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Flashcards in Atherosclerosis Meds Deck (21):

CHD risk factors

-age and gender
-lipoprotein disorders
-fam history of premature CHD


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.

-40s in men; 50s in women
-women tend to have more events later in life and are less likely to survive the events


4 lipid categories and their associated with atherosclerotic CV risk

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


Blood pressure and CVD risk

-linear, direct relationship; lower is better!


DM and CHD

-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


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

-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


Traditional risk factors confer ______ risk of heart disease.



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

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)


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

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


Clinical identification of the metabolic syndrome

-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


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

-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


6 selective emerging risk factors for atherosclerosis

-inflammatory markers
-subclinical atherosclerosis imaging
-genetic variation


List 4 inflammatory markers looked at as markers of CVD risk

-they are not causal, but mark those at higher risk
-really on CRP is used clinically


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

-no, they are not causal! just markers


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

-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


Why is screening for calcification especially beneficial?

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


2 options for DNA variants that promote risk

1. gene may increase a risk factor which increases CAD OR
2. gene may directly influence MI without operative through risk factors


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

-uncovers new targets!! like ADAMTS7
-2/3 of them have no known connections to risk factors


Potential role of ADAMTS7 in atherosclerosis

-activated ADAMTS7 turns SMCs into a synthetic phenotypes


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

-ABO locus
-O seems to be protective bc no glycosylation occurs


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

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