Hiperuricemia asintomática y enfermedad arterial coronaria / Asymptomatic hyperuricaemia and coronary artery disease

Antecedentes: El ácido úrico se ha relacionado con la tendencia de precipitarse para formar cristales, que se presenta desde manera asintomática hasta con artritis, tofos o litiasis renal. Con anterioridad, se ha asociado la hiperuricemia asintomática a la presencia de enfermedad cardiovascular. Objetivos: Determinar la asociación de enfermedad arterial coronaria compleja en pacientes con hiperuricemia asintomática. Material y métodos: Se realizó estudio observacional, transversal, retrospectivo, unicéntrico. En un hospital de tercer nivel de México, en el periodo comprendido de junio del 2017 a marzo del 2019. Se incluyó a todos los pacientes que ingresaron para realizar angiografía coronaria; se excluyó a los pacientes con gota, uso de diuréticos y enfermedad renal crónica. Resultados: Durante el periodo del estudio se seleccionó a un total de 300 pacientes, de los cuales 40% presentaron hiperuricemia. Los pacientes con hiperuricemia eran de mayor edad (59 vs. 63; p = 0,002). El grupo de pacientes con hiperuricemia asintomática tuvo mayor proporción de lesiones coronarias complejas (64 vs. 35%; p ≤ 0,0001), así como también mayor puntuación del SYNTAX I score (27 vs. 17; p ≤ 0,001). Hubo mayor probabilidad de presentar lesiones coronarias complejas en este grupo de pacientes (OR 3,4; p ≤ 0,0001). Además, en la división por grupos de nivel de ácido úrico, se relacionaba con la presencia de lesiones coronarias complejas (Q1 = 0,5; p = 0,06); (Q2 = 2; p = 0,01) y (Q3 = 3; p ≤ 0,0001). Conclusión: Los pacientes con hiperuricemia asintomática tienen mayor riesgo de presentar lesiones coronarias complejas.(AU)

Background: Uric acid has been related to a tendency to precipitate to form crystals, presenting asymptomatically, until the formation of arthritis, tophi or renal lithiasis. Previously, the presence of asymptomatic hyperuricaemia has been associated with the presence of cardiovascular disease. Objectives: To determine the association of complex coronary artery disease in patients with asymptomatic hyperuricaemia. Material and methods: An observational retrospective, transversal, unicentric study was conducted in a tertiary hospital in Mexico, in the period from June 2017 to March 2019. All patients admitted for coronary angiography were included; patients with gout, use of diuretics and chronic kidney disease were excluded. Results: During the study period, a total of 300 patients were collected, of which 40% presented hyperuricaemia. The patients with hyperuricaemia were older (59 vs. 63, P = .002). The group of patients with asymptomatic hyperuricaemia had a higher proportion of complex coronary lesions (64 vs. 35%, P ≤ .0001) as well as a higher SYNTAX I score (27 vs. 17, P ≤ .001). There was a higher probability of presenting complex coronary lesions in this group of patients (OR 3.4, P ≤ .0001). In addition, in the group division of uric acid levels, it was related to the presence of complex coronary lesions (Q1 = .5, P = .06), (Q2 = 2, P = .01) and (Q3 = 3, P ≤ .0001). Conclusion: Asymptomatic hyperuricaemia has a higher prevalence and association of presenting complex coronary lesions.(AU)

Asymptomatic hyperuricaemia and coronary artery disease. / Hiperuricemia asintomática y enfermedad arterial coronaria.

BACKGROUND: Uric acid has been related to a tendency to precipitate to form crystals, presenting asymptomatically, until the formation of arthritis, tophi or renal lithiasis. Previously, the presence of asymptomatic hyperuricaemia has been associated with the presence of cardiovascular disease. OBJECTIVES: To determine the association of complex coronary artery disease in patients with asymptomatic hyperuricaemia. MATERIAL AND METHODS: An observational retrospective, transversal, unicentric study was conducted in a tertiary hospital in Mexico, in the period from June 2017 to March 2019. All patients admitted for coronary angiography were included; patients with gout, use of diuretics and chronic kidney disease were excluded. RESULTS: During the study period, a total of 300 patients were collected, of which 40% presented hyperuricaemia. The patients with hyperuricaemia were older (59 vs. 63, P = .002). The group of patients with asymptomatic hyperuricaemia had a higher proportion of complex coronary lesions (64 vs. 35%, P ≤ .0001) as well as a higher SYNTAX I score (27 vs. 17, P ≤ .001). There was a higher probability of presenting complex coronary lesions in this group of patients (OR 3.4, P ≤ .0001). In addition, in the group division of uric acid levels, it was related to the presence of complex coronary lesions (Q1 = .5, P = .06), (Q2 = 2, P = .01) and (Q3 = 3, P ≤ .0001). CONCLUSION: Asymptomatic hyperuricaemia has a higher prevalence and association of presenting complex coronary lesions.

Long QT syndrome secondary to drug interaction between hydroxychloroquine and amiodarone / Síndrome de QT largo secundario a la interacción entre hidroxicloroquina y amiodarona

Abstract: A 67-year-old female patient with a diagnosis of heart failure with preserved ejection fraction secondary to severe mitral regurgitation in treatment with metoprolol, spironolactone, and digoxin. She was diagnosed systemic lupus erythematosus (SLE) because of the presence of arthritis, alopecia, thrombocytopenia, direct positive Coombs +++, positive ANAs 1:1,280 and positive lupus anticoagulant. The rheumatology service indicated hydroxychloroquine 200 mg every 24 hours. She presented atrial fibrillation, and amiodarone was initiated. Two weeks later the patient was admitted because of presyncope, electrocardiogram showed sinus bradycardia with long QT interval. A temporary pacemaker was placed, and hydroxychloroquine and amiodarone suspended. Twenty-four hours later, a new electrocardiogram was taken showing pacemaker rhythm with reduction of the QT interval. After 72 hours the temporary pacemaker was removed and on the fifth day the patient was discharged with an electrocardiogram in sinus rhythm with a corrected QT (Bazett) of 456 miliseconds. The hydroxychloroquine was reinitiated following discharge. She presented another episode of atrial fibrillation, and was treated with amiodarone, hydroxychloroquine was suspended previously, and she did not present prolongation of QT interval. The long QT syndrome was present when amiodarone and hydroxychloroquine interacted.(AU)

Resumen: Paciente femenina de 67 años, con diagnóstico de insuficiencia cardiaca con fracción de expulsión preservada, secundaria a insuficiencia mitral severa, en tratamiento con metoprolol, espironolactona y digoxina. Le fue diagnosticado lupus eritematoso sistémico, debido a la presencia de artritis, alopecia, trombocitopenia, Coombs directo positivo +++, anticuerpos antinucleares positivos 1:1,280 y anticoagulante lúpico positivo. El Servicio de Reumatología indicó hidroxicloroquina 200 mg cada 24 horas. Presentó fibrilación auricular, por lo que se le inició amiodarona. Dos semanas posteriores la paciente es ingresada debido a un episodio de presíncope, se le realizó electrocardiograma que demostró bradicardia sinusal con un intervalo QT prolongado. Se le colocó un marcapasos temporal, además de que se suspendió hidroxicloroquina y amiodarona. Después de 72 horas se retiró el marcapasos, y al quinto día se egresó con un electrocardiograma en ritmo sinusal con el intervalo QT corregido por Bazett de 456 milisegundos. La hidroxicloroquina fue reiniciada al egreso. La paciente presentó otro episodio de fibrilación auricular y fue tratada con amiodarona, previa suspensión de hidroxicloroquina, sin presentar prolongación del intervalo QT. El síndrome de QT largo sólo se presentó con la interacción de amiodarona con hidroxicloroquina.(AU)