Early dysfunction and long-term improvement in endothelium-dependent vasodilation in the infarct-related artery after thrombolysis
Emili Iràculis, MD*,
Angel Cequier, MD, PhD, FESC*,*,
Joan Antoni Gómez-Hospital, MD*,
Manel Sabaté, MD*,
Josepa Mauri, MD, PhD*,
Eduard Fernández-Nofrerias, MD*,
Bruno García del Blanco, MD*,
Francese Jara, MD* and
Enrique Esplugas, MD, PhD, FESC*
a Servei de Cardiologia, Hospital de Bellvitge, Universitat de Barcelona, Barcelona, Spain
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Figure 1 Percent change in arterial diameter in response to different doses of acetylcholine (ACh) in post-acute myocardial infarction (AMI) patients and the control group. At the maximum concentration of ACh the post-AMI patients showed a considerable vasoconstriction response in the infarct-related artery, indicative of endothelial dysfunction, while the control group showed a slight vasodilation response. Both groups exhibited a vasodilation response to nitroglycerin (NTG), suggesting that the nonendothelium-dependent vasodilation is conserved.
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Figure 2 Individual changes in post-acute myocardial infarction patients, in response to the maximum concentration of acetylcholine (ACh) at the time of the initial study (9 ± 2 days) and one year later. *p = 0.04; IRA = infarct-related artery. Data are expressed as mean ± SEM.
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Figure 3 Response to the maximum concentration of acetylcholine (ACh) in post-acute myocardial infarction (AMI) patients who retained infarct-related artery (IRA) patency and in the control group. Initial study was at 9 ± 2 days following infarct, and the follow-up was 12 ± 3 months later. A significant improvement in the endothelial function in the IRA was observed on follow-up. Endothelial function in the IRA at one-year follow-up was similar to the response detected initially in the control group. Data are expressed as mean ± SEM.
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Figure 4 Assessment of endothelial function in the infarct-related artery at 10 days and 9 months in the same patient post-acute myocardial infarction. At the initial assessment (A), there was a considerable vasoconstriction response to the maximum dose of acetylcholine, which indicates a marked endothelial dysfunction. In the second assessment (B), a vasodilation response to the acetylcholine was observed, which indicates a significant improvement in the grade of endothelial dysfunction in the infarct-related artery at follow-up.
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