This refers to the continuous, biological processes governing the formation, growth, stability, and potential regression of atherosclerotic plaques within the arterial walls. Plaque dynamics are clinically significant because they determine the risk of acute cardiovascular events, such as myocardial infarction or stroke, which often result from plaque rupture. Understanding these dynamics involves assessing the inflammatory state, lipid content, and fibrous cap thickness of existing lesions.
Origin
The concept arises from modern cardiology and pathology, moving beyond the static view of plaque accumulation to a dynamic, time-dependent model of vascular disease progression. The term emphasizes the continuous biological activity within the plaque structure, influenced heavily by systemic factors like hormone balance and inflammation.
Mechanism
The mechanism begins with endothelial injury, leading to the infiltration of lipoproteins and subsequent inflammatory cell recruitment, forming a fatty streak. Hormonal imbalances, such as estrogen deficiency, can accelerate this process by altering lipid profiles and promoting vascular inflammation. Plaque stabilization involves increasing the fibrous cap thickness and reducing the inflammatory burden, thereby mitigating the risk of thrombus formation upon rupture.
We use cookies to personalize content and marketing, and to analyze our traffic. This helps us maintain the quality of our free resources. manage your preferences below.
Detailed Cookie Preferences
This helps support our free resources through personalized marketing efforts and promotions.
Analytics cookies help us understand how visitors interact with our website, improving user experience and website performance.
Personalization cookies enable us to customize the content and features of our site based on your interactions, offering a more tailored experience.