AI Article Synopsis

  • The incidence of post-cardiac injury syndrome (PCIS) after primary percutaneous coronary intervention (PPCI) in acute myocardial infarction (AMI) is decreasing, but the exact causes are still unclear.
  • A case study of a 45-year-old male with AMI showed early PCIS onset, with slow blood flow in the affected arteries and no significant trauma from the intervention, suggesting a link between coronary microvascular dysfunction and PCIS.
  • The case highlights excessive inflammation and microvascular issues following ischemia-reperfusion injury, indicating a possible connection between PCIS and the effectiveness of PPCI in patients with endothelial dysfunction risks.

Article Abstract

Background: In the era of primary percutaneous coronary intervention (PPCI), the incidence of post-cardiac injury syndrome (PCIS) in patients with acute myocardial infarction (AMI) following PPCI has become less common. However, the intrinsic pathogenesis of this medical condition remains largely uncertain. Unlike the prior reports, the present paper provides new mechanistic clues concerning the pathogenesis of PCI-related PCIS.

Case Presentation: A 45-year-old male with AMI had developed an early onset of PCIS at 3 h after PPCI. A significantly slower TIMI flow (grade ≤ 2) for the culprit arteries was observed through follow-up coronary angiography (CAG); no stent thrombosis or any significant evidence of iatrogenic trauma due the intervention procedures was found. Nevertheless, the the serum level of HsCRP showed similar variation trend as the neutrophil count and troponin T in continuous blood monitoring, which suggested a potential association between PPCI-related coronary microvascular dysfunction (CMD) and pathogenesis of PCIS.

Conclusions: The reported case had excessive inflammatory reaction and CMD resulting from cardiac ischemia-reperfusion injury in an AMI patient with risk factors of endothelial dysfunction. There exists a potential reciprocal causation between PCIS and performance of PPCI in the AMI patient who was susceptible to endothelial damage.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6292035PMC
http://dx.doi.org/10.1186/s12872-018-0964-4DOI Listing

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