1. Cholesterol guidelines
2016

2. Why?
Higher cholesterol confers greater risk of death, especially in persons with ASCVD
When we lower the cholesterol, risk goes down. No matter what it was to begin with!
Statins may also have additional salutary, maybe even anti-inflammatory, effects. Magic statins.

5. ACC/AHA guideline
LDL-C is used only assess whether statin is working (are they taking it?)
High intensity statin lowers LDL-C >50%
(it is supposed to go below 100)
Moderate intensity lowers LDL-C 30-50%

6. Why not?
“the rates of rhabdomyolysis are still ‘reassuringly low’ and similar to those seen in clinical trials (about 1-2 per 10,000 patient years)” UptoDate
Raises liver enzymes. Check ALT once on initiation
Statins cause myalgias in 10-15% “Pravastatin and fluvastatin appear to be less likely to cause muscle toxicity than other statins.”

7. If adverse reaction to statin
Symptoms of rhabdo-
Check CK, myoglobinuria
Muscle pain- check for drug interactions, Vitamin D, hypothyroid,
then switch to fluvastatin, pravastatin
then lower dose, alternate day

9. If myopathy
Lower statin
Stop it if needed.
Try other things

10. Other lipid-lowering options
Bile acid sequestrants- Cause constipation
Nicotinic acid- Causes flushing
Fibrates reduce triglycerides well, and raise HDL- they cause more myopathy and rhabdomyolysis with statins
Fish oil/ omega 3 reduces triglycerides well, and raises HDL-

12. Primary prevention- Preventing a heart attack before it occurs
Secondary prevention- Preventing a heart attack in someone with known ASCVD is called secondary prevention

13. Many recommenders Many recommendations
I’ll cover what we cannot argue about here- what everyone agrees on, and give you an overview of who is recommending what, with time to play with a risk calculator, which is really cool.
USPTF for when to screen
AHA/ACC 2013 for how to treat

14. USPTF Screening
Strongly recommends screening men over 35 and women over 45 with a lipid panel, frequency not specified.
Recommends screening at risk men and women over 20 years old, and strongly recommends lipid screening for anyone with coronary heart disease risk
Other acronyms use the term atherosclerotic heart disease ASHD, Coronary artery disease CAD, JNC 8 says ACVD

15. Karen is 50 years old and having her first physician encounter in her life. Should she be screened for hyperlipidemia with a lipid panel according to USPTF?

16. according to USPTF?
Yes No
Not enough evidence to support
Yes

17. Cholesterol screening in diabetics ADA 2016
ADA guidelines require diabetics to have an initial lipid profile, then screen every 5 years However, AHA/ ACC guidelines say:
Diabetics Ages 40-75: If LDC-C is , and DM, then moderate intensity statin (unless ASCVD, or risk >7.5% then high intensity)
Diabetics <40 or >75, maybe statin
So most diabetics are on a statin, and are monitored yearly

18. Mary is an obese diabetic following up for Primary Care after a year
Mary is an obese diabetic following up for Primary Care after a year. Hba1C indicates her glucose has been under control.
Her last lipid panel was 3 years ago, normal.
Should she have a lipid panel done, according to ADA?

19. according to ADA? Yes In 2 years No Not enough evidence to support

20. Old ATP 3 ATP 3= Adult Treatment Panel III of the
Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) (ATP III) 2001
Don’t use this anymore
This is pretty old- they used tables back then. Now we have a great online calculator

21. History since ATP 3, 2001
Cardiologists added their preference to aggressively lower cholesterol with high-dose statins for any heart patients with LDL over 100, and even 70.
This effectively put almost every heart patient on a statin, which is consistent with new guidelines which track risk instead of LDL number.

22. Summary from 2014 release
Four groups most likely to benefit from statin therapy are identified:
1. Patients with any form of clinical ASCVD
2. Patients with primary LDL-C levels of 190 mg per dL or greater
3. Patients with diabetes mellitus, 40 to 75 years of age, with LDL-C levels of 70 to 189 mg per dL
4. Patients without diabetes, 40 to 75 years of age, with an estimated 10-year ASCVD risk ≥ 7.5%

23. 2014 new
There is the consideration of a statin for Patients without ASCVD, without DM, with
Risk >7.5% -unquestioned, level A evidence for a statin, moderate to high intensity
Risk 5-7.5%, Level B evidence for a statin, moderate intensity
Risk 5%, maybe statin in “select individuals”

24. Summary of AHA/ACC guidelines
Everyone should have heart healthy habits
Everyone with ASCVD on a statin
Everyone else, Based on DM, age, risk
Use algorithms and online calculator

25. If ASCVD- <75 High intensity statin
> 75 Moderate intensity statin
Is this primary or secondary prevention?
Secondary- they already have ASCVD

26. George had a heart attack 3 years ago. He is 70 years old.
His LDL-C is only 75. Should he be on a statin?
High intensity for any ASCVD<75

27. He says what about my liver?
Check ALT once, again only if hepatic symptoms

28. You are seeing a 65 year old Native American male  nonsmoker who has new onset diabetes so you order a fasting lipid panel.  His PMHx is positive for heart disease.  He had a heart attack two years ago and now has a stent in the LAD.  He does have HTN- he takes norvasc 5 mg daily.  His in-office BP is 110/80.  His lipid panel is as follows:
LDL-C= 100
total cholesterol 200
HDL = 45
Triglycerides 150
What should you do?
High intensity statin for ASCVD under 75 yo

29. No ASCVD Ages 40-75: If LDL-C >190 High intensity statin
If LDC-C , and no DM then assess 10 year risk (with an online calculator)
If risk >7.5%, then statin (level of evidence- A)
If risk %, then maybe statin,(depending on calculator), Level of Evidence B
If risk < 5%, statin “consider in select individuals”

30. Risk calculators

31. No ASCVD, and DM
Ages 40-75:
If LDC-C is , and DM, then moderate intensity statin (unless ASCVD, then high)
If <40 or >75, maybe statin
In reality, most diabetics are on a statin

33. Summary of Statin Initiation Recommendations for the Treatment of Blood Cholesterol to Reduce ASCVD Risk in Adults (See Figures 3, 4, and 5 for More Detailed Management Information).
Summary of Statin Initiation Recommendations for the Treatment of Blood Cholesterol to Reduce ASCVD Risk in Adults (See Figures 3, 4, and 5 for More Detailed Management Information). Colors correspond to the Classes of Recommendation in Table 1. Assessment of the potential for benefit and risk from statin therapy for ASCVD prevention provides the framework for clinical decision making incorporating patient preferences. *Percent reduction in LDL-C can be used as an indication of response and adherence to therapy, but is not in itself a treatment goal. †The Pooled Cohort Equations can be used to estimate 10-year ASCVD risk in individuals with and without diabetes. The estimator within this application should be used to inform decision making in primary prevention patients not on a statin. ‡Consider moderate-intensity statin as more appropriate in low-risk individuals. §For those in whom a risk assessment is uncertain, consider factors such as primary LDL-C ≥160 mg/dL or other evidence of genetic hyperlipidemias, family history of premature ASCVD with onset <55 years of age in a first-degree male relative or <65 years of age in a first-degree female relative, hs-CRP ≥2 mg/L, CAC score ≥300 Agatston units, or ≥75th percentile for age, sex, and ethnicity (for additional information, see ABI <0.9, or lifetime risk of ASCVD. Additional factors that may aid in individual risk assessment may be identified in the future. ‖Potential ASCVD risk-reduction benefits. The absolute reduction in ASCVD events from moderate- or high-intensity statin therapy can be approximated by multiplying the estimated 10-year ASCVD risk by the anticipated relative-risk reduction from the intensity of statin initiated (~30% for moderate-intensity statin or ~45% for high-intensity statin therapy). The net ASCVD risk-reduction benefit is estimated from the number of potential ASCVD events prevented with a statin, compared to the number of potential excess adverse effects. ¶Potential adverse effects. The excess risk of diabetes is the main consideration in ~0.1 excess cases per 100 individuals treated with a moderate-intensity statin for 1 year and ~0.3 excess cases per 100 individuals treated with a high-intensity statin for 1 year. In RCTs, both statin-treated and placebo-treated participants experienced the same rate of muscle symptoms. The actual rate of statin-related muscle symptoms in the clinical population is unclear. Muscle symptoms attributed to statin therapy should be evaluated (see Table 8, Safety Recommendation 8). ABI indicates ankle-brachial index; ASCVD, atherosclerotic cardiovascular disease; CAC, coronary artery calcium; hs-CRP, high-sensitivity C-reactive protein; LDL-C, low-density lipoprotein cholesterol; MI, myocardial infarction; and RCT, randomized controlled trial.
Neil J. Stone et al. Circulation. 2014;129:S1-S45
Copyright © American Heart Association, Inc. All rights reserved.

34. Initiating Statin Therapy in Individuals Without Clinical ASCVD
Initiating Statin Therapy in Individuals Without Clinical ASCVD. Colors correspond to the Classes of Recommendation in Table 1. *Fasting lipid panel preferred.
Initiating Statin Therapy in Individuals Without Clinical ASCVD. Colors correspond to the Classes of Recommendation in Table 1. *Fasting lipid panel preferred. In a nonfasting individual, a non–HDL-C level ≥220 mg/dL could indicate genetic hypercholesterolemia that requires further evaluation or a secondary etiology. If nonfasting triglycerides are ≥500 mg/dL, a fasting lipid panel is required. †The Pooled Cohort Equations can be used to estimate 10-year ASCVD risk in individuals with and without diabetes. A downloadable spreadsheet enabling estimation of 10-year and lifetime risk for ASCVD and a Web-based calculator are available at and ‡For those in whom a risk assessment is uncertain, consider factors such as primary LDL-C ≥160 mg/dL or other evidence of genetic hyperlipidemias; family history of premature ASCVD with onset <55 years of age in a first-degree male relative or <65 years of age in a first-degree female relative, high-sensitivity C-reactive protein ≥2 mg/L; CAC ≥300 Agatston units or ≥75th percentile for age, sex, and ethnicity (for additional information, see ABI <0.9; or lifetime risk of ASCVD. Additional factors that may aid in individual risk assessment could be identified in the future. §1) Potential ASCVD risk-reduction benefits. The absolute reduction in ASCVD events from moderate- or high-intensity statin therapy can be approximated by multiplying the estimated 10-year ASCVD risk by the anticipated relative-risk reduction from the intensity of statin initiated (~30% for moderate-intensity statin or ~45% for high-intensity statin therapy). The net ASCVD risk-reduction benefit is estimated from the number of potential ASCVD events prevented with a statin, compared to the number of potential excess adverse effects. 2) Potential adverse effects. The excess risk of diabetes is the main consideration in ~0.1 excess cases per 100 individuals treated with a moderate-intensity statin for 1 year and ~0.3 excess cases per 100 individuals treated with a high-intensity statin for 1 year. In RCTs, both statin-treated and placebo-treated participants experienced the same rate of muscle symptoms. The actual rate of statin-related muscle symptoms in the clinical population is unclear. Muscle symptoms attributed to statin therapy should be evaluated (see Table 8, Safety Recommendation 8). ABI indicates ankle-brachial index; ALT, alanine transaminase; ASCVD, atherosclerotic cardiovascular disease; CAC, coronary artery calcium; CK, creatine kinase; FH, familial hypercholesterolemia; LDL-C, low-density lipoprotein cholesterol; MI, myocardial infarction; RCT, randomized controlled trial; and ULN, upper limit of normal.
Neil J. Stone et al. Circulation. 2014;129:S1-S45
Copyright © American Heart Association, Inc. All rights reserved.

35. Initiating Statin Therapy in Individuals With Clinical ASCVD
Initiating Statin Therapy in Individuals With Clinical ASCVD. Colors correspond to the Classes of Recommendation in Table 1. *Fasting lipid panel preferred.
Initiating Statin Therapy in Individuals With Clinical ASCVD. Colors correspond to the Classes of Recommendation in Table 1. *Fasting lipid panel preferred. In a nonfasting individual, a non–HDL-C level ≥220 mg/dL could indicate genetic hypercholesterolemia that requires further evaluation or a secondary etiology. If nonfasting triglycerides are ≥500 mg/dL, a fasting lipid panel is required. †It is reasonable to evaluate the potential for ASCVD benefits and for adverse effects, and to consider patient preferences, in initiating or continuing a moderate- or high-intensity statin in individuals with ASCVD who are >75 years of age. ALT indicates alanine transaminase; ASCVD, atherosclerotic cardiovascular disease; CK, creatine kinase; FH, familial hypercholesterolemia; LDL-C, low-density lipoprotein cholesterol; and ULN, upper limit of normal.
Neil J. Stone et al. Circulation. 2014;129:S1-S45
Copyright © American Heart Association, Inc. All rights reserved.

36. Statin Therapy: Monitoring Therapeutic Response and Adherence.
Statin Therapy: Monitoring Therapeutic Response and Adherence. Colors correspond to the Classes of Recommendation in Table 1. *Fasting lipid panel preferred. In a nonfasting individual, a non–HDL-C level ≥220 mg/dL may indicate genetic hypercholesterolemia that requires further evaluation or a secondary etiology. If nonfasting triglycerides are ≥500 mg/dL, a fasting lipid panel is required. †In those already on a statin, in whom baseline LDL-C is unknown, an LDL-C <100 mg/dL was observed in most individuals receiving high-intensity statin therapy in RCTs. ‡See Section HDL-C indicates high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; and RCTs, randomized clinical trials.
Neil J. Stone et al. Circulation. 2014;129:S1-S45
Copyright © American Heart Association, Inc. All rights reserved.

37. 55 year old male with new onset DM.
Should you screen lipids?
Yes, fasting lipid profile
LDL-C is 100.
Should you treat?
Yes, moderate or high intensity

38. 50 year old black male without DM
Fasting lipid profile, LDL-C is 100
What now?
HDL is 90
Total cholesterol is 210
SBP is 150, he takes medication
He smokes

39. Risk calculator

40. He gets a statin and a smoke lecture

41. 55 year old Asian male with LDL-C 100
HDL is 50
Total cholesterol is 160
SBP is 120, he takes no medication
He does not smoke

42. Implementation of Risk Assessment Work Group Recommendations.
Implementation of Risk Assessment Work Group Recommendations. ACC indicates American College of Cardiology; AHA, American Heart Association; ASCVD, atherosclerotic cardiovascular disease; CV, cardiovascular; and NHLBI, National Heart, Lung, and Blood Institute.
David C. Goff, Jr et al. Circulation. 2014;129:S49-S73
Copyright © American Heart Association, Inc. All rights reserved.

44. Triglycerides (mg/dL)
< 150 Normal
Borderline high
High
500 Very high

46. Very high triglycerides
Look for other causes of dyslipidemia
Consider high glucose in patients with high triglycerides
High intensity statin
Consider fibrate and fish oil also

51. HDL For HDL, remember high is good. Low is bad. >60 is high, good
<40 is low, bad “categorical risk factor”
(HDL is an element of Metabolic syndrome if <40 in a man or <50 in a woman)

52. HMG CoA reductase inhibitors commonly cause the following side effects:
Myopathy
Constipation
Flushing
GI distress
Dyspepsia

53. HMG CoA reductase inhibitors are statins
They cause myopathy in 10-15%

54. Bile acid sequestrants commonly cause the following side effects:
Myopathy
Constipation
Flushing
GI distress
Dyspepsia

55. *
Constipation is the most common side effect of bile acid sequestrants.
Patients may also experience GI distress
Almost all medications taken by mouth can cause dispepsia

56. Nicotinic acid commonly causes the following side effects:
Myopathy
Constipation
Flushing
GI distress
Dyspepsia

57. * The flushing is dramatic.
Instructions are to take an aspirin 30 minutes before bedtime, then the nicotinic acid at bedtime.
Patients calling with this side effect need much reassurance.

58. Treatment of the metabolic syndrome
Treat underlying causes (overweight/obesity and physical inactivity):
Intensify weight management
Increase physical activity
Treat lipid and non-lipid risk factors if they persist despite these lifestyle therapies:
Treat hypertension
Use aspirin for CHD patients to reduce prothrombotic state
Treat elevated triglycerides and/or low HDL (as shown in Step 9 below)

59. Cost-Effectiveness Issues
Therapeutic lifestyle changes (TLC)
Most cost-effective therapy
Drug therapy
Dominant factor affecting costs
Cost effectiveness: one factor in the decision for drug therapy
Declining price of drugs: increases cost effectiveness
FUTURE RESEARCH

60. A patient has triglycerides of 775. What do you do?
Tell him to have a very low fat diet
Start weight management and physical activity
Start nicotinic acid
Start Fibrate
All of these

61. * All of the above for Triglycerides >500
Patients with triglycerides >500 are at risk for pancreatitis and need multiple therapies

62. Open book Quiz is hard
You are seeing a 55 year old black male  smoker who has new onset diabetes so you order a fasting lipid panel.  His PMHx is negative for heart disease.  He is a smoker.  He does have HTN- he takes norvasc 5 mg daily.  His in-office BP is 110/80.  His lipid panel is as follows:
LDL-C= 100
total cholesterol 200
HDL = 45
Triglycerides 600
What should you do?
Triglycerides over 500, high intensity statin and fibrate, fish oil

63. ATP 3 References