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Felicita Andreotti, Eliano Pio Navarese, Filippo Crea, Prolonged endogenous fibrinolysis predicts reduced survival after acute coronary syndromes, European Heart Journal, Volume 39, Issue 13, 01 April 2018, Pages 1086–1088, https://doi.org/10.1093/eurheartj/ehy118
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This editorial refers to ‘Fibrin clot properties independently predict adverse clinical outcome following acute coronary syndrome: a PLATO substudy’†, by W. Sumaya et al., on page 1078.
Awareness of the importance of coagulation in the pathogenesis of cardiovascular events is increasing. Not only have the results of COMPASS1 and ATLAS ACS 2-TIMI-512 contributed to this; so does the study in this issue of the journal.3 In a PLATO substudy of 4354 acute coronary syndrome patients, Sumaya and colleagues associate prolonged endogenous fibrinolysis, measured at hospital discharge, with a 20% relative increase in the risk of cardiovascular and all-cause death at 1-year follow-up.3 The finding emerges regardless of traditional risk factors, antiplatelet regimen, invasive or conservative management, and established prognostic markers.3 The results are biologically plausible and consistent with long-standing previous research.
Fibrin clots were reported to obstruct epicardial arteries in patients dying of heart attacks in 1969, although 50 years ago the observation was considered a post-mortem artefact.4 In 1980, a follow-up of 1510 middle-aged men identified plasma fibrinogen and coagulation factor VII as independent predictors of fatal and non-fatal coronary events, with a stronger relationship than for cholesterol, blood pressure, or smoking.5 The relevance of this association was probably under-rated at that time. In parallel, a placebo-controlled trial of 878 patients reported a dramatic effect of warfarin in reducing deaths and recurrent infarctions over a 2-year follow-up.6 In 1985, impaired vascular release of tissue-type plasminogen activator (t-PA) and elevated circulating plasminogen activator inhibitor-1 (PAI-1) were found to characterize young survivors of heart attacks, particularly if hypertriglyceridaemic.7 In 1986, fibrinolytic therapy vs. placebo in acute heart attack patients significantly improved survival.8 In the long term, anticoagulation, alone or with aspirin, reduced ischaemic outcomes vs. aspirin alone up to 4 years after a first heart attack.9 In primary prevention, in a high-risk population, low-intensity warfarin, aspirin, or their combination reduced adverse cardiac outcomes vs. placebo, with warfarin acting chiefly on fatal events.10 More recently, low-dose rivaroxaban vs. placebo, on top of dual antiplatelet therapy, was found to prevent fatal outcomes during the first year after an acute coronary syndrome, albeit at an increased risk of major bleeding.2 The same low-dose rivaroxaban on top of aspirin prevented fatal and non-fatal events in stable cardiovascular disease patients compared with aspirin alone.1 Thus, excessive fibrin formation and delayed fibrin dissolution have repeatedly emerged as affecting cardiovascular events, particularly fatal ones. And treatments altering these biochemical processes have consistently reduced the occurrence of adverse events (Figure 1).
