[Leucocytosis associated with higher incidence of adverse cardiovascular events in myocardial infarcts]. / Leucocitosis y su asociación con eventos cardiovasculares adversos en sujetos con infarto y elevación de ST sometidos a intervención coronaria percutánea.

UNLABELLED: In acute phase leukocytes has been related with higher incidence of major adverse cardiovascular events, (MACE) this evidence in AMI ST elevation after mechanical reperfusion is poor. We study prospectively this group to relationship among mechanical reperfusion, leukocytes and MACE. Two groups were considered < 10,000/microL or > 10,000/microL; 271 patients had full inclusion criteria in a 5 year period; 93 had < 1 0,000/microL leukocytes. (8,300 +/- 1,254/microL) and 178 > 10,000/microL. (13,810 +/- 3,192/microL, p 0.0001). We did not observe any difference between both groups regarding demographic characteristics. At beginning leukocytosis group had higher flow TIMI 0 - 1 incidence (89% vs 75%, p 0.004) and in-hospital major cardiovascular adverse events (32% vs 14%, p 0.001) and in follow-up (5% vs 2%, p 0.04). Logistic regression model include > 60 years-old, diabetes, extensive anterior or inferior infarction, TIMI flow 0, 1, or 2, cardiogenic shock, leukocytosis and neuthrophilia, had close relationship with mortality (p = 0.0007, RM 1.40, IC 95% 0.410 - 4.841). Multiple regression that include leukocytosis and neuthrophlia had stronger correlation with major cardiovascular adverse events (mortality, r = 0.34 and cardiogenic shock, r = 0.27) and abnormal TIMI flow (r = 0.20). CONCLUSION: Our results confirm close relationship among leukocitosis, thrombosis and major cardiovascular adverse events and extend this knowledge to acute phase and follow- up in acute myocardial infarction ST elevation under percutaneous coronary intervention. These results could be considered as evidence that connecting between endotelial dysfunction (inflammation-atherothrombosis) and cardiovascular disease.

Leucocitosis y su asociación con eventos cardiovasculares adversos en sujetos con infarto y elevación de ST sometidos a intervención coronaria percutánea / Leucocytosis associated with higher incidence of adverse cardiovascular events in myocardial infarcts

En la fase aguda de un infarto miocárdico los leucocitos se han relacionado con eventos cardiovasculares mayores adversos, (ECMA) esta asociación en pacientes llevados a reperfusión mecánica no se ha determinado con exactitud. Se estudió prospectivamente si existe asociación entre reperfusión mecánica, leucocitos y ECMA. En 5 años se ingresaron 271 pacientes con infarto agudo; 93 con < 10,000/µL leucocitos (8,300 ± 1,254/µL) y 178 tuvieron > 10,000/µL (13,810 + 3,192/µL, p 0.0001). No se observó diferencia estadísticamente significativa entre ambos grupos en las variables demográficas. El grupo con leucocitosis tuvo la mayor incidencia de flujo TIM I 0 - 1, (89% vs 75%, p 0.004) y ECMA hospitalarios (32% vs 14%, p 0.001) y en el seguimiento (5% vs 2%, p 0.04). La regresión logística que incluyó: edad > 60 años, diabetes, infarto anterior o inferior extenso, flujo TIMI (0, 1 y 2), choque cardiogénico, leucocitosis y neutrofilia tuvo mayor relación con mortalidad (p = 0.0007, RM 1.40, IC 95% 0.410-4.841). La regresión múltiple con leucocitosis y neutrofilia tuvo la correlación más fuerte para ECMA (mortalidad, r = 0.34 y choque, r = 0.27) y flujo TIMI basal subóptimo (r = 0.20). Conclusión: Los resultados establecen una asociación entre leucocitosis, trombosis y EMCA y extienden este conocimiento a la fase aguda y en el seguimiento de un infarto con elevación del ST llevado a ICP Estos hallazgos podrían considerarse como una evidencia más de la interacción entre disfunción endotelial (inflamación-aterotrombosis) y enfermedad cardiovascular.

In acute phase leukocytes has been related with higher incidence of major adverse cardiovascular events, (MACE) this evidence in AMI ST elevation after mechanical reperfusion is poor. We study prospectively this group to relationship among mechanical reperfusion, leukocytes and MACE. Two groups were considered < 10,000/µL or > 10,000/µL; 271 patients had full inclusion criteria in a 5 year period; 93 had < 10,000/µL leukocytes. (8,300 ±1,254/µL) and 178 > 10,000/µL (13,810 + 3,192/µL, p 0.0001). We did not observe any difference between both groups regarding demographic characteristics. At beginning leukocytosis group had higher flow TIMI 0 - 1 incidence (89% vs 75%, p 0.004) and in - hospital major cardiovascular adverse events (32% vs 14%, p 0.001) and in follow- up (5% vs 2%, p 0.04). Logistic regression model include > 60 years - old, diabetes, extensive anterior or inferior infarction, TIMI flow 0, 1, or 2, cardiogenic shock, leukocytosis and neuthrophilia, had close relationship with mortality (p = 0.0007, RM 1.40, IC 95% 0.410 -4.841). Multiple regression that include leukocytosis and neuthrophlia had stronger correlation with major cardiovascular adverse events (mortality, r = 0.34 and cardiogenic shock, r = 0.27) and abnormal TIMI flow (r = 0.20). Conclusion: Our results confirm close relationship among leukocitosis, thrombosis and major cardiovascular adverse events and extend this knowledge to acute phase and follow- up in acute myocardial infarction ST elevation under percutaneous coronary intervention. These results could be considered as evidence that connecting between endotelial dysfunction (inflammation-atherothrombosis) and cardiovascular disease.

Assembly of archaeal cell division protein FtsZ and a GTPase-inactive mutant into double-stranded filaments.

We have studied the assembly and GTPase of purified FtsZ from the hyperthermophilic archaeon Methanococcus jannaschii, a structural homolog of eukaryotic tubulin, employing wild-type FtsZ, FtsZ-His6 (histidine-tagged FtsZ), and the new mutants FtsZ-W319Y and FtsZ-W319Y-His6, with light scattering, nucleotide analyses, electron microscopy, and image processing methods. This has revealed novel properties of FtsZ. The GTPase of archaeal FtsZ polymers is suppressed in Na+-containing buffer, generating stabilized structures that require GDP addition for disassembly. FtsZ assembly is polymorphic. Archaeal FtsZ(wt) assembles into associated and isolated filaments made of two parallel protofilaments with a 43 A longitudinal spacing between monomers, and this structure is also observed in bacterial FtsZ from Escherichia coli. The His6 extension facilitates the artificial formation of helical tubes and sheets. FtsZ-W319Y-His6 is an inactivated GTPase whose assembly remains regulated by GTP and Mg2+. It forms two-dimensional crystals made of symmetrical pairs of tubulin-like protofilaments, which associate in an antiparallel array (similarly to the known Ca2+-induced sheets of FtsZ-His6). In contrast to the lateral interactions of microtubule protofilaments, we propose that the primary assembly product of FtsZ is the double-stranded filament, one or several of which might form the dynamic Z ring during prokaryotic cell division.