[Enterovirus infection as a risk factor of acute coronary syndrome and its complications]
Insights
Enterovirus infection is a key factor in acute coronary syndrome (ACS), directly contributing to its pathogenesis. This viral presence promotes the development of severe complications like cardiogenic shock and cardiac rupture in patients.
Area of Science:
- Cardiology
- Virology
- Pathogenesis
Context:
- Acute coronary syndrome (ACS) encompasses conditions like myocardial infarction (MI) and unstable angina (UA).
- Cardiogenic shock and cardiac rupture are severe, often fatal, complications of MI.
- The role of viral infections, specifically enteroviruses, in ACS pathogenesis is an area of ongoing research.
Purpose:
- To quantitatively detect enterovirus antigens in patients with ACS.
- To investigate the correlation between enterovirus antigen levels and the severity of ACS, including complications like cardiogenic shock and cardiac rupture.
- To determine if enterovirus infection is a contributing factor to ACS and its severe outcomes.
Summary:
- Enterovirus antigens were detected in blood (49%), coronary artery (95.8%), and heart tissues (54.3%) of ACS patients.
- Elevated relative levels of enterovirus antigen in blood (RLEVA) were observed in patients with MI, particularly those with cardiogenic shock/cardiac rupture, compared to UA patients.
- Higher RLEVA was found in necrotized myocardial areas and associated coronary vessels in patients with MI complicated by cardiogenic shock/cardiac rupture.
Impact:
- Enterovirus infection is identified as a significant factor in ACS.
- The findings suggest direct involvement of enteroviruses in the pathogenesis of ACS.
- Enterovirus infection appears to promote the development of cardiogenic shock and/or cardiac rupture, highlighting potential therapeutic targets.
Abstract:
Antigens of enteroviruses were detected quantitatively in the modified complement-binding reaction in blood samples from 102 of the 208 (49%) patients with ACS, in coronary artery tissues from 23 of 24 and heart from 51 of 94 (54.3%) patients with MI who died from cardiogenic shock and/or cardiac rupture. The relative level of enterovirus antigen (RLEVA) in the blood of patients with MI complicated and uncomplicated by cardiogenic shock and/or cardiac rupture was 0.42 +/- 0.04 and 0.29 +/- 0.02 arbitrary units respectively (p = 0.032) compared with 0.21 +/- 0.07 in patients with unstable angina (UA) (p = 0.0001). RLEVA in patients with UA was significantly lower than in those with uncomplicated MI (p < 0.011). RLEVA in necrotized myocardial areas after death from cardiogenic shock (0.54 +/- 0.18) and/or cardiac rupture (0.46 +/- 0.15) was higher than outside MI zones (0.30 +/- 0.14 and 0.26 +/- 0.10 respectively) (p < 0.01). RLEVA in coronary vessels feeding the necrotic zones of patients with MI complicated by cardiogenic shock (0.44 +/- 0.18) was higher (p = 0.03) than in the vessel feeding tissues outside the MI zone (0.29 +/- 0.19). It is concluded that enterovirus infection is a factor of ACS; it is directly involved in its pathogenesis and promotes the development of cardiogenic shock and/or cardiac rupture.
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