Difference in fibrinolytic activity between multivessel coronary spasm and one-vessel coronary spasm

H Ogawa1, H Suefuji, K Takazoe

  • 1Department of Cardiovascular Medicine, Kumamoto University School of Medicine, Japan. ogawah@kumamoto-u.ac.jp

Insights

Patients with multivessel coronary spasm show higher plasminogen activator inhibitor activity, indicating a more impaired fibrinolytic system. This may correlate with increased angina and cardiac events.

Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Biochemistry

Background:

  • Coronary artery spasm is a significant cause of angina.
  • The fibrinolytic system plays a crucial role in maintaining vascular patency.
  • Impairment of the fibrinolytic system may contribute to adverse cardiovascular outcomes.

Purpose of the Study:

  • To investigate the activity of plasminogen activator inhibitor (PAI) and tissue plasminogen activator (t-PA) antigen in patients with multivessel coronary spasm compared to single-vessel spasm and controls.
  • To explore the relationship between fibrinolytic system activity and clinical outcomes in coronary spasm patients.

Main Methods:

  • Assessed plasminogen activator inhibitor activity in patient plasma samples.
  • Measured tissue plasminogen activator antigen levels.
  • Compared these levels across three groups: multivessel spasm, 1-vessel spasm, and control patients.

Main Results:

  • Plasminogen activator inhibitor activity was significantly higher in patients with multivessel spasm (n=18) than in those with 1-vessel spasm (n=20) and control patients (n=22).
  • Tissue plasminogen activator antigen levels were also elevated in multivessel spasm patients compared to the other two groups.
  • These findings suggest a more pronounced impairment of the fibrinolytic system in multivessel coronary spasm.

Conclusions:

  • Multivessel coronary spasm is associated with increased plasminogen activator inhibitor activity, indicating a more severely impaired fibrinolytic system.
  • This fibrinolytic impairment may contribute to the higher incidence of refractory angina and adverse cardiac events observed in these patients.
  • Further research is warranted to elucidate the precise mechanisms and therapeutic implications.

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