Myocardial infarction accelerates atherosclerosis.

Area of Science:

• Cardiovascular Science
• Immunology
• Hematology

Background:

• Myeloid cells contribute to atherosclerotic plaque rupture, leading to myocardial infarction and stroke.
• Recurrent cardiovascular events are common in survivors due to unknown mechanisms.

Purpose of the Study:

• To investigate how systemic responses to ischemic injury, such as myocardial infarction or stroke, affect chronic atherosclerosis.
• To identify the source of increased monocyte recruitment in atherosclerotic plaques after ischemic events.

Main Methods:

• Utilized Apoe-/- mice models subjected to myocardial infarction or stroke.
• Analyzed atherosclerotic lesion size and morphology.
• Investigated monocyte recruitment and hematopoietic stem and progenitor cell mobilization.
• Examined the role of sympathetic nervous system signaling.

Main Results:

• Ischemic injury accelerated atherosclerosis, resulting in larger, more advanced lesions in Apoe-/- mice.
• Monocyte recruitment significantly increased in plaques weeks after myocardial infarction or stroke.
• Myocardial infarction triggered the release of hematopoietic stem and progenitor cells from bone marrow via sympathetic nervous system signaling.
• These progenitors migrated to the spleen, leading to sustained elevated monocyte production.

Conclusions:

• Systemic response to ischemic injury exacerbates atherosclerosis by boosting monocyte production.
• Sympathetic nervous system signaling plays a key role in mobilizing hematopoietic stem and progenitor cells after myocardial infarction.
• This study reveals a novel mechanism linking ischemic events to accelerated atherogenesis and suggests potential therapeutic targets.