Shortening in the Tp-e/QTc ratio after angioplasty in patients with acute coronary syndrome. / Acortamiento en la relación Tp-f/QTc tras angioplastia en pacientes con síndrome isquémico coronario agudo.

Objetivo: La dispersión transmural de la repolarización ventricular (DTMRV) es un factor de riesgo para muerte en pacientes con síndrome isquémico coronario agudo (SICA). Con el objetivo de conocer el efecto de la realización de angioplastia sobre la DTMRV, se estudió la relación Tp-f/QTc en pacientes con SICA sometidos a angioplastia. Método: Se diseñó un estudio observacional, retrospectivo y descriptivo. Se incluyeron 150 pacientes (N = 150) con diagnóstico de SICA. Se valoró la relación Tp-f/QTc inicial y se evaluó su acortamiento posangioplastia. Como objetivo secundario, se comparó la asociación de dichos cambios en la relación Tp-f/QTc con la mortalidad cardiovascular y los eventos adversos cardiovasculares. Resultados: El promedio en la relación Tp-f/QTc inicial fue de 0.2529, mientras que posangioplastia fue de 0.2397. Por medio de prueba de rangos de Wilcoxon se evidenció un descenso significativo en la relación Tp-f/QTc posterior a la angioplastia, con un valor Z de -2.051 y una p < 0.04. En el análisis secundario se encontró que una Tp-f/QTc ≥ 0.29 posangioplastia es factor de riesgo para presentación de los siguientes eventos adversos: muerte intrahospitalaria (7.4 vs 0%; p < 0.003), nuevo SICA en seguimiento a 1 año (25.9 vs. 18.5%; p < 0.006) y reintervención en seguimiento a 1 año (29.6 vs. 15.0%; p < 0.002). Conclusiones: Existe un acortamiento significativo en la relación Tp-f/QTc posangioplastia en pacientes con SICA. Esta medida de la DTMRV puede servir como un predictor de muerte intrahospitalaria, eventos cardiovasculares y reintervención a 1 año en pacientes con SICA tratados con angioplastia. Objective: Transmural Dispersion of Repolarization (TDR) is a Risk factor for Death in patients with Acute Coronary ­Syndrome (ACS). In order to know the effect of angioplasty on TDR, the Tp-e/QTc ratio was studied in patients with ACS undergoing angioplasty. Method: An observational, retrospective and descriptive study was designed. 150 patients (N = 150) with diagnosis of ACS were included. The initial Tp-e/QTc ratio was assessed and then its post-angioplasty shortening was evaluated. As a secondary objective, we compared the association of these Tp-e/QTc ratio changes with cardiovascular mortality and cardiovascular adverse events. Results: The average in the initial Tp-e/QTc ratio was 0.2529, while post-angioplasty was 0.2397. Through a Wilcoxon rage test, a significant decrease in the Tp-e/QTc ratio after angioplasty was observed, with a Z value of −2.051 and p < 0.04. In the secondary analysis, it was found that a Tp-e/QTc ≥ 0.29 post-angioplasty is a risk factor for presenting the following adverse events: in-hospital death (7.4 vs. 0%; p < 0.003), new ACS in 1-year follow-up (25.9 vs. 18.5%; p < 0.006), and reintervention in 1-year follow up (29.6 vs. 15%; p < 0.002). Conclusions: There is a significant shortening in the Tp-e/QTc ratio post-angioplasty in patients with ACS. This measure of TDR can serve as a predictor of in-hospital death, cardiovascular events and 1-year reintervention in patients with ACS treated initially by angioplasty.

Acortamiento en la relación Tp-f/QTc tras angioplastia en pacientes con síndrome isquémico coronario agudo / Shortening in the Tp-e/QTc ratio after angioplasty in patients with acute coronary syndrome

Resumen Objetivo: La dispersión transmural de la repolarización ventricular (DTMRV) es un factor de riesgo para muerte en pacientes con síndrome isquémico coronario agudo (SICA). Con el objetivo de conocer el efecto de la realización de angioplastia sobre la DTMRV, se estudió la relación Tp-f/QTc en pacientes con SICA sometidos a angioplastia. Método: Se diseñó un estudio observacional, retrospectivo y descriptivo. Se incluyeron 150 pacientes (N = 150) con diagnóstico de SICA. Se valoró la relación Tp-f/QTc inicial y se evaluó su acortamiento posangioplastia. Como objetivo secundario, se comparó la asociación de dichos cambios en la relación Tp-f/QTc con la mortalidad cardiovascular y los eventos adversos cardiovasculares. Resultados: El promedio en la relación Tp-f/QTc inicial fue de 0.2529, mientras que posangioplastia fue de 0.2397. Por medio de prueba de rangos de Wilcoxon se evidenció un descenso significativo en la relación Tp-f/QTc posterior a la angioplastia, con un valor Z de −2.051 y una p < 0.04. En el análisis secundario se encontró que una Tp-f/QTc ≥ 0.29 posangioplastia es factor de riesgo para presentación de los siguientes eventos adversos: muerte intrahospitalaria (7.4 vs 0%; p < 0.003), nuevo SICA en seguimiento a 1 año (25.9 vs. 18.5%; p < 0.006) y reintervención en seguimiento a 1 año (29.6 vs. 15.0%; p < 0.002). Conclusiones: Existe un acortamiento significativo en la relación Tp-f/QTc posangioplastia en pacientes con SICA. Esta medida de la DTMRV puede servir como un predictor de muerte intrahospitalaria, eventos cardiovasculares y reintervención a 1 año en pacientes con SICA tratados con angioplastia.

Abstract Objective: Transmural Dispersion of Repolarization (TDR) is a Risk factor for Death in patients with Acute Coronary Syndrome (ACS). In order to know the effect of angioplasty on TDR, the Tp-e/QTc ratio was studied in patients with ACS undergoing angioplasty. Method: An observational, retrospective and descriptive study was designed. 150 patients (N = 150) with diagnosis of ACS were included. The initial Tp-e/QTc ratio was assessed and then its post-angioplasty shortening was evaluated. As a secondary objective, we compared the association of these Tp-e/QTc ratio changes with cardiovascular mortality and cardiovascular adverse events. Results: The average in the initial Tp-e/QTc ratio was 0.2529, while post-angioplasty was 0.2397. Through a Wilcoxon rage test, a significant decrease in the Tp-e/QTc ratio after angioplasty was observed, with a Z value of −2.051 and p < 0.04. In the secondary analysis, it was found that a Tp-e/QTc ≥ 0.29 post-angioplasty is a risk factor for presenting the following adverse events: in-hospital death (7.4 vs. 0%; p < 0.003), new ACS in 1-year follow-up (25.9 vs. 18.5%; p < 0.006), and reintervention in 1-year follow up (29.6 vs. 15%; p < 0.002). Conclusions: There is a significant shortening in the Tp-e/QTc ratio post-angioplasty in patients with ACS. This measure of TDR can serve as a predictor of in-hospital death, cardiovascular events and 1-year reintervention in patients with ACS treated initially by angioplasty.

Venous thromboembolism: thrombosis, inflammation, and immunothrombosis for clinicians.

Venous thromboembolism (VTE) is a worldwide disease related with mortality, cardiovascular disability, impaired quality of life and, cause major long-term complications. Clinicians related to the acute and long-term patients care must be involved in the molecular mechanisms of thrombosis. The vessel wall and its inner lining of the endothelium are critical to the maintenance of a patent vasculature. After endothelial disruption, collagen (first line of endothelial defense) and intravascular tissue factor (second line of endothelial defense) are exposed to blood flow, starting the formation of a thrombus. Anticoagulant endovascular proteins and endogenous fibrinolysis have an active role in hemostasis. Currently, the process of coagulation is a cell surface-based model that includes three overlapping phases: initiation, amplification, and propagation. From a simple view, inflammation is one of the first responses of the immune system to infection; inflammation is driven by eicosanoids and cytokines, which are released by injured or infected cells. Common cytokines, which regulate inflammatory response, include interleukins (mainly interleukin-6) that are responsible for communication among white blood cells, chemokines that promote chemotaxis, and interferons that have anti-viral effects. Acute infections have been associated with a transient increase in the risk of myocardial infarction, stroke and recently with venous thrombosis, supporting the notion that systemic and respiratory infections increase the risk of thromboembolic events. Recently, immunothrombosis, another thrombosis mechanism that includes innate immune mechanisms, the neutrophil extracellular genetic traps, and the immunothrombosis dysregulation, could explain some cases of "unprovoked" VTE especially in elderly, a high-risk population for thrombosis.

Inferior vena cava filters in pulmonary embolism: A historic controversy / Filtros de vena cava inferior en tromboembolia pulmonar: Una controversia histórica

Abstract: Objective: Rationale for non-routine use of inferior venous cava filters (IVCF) in pulmonary embolism (PE) patients. Methods: Thrombosis mechanisms involved with IVCF placement and removal, the blood-contacting medical device inducing clotting, and the inorganic polyphosphate in the contact activation pathway were analyzed. In addition, we analyzed clinical evidence from randomized trials, including patients with and without cancer. Furthermore, we estimated the absolute risk reduction (ARR), the relative risk reduction (RRR), and the number needed to treat (NNT) based on the results of each study using a frequency table. Finally, we analyzed the outcome of our PE patients that were submitted to thrombolysis with short and long term follow-up. Results: IVCF induces thrombosis by several mechanisms including placement and removal, rapid protein adsorption, and simultaneous surface-induced activation via the contact activation pathway. Also, inorganic polyphosphate has an important role as a procoagulant, reversing the effect of anticoagulants. Randomized control trials included 904 cancer and non-cancer PE patients. In terms of ARR, RRR, and NNT, there is no evidence for routine use of IVCF. In 290 patients with proved PE, extensive thrombotic burden and right ventricular dysfunction under thrombolysis and oral anticoagulation, we observed a favorable outcome in a short- and long-term follow-up; additionally, IVCF was only used in 5% of these patients. Conclusion: Considering the complex mechanisms of thrombosis related with IVCF, the evidence from randomized control trials and ARR, RRR, and NNT obtained from venous thromboembolism patients with and without cancer, non-routine use of IVCF is recommended.

Resumen: Objetivo: Racionalidad para no utilizar en forma rutinaria filtros de vena cava inferior (FVCI) en pacientes con tromboembolia pulmonar (TEP). Métodos: Analizamos mecanismos de trombosis relacionados con la colocación o retiro de estos dispositivos médicos, incluyendo la importancia del polifosfato inorgánico en la vía de activación de contacto. Analizamos evidencia clínica de estudios aleatorizados controlados en pacientes con y sin cáncer. Mediante tablas de frecuencia estimamos de cada estudio reducción del riesgo absoluto (RRA) y relativo (RRR) y el número necesario a tratar (NNT). Finalmente, examinamos la evolución de nuestros pacientes con TEP llevados a trombolisis con seguimientos a corto y largo plazo. Resultados: FVCI inducen trombosis por diferentes mecanismos: colocación y retiro, adsorción rápida de proteínas y activación de superficie inducida en la vía de activación de contacto. El polifosfato inorgánico es un procoagulante importante para la anticoagulación. Estudios aleatorizados controlados incluyeron 904 pacientes con TEP con y sin cáncer. En términos de RRA, RRR y NNT no existe evidencia para el uso rutinario. En 290 pacientes con TEP probada, importante carga de trombo y disfunción del ventrículo derecho llevados a trombolisis y anticoagulación observamos una evolución favorable en seguimientos a corto y largo plazo. En estos pacientes los FVCI se utilizaron solo en el 5%. Conclusión: Considerando los mecanismos complejos de trombosis relacionados con los FVCI, la evidencia obtenida de los estudios aleatorizados y controlados, así como la RRA, RRR y NNT en pacientes con tromboembolismo venoso con y sin cáncer, no recomendamos el uso rutinario de FVCI.

Inferior vena cava filters in pulmonary embolism: A historic controversy.

OBJECTIVE: Rationale for non-routine use of inferior venous cava filters (IVCF) in pulmonary embolism (PE) patients. METHODS: Thrombosis mechanisms involved with IVCF placement and removal, the blood-contacting medical device inducing clotting, and the inorganic polyphosphate in the contact activation pathway were analyzed. In addition, we analyzed clinical evidence from randomized trials, including patients with and without cancer. Furthermore, we estimated the absolute risk reduction (ARR), the relative risk reduction (RRR), and the number needed to treat (NNT) based on the results of each study using a frequency table. Finally, we analyzed the outcome of our PE patients that were submitted to thrombolysis with short and long term follow-up. RESULTS: IVCF induces thrombosis by several mechanisms including placement and removal, rapid protein adsorption, and simultaneous surface-induced activation via the contact activation pathway. Also, inorganic polyphosphate has an important role as a procoagulant, reversing the effect of anticoagulants. Randomized control trials included 904 cancer and non-cancer PE patients. In terms of ARR, RRR, and NNT, there is no evidence for routine use of IVCF. In 290 patients with proved PE, extensive thrombotic burden and right ventricular dysfunction under thrombolysis and oral anticoagulation, we observed a favorable outcome in a short- and long-term follow-up; additionally, IVCF was only used in 5% of these patients. CONCLUSION: Considering the complex mechanisms of thrombosis related with IVCF, the evidence from randomized control trials and ARR, RRR, and NNT obtained from venous thromboembolism patients with and without cancer, non-routine use of IVCF is recommended.