Thank you to Dr Paul Williams for the many words of wisdom!
Check it out on Class Capture through our Lecture Database.
“Lipids. What are they good for? Absolutely nothin’. Huh”
Hypercholesterolemia leads to LDL accumulation in vessel intima, results in oxidative modification of lipoproteins, which triggers an inflammatory response. Monocytes invade the intima and become foam cells which also trigger smooth muscle cells to migrate from the media to intima.
Rupture of the plaque causes there to be contact of coagulation factors in the blood with the thrombogenic tissue factors.
Statin Drug Information
Statins lead to decreased cholesterol synthesis and hepatic cholesterol concentrations by inhibiting HMG-CoA reductase. They may also have anti-inflammatory effects by acting on Ras and Rho synthesis.
Statin intolerance can be manifested by myalgia, asymptomatic myopathy, myositis, and rhabdomyolysis. Risk factors include age >80, female sex, frailty, hypothyroidism, CKD, DM-2, EtOH abuse, infection, high doses of statins. If there is an elevated CK, statin should be avoided if CK >10 times upper limit of normal. ACC/AHA recommends niacin or cholestyramine if this occurs. Patients with normal CK and myalgias can stop the statin for two weeks and then restart to see if symptoms recur or reduce the dosage or change to fluvastatin or rosuvastatin.
Statins can also modestly increase the incidence of type 2 diabetes, in patients with risk factors for diabetes (metabolic syndrome, impaired fastin glucose, BMI >30, A1c >6%)
Current statin therapy are influenced by the 2013 ACC/AHA practice guidelines. Takeaway points include:
- patients with clinical ASCVD should be on a high-intensity statin
- those with an LDL >190 mg/dL should be on a high intensity statin
- patients with diabetes with LDL between 70-190 should be on a moderate intensity statin (if 10 year ASCVD risk >7.5% should be on a high intensity statin)
- patients with a 10 year ASCVD risk >7.5% should be on a moderate or high intensity statin.