From plaque biology to clinical setting

Area of Science:

• Cardiovascular Medicine
• Pathology
• Infectious Diseases

Background:

• Coronary atherosclerosis underlies acute and chronic ischemic syndromes.
• Acute events involve plaque rupture or erosion, leading to thrombosis.
• Plaque vulnerability is influenced by inflammation and potential infectious triggers.

Purpose of the Study:

• To explore the role of infectious agents in coronary plaque inflammation and vulnerability.
• To investigate the link between infections and acute coronary syndromes.
• To understand how local and systemic inflammation interact in atherothrombosis.

Main Methods:

• Review of existing literature on plaque pathology and infectious triggers.
• Analysis of microbiological, ultrastructural, immunohistochemical, and molecular findings in plaque samples.
• Examination of systemic inflammatory markers and their association with infections.

Main Results:

• Plaque rupture and erosion are key mechanisms in acute coronary syndromes.
• Infectious agents, such as Chlamydia pneumoniae and Helicobacter pylori, are implicated in plaque inflammation.
• Infections increase local thrombogenicity and are associated with systemic inflammation markers.
• Infected circulating cells may contribute to local inflammation upon specific triggers.

Conclusions:

• Infectious agents are significant contributors to coronary plaque inflammation, activation, and vulnerability.
• These infections can bridge local and systemic inflammatory processes in atherothrombosis.
• Understanding infectious triggers is crucial for managing acute coronary syndromes and vulnerable plaques.