coronary graft.</p>

Asunto(s)

Femenino , Humanos , Masculino , Persona de Mediana Edad , Factores Biológicos , Metabolismo , Células Endoteliales , Metabolismo , Fisiología , Endotelio Vascular , Biología Celular , Metabolismo , Potenciales de la Membrana , Fisiología , Óxido Nítrico , Metabolismo , Arteria Radial , Biología Celular , Vena Safena , Biología Celular

RESUMEN

<p><b>OBJECTIVE</b>To observe the coronary vessel lumen diameter and bifurcation angle in subjects with normal CT coronary angiography (CTCA) imaging.</p><p><b>METHODS</b>64-row CT coronary angiography imaging from 526 adult people with excellent image quality and normal vascular image were analyzed in this study. The lumen diameter from the origin to distal with 2 mm lumen of left main coronary artery (LM), anterior descending branch (LAD), left circumflex branch (LCX) and right coronary artery (RCA) was measured at 1 cm interval in CPR image. The vascular tapered ratio was calculated. The bifurcation angle in the diagonal branch, obtuse marginal branch, posterior descending branch, acute marginal branch as well as the origin diameter was also measured in VR image.</p><p><b>RESULTS</b>The LAD average length was 13 cm and lumen diameter was 3.92 mm at origin and 2.10 mm at distal. The average decremented ratio of LAD was 7.7% (male 7.0%, female 8.4%). The maximal decremented ratio 8.0% - 10.0% occurred at 3 - 5 cm apart from the origin of LAD. The LCX average length was 13 cm and lumen diameter was 3.57 mm at origin and 2.10 mm at distal. The average decremented ratio of LCX was 9.7% (male 9.6%, female 9.7%). Lumen decremented ratio was less than 3.0% between origin and proximal 3 cm and 8.3% - 10.7% in the rest portion of the LCX. The RCA average length was 18 cm and lumen diameter was 3.97 mm at origin and 2.15 mm at distal. The average decremented ratio of RCA was 5.1% (male 4.9%, female 5.3%). The decremented ratio of RCR was less than 4.0% between origin and proximal 10 cm and 6.1% - 15.2% in the rest portion. The bifurcation angle was 50, 55, 66 and 76 degree for LAD with diagonal branch, LCX with obtuse marginal branch, RCA with posterior descending branch and RCA with obtuse marginal branch respectively.</p><p><b>CONCLUSION</b>Coronary artery length, lumen diameter and decremented ratio as well as bifurcation angel could be identified in 64 row CTCA image in vivo. This information could help us to understand the in vivo coronary artery anatomy.</p>

Asunto(s)

Adulto , Anciano , Anciano de 80 o más Años , Femenino , Humanos , Masculino , Persona de Mediana Edad , Angiografía Coronaria , Estenosis Coronaria , Diagnóstico por Imagen , Vasos Coronarios , Diagnóstico por Imagen , Tomografía Computarizada Espiral

RESUMEN

<p><b>OBJECTIVE</b>To prepare a biodegradable drug-eluting stent in myocardium channel and evaluate its effect on myocardium channel after transmyocardial revascularization (TMR).</p><p><b>METHODS</b>A biodegradable drug-eluting stent was prepared using poly (epsilon-caprolactone) (PCL), bovine serum albumin (BSA), and poly (D, L-lactide-co-glycolide) (PLGA) as material of stent, model protein drug, and drug carrier respectively. The amount of BSA in stent and in vitro released BSA of stent were determined by the Coomassie brilliant blue assay. The mechanical strength of stent was tested by universal material testing machines. The material and structure of stent was characterized by nuclear magnetic resonance spectroscopy. The effect of stent on myocardium channel after TMR was evaluated in vivo by a standard animal model of chronic myocardial ischemia in miniswine.</p><p><b>RESULTS</b>The stent could carry 13.1 microg BSA per mg of stent and the stent could release about 95% of BSA after 30 days. The stent diminished 80% of initial scale under the stress of 1.7 Mpa. It also kept the myocardium channel patency after TMR.</p><p><b>CONCLUSIONS</b>A biodegradable drug-eluting stent in myocardium channel was successfully prepared. It can sustain the pressure from the heart and achieve the controlled release of drug. The stent can ensure the myocardium channel patency after TMR.</p>

Asunto(s)

Animales , Humanos , Materiales Biocompatibles , Química , Prótesis Vascular , Caproatos , Química , Procedimientos Quirúrgicos Cardíacos , Modelos Animales de Enfermedad , Sistemas de Liberación de Medicamentos , Corazón , Lactonas , Química , Isquemia Miocárdica , Quimioterapia , Cirugía General , Revascularización Miocárdica , Distribución Aleatoria , Porcinos , Porcinos Enanos