Angiographic no-reflow during primary PCI procedures occurs at relatively high rate (25%) and is associated with worsening of long term morbidity and mortality. The exact mechanism of no-reflow is not fully understood, yet it is believed to be multifactorial including microvascular plugging with activated platelets and thrombotic debris in addition to the microvascular dysfunction from the ischaemia-reperfusion injury.
Despite a theoretical advantage of glycoprotein IIb/IIIa inhibitors (GPi) (like; Tirofiban) to suppress the intense platelets' activation/reaction; their use did not lead to a significant net benefit, because it was opposed by increased risk of bleeding.
However, the bleeding that plagued GPi use was predominantly related to vascular access in the era femoral approach was the default. Moreover, there are some recent data suggesting that small intracoronary bolus of GPi was non-inferior to intravenous bolus-infusion dose with less bleeding events.
This study plans to assess upfront premedication with small doses of GPi + Nitroglycerin ± Verapamil, with staged restoration of flow (repeated balloon inflation) to reduce angiographic no-reflow and CMR assessed microvascular occlusion (MVO).
STEMI patients with time from symptom onset of < 24 hours duration.
Large thrombus burden confirmed after initial wiring.
Radial vascular access.
STEMI patients receiving successful fibrinolytic therapy.
TIMI flow ≥ 1 or TIMI thrombus grade ≤ 3 at initial wiring.
Refusal to participate int the study, or unable to be consented (unconscious or comatose patients).
Femoral access.
Cairo University
Lead sponsor
Aswan Heart Centre
Collaborator