The following are key points to remember from this review on medical therapy for long-term prevention of atherothrombosis following an acute coronary syndrome (ACS):

1. There is a heightened predisposition to recurrent atherothrombotic events for months to years after an ACS.
2. Despite current guideline-directed medical therapy (GDMT), a consistent proportion of post-ACS patients experience recurrent atherothrombotic events due to unaddressed “residual risk.”
3. The risk of myocardial infarction (MI) after an ACS is greatest during the first 30 days and remains significantly elevated in the first year, with reported rates of 5-7%.
4. Contemporary clinical trials underline the pivotal role of platelets, coagulation, cholesterol, and systemic inflammation and provide a perspective on a personalized, targeted approach to reducing future events.
5. While the overall incomplete adoption of GDMT in practice likely contributes to these findings, the high event rates reported in the optimally-treated randomized controlled trial populations demonstrate that substantial residual risk remains despite current optimal management.
6. Overall, patients with a high atherosclerotic burden (e.g., with peripheral artery disease, cerebrovascular disease, or diffuse coronary disease) and a low bleeding risk (PRECISE-DAPT score <25 and no bleeding events) may gain the greatest benefit from a long-term dual antiplatelet (DAPT) strategy. Currently, genetic testing does not constitute a promising strategy to tailor antiplatelet therapy.
7. Pending a direct comparison of antiplatelet plus anticoagulant agent versus DAPT regimens in the post-MI stable coronary artery disease setting, the anticoagulant approach appears very promising to reduce thrombotic risk further.
8. Available data suggest that a nonstatin agent combined with the maximally tolerated statin dose regardless of baseline low-density lipoprotein cholesterol (LDL-C) levels can further reduce recurrent atherothrombotic events.
9. Clinicians should always aim to achieve the goals recommended by GDMT, as mere drug compliance does not ensure their attainment, for example, of recommended cholesterol goals.
10. Finally, a fine tuning of optimal antithrombotic duration, a platelet function testing guided approach to antiplatelet therapy, the best combination of antiplatelet with anticoagulant drugs with a long-term perspective, more aggressive lipid-lowering based on an “as-low-as-achievable with maximally tolerated therapy LDL-C value” approach, and novel direct anti-inflammatory agents may offer potentially effective strategies to reduce/minimize residual atherothrombotic risk.

Keywords: Acute Coronary Syndrome, Anticoagulants, Anti-Inflammatory Agents, Atherosclerosis, Blood Coagulation, Cerebrovascular Disorders, Cholesterol, LDL, Coronary Artery Disease, Dyslipidemias, Genetic Testing, Inflammation, Myocardial Infarction, Myocardial Ischemia, Peripheral Arterial Disease, Platelet Aggregation Inhibitors, Platelet Function Tests, Primary Prevention, Thrombosis

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