6.1 Pathophysiology of Atherosclerosis and Hypertension

Atherosclerosis and hypertension are major players in cardiovascular disease. They're like troublemakers in your blood vessels, causing inflammation, plaque buildup, and high blood pressure. These conditions can lead to serious health problems if left unchecked.

Understanding how these diseases work is key to preventing and treating them. We'll look at how plaques form in arteries, what causes high blood pressure, and how your body's systems can go haywire. This knowledge is crucial for managing cardiovascular health.

Atherosclerosis Pathophysiology

Plaque Formation and Endothelial Dysfunction

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• Atherosclerosis develops as a chronic inflammatory response in arterial walls
• Plaque formation begins with endothelial dysfunction caused by various factors (high blood pressure, smoking, high cholesterol)
• Damaged endothelium allows lipids and inflammatory cells to enter the arterial wall
• Lipid accumulation in the arterial wall triggers an immune response
• Macrophages attempt to engulf excess lipids, transforming into foam cells
• Smooth muscle cells migrate to the site and proliferate, contributing to plaque growth
• Over time, plaques can narrow arteries and restrict blood flow to organs and tissues

Inflammation and Arterial Stiffness

• Chronic inflammation plays a crucial role in atherosclerosis progression
• Inflammatory mediators (cytokines, chemokines) promote further recruitment of immune cells
• T-cells and other immune cells contribute to ongoing inflammation within the plaque
• Arterial stiffness increases as plaques develop and calcify
• Reduced arterial elasticity leads to higher pulse pressure and increased cardiovascular risk
• Advanced plaques may develop a fibrous cap, which can rupture and cause thrombosis
• Plaque rupture can lead to acute cardiovascular events (heart attacks, strokes)

Hypertension Pathophysiology

Blood Pressure Components and Measurement

• Hypertension refers to persistently elevated blood pressure in the arteries
• Blood pressure consists of two components: systolic and diastolic pressure
• Systolic pressure measures the force exerted on artery walls during heart contraction
• Diastolic pressure represents the pressure in arteries between heartbeats
• Normal blood pressure falls below 120/80 mmHg (systolic/diastolic)
• Hypertension diagnosed when blood pressure consistently exceeds 130/80 mmHg
• Various factors influence blood pressure (cardiac output, peripheral resistance, blood volume)

Vascular Changes and Hemodynamics

• Vasoconstriction narrows blood vessels, increasing peripheral resistance
• Chronic vasoconstriction leads to structural changes in blood vessels
• Arterial remodeling occurs, with thickening of vessel walls and reduced lumen diameter
• Increased peripheral resistance raises blood pressure, especially diastolic pressure
• Endothelial dysfunction contributes to impaired vasodilation and increased vasoconstriction
• Baroreceptors in the carotid sinus and aortic arch regulate short-term blood pressure
• Long-term hypertension can reset baroreceptor sensitivity, maintaining elevated pressure

Hypertension Mechanisms

Renin-Angiotensin-Aldosterone System (RAAS)

• RAAS plays a crucial role in blood pressure regulation and fluid balance
• Renin released by juxtaglomerular cells in response to low blood pressure or sodium levels
• Renin converts angiotensinogen to angiotensin I
• Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II
• Angiotensin II causes vasoconstriction and stimulates aldosterone release
• Aldosterone promotes sodium and water retention in the kidneys
• Overactivity of RAAS contributes to chronic hypertension
• RAAS inhibitors (ACE inhibitors, ARBs) effectively treat hypertension

Sodium Retention and Cardiovascular Risk Factors

• Increased sodium retention leads to expanded blood volume and elevated blood pressure
• Kidneys play a crucial role in regulating sodium balance and blood pressure
• Impaired pressure natriuresis contributes to sodium retention in hypertension
• Obesity associated with increased sodium retention and RAAS activation
• Insulin resistance can promote sodium retention and sympathetic nervous system activation
• Endothelial dysfunction impairs nitric oxide production, reducing vasodilation
• Oxidative stress contributes to vascular damage and reduced nitric oxide bioavailability
• Lifestyle factors (high-sodium diet, physical inactivity) increase hypertension risk