CVD 3 Flashcards
Hard vs soft outcomes
Soft outcomes: Total Chol, LDL-C, HDL-C, TG, non-HDL-C and apoB
- easy and fast to respond
Hard: CVD and CHD events, and CV associated mortality
- Long term, slow to change, strongest evidence
Why is LDL-C used as a soft outcome to reduce risk of heart disease?
Because a longitudinal study which demonstrated a linear improvement in reduction in risk of CHD proportional to magnitude of exposure to lower LDL-C
Why statins are used and who they should be used for
When to discuss add on therapy
1 mmol/L decrease in LDL-C is associated with 20-25% RR reduction for CV risk
High risk group recommended: FRS > 20% and Intermediate risk
Not recommended for low-risk group not recommended
Always discuss behavior modification first
Discuss add on therapy if following LDL reduction therapy LDL-C > 2 or ApoB >.8 or non-HDL > 2.6 on max statin dose
Ezetimibe as first-line add on
Define the intermediate risk group for CVD
FRS 10-19.9% AND
LDL-C >3.5 mmol/L or
Non-HDL-C >4.2 mmol/L or
ApoB > 1.05 g/L or
Men >50/women >60 w/ additional risk factor or
Presence of other risk modifers like hsCRP >2, CAC >0, family history of premature CAD, lp(a) >50
Lifestyle modification approach for dyslipidemia
Weight management: 5-10% loss + reduced abdominal obesity (not first line recommended)
Reduced risk of CVD by 6% per 4.5 BMI and 9% by 12.6 lower cm WC
PA: 30-60 minutes mod/vig per day
Variable effects alone, accentuated with weight loss, minimal effect of resistance training (VO2 link)
20-30% decrease in CVD events
Smoking cessation
Combined health behaviors decrease by 75% risk of CVD events
Dietary cholesterol and serum cholesterol: Ancel Keys (and limitations)
Current knowledge of relationship and limitations of studies
Ancel Keys studies found a relationship from which an equation for CVD risk prevention was formed
Limitations: grouped all SFAs, predicted only total cholesterol, assumed neutrality of MUFAs and CHO and effects may not be linear
Now we know saturated fat raises serum cholesterol more than dietary cholesterol from animal foods
100 mg/d ↓ in dietary chol –> ↓ 0.05-0.2 mmol/L ↓ in total-C
Limitations: not many very high cholesterol studies and it is just one component in the diet
Mechanistic effect of dietary cholesterol on dyslipidemia (4 points)
↓ synthesis/activity of hepatic LDL-R
↑ chylomicron cholesterol which is more atherogenic and ↑ hepatic delivery
↑ VLDL cholesterol which is more atherogenic
Interferes w/ HDL’s ability to clear cholesterol
Very high cholesterol foods
Compensators and non-compensators what does it mean?
Brains, pancreas, kidney, liver, heart, veal, shrimp, oysters
Compensators (2/3) and non-compensators (1/3) difference in sensitivity to dietary cholesterol intake
AMDR total fat
25-35% of calories - helps reduce total calories and saturated fat intake
Very low fat can ↓ HDL
Current intake 34-37% of kcal
Type matters more than amount
Saturated fat mechanism of ↑ LDL
Reduced LDL-R synthesis and activity
Delayed VLDL clearance
Increased conversion of VLDL remnants –> LDL
Dietary saturated fats current information and recommendations from Heart & Stroke and CFG 2019
Data directly connecting high SFA diet to CVD risk does not exist, only association ↑ LDL-C which is associated with ↑ CVD risk
BUT Dietary SFA also ↑ HDL
More about what SFA is replaced with: MUFA/PUFA replacement improves lipids and CVD risk
Replace “other foods” category to reduce SFA intake before changing central food patterns
Reducing SFA ↓ LDL-C large particles mostly, atherogenic small particles less effected
Replacing SFA w/ CHO –> no benefit on CVD
Heart & Stroke: no limit, focus on healthy balanced diet
CFG: < 10% total energy intake
Effect of SFA, PUFA, MUFA and trans fats on LDL and HDL
SFA increases LDL-C + HDL-C (less), no VLDL-TG
- Especially lauric (but ↑ HDL-C more, found in coconut oil), myristic and palmitic (in presence of dietary chol)
- Stearic is neutral
- MCT no effect on serum chol
MUFA Increases HDL-C and decreases LDL-C
PUFA Increases HDL-C and decreases LDL-C
Trans fats increase LDL-C and decrease HDL-C
Does the source of SFA matter?
Specific food examples
Yes. The food matrix and other benefits of whole food sources matters
SFA from dairy products ↓ CVD risk compared to meat sources and cheese ↑ LDL-C less than butter
Yogurt and cheese inverse association w/ CVD risk (higher C15:0 and C17:0)
Dark chocolate is neutral (stearic C18:0)
Process meats ↑ CVD risk but maybe not unprocessed meats
High risk hypertension group definition
≥ 50 years old + SBP 130-180 mmHg +
1) sub/clinical CVD or
2) CKD or
3) FRS score ≥ 15% or
4) ≥ 74 years old
Low risk hypertension group definition
no target organ damage or CVD risk factors
FRS <10%
