ADN libre y daño microvascular en el infarto agudo de miocardio con elevación del segmento ST tratado con intervención coronaria primaria / Cell-free DNA and microvascular damage in ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention

Introducción y objetivos: En el infarto agudo de miocardio con elevación del segmento ST, el ADN libre circulante podría originarse de los leucocitos activados en la lesión coronaria. El objetivo fue investigar la relación entre el ADN libre y la reperfusión coronaria. Métodos: Se incluyó a 116 pacientes, tratados con angioplastia primaria y tromboaspiración. Se cuantificó el ADN libre coronario (durante la aspiración) y periférico (al final del procedimiento), así como la troponina T ultrasensible y la mieloperoxidasa. El objetivo primario fue la no resolución del segmento ST (RST) (≥ 70%) y el secundario la ausencia de flujo Thrombolysis In Myocardial Infarction 3 (TIMI 3) final. Resultados: Se obtuvo RST en 51 (44%) pacientes y flujo TIMI 3 en 97 (84%). Los pacientes sin RST y flujo TIMI 3 tuvieron un menor gradiente ADN libre periférico-coronario (p = 0,02 y p = 0,04, respectivamente). Un gradiente pequeño de ADN libre (< 1,82 ng/ml) se asoció a una mayor frecuencia de no RST (65 frente al 30%; p = 0,001) y de falta de flujo TIMI 3 (21 frente al 3%; p = 0,05. Tras el ajuste multivariable, un gradiente de ADN libre pequeño fue predictivo de no RST (OR = 4,50; IC95%, 1,60-12,62; p = 0,004), en tanto que hubo una tendencia no significativa para el flujo TIMI 3 (p = 0,14). El ADN libre no se correlacionó con la troponina o la mieloperoxidasa. Conclusiones: Un gradiente pequeño de ADN libre periférico-coronario, como expresión de una alta carga de ADN libre coronario, se asocia con no RST en el infarto agudo de miocardio. El ADN libre coronario podría reflejar la activación de los neutrófilos. La potencial contribución de este fenómeno al fracaso de la tromboaspiración requiere nuevos estudios

Introduction and objectives: Cell-free DNA (cfDNA) in ST-segment elevation myocardial infarction might originate from hyperactivated leukocytes at the coronary lesion. Our aim was to investigate the relationship between cfDNA and coronary reperfusion. Methods: We studied 116 patients treated with primary angioplasty using thrombus aspiration. Coronary (during aspiration) and peripheral (at the end of the procedure) blood samples were drawn for cfDNA, as well as high-sensitivity troponin T and myeloperoxidase quantification. The primary endpoint was no ST-segment resolution (STR) (≥ 70%) and the secondary endpoint was lack of final Thrombolysis In Myocardial Infarction flow 3 (TIMI 3). Results: ST-segment resolution was achieved in 51 (44%) patients and TIMI 3 flow in 97 (84%). Patients without STR and TIMI 3 flow had a smaller peripheral-coronary cfDNA gradient (P = .02 and P = .04 respectively). A small cfDNA gradient (< 1.82 ng/mL) was associated with a higher rate of no STR (65% vs 30%; P = .001) and lack of TIMI 3 flow (21% vs 3%; P = .05). After multivariable adjustment, the small cfDNA gradient was predictive of no STR (OR, 4.50; 95%CI, 1.60-12.62; P = .004), while there was a nonsignificant trend for final TIMI 3 flow (P = .14). Cell-free DNA levels did not correlate with troponin T or myeloperoxidase. Conclusions: A small peripheral-coronary cfDNA gradient, as an expression of high coronary cfDNA burden, is associated with no STR in acute myocardial infarction. Intracoronary cfDNA might reflect neutrophil activation. Whether this phenomenon contributes to thrombus aspiration failure requires further study

Cell-free DNA and Microvascular Damage in ST-segment Elevation Myocardial Infarction Treated With Primary Percutaneous Coronary Intervention.

INTRODUCTION AND OBJECTIVES: Cell-free DNA (cfDNA) in ST-segment elevation myocardial infarction might originate from hyperactivated leukocytes at the coronary lesion. Our aim was to investigate the relationship between cfDNA and coronary reperfusion. METHODS: We studied 116 patients treated with primary angioplasty using thrombus aspiration. Coronary (during aspiration) and peripheral (at the end of the procedure) blood samples were drawn for cfDNA, as well as high-sensitivity troponin T and myeloperoxidase quantification. The primary endpoint was no ST-segment resolution (STR) (≥ 70%) and the secondary endpoint was lack of final Thrombolysis In Myocardial Infarction flow 3 (TIMI 3). RESULTS: ST-segment resolution was achieved in 51 (44%) patients and TIMI 3 flow in 97 (84%). Patients without STR and TIMI 3 flow had a smaller peripheral-coronary cfDNA gradient (P = .02 and P = .04 respectively). A small cfDNA gradient (< 1.82 ng/mL) was associated with a higher rate of no STR (65% vs 30%; P = .001) and lack of TIMI 3 flow (21% vs 3%; P = .05). After multivariable adjustment, the small cfDNA gradient was predictive of no STR (OR, 4.50; 95%CI, 1.60-12.62; P = .004), while there was a nonsignificant trend for final TIMI 3 flow (P = .14). Cell-free DNA levels did not correlate with troponin T or myeloperoxidase. CONCLUSIONS: A small peripheral-coronary cfDNA gradient, as an expression of high coronary cfDNA burden, is associated with no STR in acute myocardial infarction. Intracoronary cfDNA might reflect neutrophil activation. Whether this phenomenon contributes to thrombus aspiration failure requires further study.