Atherosclerosis Meds Flashcards

1
Q

CHD risk factors

A
  • age and gender
  • lipoprotein disorders
  • HTN
  • DM
  • fam history of premature CHD
  • smoking
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2
Q

In the general population, clinical atherosclerosis CVD is strongly related to age, in a gender dependent manner, increasing in the ______ in men and ______ in women.

A
  • 40s in men; 50s in women

- women tend to have more events later in life and are less likely to survive the events

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3
Q

4 lipid categories and their associated with atherosclerotic CV risk

A
  • total and LDL-C: direct
  • HDL-C: inverse
  • TGs: direct
  • Lpa: direct; genetic biomarker of risk
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4
Q

Blood pressure and CVD risk

A

-linear, direct relationship; lower is better!

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5
Q

DM and CHD

A
  • diabetes is a heart disease “equivalent” because it confers as much risk of future CVD as existing heart disease without DM
  • combination of DM and existing heart disease carries remarkable risk of future MI
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6
Q

T/F: Genetics only play a role in early heart disease.

A
  • false; family history of atherosclerotic heart disease, particularly early onset in 1st degree relatives is a major risk factor for future heart disease independent of other factors
  • still genetics influencing events happening over the age of 65, but most telling at younger ages
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7
Q

Traditional risk factors confer ______ risk of heart disease.

A

-additive

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8
Q

4 patient groups that guidelines recommend high or moderate intensity statins for

A
  1. clinical ASCVD
  2. LDL-C >/ 190 mg/dL
  3. DM
  4. 10 year risk >/7.5% (meant to capture those with strong family histories)
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9
Q

The fact that 30-40% of subjects with premature CHD are not considered high-risk tells us what?

A
  • traditional risk factors do not identify all high-risk subjects
  • there are still unknown risk factors we need to uncover!!
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10
Q

Clinical identification of the metabolic syndrome

A
  • abdominal obesity in men >102 cm, women >88 cm
  • TGs >150
  • HDL in men 130/>85
  • fasting glucose >110 mg/dL
  • 3/5= metabolic syndrome and high risk for CHD
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11
Q

Why is it important to measure more than just LDL-C?

A
  • TGs were shown to be an independent, atherogenic risk factor; and thus remnants carrying high TGs are also atherogenic and need to be measured
  • basically, all non-HDL-C= atherogenic
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12
Q

6 selective emerging risk factors for atherosclerosis

A
  • Lpa
  • homocysteine
  • fibrinogen
  • inflammatory markers
  • subclinical atherosclerosis imaging
  • genetic variation
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13
Q

List 4 inflammatory markers looked at as markers of CVD risk

A
  • CRP
  • SAA
  • siCAM-1
  • IL-6
  • they are not causal, but mark those at higher risk
  • really on CRP is used clinically
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14
Q

If someone is born with a gene that raises their CRP level, are they are heightening risk of CVD?

A

-no, they are not causal! just markers

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15
Q

Methods for non-invasive imaging of atherosclerosis as a way to measure subclinical atherosclerosis

A
  • B-mode ultrasound of carotids: intimal-medial thickness
  • electron beam tomography of coronaries: look for coronary artery calcification; more Ca = more plaque= higher risk
  • magnetic resonance imaging of aorta, carotids, coronaries: plaque size and morphology
  • molecular imaging
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16
Q

Why is screening for calcification especially beneficial?

A

-Ca in coronaries tends to detect events 10 years before they happen!; so check women in their 40s

17
Q

2 options for DNA variants that promote risk

A
  1. gene may increase a risk factor which increases CAD OR

2. gene may directly influence MI without operative through risk factors

18
Q

GWAS studies >100,000 people have uncovered 95 lipid loci. Why is this so important?

A
  • uncovers new targets!! like ADAMTS7

- 2/3 of them have no known connections to risk factors

19
Q

Potential role of ADAMTS7 in atherosclerosis

A

-activated ADAMTS7 turns SMCs into a synthetic phenotypes

20
Q

ADAMTS7 plays a role in atherosclerosis formation, while ______ is thought to maybe play a role in plaque rupture/thrombosis.

A
  • ABO locus

- O seems to be protective bc no glycosylation occurs

21
Q

GWAS is importantly utilized in uncovering common variants conferring small effects. While ________ helps find the rare/mendelian variants conferring strong effects on risk.

A
  • sequencing/exome sequencing
    ex: PCSK9, FH
  • we now try to target PCSK9 with small mlc inhibitors, ASO