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Cardio Exam 2 > Lecture 4 > Flashcards

Lecture 4 Flashcards

1
Q

class I of recomenation

A

benefits»> risk

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2
Q

Level A of evidence

A

multiple populations; data from multiple randomized, controlled trials or meta- analysis

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3
Q

Level B of evidence

A

limited populations & single RCT or non-controlled trials

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4
Q

Level C of evidence

A

very limited populations; consensus option

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5
Q

class IIa of recomenation

A

benefits»risk

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6
Q

class IIb of recomenation

A

benefit>/= risk

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7
Q

class III of recomenation

A

no benefit or harm

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8
Q

dietary advice for LDL lowering

A
  1. emphasize intake of veggies, fruits, whole grains, low-fat dairy, poultry, fish, legumes, non-tropical veggie oils & nuts
  2. limit intake of sweets & red meats
  3. 5-6% of total calories from saturated fats
  4. reduce % calories from saturated fat
  5. reduce % calories from trans fat
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9
Q

exercise for dyslipidemia

A
  1. aerobic physical activity
  2. dec. LDL and inc. HDL
  3. 3-4 sessions/wk (120-160min/wk)
  4. moderate to vigorous activity
  5. resistance-training may dec. LDL, TG, & non-HDL (no effect)
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10
Q

optimal lipid panel

A

LDL <200

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11
Q

TC=

A

LDL+ HDL+ TGs

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12
Q

CK labs done in selected individuals who may be at increased risk

A
  1. personal history of statin intolerance
  2. family history of statin intolerance or muscle disease
  3. concomitant drug therapy that may incr. risk
  4. clinical presentation (e.g. elderly, high dose-statin therapy)
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13
Q

secondary causes of dyslipidemia

A

diet
drugs
diseases
disorders & altered metabolism

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14
Q

diet

A
  • elevated LDL: saturated or trans fats, weight gain, anorexia
  • elevated TG: weight gain, very low-fat diets, high intake of refined carbs, excessive alcohol intake
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15
Q

drugs

A
  • elevated LDL: diuretics, cyclosporine, glcocorticoids, amiodarone
  • elevated TG: oral estrogens, glucocorticoids, bile acid sequestrants, protease inhibitors, retinoic acid, anabolic steroids, sirolimus, raloxifene, tomxifen, BB (not carvedilol), thiazides
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16
Q

diseases

A
  • elevated LDL: biliary obstruction, nephrotic syndrome

- elevatedTG: nephrotic syndrome, chronic renal failure, lipodystrophies

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17
Q

disorders & altered metabolism

A
  • elevated LDL: hypothyroidism, obesity, prego

- elevated TG: poorly controlled DM, hypothyroidism, obesity, prego

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18
Q

what does ASCVD stand for?

A

atherosclerotic cardiovascular disease

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19
Q

additional risk factors for ASCVD

A
  1. 1* LDL>160mg/dL or evidence of genetic hyperlipidemia
  2. premature ASCVD in 1* (/=2mg/dL)
  3. elevated coronary artery calcium (CAC) score >300units or >75 percentile
  4. ankle-brachial index<0.9
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20
Q

focus is on

A

intensity of statin therapy

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21
Q

primary therapy

A

statin-based

  • outcomes-based trials
  • decreased risk of future events & decreased mortality
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22
Q

primary therapy, data demonstrating

A
  • decreased morbidity/mortality related to ASCVD
  • strong evidence: decr. LDL
  • some evidence: incr. HDL & decr. TG
  • not proven: dec, il(a), CRP & homocysteine
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23
Q

statin therapy does not have a

A

specific LDL target

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24
Q

high-intensity

A

<75 yo w/out CI or drug-drug interactions or history of intolerance

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25
Q

moderate-intensity

A

> 75yo or not able to tolerate high-intensity

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26
Q

if TG >500 assess underlying causes & target 1st due to

A

risk of pancreatitis

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27
Q

clinical ASCVD inclusion criteria

A
  • ACS (acute coronary syndrome)
  • history of MI
  • stable or unstable angina
  • coronary or other arterial revascularization procedures
  • stroke or TIA
  • PAD presumed to be atherosclerotic in origin
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28
Q

high-intensity statin therapy

A

atorvastatin (40-80mg)

rosuvastatin (20-40)

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29
Q

primary evaluations in adults >21 with >190mg/dL

A
  • pt at high risk of ASCVD due to lifetime exposure to high LDL 2* to genetic causes (FH)
  • at 21 should receive statin, if not already on one
  • high intensity
  • reasonable to intensify statin therapy to at least 50% LDL reduction
  • after max intensity of statin is achieved, addition of non-statin may be considered to further lower LDL
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30
Q

primary prevention in DM age 40-75 w/ LDL 70-189mg/dL

A
  • use at least moderate intensity
  • if DM & 10-yr risk >7.5%, consider high-intensity
  • 75, weigh benefits & risks when deciding to initiate therapy
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31
Q

primary prevention (no ASCVD or DM) w/ LDL 70-189mg/dL

A
  • estimate 10-yr risk
  • > 7.5%: moderate to high intensity
  • 5-7.5%: can consider moderate-intensity
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32
Q

cholesterol effects of statins

A

< LDL 18-63%
< TG 7-30%
>HDL 5-15%

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33
Q

Statin-induced myalgia

A

muscle aches, soreness or weakness with minimal or no evalution in CK

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34
Q

statin-induced myopathy

A

muscle symptoms associated with elevations in CK >10 X ULN (normal 22-198).
- also, pts who hve intolerable muscle symptoms but CK not 10 X ULN, may be considered to have myopathy

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35
Q

statin-induced rhabdomyolysis

A
  • CK >10,000IU/L or CK >10X ULN with an elevation in SCr or requiring IV hydration therapy. Myopathy extensive enough to cause spillage of myoglobin into the urine & may cause renal failure
36
Q

statin induced myotoxicities

A
  • include myalgia, myopathy & rhabdomyolysis
  • dose related
  • greater risk w/ lovastatin & simvastatin
  • incr. risk when combined with fibrates (gemfibrozil)
37
Q

management if pain, tenderness, stiffness, cramping, weakness or fatigue in statin-treated pts

A
  • establish baseline before starting statins (CK)

- determine severity of new onset pain

38
Q

if unexplained & severe pain

A

DC statin & evaluate CK, SCr& myoglobinuria for possible rhabdomyolysis

39
Q

if mild-moderate pain

A
  • DC statin until symptoms can be evaluated
  • evaluate for other causes
  • if muscle symptoms resolve, give original or lower does of same statin to establish causal relationship
  • if causal relationship, DC statin & switch to low dose of another statin & gradually increase as tolerated
40
Q

new onset DM with statin use

A
  • benefit from statins far outweigh the risk of DM
41
Q

contraindications to statin use

A

liver disease
unexplained LFTs
pregnancy category X

42
Q

drug interactions with statins

A

warfarin
strong CYP3A4 inhibitors (itraconazole, erythromycin)
grapefruit juice may > sim/ator/lovastatin
-agents that increase risk of myopathy

43
Q

monitoring for efficacy of statins

A
  • after baseline & initiation of statin, recheck FLP in 4-12 wks to determine adherence
  • then 3-12 months as clinically indicated
  • reinforce adherence at each visit
44
Q

fibric acid derivatives is primarily for

A

hyperTGemia

45
Q

cholesterol effects of fibric acid derivatives

A

HDL 10-20%

<LDL 5-20%

46
Q

gemfibrozil outcomes data

A

primary prevention of CHD & secondary prevention of cardiac events in med with low HDL

47
Q

gemfibrozil frequency

A

BID

48
Q

fenofibrate frequenct

A

once daily

49
Q

gemfibrozil should not be given with

A

statins, esp lovastatin and simvastatin

50
Q

which fibrate can you use with a statin?

A

fenofibrate

51
Q

adverse effects of fibrates

A
  • GI
  • rash
  • hepatotoxicity-monitor LFTs baseline, 6-12 wjs then annually
  • myalgias (esp w/ statins)
  • drug interactions (may sug >warfarin)
    renal function (SCr & eGFR at baseline, w/in 3 months then Q6mo)
52
Q

clinical pearls of fibrates

A
  • 1st line therapy for pts w/ significant hypertriglyceridemia (>500mg/dL)
  • fenofibrate is preferred when using a statin
  • monitor renal function, esp. fenofibrate & potentially adjust dose
53
Q

bile acid sequestrants are primarily used

A

to lower LDL

54
Q

cholesterol effects of bile acid sequestrants

A

<HDL 3-5%

TG+/-

55
Q

outcomes data on bile acid sequestrants

A
  • primary prevention in men reduces need for bypass, CHD, death & nonfatal MI
  • secondary prevention in men w/ diet, reduces cardiac events compared to usual care
56
Q

bile acid sequestrant drugs

A

cholestyramine resin
micronized colestipol
colesevelam

57
Q

adverse effects of bile acid sequestrants

A
  • GI: constipation & dyspepsia
  • CI in complete bowel obstruction
  • not absored, so 300 & use caution if 250-299
  • check FLP at baseline, 3 mo, & Q6-12mo
58
Q

drug interactions with bile acid sequestrants

A
  • may sig < absorption of other meds
  • tk 1 hour before or 4 hours after
  • supplements with vitamins ADEK, folic acid and Fe may ne required
59
Q

bile acid sequestrant clinical pearls

A
  • limited use to do tolerability & efficacy (outcomes data)

- options for pts with CI to statin due to liver impairment or another issue

60
Q

niacin has positive effects on

A

all lipid parameters

61
Q

niacin cholesterol effects

A

HDL 15-35%

<TG 20-50%

62
Q

outcomes data for niacin

A

inconsistent demonstrating benefit

63
Q

do not use niacin if

A
  • hepatic transaminases >2-3X ULN
  • persistent cutaneous symptoms
  • persistent hyperglycemia, acute gout or unexplained abdominal pain of GI symptoms
64
Q

adverse effects of niacin

A
  • flushing & itching: tk 325mg ASA 30 minutes before
  • may > uric acid & blood glucose in pts with gout & DM
    -hepatotoxicity
    -GI: N/V/D, gas, dyspepsia (avoid if peptic ulcer)
    -
65
Q

lab monitoring for niacin

A

baseline hepatic transaminases, fasting blood glucose or A1C & uric acid before initiating and again during titration & Q6mo

66
Q

niacin drug interactions

A
  • statins may > risk of myopathy

- cholestyramine < absorption 10-30%

67
Q

niacin clinical pearls

A
  • most potent agent to >HDL but may not translate to outcomes
  • limited use, secondary to lack of data& tolerability, esp IR
  • do not use no flush niacin. incr risk of hepatotoxicity
68
Q

ezetimibe cholesterol effects

A

<TG 8%

HDL +/-

69
Q

adverse effects of ezetimibe

A
  • generally well tolerated

- case reports of myopathy & increased LFTs as monotherapy & in combo with statins

70
Q

drug interactions with ezetimibe

A
  • case reports of > warfarin
  • < conc. with bile acid sequestrants
  • > conc. with cyclosporine
71
Q

clinical pearls of ezetimibe

A
  • modest reduction in outcomes; questionable clinical values vc high intensity statin
  • expensive!
72
Q

fatty acid drugs

A 
omega 3 ethyl acid esters (lovaza)
icosapent ethyl (EPA) (Vascepa)
73
Q

fatty acids are FDA approved for

A

severe TG >500

74
Q

cholesterol effects of fatty acids

A

TG: 9%w/L; 45% w/ L; <5% w/ V

75
Q

fatty acid outcomes data

A
  • generally lacking
  • secondary prevention: may reduce CV death, sudden death, nonfatal MI & nonfatal stroke
  • no head to head vs statin
76
Q

adverse effects of fatty acids

A
  • GI: belching

- taste perversion (fishy)

77
Q

clinical pearl of fatty acids

A
  • may consider in pts w/ high TGs
  • decreased risk hepatotoxicity & P450 interactions
  • Vascepa does not increase LDL
  • Vascepa not as effective at lowering TGs as lovaza
78
Q

statin + bile acid sequestrants use

A

improved LDL reduction

79
Q

Stain + ezetimibe use

A

improved LDL reductions

  • up to ~60%
  • ezetimibe/simvastatin (vytorin)
  • ezetimibe/ atorvastatin (liptruzet)
80
Q

statin + fibrate use

A

decrease TG & likely LDL depending on agent

- fenofibrate/rosuvastatin being developed

81
Q

statin + niacin use

A
  • improved LDL & TG
  • niacin/lovastatin (advicor)
  • niacin/simvastatin ( simcor)
82
Q

niacin + bile acid sequestrant use

A

improved LDL

83
Q

other combos

A
  • atorvastatin/amlodipine (caduet)

- buffered ASA/pravastatin (Pravigard)

84
Q

clinical ASCVD

A
  • high intensity statin if 75 or not a candidate
85
Q

LDL >190

A

high intensity statin

86
Q

DM

age 40-75

A
  • moderate intensity statin

- high intensity statin if 10y ASCVD risk >7.5%

87
Q

> 7.5% ASCVD 10 yr risk & age 40-75

A

moderate to high intensity statin

Cardio Exam 2 (12 decks)

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