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Cardio > LIPIDS > Flashcards

LIPIDS Flashcards

1
Q

Population of Europe 2016 roughly

A

0.7 billion

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2
Q

Population of US roughly 2016

A

0.3 billion

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3
Q

Population in low income countries roughly 2016

A

0.6 billion

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4
Q

Population in high income countries 2016 roughly

A

1.2 billion

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5
Q

Total no of deaths worldwide 2016 roughly

A

Near 60 million

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6
Q

Percentage and number of deaths due to cardiovascular disease worldwide

A

30% and 17.5 million in 2015-16 . In US also 30%, but in Europe nearly 50% . I don’t know the reason

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7
Q

Most common types of cardiovascular disease

A

80% heart attack and strokes

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8
Q

_______% of reduction seen in CVD is due to change in risk factors and ______% due to improved treatment.

A

50 & 40

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9
Q

SCORE system is not required for assessing risk in

A
  1. CVD
  2. Diabetes
  3. CKD
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10
Q

SCORE estimates

A

First FATAL Heart attack, stroke, other occlusive arterial disease, SCD

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11
Q

How to convert SCORE risk estimate to total CVD event risk

A

Multiply with 3 for males
With 4 for females
Lower in older persons

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12
Q

Most frequent monogenic disorder a/w premature CVD

A

Familial hypercholesterolemia

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13
Q

——is technically not fat

A

Cholesterol = steroid plus alcohol

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14
Q

Incidence of DM with statins

A

1in 500

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15
Q

SGPT and statins

A

> 3 times change or reduce

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16
Q

CPK and statins

A

> 10 times stop??

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17
Q

Statins for Diabetes at less than 40 yrs

A

Consider if multiple risk factors

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18
Q

Role of statins in pregnancy

A

CONTRA INDICATED

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19
Q

Why statins not used for primary prevention in young age 20s& 30s

A
  1. SAFETY of statins over decades of therapy uncertain .
  2. Also uncertain whether long term treatment leads to better OUTCOMES compared with postponing treatment until CV risk rises to an absolute level where treatment becomes warranted .
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20
Q

Mobile and precautions of PPI

A
  1. Don’t keep on same side pocket
  2. Keep on opposite ear
  3. May be keep 15-20 cm away from PG
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21
Q

Bile salts are made from

A

Cholesterol

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22
Q

—-% of bile acids are re absorbed

A

95% by enterohepatic circulation

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23
Q

Indications for statin treatment in children with hyperlipidemia

A

LDL above 190 and AGE 8 yrs or above not controlled with diet

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24
Q

Incidence of FH-hetero and homo

A

Heterozygous 1:200-500

Homo-1: 1 million

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25
Q

3 conditions where statin treatment is considered as secondary prevention (other than CAD &stoke)

A
  1. Peripheral arterial disease
  2. Multiple risk factors that confer a 10-year risk of CVD >20%
  3. Chronic kidney disease with estimated GFR <45 mL/min per 1.73 m2*
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26
Q

Effect of diet on LDL Cholesterol

A

In occasional patients with poor baseline diets, marked dietary change can lower LDL-C by as much as 30 percent

Otherwise around 5_7%

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27
Q

Framingham is a place in

A

Northeastern US

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28
Q

Why statins are given at night

A

The majority of cholesterol synthesis appears to occur at night

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29
Q

Criteria for FH Diagnosis-3 types

A
  1. Dutch lipid clinical network criteria - commonly used
  2. Simon Broom register criteria
  3. WHO criteria
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30
Q

Total cholesterol level beyond which FH is to be suspected

A

310

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31
Q

Gall stones are an indication to stop treatment with……….

A

Fenofibrate

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32
Q

USPSTF 2016 recommendations for primary prevention with statins

A 
ASCVD risk more than 10 % and at least one risk factor::
(Age40-75)
Risk factors 
1. Dyslipidemia-LDL > 130; or HDL <40
2.DM
3.HTN
4.Smoking

NOT FOR LDL>190 or FH

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33
Q

NNT to prevent one major adverse CV event or death with statin primary prevention

A

50-200

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34
Q

Total cholesterol level in Homozygous FH

A

More than 500

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35
Q

Homozygous FH patients develop —– before 20

A

CAD and Aortic stenosis before 20 and die before 30

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36
Q

Lomitapide is

A

Microsomal Triglyceride Transfer Protein

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37
Q

If left untreated Heterozygous FH will develop CAD before

A

55/60- males/ females

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38
Q

Frequency of Heterozygous FH

A

1/500 to 1/200

Around 14-34 million estimated pts worldwide

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39
Q

The risk of CHD in definite or probable Heterozygous FH

A

At least 10 fold

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40
Q

Incidence of FCH( familial combined hyperlipidemia)

A

1:100

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41
Q

Useful criteria for diagnosis of FCH

A

Apo B > 120 +TG>133 +family h/o of premature CAD

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42
Q

LDL particle number starts increasing when TG is more than

A

133 i.e. 1.5 mmol/l

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43
Q

SCORE risk assessment is for people without

A

DM,CKD, or FH

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44
Q

Name a bile acid sequestrant

A

ColeSEVelam

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45
Q

Role of statins in NAFLD/NASH

A

Statins are safe and may help Resolution of liver disease

Reduces ASCVD more than in people with normal liver function

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46
Q

Risk of new onset DM with moderate intensity statins

A

1 per 1000 pt years

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47
Q

Incidence of permanent liver damage with statins

A

1 in 2 million treated subjects

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48
Q

Moderate intensity statins should be able to reduce LDL cholesterol by

A

> 30-<50%

High intensity 50% or more

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49
Q

Effect of statins on HDL

A

5-15% increase

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50
Q

Effect of Alcohol consumption in South asians in INTERHEART study

A

No protective effec

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51
Q

INTERHEART study population

A

Acute MI patients in 52 countries- case control study

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52
Q

Atherogenic dyslipidemia of South Asians

A

High TG + Low HDL

But total cholesterol and LDL are lower than western popln

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53
Q

CKD Stage 3 b is

A

GFR- 30-44 ml/mt

Stg 3A is 45-59ml/mt

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54
Q

Ankle brachial index of — is considered as ASCVD

A

<0.9

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55
Q

Coronary artery calcium score more than—-puts pt at high risk of coronary disease

A

300 or more (above 100 is moderate risk)

Also non stenotic carotid plaque

Lp(a) 50 or more (Above 20 moderate risk)

Indian guidelines

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56
Q

When to start statins in Diabetes

A

Age of 40yrs

Or if DMof > 15 yrs and Age of 30 yrs

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57
Q

Documented CAD by angiography means

A

> 10% stenosis

Canadian lipid guidelines

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58
Q

If triglycerides more than ——don’t use friedwald formula

A

400

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59
Q

Apo B is equivalent of

A

Non HDL cholesterol

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60
Q

Even direct assessment of HDL or LDL is accurate only if

A

TG is normal

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61
Q

Seasons and cholesterol

A

TC and HDL high during winter

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62
Q

CVD risk assessment is not required if TC is

A

More than 290 or inFH

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63
Q

Non HDL Cholesterol =

A

Total number of atherogenic lipoproteins in plasma

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64
Q

Lipoprotein (a) is

A

LDL + apoprotein(a)

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65
Q

Effect of high TG on Sodium

A

Pseudohyponatremia

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66
Q

Apo lipoprotein assay and fasting

A

Not required

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67
Q

If u suspect if high concentration of small dense ldl is suspected

A

Do Apolipoprotein B assay

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68
Q

Apo C III is

A

A new Cardiac risk factor

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69
Q

Role of Apo B in risk prediction

A

Apo B= LDL=Non HDL cholesterol

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70
Q

Apo A level corresponding to low HDL

A

Less than 120 ms/dl and 140 males and females respectively

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71
Q

Effect of high TG on HDL and LDL

A

Decrease HDL and increase SMALL DENSE LDL

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72
Q

External manifestations of FH

A

Xanthoma, Xanthelema, Arcus cornealis before 45

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73
Q

How to do CVD risk scoring in CKD

A

No risk scoring required

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74
Q

Treatment principles of high LDL

A

If low risk- treat if LDL > 190
High risk category treat LDL >100
Very high risk category treat if LDL > 70

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75
Q

Markers of sub clinical atherosclerotic vascular damage

A

ABI, Coronary Artery calcfn,Carotid USG

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76
Q

CPK and stopping statins

A

> 10 times-STOP
Plenty of water
Weaker statins-Fluva/Prava after CK is normal

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77
Q

Statins dose and muscle toxicity

A

PRIMARILY at high doses

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78
Q

Cholesterol has the structure of —

A

Steroid

It is called a STEROL as it is Steroid plus AlcohOL

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79
Q

Pseudo hypertriglyceridemia is seen in

A

Hyperglycerolemia. The methods used estimate glycerol and triglycerides

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80
Q

Treatment goal in familial hypercholestrolemia

A

LDL <100 or less than 50% of original value ( for HeFH)

For Homozygous FH LDL<150 is the target

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81
Q

Incidence of FH

A

1 in 250 Heterozygous

1 in 1 million Homozygous

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82
Q

Difference between criteria for FH Homozygous and Heterozygous

A

Homozygous- LDL>500 or treated LDL>300 with clinical criteria

Heterozygous- Simon Broom or Dutch Lipid clinic criteria

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83
Q

Total number of FH patients in world

A

10 million

of these 7000 pts will be Homozygous😏 ( 1in 1 million incidence; total world popln of 7 billion)

So majority HeFH.

85% of males and 50% of these females will develop ASCVD before 65 yrs if proper care not taken

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84
Q

Cholesterol levels in pregnancy

A

Increase by 25-50%.

B/w 18-36 wks of pregnancy

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85
Q

Only cholesterol medicines permitted in pregnancy

Also lactation

A

Bile acid Sequestrants.

Not absorbed into blood

Reduce LDL by 15%

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86
Q

LDL apheresis during pregnancy frequency..

A

Weekly or biweekly

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87
Q

FH is suspected when LDL is above ……. in adults and above…. in children

A

190/ 160

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88
Q

Cascade screening means

A

Testing the family members for same illness

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89
Q

PCSK9 inhibitors work by

A

Preventing LDL Receptor degradation inside liver cells thus increasing LDL Receptors on liver surface

So more and more LDL from extra cellular fluid is removed

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90
Q

Patients with FH has a ….times higher risk of heart disease

A

20 times

FH foundation

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91
Q

In HeFH , the time by which pts develop heart disease

A

50% by 50 yrs males

30% by 60 yrs in females

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92
Q

Effect of cetp inhibitors on cardiac risk

A

Cetrapibs - Neutral or Negative

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93
Q

1% reduction in LDL reduces CAD risk by

A

1%

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94
Q

Statin studies in ACS population

A

MIRACL,PROVE IT,A-Z,IMPROVE IT

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95
Q

LDL Goal in high risk patients-American guidelines

1988 ATP 1

1993 ATP 2
2001ATP 3
2004ATP 3 update
2006 AHA ACC update

A

1988-130 less than FRAMINGHAM

1993-100 equal to or less than

2001- 100 less than

2004- 70 optional - less than ( HPS, PROVE IT, ASCOT LLA,PROSPER, ALLHAT LLT)

2006- reasonable (TNT,IDEAL)

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96
Q

Change Lipid guidelines in 2013 and 2016

A

2013- ACC AHA removed targets

2016- ESC- came back to Lower the better slogan

Also new entry of 50% or more reduction from baseline in very high and high risk subsets

Primary target in moderate and low risk is <115

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97
Q

Serum levels of LDL is predominantly controlled by ….

A

Hepatic LDL receptor

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98
Q

LDL receptor binds to …….. on the LDL

A

Apo B 100

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99
Q

PCSK 9 reduces LDL by what %

A

57% evolucumab

50-57 Alirocumab

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100
Q

Severe myopathy incidence with statins

A

0.1%

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101
Q

Increase in creatinine to say rhabdomyolysis

A

0.5 mg/dL

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102
Q

Statins with less penetration into muscle

A

Pravastatin, Rosuvastatin- water soluble statins

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103
Q

eGFR and cardiovascular risk

A

GFR<60- high risk of CAD

GFR < 30– very high risk

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104
Q

PCSK9 inhibitors approved for use in US and Europe

A

Evolocumab and Alirocumab

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105
Q

Lipoprotein small a is

A

LDL like particle PLUS apo lipoprotein small a which is attached to apo B of the LDL like particle

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106
Q

When to interrupt Statin therapy

A

CPK > 5 Times Normal, SGPT >3 Times Normal

Annals of Pediatric cardio 2014

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107
Q

What happens in liver with PCSK9 inhibitors

A

There will be more cholesterol UPTAKE by liver(as LDL-R in liver is unregulated)and liver will convert these to more bile acids.

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108
Q

INCLISIRAN is ————

Its given as a ——————

A

PCSK9 synthesis inhibitor.(not Mab like alirocumab etc)

It’s given as twice YEARLY injection

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109
Q

% of 0-14 yr population in world

A

26%

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110
Q

2017 ORION 1 Trial is with

A

INCLISIRAN- PCSK9 synthesis inhibitor

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111
Q

Study of CETP inhibitor Evacetrapib inCVD

A

2017 ACCELERATE study

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112
Q

INCLISIRAN lowers LDL by

A

50%

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113
Q

CETP inhibitor Evacetrapib reduces LDL by

A

Around 40% - 2017 ACCELERATE trial

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114
Q

Trials which showed LDL can be reduced to 20 without CNS or Liver problem

A

IMPROVE-IT( ezetemibe)

FOURIER ( Evolocunab)

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115
Q

Ticagrelor needs to be stopped how many days prior to surgery

A

3 days( previously 5)

ESC 2017

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116
Q

Difference inDAPT duration between BMS&DES was removed in

A

ESC 2017

117
Q

Short term DAPT means

Ultra Short term means

A

Short:3-6 months
Ultra Short:1 month

New generation DES superior to BMS in both settings

ESC 2017

118
Q

DAPT duration in bioreabsorbable scaffolds

A

At least 1 year

119
Q

Role of PCSK9 in platelet function

A

Co activator

ESC 2017

120
Q

PCSK9 function

A

Degrades LDL receptor

121
Q

Study which showed lowering inflammation independent of cholesterol reduced Cardiovascular risk

A

2017 CANTOS trial with Canakinumab( IL-1 beta inhibitor)

122
Q

…….. of the heart attacks occur in people who do not have high cholesterol

A

Half

ESC 2017 leaflet

123
Q

LDL levels as low as <8mg were achieved in ———trial

A

FOURIER

with PCSK9

124
Q

Common cut offs for liver enz and CPK in statin trials

A

OT/PT- x 3 Times Normal

CPK- x5 Times Normal

125
Q

Which study showed LDL as low as 8mg is safe with no safety concerns

A

FOURIER study with PCSK9

126
Q

PURE study was done in

A

135,000 patients from 18 countries. Median fu of 7 yrs

Study showed high carb intake- worse total mortality
High fat intake associated with lower risk

127
Q

Effect of saturated fat on cholesterol according to 2017 PURE study

A

LDL And HDL increases
But HDL increases more
So Total cholesterol/HDL ratio becomes better

128
Q

2017 PURE study suggests use of ——— instead of LDL to assess effect of saturated cholesterol on cardiovascular risk

A

Apo B/Apo A1 ratio

129
Q

In 2017 PURE study higher saturated fat intake was associated with———-in stroke risk

A

21% DECREASE in stroke risk🤯

130
Q

Mortality risk reduction with

  1. Saturated fat
  2. Monounsaturated fat
  3. PUFA
A
  1. 14%
  2. 19%
  3. 20%
131
Q

Recommended fat intake by 2017 PURE trialists

A

35%

Up from less than 30 in Guidelines

132
Q

Which study showed LDL is not reliable in predicting effects on saturated fatty acids on future cardiovascular events

A

2017 PURE Trial

133
Q

A study which showed reducing SBP below 120 is not useful

A

2016 HOPE study

Optimal BP in the trial appeared to be 130/80

134
Q

Main procedural difference in 2017 SPYRAL HTN OFF trial was

A

Renal denervation was extended to the Branch vessel s

135
Q

Very high or high risk groups who doesn’t need SCORE risk charts

ESC2017

A

Very High Risk

  1. CKD
  2. T2DM(as such)/ T1DM
  3. Documented CVD including Carotid plaques
  4. SCORE risk-10%

High risk

  1. SCORE risk-5%
  2. Markedly elevated single risk factor-Eg: Severe HTN, Familial dyslipidemia
136
Q

SCORE risk estimates

A

10 yr risk of first FATAL atherosclerotic event(any CAD,PAD,ischemic stroke etc)

ESC 2017 claims most others estimate CAD risk only

137
Q

How to convert fatal CVD risk to total(fatal +non fatal)

A

Men- x 3 times
Women- x 4 Times
Elderly- lower values.

ESC 2016 lipid Guidelines

138
Q

Impact of DM on CVD risk

A

Men-x3 Times risk
Women-x 5 Times risk

According to SCORE risk( More risk than in Framingham cohorts)

ESC 2011

139
Q

How to convert mmol of Cholesterol to mg

A

Mmol x 4 - 10:: my equation for ease

140
Q

Stopping smoking reduces CVD risk by ….,,,

A

Half

ESC 2017

141
Q

Family history of premature CVD increases the risk of. CVD by

A

Males -x 2 Times

Females- x1.7 Times

142
Q

SCORE risk of 1% means———- risk

A

Moderate risk

Check - Abdominal obesity,Lp(a), Homocysteine, Fibrinogen, Apo B etc

143
Q

Risk factor screening should start at——-age according to ESC 2017 lipid Guidelines

A

Males-40 yrs
Females-50 yrs

Family history, DM, Any e/o CVD in any vascular bed , HTN,Central Obesity Or BMI> 25 ,CKD-GFR<60,Autoimmune chronic inflammation (RA,SLE), Psoriasis, xanthomas, xanthelesma, premature arcus , antiretroviral therapy , premature CAD etc- early screening
Also Smoking

144
Q

Definition of central obesity

A

Males- 90 cm waist
Females- 80 cm waist

European males-94

ESC 2017

145
Q

Exponential increase in CVD when BMI is

A

27 or more

ESC 2017

146
Q

Most common monogenic disorder associated with premature CAD

A

FH

147
Q

Fried real dd formula not used if TG is

A

400 or more

148
Q

Fasting is required only for which all lipid parameters

A

Only TG

Even Apo A1 , B etc no need of fasting

149
Q

Lipid change happening in winter

A

Higher Total cholesterol and HDL cholesterol

150
Q

Most risk estimates and almost all drug trials are based on

A

Total cholesterol and LDL cholesterol

151
Q

Conditions with high cholesterol where risk scoring not required

A

Total cholesterol > 310, FH And FCH

Risk is always high

ESC 2017

152
Q

Non HDL -C provide better risk estimates especially in

A

when high TG as in DM, CKD, MetS

Apo B also useful in this situation where small dense LDL would be high

153
Q

False high TG levels are seen in

A

Hyperglycerolemia

154
Q

Plasma Apo A1 levels which are considered to be equal to HDL levels

A

<120- males

<140- females

155
Q

The lipid which is genetically determined to a major extent

A

Lp(a)

156
Q

Lp(a) is like LDL which contains

A

A Unique Protein called-
Apolipoprotein (a) .

This is structurally different from other Apolipoproteins

157
Q

Apo E mutation causes

A

Familial dysbetalipoproteinemia- Apo E2 Homozygous

High TG, low HDL, high TC(FCH)

Xanthoma striatum palmaris, Tuberoeruptive xanthoma etc

158
Q

Every 40 mg reduction in LDL reduces CVD risk by

A

22%

ESC 2011

159
Q

SCORE project was done in

A

2003

160
Q

NICE guidelines suggest evaluation for FH when

A

TC> 290

Use Simon Broome Criteria or DLCN Criteria

161
Q

LDL targets in Very high risk and High risk subsets in ESC 2017

A

Very high risk-< 70 or 50% from baseline

High- <100

162
Q

Apo B treatment targets in Very high risk and High risk subsets

A

80 mg/dL And 100 respectively

Better than LDL alone in pts with HIGH TG

ESC2017

163
Q

Specific target for hs crp May be useful is based on which all trials

A

2004 PROVE-IT TIMI 22
2004 to Z trial
2008 Jupiter trial

164
Q

When to refer for DNA testing in FH

A

Simon Broome- Possible or Definite

DLCN- score 6

NICE guidelines

165
Q

A diagnosis of Homozygous FH is considered when

A 
LDL cholesterol ( not total cholesterol) > 500 in 16 years or older 
> 425 in under 16
166
Q

Every 10 kg loss LDL comes down by

A

8mg/dl In grossly obese

Effect is rather small

Even smaller is the reduction by regular exercise

ESC2017

167
Q

The dietary factor with strongest impact on LDL

A

Dietary SFA

1.6 mg/dl for every 1% additional energy from saturated fat

168
Q

SFA which will not increase TC

A

Stearic acid

169
Q

Trans fatty acids in limited amounts is seen in natural foods like

A

Dairy products, Meat of ruminants

170
Q

Effect of dietary cholesterol on CAD mortality

2. On cholesterol levels

A
  1. Positive relation with CAD mortality partly independent of TC levels
  2. Marked inter individual variability
171
Q

Effect of dietary carbs on LDL

A

Neutral

172
Q

PUFA effect on cholesterol

A

n3 series-no direct hypocholesterolemic effect

N6 PUFA- decreases LDL by 2 mg/dl for every 1% energy substitution of SFA with PUFA

173
Q

Effect of habitual fish consumption on C.V. risk and lipids

A

Is associated with reduced C.V. risk that is mostly independent of any effect on lipids

174
Q

A mono unsaturated fat effect other than on lipids

A

Significantly improves insulin sensitivity

So will reduce post prandial TG

175
Q

In patients with high TG with chylomicrons the use of ——- avoid formation of chylomicrons

A

Medium chain TG

As these are directly transported to metabolized in liver

Long chain TG are transported as chylomicrons through lymphatic system while medium chain directly to the Portal system to Liver

176
Q

Does dietary Fructose increase TG

A

Yes

ESC 2017

177
Q

Effect of weight reduction on TG

A

20-30% reduction

178
Q

Moderate consumption of Alcohol is

A

10-30g/day

1-2 drinks/day

179
Q

Difference between SFA and Trans FA on Lipid

A

SFA- HDL and LDL increases

Trans FA-HDL decreases and LDL increases

180
Q

How phytosterols help in dyslipidemia

A

They compete with Cholesterol for intestinal absorption

181
Q

Phytosterols can reduce TC&LDL by——-

A

upto 10%

182
Q

Soy protein effect on LDL

A

Upto 5% reduction

183
Q

Omega 3 can reduce TG by

A

30%

May increase LDL by 5%

184
Q

Low intake of fats and oil will reduce

A

Vitamin E and Essential fatty acids

185
Q

N3 PUFA sources

A

Fish, Nuts, Soy, Flaxseed oil

186
Q

Factors modifying SCORE risk

A

LVH,AFib, OSA, AI diseases, Central Obesity among others

187
Q

Eliminating health risk behaviors can prevent …….%CVD and …….% cancers

A

80& 40

ESC 2011 lipid Guidelines

188
Q

Poly pill approach is for people more than ….yrs

A

55

ESC 2016 lipid Guidelines

189
Q

Markers of sub clinical vascular damage

A
  1. ABI
  2. Carotid USG
  3. CAC- Coronary Artery calcification

ESC 2016 lipid Guidelines

190
Q

Markers indicating higher cardiac risk in intermediate SCORE patients

A 
hsCRP
Lp(a)
Apo B
Albuminuria
High TG
ABI 1.4
Carotid plaques 
CAC>400
191
Q

How to know pretreatment cardiac risk

A

Multiply by 3/2

Risk is usually reduced 1/3 by treatment

ESC 2016 lipid Guidelines

192
Q

Stopping smoking in general will reduce……% of CVD risk

A

50%

193
Q

Age for risk factor screening without any pre existing problem s

A

40- males

50- females or menopause

194
Q

European statistics on male female ratio of CVD

A

Total CVD death: Male:Female-45:55

In less than 65 age group -approx 70:30!ratio

195
Q

Markedly elevated single risk factors which will include in high risk category to take statin

A

TC-> 310
BP>=180/110
Most people with DM
GFR-30-59

DM with end organ damage is in -Very high risk category
Severe CKD-GFR<30-Very high risk
Documented significant plaque

ESC 2016 lipid Guidelines

196
Q

Premature at us cornealis means

A

<45 yr olds

197
Q

An alternative to non HDL C is

A

Apo-B

ESC 2016 lipid Guidelines

198
Q

Effect of DM on non fasting LDL levels

A

May show around 20 mg less

199
Q

HDL C at increased risk of CVD is if less than

A

Males-40

Females-50

200
Q

Apo A1 levels corresponding to HDL levels of 40/50

A

<120/140

201
Q

Lipoprotein (a) is

A

Routine LDL in which the ApoB protein of LDL is attached to another protein called Apolipoprotein small a. This small a has similarity to Plasminogen.

Hence this will compete with Fibrinogen and prevent thrombolysis

202
Q

Drugs which can reduce Lipoprotein (a)

A

PCSK9 inhibitors And Nicotinic acid

Reduce upto 30% . Clinical effect not known

203
Q

The BP And DM targets to reduce risk of CVD according to 2016 lipid Guidelines

A

BP-<140/90

DM-<7 HbA1c

204
Q

In addition to the goals set for LDL the ESC lipid Guidelines also says

A

The LDL C should be reduced by at least 50%

205
Q

Effect of dietary carbohydrates on HDL

A

Reducing Carbs can increase HDL

206
Q

Mediterranean diet supplemented with extra virgin oil or Nuts reduced incidence of major CV events by

A

30%

ESC lipid Guidelines 2016 or 17

207
Q

Relation between dietary cholesterol and CAD

A

Positive relationship exists between dietary cholesterol and CAD mortality which is
Partly independent of TC levels

208
Q

Effect of carbohydrate on lipid profile

A

LDL-C- neutral
TG- increases
HDL-C - decreases

But fiber has a direct hypocholesterolemic effect

So use carb with fiber

209
Q

For every 10 kg weight loss the LDL comes down by

A

8 mg

Regular exercise causes even smaller reductions in LDL

But exercise and weight loss goes beyond LDL reduction to reduce CV risk

210
Q

SFA replaced by MUFA /n6PUFA/n3PUFA on HDL

A

MUFA-Neutral
N6- Slight decrease
N3- Almost neutral

211
Q

Effect on HDL with 10 kg weight reduction

A

4 mg increase in HDL

212
Q

Physical activity to increase HDL-C

A

5 km brisk walk / 5!days per week will roughly increases HDL by 5 mg

Roughly 1500-2000kcal / week

213
Q

Calorie reduction for weight loss

A

300-500kcal/ day

214
Q

Position of very low carbohydrate diet as per ESC LIPID GUIDELINES 2016

A

Not recommended

215
Q

80% intake of trans fatty acids is from

A

Partial hydrogenated vegetable oils

216
Q

Low intake of fats and oils causes

A

Low Vit E/Essential fatty acids/reduce HDL

217
Q

Fatty acid intake as advised by ESC 2016

A

Predominantly from MUFA/N6PUFA(<10%_ to reduce lipid peroxidation and avoid decrease in HDL)/ N3PUFA
Cholesterol to< 300 mg esp in people with high cholesterol

ESC 2016

218
Q

Moderate alcohol consumption according to ESC 2016 lipid Guidelines

A

Males- upto 20 gm( 2 drinks)

Females-10 gms (1 drink)

219
Q

2 GM of phytosterols daily can reduce LDL by

A

10%

HDL&TG- no effect

220
Q

Which meta analysis showed that LDL reduction translates into lower CV events independent of mechanism involved

A

2009 Robinson Rt al JACC

221
Q

Adverse effect if excess phytosterols

A

Decrease in carotenoids and fat soluble vitamin levels by the sterols

222
Q

Bioactive ingradient in Red Yeast Rice

A

Monacolins

Similar to statins

223
Q

Dietary fiber which reduces LDL-C

A

Water soluble fiber from oats
Barley beta glucan

At least 3 GM/ day

224
Q

Omega 3 may reduce TG upto

A

30% ( Veg N3 are less effective)

At doses of 2-3 GM/ day

At higher doses may increase LDL

225
Q

Study which supports Mediterranean diet forvCVD prevention

A
  1. PREDIMED trial
226
Q

ESC LIPID GUIDELINES 2016 position on omega 3 for secondary prevention of CVD

A

No longer recommended

227
Q

Recommended salt intake as per ESC 2016 LIPID GUIDELINES

A

< 5 gm salt

228
Q

Tropical vegetable oils means

A

Palm oil and Coconut oil

229
Q

For which group of patients according to ESC 2016 lipid Guidelines >50% LDL reduction is to be achieved

A

Very high risk and High risk

230
Q

Effect of statins on TG and HDL

A

Reduce TG by 30-50%

HDL increases by 5-10%

231
Q

Statins which are pro drugs

A

Lovastatin and Simvastatin

232
Q

In rhabdomyolysis CK levels are elevated at least

A

10 Times

233
Q

Frequency of muscle related complaints with statins 2013 circulation article

A

5%

10-15% in some observational studies

234
Q

Mild ALT elevation occurs in ——% of patients On statins

A

0.5-2%

235
Q

Clinically relevant SGPT elevation with statins

A

3 Times ULN On two occasions

236
Q

mild ALT elevations due to steatosis- statins will…

A

No indication that statins cause worsening of Liver disease

ESC 2016 lipid Guidelines

237
Q

The number needed to cause one case of DM with statin use

A

255 pts over 4 years

ESC 2016 lipid Guidelines

Relative risk increases 9%
Absolute risk 0.2%

238
Q

Proteinuria and Statins

A

Increased frequency with all Statins

12% with 80 mg Rosuvastatin
At 40 mg it is similar to other statins

ESC 2016 lipid Guidelines

239
Q

The apparent reason for proteinuria with statins

A

Due to reduced tubular reabsorption and not due to glomerular dysfunction

240
Q

Statins not undergoing Hepatic metabolism via CYP

A

Pravastatin, Rosuvastatin, Pitavastatin

241
Q

CCBs which may increase statin toxicity

A

Amlodipine/Verapamil/ Diltiazem

By CYP3A4 interaction
ESC 2016 lipid Guidelines

Ranolazine And Amiodarone also

242
Q

Most of the bile acids are reabsorbed and returned to liver by

A

Active absorption at terminal ileum

243
Q

Bile acid sequestrants- the 2 older ones and the new one

A

Cholestyramine, Colestipol- resins

New- Colesevelam- a synthetic drug

244
Q

Action on blood sugar by Colesevelam

A

Reduces blood sugar

245
Q

Effect of bile acid sequestrants on LDL,HDL,TG

A

LDL-20% decrease
HDL-neutral
TG- may increase in some predisposed pts

246
Q

Precautions with bile acid sequestrants

A

Take 4 hr before or 1 hour after other drugs With PLENTY of Water

Fat soluble Vitamin deficiency can happen

247
Q

The drug which reduces intestinal absorption of dietary and biliary cholesterol without affecting absorption of fat soluble nutrients

A

EZETEMIBE

By acting on NMC1L1- Neimann-Pick C1Like Protein

248
Q

EZETEMIBE reduces LDL by

A

20%

249
Q

EZETEMIBE studied after ACS

A

2015 IMPROVE IT

250
Q

Two studies which showed EZETEMIBE was effective in reducing CV events

A

2008 SEAS trial- Aortic Stenosis

2011 SHARP trial- CKD

251
Q

Most frequent adverse effect of EZETEMIBE

A

Muscle pain & Moderate elevation in liver enzymes

252
Q

PCSK9 reduces LDL by

A

60%

No effect on HDL and TG

253
Q

The subset which doesn’t respond to PCSK9 inhibitors

A

LDL -R deficient Ho FH

254
Q

PCSK9 adverse effects

A

Flu like symptoms
Itching at injection site
Pt reported neuro cognitive effects- needs more scrutiny

255
Q

Nicotine can acid effect on LDL,HDL,TG

A

LDL-15%
HDL-25% increase

TG-30%

At 2gm/day

256
Q

ESC 2016 lipid Guidelines recommendation level for PCSK9 in statin intolerant pts

A

2b

257
Q

Remnant cholesterol is calculated as

A

TC- HDL+LDL

258
Q

Percentage of people with TH> 150

A

1/3 rd If adults

259
Q

Effect of pregnancy on TG

A

Double during 3rd trimester

260
Q

Moderate TG definition as in ESC 2016 lipid Guidelines

Adapted from EAS

A

150- 880. (10 mmol/l)

261
Q

Recommendation for drug treatment in HTG- ESC 2016 lipid Guidelines

A

> 200
High risk for CVD
Class 2a- drug treatment to be considered

DOC- Statin Class 2 b

If >200 despite statin add fibrate- 2b

262
Q

Dosage of PCSK9 is every

A

TWO weeks

Ie Monthly 2 injections

263
Q

Relationship between carbohydrate intake and MI occurrence as per 2017 PURE study

A

No relation

Also no relation to Stroke

264
Q

Relation between fat intake and MI as per PURE 2017 study

A
  1. No relation with MI
  2. Sat fat reduced stroke
  3. Total mortality reduced with increased fat intake

But increased carb intake increased mortality

The difference in mortality in both groups were due to changes in non CVD mortality

265
Q

PURE Study 2017 was done with > …….number of cases from ….. countries

A 
135,000
18 countries 
35-70 yrs population 
2003-2013 recruitment 
Median fu- 7.5 years

6000- total mortality
5000–CVD events

266
Q

Countries like Finland have a very high intake of saturated fats in the range of

A

20% of total energy

From PURE 2017 study discussions

Guidelines as of 2017 recommend <10% of saturated fat intake

267
Q

Argument against using only LDL as the marker in assessing effect of Saturated fat intake

A
  1. Cholesterol/HDL ratio may be changed favorably
  2. Effect on Apolipoproteins is not known
  3. May have effects on BP

The 3 arguments presented in PURE 2017 discussion

268
Q

The only 3 high income countries in PURE 2017 study

A

UAE
Canada
Sweden

269
Q

What % of the PURE 2017 cohort had CVD and were excluded from study

A

5%

Around 7000 had CVD

270
Q

Percentage of Carb/Fat/Protein intake in South Asia in PURE 2017
Study

A

65/20/10 roughly

271
Q

Relation between total mortality and PUFA/MUFA/Sat FA

A

Reduced with more intake of PUFA and MUFA and Sat fats

PURE 2017 study

272
Q

Highest quintile of fat and sat fat intake in PURE 2017 study

A

33-38% for total fat

12-15% for sat fats

Both of total energy

273
Q

Total mortality increased with carb when intake was more than…. in PURE2017 study

A

65% ie 4th and 5th quintiles

274
Q

As per PURE 2017 study sat Fat intake of ….. reduced stroke

A

12-15% roughly

275
Q

Effect of high Carbohydrate intake on Dyslipidemia

From PURE 2017 Discussion

A
  1. High TG and low HDL
  2. Apo B/Apo A ratio increased
    3.Increased small dense LDL
    And also increases BP
276
Q

The relation between low Carb intake and mortality in PURE study of 2017

A

<50% energy quartile didn’t show any risk reduction

So not advisable as such

So the authors suggest moderate intake in range of 50-55%

Total fat they suggest- about 35%

277
Q

First large study to show the effect of low level Sat fat intake and mortality and CVD events

A

PURE 2017

Doesn’t reduce total mortality or stroke and this quintile when compared to 15% had higher events

So less than 7% may be harmful as per PURE discussion

278
Q

Strongest risk predictor of MI and stroke as per PURE 2017 discussion

A

ApoB/ApoA1 ratio

279
Q

The 2017 study which showed that there is no detrimental effect of fat intake in CVD events

A

PURE study

280
Q

The effect of increasing carb intake and fat intake on cardiovascular mortality or on major CVD as per 2017 PURE study

A

No effect

The effect was on total mortality and non cardiovascular mortality

281
Q

Mortality benefit was maximum when carbohydrates were replaced with… ……in PURE 2017 study

A

PUFA

Still no effect on CVD.

Effects minimal when replaced with sat fat, MUFA or proteins

282
Q

The simplistic thinking that is questioned by PURE 2017

A

Can the effect of diet be captured by a single bio marker eg. like LDL or BP alone..It’s much much more complex. Multiple bio markers should be always considered in assessing effect of diet.

Similar Pr. Yusuf

283
Q

Arguments against PURE 2017

Some thoughts

A

Comparing lowest BMI to highest BMI is not the right thing to do. Here they have compared the quintile 1 to 5.
The sweet spot may be somewhere in between

It may be a U shaped relation

Also didn’t swap PUFA for sat fat. Did only for carb.

Used a single questionnaire to assess food intake over 7 years in addition to possible recall bias
Also only one blood sample at the start of the study

Also risk ratios of less than 2 may be questionable

It’s only an observational study

It’s good to have aHealthy dose of HUMILITY in dietary advices

284
Q

Argument against AHA 2017 guidelines on sat fat intake based on PURE study

A

AHA suggests less than 6% sat fat intake. But in PURE study it was linked to higher mortality ( only the 4th and 5th quintiles were good

285
Q

Effect of saturated fat on BP in PURE 2017 substudy

A

Increases. Also carbs

Protein a/w decrease in BP

286
Q

Mean saturated fat intake in North America and Europe

A

11%

China around 6%

287
Q

SCORE risk grading

A

Low-<1%
Moderate-1-5%
High<10%
V.high-10%

288
Q

Alirozumab and Evolocumab was approved by US FDA in

A

2015

Cardio (36 decks)

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