Explorar la asociación entre consumo de estatinas (CE) y desarrollo de síndrome postrombótico (SPT).
Cohorte retrospectiva con pacientes con primer episodio de trombosis venosa profunda (TVP) entre el 06/2006 y el 12/2017, incluidos en el Registro Institucional de Enfermedad TromboEmbólica (RIET) del Hospital Italiano de Buenos Aires. Se consideró exposición al CE entre los 30 días previos y hasta 180 días posterior al diagnóstico de TVP. Se definió SPT según constaba este dato en la base de seguimiento del RIET. Se evaluó el desarrollo de SPT con un modelo de riesgos proporcionales de Cox, reportando hazard ratios (HR) crudas y ajustadas. Se consideró la confusión por indicación del CE y se utilizó un propensity score (PS) para el ajuste del riesgo estimado, reportando los HR con sus intervalos de confianza del 95% (IC 95%).
Se incluyeron 905 pacientes, de los cuales 273 fueron CE y 632 no consumidor de estatinas (NCE). Al seguimiento, la incidencia de SPT fue: 6.59% (18) en el grupo CE y 8.07% (51) en el grupo NCE, con p = 0.412. La razón de riesgo para el desarrollo de SPT de CE resultó no significativa (HR cruda: 0.78; IC 95%: 0.43-1.41; p = 0.414). La HR de CE ajustada por edad, sexo, antiinflamatorios no esteroideos, corticosteroides, inmovilidad, anticoagulante, hipertensión arterial, diabetes, dislipidemia, insuficiencia renal crónica, enfermedad coronaria, accidente cerebrovascular, insuficiencia cardiaca y enfermedad oncológica fue 0.45 (IC 95%: 0.13-1.5; p = 0.196). La HR del CE ajustado por edad, sexo, antiinflamatorios no esteroideos, corticosteroides, inmovilidad, tratamiento anticoagulante, enfermedad oncológica y PS fue de 0.52 (IC 95%: 0.17-1.66; p = 0.272).
El CE no se asoció con menor SPT, aunque hubo escaso número de eventos detectados.
To evaluate the association between statin consumption and development of post-thrombotic syndrome (PTS).
Retrospective cohort study which included patients with a first episode of deep vein thrombosis (DVT) between 06/2006 and 12/2017, included in the Institutional Registry of ThromboEmbolic Disease of the Italian Hospital of Buenos Aires, Argentina. Exposure to statin use (SU) was considered between the 30 days before and up to 180 days after the diagnosis of DVT. PTS was defined as recorded dataset on registry. The development of PTS was evaluated with Cox proportional hazards model, raw and adjusted hazard ratios (HR) were reported. Confusion was considered by indication of SU and a propensity score (PS) was used for adjustment. We reported HR with their 95% confidence interval (CI); p value < 0.05 was considered statistically significant.
Of 1393 patients, 905 were included for the analysis, of which 273 were SU and 632 non-statin users (NSU). At follow-up, incidence of PTS was: 6.59% (18) in the SU group and 8.07% (51) in the NSU group, with p = 0.412. Crude HR for PTS for SU was not significant (0.78; 95% CI: 0.43-1.41; p = 0.414). Adjusted HR of SU by age, sex, non-steroidal anti-inflammatory drugs, corticosteroids, immobility, anticoagulant, high blood pressure, diabetes, dyslipidemia, chronic renal failure, coronary heart disease, stroke, heart failure and cancer disease was 0.45 (95% CI: 0.13-1.5; p = 0.196) for PTS. While HR for the development of PTS adjusted by age, sex, non-steroidal anti-inflammatory drugs, corticosteroids, immobility, anticoagulant treatment, cancer disease and PS of the SU was 0.52 (95% CI: 0.17-1.66; p = 0.272).
No statistically significant association was found between CE and the development of SPT, although there were a small number of events detected in both groups.

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