Mariama Akodad1, Benoît Lattuca1, Nicolas Nagot2, Vera Georgescu2, Mathilde Buisson2, Jean-Paul Cristol3, Florence Leclercq1, Jean-Christophe Macia1, Richard Gervasoni1, Thien-Tri Cung1, Stéphane Cade1, Frédéric Cransac1, Jessica Labour1, Anne-Marie Dupuy4, François Roubille5. 1. UFR de médecine, cardiology department, hôpital Arnaud-de-Villeneuve, université Montpellier 1, CHU de Montpellier, 371, avenue du Doyen-Gaston-Giraud, 34295 Montpellier cedex 05, France. 2. UFR de médecine, medical information department, université Montpellier 1, CHU de Montpellier, 34295 Montpellier, France. 3. UFR de médecine, department of biochemistry, université Montpellier 1, CHU de Montpellier, 34295 Montpellier, France; PhyMedExp, Inserm U1046, CNRS UMR 9214, university of Montpellier, 34295 Montpellier, France. 4. UFR de médecine, department of biochemistry, université Montpellier 1, CHU de Montpellier, 34295 Montpellier, France. 5. UFR de médecine, cardiology department, hôpital Arnaud-de-Villeneuve, université Montpellier 1, CHU de Montpellier, 371, avenue du Doyen-Gaston-Giraud, 34295 Montpellier cedex 05, France; PhyMedExp, Inserm U1046, CNRS UMR 9214, university of Montpellier, 34295 Montpellier, France. Electronic address: francois.roubille@gmail.com.
Abstract
BACKGROUND: Inflammation is involved during acute myocardial infarction, and could be an interesting target to prevent ischaemia-reperfusion injuries. Colchicine, known for its pleiotropic anti-inflammatory effects, could decrease systemic inflammation in this context. AIMS: To evaluate the impact of colchicine on inflammation in patients admitted for ST-segment elevation myocardial infarction (STEMI). METHODS:All patients admitted for STEMI with one of the main coronary arteries occluded, and successfully treated with percutaneous coronary intervention, were included consecutively. Patients were randomized to receive either 1mg colchicine once daily for 1 month plus optimal medical treatment or optimal medical treatment only. C-reactive protein (CRP) was assessed at admission and daily until hospital discharge. The primary endpoint was CRP peak value during the index hospitalization. RESULTS:Forty-four patients were included: 23 were treated withcolchicine; 21 received conventional treatment only. At baseline, both groups were well balanced regarding age, sex, risk factors, thrombolysis in myocardial infarction flow and reperfusion delay. The culprit artery was more often the left anterior descending artery in the colchicine group (P=0.07), reflecting a more severe group. There was no significant difference in mean CRP peak value between the colchicine and control groups (29.03mg/L vs 21.86mg/L, respectively; P=0.36), even after adjustment for type of culprit artery (26.99 vs 24.99mg/L, respectively; P=0.79). CONCLUSION: In our study, the effect of colchicine on inflammation in the context of STEMI could not be demonstrated. Further larger studies may clarify the impact of colchicine in acute myocardial infarction.
RCT Entities:
BACKGROUND:Inflammation is involved during acute myocardial infarction, and could be an interesting target to prevent ischaemia-reperfusion injuries. Colchicine, known for its pleiotropic anti-inflammatory effects, could decrease systemic inflammation in this context. AIMS: To evaluate the impact of colchicine on inflammation in patients admitted for ST-segment elevation myocardial infarction (STEMI). METHODS: All patients admitted for STEMI with one of the main coronary arteries occluded, and successfully treated with percutaneous coronary intervention, were included consecutively. Patients were randomized to receive either 1mg colchicine once daily for 1 month plus optimal medical treatment or optimal medical treatment only. C-reactive protein (CRP) was assessed at admission and daily until hospital discharge. The primary endpoint was CRP peak value during the index hospitalization. RESULTS: Forty-four patients were included: 23 were treated with colchicine; 21 received conventional treatment only. At baseline, both groups were well balanced regarding age, sex, risk factors, thrombolysis in myocardial infarction flow and reperfusion delay. The culprit artery was more often the left anterior descending artery in the colchicine group (P=0.07), reflecting a more severe group. There was no significant difference in mean CRP peak value between the colchicine and control groups (29.03mg/L vs 21.86mg/L, respectively; P=0.36), even after adjustment for type of culprit artery (26.99 vs 24.99mg/L, respectively; P=0.79). CONCLUSION: In our study, the effect of colchicine on inflammation in the context of STEMI could not be demonstrated. Further larger studies may clarify the impact of colchicine in acute myocardial infarction.
Authors: Yao Neng Teo; Yao Hao Teo; Nicholas L Syn; Ming Wei Goh; Celine Shuen Yin Yoong; Chi-Hang Lee; Mark Yan-Yee Chan; Ping Chai; Tiong-Cheng Yeo; Ching-Hui Sia Journal: High Blood Press Cardiovasc Prev Date: 2021-05-18