3/23/2023 0 Comments Timi 1 flowCardiogenic shock (p=0.001), age (p=0.008), baseline SYNTAX Score II (p=0.006), and SYNTAX Revascularization Index (p=0.046) were independent mortality predictors at one-year follow-up. 30-day, 1-year, and long-term outcomes were analyzed in a cohort of retrospectively selected, 81 consecutive patients with STEMI, and primary PCI on UPLMCA. Previous studies on primary PCI in UPLMCA have identified cardiogenic shock, TIMI 0/1 flow, and cardiac arrest, as prognostic factors of an unfavourable outcome, but the complexity of coronary artery disease and the extent of revascularization have not been thoroughly investigated in these high-risk patients. The study evaluated the correlation between baseline SYNTAX Score, Residual SYNTAX Score, and SYNTAX Revascularization Index and long-term outcomes in ST-elevation myocardial infarction (STEMI) patients with primary percutaneous coronary intervention (PCI) on an unprotected left main coronary artery lesion (UPLMCA). Don’t hype exceptions and undermine the importance of a great concept ! Exceptions and rules are directly related to our experience we have accrued.Objectives. One may argue this is an exceptional case in STEMI intervention. This I call as Para cardiology : Heart facts without evidence ! The science of myocardial re-perfusion is a perfect example. But in this patient I believe, the common sense was proved wrong ! When it comes to the heart it must be done in an urgent basis That is the essence of primary angioplasty. Īnother possibility is the opening the LAD lesion some how impact on remote lesional flow as well (PDA in this patient )Įven a transient hypo- tension can have devastating effect in the hemo -dynamics of non IRA territory especially if it harbors a critical lesion !Ĭoming to the title question, Is no – flow better than slow- flow in late presenters of STEMI ?Ĭommon sense dictates whenever an artery is obstructed just get rid of it. Interference with remote lesion Hemodynamics. This a very critical time for the myocardium where antegrade and retrograde flow are kept in a fine balance. This raises the local hydrostatic pressure (Myocardial edema) and further impede the incoming micro collateral flow. Once you poke the lesion the coronary vascular bed which had dilated (as a response to total occlusion ) may react with inappropriate vasoconstriction. The acute collaterals to LAD may be interrupted during primary PCI. In some it can even salvage significant mass of myocardium. We know collaterals can be recruited within 12 hours in many STEMI patients. One more mechanism which we feel that might have contributed to death here is the “collateral damage”. Unfortunately if any cardiologist talks about it in 2012, he is at risk of labeled as old fashioned ! There are lots of reasons for stunning to be a clinically relevant phenomenon. It is part of the once famous concept called myocardial stunning. If it is mechanical outcome is bad ! This is not a new concept. If re-perfusion Injury is simply an electrical event like VF, it can be resuscitated. The LV came to standstill and the patient died. The moment a trickle of flow was established, some thing happened and the whatever little mechanical function his LV had was also interrupted. In this particular patient even though there was a total LAD occlusion, the segments supplied by the LAD was partially functional and it was contributing to LV pump function. Is re-perfusion injury electrical, mechanical or both ? Re-perfusion Injury ? How relevant it is in cath lab ? Physiological de-stabilisation of Contra -Lateral lesion (Remote lesions ).Why it was triggered after opening the IRA ? What is the mechanism of death here ? Expert STEMI interventionist from core labs may answer this !Īn acute ischemic MR with myocardial disruption was suggested. Even after a 30 minutes of heart (Fire ) fighting he could not be resuscitated. The moment LAD was opened he developed severe acute LVF / flash pulmonary edema. The septum was hypo-kinetic but did not appear severely dysfunctional. He had a total occlusion of LAD with TIMI zero flow. He was other wise stable and free from angina but had persistent ST elevation (5mm in V 1 to V 5 ). A patient with extensive anterior STEMI presented 18 hours after onset of chest pain.
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