Identifying the vulnerable patient with rupture-prone plaque.

Area of Science:

• Cardiovascular Medicine
• Biochemistry

Background:

• Atherosclerotic cardiovascular disease is a leading cause of death in the US, with rising prevalence due to obesity and an aging population.
• Current risk assessment models explain less than 50% of cardiovascular risk variability.
• Atherosclerosis is now viewed as a systemic disease involving endothelial dysfunction and plaque inflammation, not just severe stenosis.

Purpose of the Study:

• To highlight the need for improved cardiovascular risk identification strategies.
• To introduce Lipoprotein-associated phospholipase A2 (Lp-PLA2) as a specific marker for plaque inflammation.
• To evaluate Lp-PLA2's potential in assessing rupture-prone plaques and guiding prevention.

Main Methods:

• Review of current understanding of atherosclerosis and risk assessment.
• Discussion of the role of Lp-PLA2 as a marker of vascular inflammation.
• Emphasis on the noninvasive and cost-effective measurement of Lp-PLA2 levels.

Main Results:

• Lp-PLA2 is identified as a specific marker of plaque inflammation.
• Lp-PLA2 may play a direct role in the development of rupture-prone plaques.
• Traditional risk factors and imaging do not directly assess acute ischemic potential.

Conclusions:

• Lp-PLA2 measurement offers a noninvasive and inexpensive method to assess atherosclerotic disease activity.
• Lp-PLA2 levels can provide clinically relevant information on vascular inflammation and progression to high-risk plaques.
• This marker may enhance the identification of patients at increased risk for heart attack and stroke.