The correct answer could be any of the above , depending upon the level of your knowledge.
Ever since Herrick reported coronary thrombosis as a cause for MI and Davies documented it by angiogram many decades later (1980) ,the fate of thrombus and the mechanism of its dissolution is the key to our understanding of ACS.
Even though we are now able to take on this thrombus in a direct fight by aspiration techniques ,still the hematological aftermath and the aberrant coronary behavior can fool us at any time ! The major lesson learnt in recent times is the success of pPCI is not in clearing the thrombus but ensure it never accumulates again at the site in the future .This is why there is whole big industry working on post PCI anti coagulation and anti platelet strategies .
Clinical correlates of poor perfusion in micro circulation.
Plugging of micro circulation is the most under-recognised issue.This results in no reflow in acute fashion or LV dysfunction and micro-vascular angina in long term . Late recovery of LV function is attributed to late clearance of thrombotic debri.
RCA vs LCA thrombus load.
*One interesting observation is RCA thrombus clears more slowly as it has no well formed venous circuits .most RCA blood drains through thebesian veins which traverses RV myocardium .this can be hemodynamic hurdle unlike the LCA venous drainage