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Sino-atrial nodal artery occlusion causing acute sinus node dysfunction after percutaneous coronary intervention: Case report and systematic review.
Pacing and Clinical Electrophysiology : PACE 2024 June 23
BACKGROUND: New antithrombotic medications and improved stent designs have reduced branch occlusion, although the sino-atrial nodal artery (SANA) may still be occluded after a percutaneous coronary intervention (PCI), causing sinus node dysfunction (SND). Ischemic sinus nodes are usually asymptomatic but can cause sinus arrest sometimes requiring pacemaker placement. In rare cases, junctional escape rhythms, a manifestation of sinus exit blocks after PCI, can predict cardiogenic shock.
METHODS: We present a case study of a patient who underwent bifurcation PCI to the LMCA to the LCX but subsequently developed cardiogenic shock as a result of SND, a junctional escape rhythm required substantial inotropic support. This case offers an exemplification of a sparsely documented, yet infrequent manifestation of iatrogenic ischemic SND at an unorthodox site, the confluence of the LMCA-LCX. In addition, we conducted a comprehensive analysis of 22 scholarly works pertaining to the subject of sinus node dysfunction (SND) subsequent to PCI resulting from ischemia caused by stenosis or occlusion of the SANA.
RESULTS: RCA was responsible for 96.1% of SND cases, whereas LCX was responsible for 3.9%. SND was asymptomatic in 49.3% of cases and junctional escape rhythm in 37.6% of symptomatic cases. 28% needed a temporary transvenous pacemaker, while 7.8% needed a permanent one. Interventional management recanalized the SANA in 5.2% of patients, restoring flow.
CONCLUSION: Transient sino-atrial node ischemia after PCI can cause acute SND. Before stent implantation, doctors should consider SND. Complete plaque evaluation around the SANA is needed before choosing the best PCI procedure.
METHODS: We present a case study of a patient who underwent bifurcation PCI to the LMCA to the LCX but subsequently developed cardiogenic shock as a result of SND, a junctional escape rhythm required substantial inotropic support. This case offers an exemplification of a sparsely documented, yet infrequent manifestation of iatrogenic ischemic SND at an unorthodox site, the confluence of the LMCA-LCX. In addition, we conducted a comprehensive analysis of 22 scholarly works pertaining to the subject of sinus node dysfunction (SND) subsequent to PCI resulting from ischemia caused by stenosis or occlusion of the SANA.
RESULTS: RCA was responsible for 96.1% of SND cases, whereas LCX was responsible for 3.9%. SND was asymptomatic in 49.3% of cases and junctional escape rhythm in 37.6% of symptomatic cases. 28% needed a temporary transvenous pacemaker, while 7.8% needed a permanent one. Interventional management recanalized the SANA in 5.2% of patients, restoring flow.
CONCLUSION: Transient sino-atrial node ischemia after PCI can cause acute SND. Before stent implantation, doctors should consider SND. Complete plaque evaluation around the SANA is needed before choosing the best PCI procedure.
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