The Struggle against Death – The “Clot” War
Dr. Kent Chak-yu SO
Case Presentation
A 71-yr-old male presented with chest pain and LOC, ECG showed 5mm STE over inferior and V3R-V6R leads (Figure 1, Figure 2). He was in cardiogenic shock required Dopamine support. However, he developed PEA arrest while transferring to cath lab for primary PCI. Aspirin 320mg only was given before the patient developed cardiac arrest after arrival.
Progress
IABP was inserted immediately before coronary angiogram, which showed mRCA totally occluded, pLAD with a critical 95% stenosis and pLCx 60% stenosis. (Movie 1, Movie 2)
PCI to RCA was performed and 2 overlapping DES were implanted successfully. (Movie 3)
However, the patient still required high dose inotropic support with borderline low BP, despite the successful revascularization of RCA. While preparing for the ECMO, PCI to pLAD critical lesion was performed with another DES implanted. (Movie 4)
Patient developed sudden hypotension and bradycardia. Transvenous pacing wire and ECMO were inserted for supporting the haemodynamics. ST elevation was observed over inferior leads again and coronary angiogram via left radial access was done again and showed acute stent thrombosis over RCA. (Movie 5)
Thrombus aspiration was done. GP2B3A inhibitor was given. IVUS guided post-dilation of RCA and LAD stent was performed for the suboptimal stent apposition.
Discussion
The cause of acute stent thrombosis was probably multifactorial:
- Inadequate haemodynamic support –> Adequate inotropes, IABP and early ECMO were important
- Inadequate antiplatelet loading –> Adequate antiplatelet loading peri-stent insertion, or use of IC GP2B3A inhibitor if inadequate loading is forseen
- Under-optimized stent apposition –> image guided stent optimization if time allows
References
JACC 2005;95:1466–1468
J Interv Cardiol. 2013;26:215–220
Cardiovasc Interv. 2013;6:36–43
J Thrombosis and Haemostasis, 8: 2385–2393