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Hyperlipidemia/CAD

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by

Michael Torres

on 4 October 2012

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Transcript of Hyperlipidemia/CAD

Hyperlipidemia/CAD Michael Torres, D.O. Chemical compound derived from fat only found in the cell walls of eukaryote cell membranes

Keeps the cell wall fluid and maintains the membrane permeability

Not water soluble, transported in blood by lipoproteins Cholesterol Lipoproteins Chylomicrons - transport fats from the intestine directly to mucles

VLDL - produced by the liver. Blood vessels cleave parts of the molecule eventually leading to...

LDL - the major carrier of cholesterol in the blood. LDL Contain a molecule of apolipoprotein B100
-recognized by surface receptors
-regulate uptake of LDL into peripheral tissue

An excess of LDL can lead to oxidization and uptake into macrophages
-oxidized LDL can cause endothelial damage and inflammation
-initially a protective response
-macrophages become engorged, termed "foam cells"
-foam cells release inflammatory cytokines and growth factors HDL "Good cholesterol"
-associated with better health outcomes

Transports cholesterol back to liver for excretion
-other tissues can use to synthesize hormones
-"reverse cholesterol transport" Cardiovascular Disease Number one cause of deaths worldwide

Risk factors:
-smoking
-HTN (BP>140/90 or on antihypertensives)
-HDL < 40
-Family history of premature CHD
-Age (men>45, women>55)

Obesity used to be a risk factor

Framingham Heart Study
-lifetime risk at age 40: 49% in men, 32% in women
-at age 70: 35% in men, 24% in women Coronary Heart Disease Stable vs Unstable Plaque Cardiovascular Disease NOT just a cardiac concern

CVD includes 4 major areas:
-Coronary Heart Disease: MI, angina pectoris, heart failure and coronary death
-Cerebrovascular Disease: stroke, TIA
-Peripheral Artery Disease: claudication
-Aortic atherosclerosis: thoracic or abdominal aortic aneurysm Risk with Hyperlipidemia Cadiovascular Deaths Role of LDL in Atherosclerosis Risk with Hyperlipidemia HDL Inverse Relationship HDL and Triglycerides Triglyceride induced hypercoaguable state may also cause endothelial damage and inflammation ATP III Guidelines for Tx Start with Risk Assesment:

1. Obtain a fasting lipid profile 2. Identify CHD equivalents
-Factors that place the patient at a similar risk for CHD events as CHD itself
Main Equivalents:
-Diabetes Mellitus
-Symptomatic carotid artery disease
-Peripheral Artery Disease
-Abdominal aortic aneurysm
-Multiple risk factors that confer a 10 year risk of CHD>20%

3. Identify other CHD factors other than elevated LDL
-smoking
-HTN (BP > 140/90, pt on antihypertensives)
-Low HDL cholesterol (<40 mg/dL)
-Family hx premature CHD (first degree male <55, female <65)
-Age (men>45, women>55)
HDL >60 is a "negative risk factor" and removes one risk from the total count Risk Assesment Risk Assesment 4. If two or more risk factors are present, other than LDL, without CHD or CHD risk factors, 10 year risk calculated with Framingham Risk table: Framingham Accurate for Caucasians and African Americans. May overestimate risk in Asian and Hispanic men and Native American women Risk Assesment 5. Determine risk category that establishes LDL goals Treat the LDL first
- Lifestyle modification is recommended for all patients with elevated LDL:
-weight loss in obese patients
-aerobic exercise
-dietary changes

-studies have found diet and exercise more effective than diet alone
-exercise alone seemed to be comparable to diet and exercise in a few studies

Cons: compliance, dietary changes less effective for larger BMIs, may not be an absolute decreased risk in cardiovascular mortality Treatment Medication
-statin vs non-statin:
-early lipid lowering studies using non-statin medication showed increased noncardiovascular mortality

-recent studies have shown statins may even be cardioprotective for people with LDL already in target range but with risk factors

-Multiple studies have shown effective CHD reduction by lowering LDL with statins in patients without CHD

(WOSCOPS - pravastatin, AFCAPS/TexCAPS - lovastatin, ASCOT LLA - atorvastatin, JUPITER - rosuvastatin)
-showed decreased rates of first major cardiovascular events and all cause mortality Treatment Statins
-Possible other effects of statins aside from lowering LDL:

Reduction in plaque size
-changes seen at 12 months can include a regression of the plaque as well as increased artery luminal diameter

Plaque stabilization
-seems to be a change of plaque composition from lipid rich to fibrotic and calcified
-inhibition of macrophage proliferation

Reduced inflammation
-studies have shown a decrease in inflammatory markers after administration of a statin
-fall in serum CRP can be seen after 14 days
-a study with RA pts reported improvement after starting atorvastatin
Statins
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