====== Antilipemics ======

Antilipemics are drugs that reduce atherogenic lipoproteins — primarily LDL cholesterol — in order to reduce atherosclerotic cardiovascular disease (ASCVD).

This module focuses on:

• Drug mechanisms  
• LDL reduction potency  
• Outcome data  
• Adverse effects  
• Clinical selection strategies  

In cardiovascular pharmacology, lipid drugs are long-term mortality drugs.

They do not relieve symptoms.
They prevent events.

----

===== Drug Classes Overview =====

^ Class ^ Primary Mechanism ^ LDL Reduction ^ Mortality Benefit ^
| [[cardio:lipids:statins|Statins]] | HMG-CoA reductase inhibition → ↑ LDL receptors | ↓↓ (30–60%) | Strong |
| [[cardio:lipids:ezetimibe|Ezetimibe]] | ↓ Intestinal cholesterol absorption | ↓ (~15–20%) | Moderate (add-on) |
| [[cardio:lipids:pcsk9|PCSK9 Inhibitors]] | Prevent LDL receptor degradation | ↓↓↓ (50–60%) | Strong (high-risk pts) |
| [[cardio:lipids:bempedoic|Bempedoic Acid]] | ATP citrate lyase inhibition | ↓ (~15–20%) | Emerging |
| [[cardio:lipids:fibrates|Fibrates]] | PPAR-α activation → ↓ TG | Minimal LDL effect | Limited |
| [[cardio:lipids:omega3|Omega-3 / Icosapent]] | ↓ VLDL production | TG lowering | Select benefit |

----

===== 1. Statins – Foundation Therapy =====

Statins are first-line therapy for ASCVD prevention.

Mechanism:
• Inhibit HMG-CoA reductase  
• Decrease hepatic cholesterol synthesis  
• Upregulate LDL receptors  
• Increase LDL clearance  

Clinical effects:
• ↓ MI  
• ↓ Stroke  
• ↓ Cardiovascular mortality  

→ [[cardio:lipids:statins|Go to Statins]]

----

===== 2. Cholesterol Absorption Inhibition =====

==== Ezetimibe ====

Mechanism:
• Blocks NPC1L1 transporter in intestine  
• Reduces dietary and biliary cholesterol absorption  

Used:
• Add-on to statin  
• Statin intolerance  

→ [[cardio:lipids:ezetimibe|Go to Ezetimibe]]

----

===== 3. PCSK9 Inhibitors =====

Mechanism:
• Monoclonal antibodies that prevent LDL receptor degradation  
• Dramatically increase LDL clearance  

Used:
• Secondary prevention  
• Familial hypercholesterolemia  
• Very high-risk patients  

→ [[cardio:lipids:pcsk9|Go to PCSK9 Inhibitors]]

----

===== 4. ATP Citrate Lyase Inhibition =====

==== Bempedoic Acid ====

Mechanism:
• Inhibits cholesterol synthesis upstream of HMG-CoA reductase  
• Liver-selective activation  

Used:
• Statin intolerance  
• Add-on therapy  

→ [[cardio:lipids:bempedoic|Go to Bempedoic Acid]]

----

===== 5. Triglyceride-Focused Therapy =====

==== Fibrates ====

Mechanism:
• Activate PPAR-α  
• Increase lipoprotein lipase activity  
• Reduce triglycerides  

→ [[cardio:lipids:fibrates|Go to Fibrates]]

----

==== Omega-3 Fatty Acids / Icosapent Ethyl ====

Mechanism:
• Reduce hepatic VLDL production  

Used:
• Severe hypertriglyceridemia  
• Select ASCVD risk reduction  

→ [[cardio:lipids:omega3|Go to Omega-3 Therapy]]

----

===== Clinical Strategy =====

Lipid therapy is risk-based.

Primary Prevention:
• Statin intensity based on ASCVD risk

Secondary Prevention:
• High-intensity statin
• Add ezetimibe if LDL above goal
• Consider PCSK9 for very high risk

This module teaches you to:

✔ Choose statin intensity  
✔ Manage statin intolerance  
✔ Add second-line therapy appropriately  
✔ Understand LDL percent reductions  
✔ Recognize major adverse effects  

----

Return to the main cardiovascular section:

→ [[cardio:start|Back to Cardiovascular Pharmacology]]