In the cath lab, how is acute stent thrombosis typically treated?

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Multiple Choice

In the cath lab, how is acute stent thrombosis typically treated?

Explanation:
When a stent thromboses, the blockage is due to a fresh clot inside a recently placed scaffold, causing sudden loss of blood flow and ongoing heart muscle ischemia. The fastest and most reliable way to restore patency is urgent repeat PCI to mechanically reopen the stented artery. This is done by re-crossing the lesion, removing or compressing the thrombus, and optimizing the vessel with balloon inflation and, if needed, additional stenting. Simultaneously, aggressive antiplatelet and anticoagulant therapy is given to prevent further clot formation and sustain patency during and after the procedure. In practice, this often includes aspirin plus a potent P2Y12 inhibitor, along with anticoagulation such as heparin, and may involve glycoprotein IIb/IIIa inhibitors as an adjunct to improve flow and reduce microvascular thrombosis. Systemic thrombolysis is not ideal here because it carries bleeding risk and is less reliable for a stented segment, and it does not address the mechanical occlusion promptly. Conservative medical therapy with beta-blockers or observation without intervention would not resolve the acute blockage and could lead to continued myocardial injury.

When a stent thromboses, the blockage is due to a fresh clot inside a recently placed scaffold, causing sudden loss of blood flow and ongoing heart muscle ischemia. The fastest and most reliable way to restore patency is urgent repeat PCI to mechanically reopen the stented artery. This is done by re-crossing the lesion, removing or compressing the thrombus, and optimizing the vessel with balloon inflation and, if needed, additional stenting. Simultaneously, aggressive antiplatelet and anticoagulant therapy is given to prevent further clot formation and sustain patency during and after the procedure. In practice, this often includes aspirin plus a potent P2Y12 inhibitor, along with anticoagulation such as heparin, and may involve glycoprotein IIb/IIIa inhibitors as an adjunct to improve flow and reduce microvascular thrombosis.

Systemic thrombolysis is not ideal here because it carries bleeding risk and is less reliable for a stented segment, and it does not address the mechanical occlusion promptly. Conservative medical therapy with beta-blockers or observation without intervention would not resolve the acute blockage and could lead to continued myocardial injury.

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