RESUMEN
OBJECTIVE: We aimed to confirm whether serum on admission homocysteine level (HCY) and red cell distribution width (RDW) value are independent risk factors for MACE incidence in patients with STEMI myocardial infarction treated by percutaneous coronary intervention (PCI), as well as the possibility of their joint assessment in order to enhance the risk stratification for major adverse cardiac events (MACE). PATIENTS AND METHODS: A total of 80 patients with acute myocardial infarction (AMI) were included in the study and tested for blood HCY and RDW values. Patients were followed up for six months after discharge and evaluated for MACE occurrence. RESULTS: The RDW value was significantly associated with HCY level (r=0.267, p=0.026). Univariate logistic regression analysis identified both the RDW and HCY as independent predictors of MACE (OR 2.179; CI 95% 1.250 to 3.797; p=0.006 and OR 1.108; CI 95% 1.013 to 1.213; p=0.025, respectively), naming RDW as a stronger predictor of unfavorable prognosis in AMI patients. Addition of HCY to RDW value in receiver operating characteristic (ROC) curve analysis increased the area under the curve (AUC) from 0.705 to 0.730 (p=0.007), while risk prediction model, which also included traditional risk factors, increased AUC up to 0.806, implying this model as good predictor of MACE both in low-risk and high-risk STEMI patients. CONCLUSIONS: A high baseline HCY level and RDW value in patients with STEMI undergoing PCI is independently associated with increased risk for MACE outcome. Their joint assessment increases risk prediction ability.
Asunto(s)
Índices de Eritrocitos , Homocisteína/sangre , Intervención Coronaria Percutánea , Infarto del Miocardio con Elevación del ST/sangre , Infarto del Miocardio con Elevación del ST/cirugía , Anciano , Bosnia y Herzegovina , Femenino , Humanos , Masculino , Persona de Mediana Edad , Medición de Riesgo , Factores de RiesgoRESUMEN
Surgically perforated stomach (since direct injury in rats until persisting defect and huge adhesions (day 1, day 7)) fairly represent an unresolved cytoprotection issue, and thereby, we focused resolving of the immediate triad, particular vascular failure (vessels 'disappear'/empty), prolonged bleeding, debilitated defect large widening. Agents (mg/kg) or saline (controls) were given at 1 min post-injury as an abdominal bath (10 ml/rat throughout 2 min). Within 1 - 15 min post-injury period, with cytoprotective BPC 157 (0.01 µg), the rapidly restored vessels 'run' (vessels filled/reappeared) toward the perforated defect, and there is less bleeding, and defect contraction; advanced perforated lesion healing (day 1) to complete healing (day 7), and less adhesions. With pantoprazole (10 mg), early (vessels (worsening), bleeding (prolongation), defect (attenuated widening)) effect means eventual lesions and adhesions severity as in controls. Ranitidine (10 mg) early effect (vessels (improvement), bleeding (less bleeding), defect (eliminated widening, defect not changed)) means final lesions attenuation, but not complete healing, less adhesions. L-NAME (5 mg) early (vessels worsening, less bleeding, attenuated defect widening) and final (lesions aggravation, more adhesions) effect, versus L-arginine (100 mg) early (vessels improvement, more bleeding, attenuated defect widening) and final (lesions attenuation, less adhesions) effect, combined few simultaneously occurring nitric oxide (NO)-system distinct processes. Finally, in the stomach tissue surrounding defect, increased malondialdehyde (MDA)- and decreased NO-values, BPC 157 reversed to the normal healthy values, and mRNA expression studies (Cox2, VEGFa, Nos1, Nos 2, Nos3, Nkap (NF-kappa-B-activating protein gene)), done at that very early post-perforation-time, indicate a way how BPC 157 may act beneficially in the perforated stomach lesion throughout NO- and prostaglandinds-system.
Asunto(s)
Óxido Nítrico , Gastropatías , Animales , Arginina/farmacología , Arginina/uso terapéutico , Citoprotección , Hemorragia , NG-Nitroarginina Metil Éster , Óxido Nítrico/metabolismo , Pantoprazol/farmacología , Pantoprazol/uso terapéutico , Fragmentos de Péptidos , Proteínas , Ranitidina , Ratas , Ratas WistarRESUMEN
In contrast to the strawberry fruits, strawberry leaves as a source of bioactive compounds with potentially beneficial biological effects have been largely overlooked. In this study we examined direct, dose-dependent effects of wild strawberry (Fragaria vesca, L.) leaves aqueous extract, in two experimental models and animal species, the isolated guinea pig hearts and rat aortic rings. Vasodilatory potential of the wild strawberry leaves extract was compared with vasodilatory activity of aqueous extract of hawthorn (Crataegus oxycantha, L) leaves with flowers, which can be regarded as a reference plant extract with a marked vasodilatory activity. The extracts were analysed by their "phenolic fingerprints", total phenolic content and antioxidative capacity. Their vasodilatory activity was determined and compared in the isolated aortic rings from 24 rats that were exposed to the extracts doses of 0.06, 0.6, 6, and 60 mg/100ml. Both extracts induced similar, dose-dependent vasodilation. Maximal relaxation was 72.2+/-4.4% and 81.3+/-4.5%, induced by the strawberry and hawthorn extract, respectively. To determine vasodilatory mechanisms of the wild strawberry leaves extract, endothelium-denuded and intact rings exposed to nitric oxide (NO) synthase inhibitor L-NAME or cyclooxygenase inhibitor indomethacin were used. Removal of the endothelium prevented and exposure to L-NAME or indomethacin strongly diminished the vasodilatatory response to the extract. In the isolated hearts (n=12), the wild strawberry extract was applied at concentrations of 0.06, 0.18, 0.6, and 1.8 mg/100ml. Each dose was perfused for 3.5 min with 15 min of washout periods. Heart contractility, electrophysiological activity, coronary flow and oxygen consumption were continuously monitored. The extract did not significantly affect heart rate and contractility, main parameters of the cardiac action that determine oxygen demands, while coronary flow increased up to 45% over control value with a simultaneous decrease of oxygen extraction by 34%. The results indicate that the aqueous extract of wild strawberry leaves is a direct, endothelium-dependent vasodilator, action of which is mediated by NO and cyclooxygenase products and which potency is similar to that of the hawthorn aqueous extract.
Asunto(s)
Antioxidantes/farmacología , Fragaria/química , Contracción Miocárdica/efectos de los fármacos , Óxido Nítrico/antagonistas & inhibidores , Fenoles/farmacología , Extractos Vegetales/farmacología , Vasodilatadores/farmacología , Animales , Aorta Torácica/efectos de los fármacos , Circulación Coronaria/efectos de los fármacos , Crataegus , Relación Dosis-Respuesta a Droga , Endotelio Vascular/efectos de los fármacos , Flavonoides/análisis , Flavonoides/farmacología , Cobayas , Frecuencia Cardíaca/efectos de los fármacos , Técnicas In Vitro , Masculino , Fenoles/análisis , Extractos Vegetales/química , Hojas de la Planta/química , Ratas , Ratas WistarRESUMEN
Direct, dose dependent effects of the nose-horned vipers (Vipera ammodytes ammodytes) venom on various parameters of cardiac action in isolated rat hearts were examined. Biochemical (protein content, SDS polyacrylamide gel electrophoresis) and biological (minimum haemorrhagic and necrotizing dose and lethal dose (LD(50))) characterization of the venom was performed before testing. The hearts were infused with venom doses of 30, 90 and 150 microg/mL for 10 min followed by 30 min of wash out period. Left ventricular pressure, coronary flow, heart rate, atrioventricular conduction, myocardial oxygen consumption, incidence and duration of arrhythmias were measured and relative cardiac efficiency was calculated. Cardiac CPK, LDH, AST and troponin I were measured as biochemical markers of myocardial damage. The venom caused dose dependent electrophysiological instability and depression of contractility and coronary flow. Effects on the heart rate were biphasic; transient increase followed by significant slowing of the frequency. Relative cardiac efficiency decreased as oxygen consumption remained high relative to the heart rate-contractility product, indicating purposeless expenditure of oxygen and energy. Effects by the dose of 30 microg/mL were highly reversible while the dose of 90 mug/mL caused damages that were mostly irreversible. The dose of 150 mug/mL induced irreversible asystolic cardiac arrest.