Cardio Exam 2 > Lecture 4 > Flashcards

Lecture 4 Flashcards

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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
moderate-intensity
>75yo or not able to tolerate high-intensity
26
if TG >500 assess underlying causes & target 1st due to
risk of pancreatitis
27
clinical ASCVD inclusion criteria
- 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
28
high-intensity statin therapy
atorvastatin (40-80mg) | rosuvastatin (20-40)
29
primary evaluations in adults >21 with >190mg/dL
- 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
30
primary prevention in DM age 40-75 w/ LDL 70-189mg/dL
- use at least moderate intensity - if DM & 10-yr risk >7.5%, consider high-intensity - 75, weigh benefits & risks when deciding to initiate therapy
31
primary prevention (no ASCVD or DM) w/ LDL 70-189mg/dL
- estimate 10-yr risk - >7.5%: moderate to high intensity - 5-7.5%: can consider moderate-intensity
32
cholesterol effects of statins
< LDL 18-63% < TG 7-30% >HDL 5-15%
33
Statin-induced myalgia
muscle aches, soreness or weakness with minimal or no evalution in CK
34
statin-induced myopathy
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
35
statin-induced rhabdomyolysis
- 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
statin induced myotoxicities
- include myalgia, myopathy & rhabdomyolysis - dose related - greater risk w/ lovastatin & simvastatin - incr. risk when combined with fibrates (gemfibrozil)
37
management if pain, tenderness, stiffness, cramping, weakness or fatigue in statin-treated pts
- establish baseline before starting statins (CK) | - determine severity of new onset pain
38
if unexplained & severe pain
DC statin & evaluate CK, SCr& myoglobinuria for possible rhabdomyolysis
39
if mild-moderate pain
- 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
new onset DM with statin use
- benefit from statins far outweigh the risk of DM
41
contraindications to statin use
liver disease unexplained LFTs pregnancy category X
42
drug interactions with statins
warfarin strong CYP3A4 inhibitors (itraconazole, erythromycin) grapefruit juice may > sim/ator/lovastatin -agents that increase risk of myopathy
43
monitoring for efficacy of statins
- 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
fibric acid derivatives is primarily for
hyperTGemia
45
cholesterol effects of fibric acid derivatives
HDL 10-20% |
46
gemfibrozil outcomes data
primary prevention of CHD & secondary prevention of cardiac events in med with low HDL
47
gemfibrozil frequency
BID
48
fenofibrate frequenct
once daily
49
gemfibrozil should not be given with
statins, esp lovastatin and simvastatin
50
which fibrate can you use with a statin?
fenofibrate
51
adverse effects of fibrates
- 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
clinical pearls of fibrates
- 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
bile acid sequestrants are primarily used
to lower LDL
54
cholesterol effects of bile acid sequestrants
55
outcomes data on bile acid sequestrants
- 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
bile acid sequestrant drugs
cholestyramine resin micronized colestipol colesevelam
57
adverse effects of bile acid sequestrants
- 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
drug interactions with bile acid sequestrants
- 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
bile acid sequestrant clinical pearls
- limited use to do tolerability & efficacy (outcomes data) | - options for pts with CI to statin due to liver impairment or another issue
60
niacin has positive effects on
all lipid parameters
61
niacin cholesterol effects
HDL 15-35% |
62
outcomes data for niacin
inconsistent demonstrating benefit
63
do not use niacin if
- hepatic transaminases >2-3X ULN - persistent cutaneous symptoms - persistent hyperglycemia, acute gout or unexplained abdominal pain of GI symptoms
64
adverse effects of niacin
- 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
lab monitoring for niacin
baseline hepatic transaminases, fasting blood glucose or A1C & uric acid before initiating and again during titration & Q6mo
66
niacin drug interactions
- statins may > risk of myopathy | - cholestyramine < absorption 10-30%
67
niacin clinical pearls
- 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
ezetimibe cholesterol effects
69
adverse effects of ezetimibe
- generally well tolerated | - case reports of myopathy & increased LFTs as monotherapy & in combo with statins
70
drug interactions with ezetimibe
- case reports of > warfarin - < conc. with bile acid sequestrants - > conc. with cyclosporine
71
clinical pearls of ezetimibe
- modest reduction in outcomes; questionable clinical values vc high intensity statin - expensive!
72
fatty acid drugs
``` omega 3 ethyl acid esters (lovaza) icosapent ethyl (EPA) (Vascepa) ```
73
fatty acids are FDA approved for
severe TG >500
74
cholesterol effects of fatty acids
TG: 9%w/L; 45% w/ L; <5% w/ V
75
fatty acid outcomes data
- generally lacking - secondary prevention: may reduce CV death, sudden death, nonfatal MI & nonfatal stroke - no head to head vs statin
76
adverse effects of fatty acids
- GI: belching | - taste perversion (fishy)
77
clinical pearl of fatty acids
- 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
statin + bile acid sequestrants use
improved LDL reduction
79
Stain + ezetimibe use
improved LDL reductions - up to ~60% - ezetimibe/simvastatin (vytorin) - ezetimibe/ atorvastatin (liptruzet)
80
statin + fibrate use
decrease TG & likely LDL depending on agent | - fenofibrate/rosuvastatin being developed
81
statin + niacin use
- improved LDL & TG - niacin/lovastatin (advicor) - niacin/simvastatin ( simcor)
82
niacin + bile acid sequestrant use
improved LDL
83
other combos
- atorvastatin/amlodipine (caduet) | - buffered ASA/pravastatin (Pravigard)
84
clinical ASCVD
- high intensity statin if 75 or not a candidate
85
LDL >190
high intensity statin
86
DM | age 40-75
- moderate intensity statin | - high intensity statin if 10y ASCVD risk >7.5%
87
>7.5% ASCVD 10 yr risk & age 40-75
moderate to high intensity statin
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