Module 7: CV Risk Assessment Flashcards
Describe the main steps to completing a medical history form
- Initial interaction and history of ischemic vascular disease
- Dyslipidemia
- Smoking
- Elevated blood glucose or known diabetes
- High blood pressure (hypertension)
- Exercise
- Weight history
- Alcohol intake
- Psychosocial stress
- Other past history
- Medications
- Dietary assessment
How is premature CVD in a first degree relative defined as?
evidence of vascular disease or event in the patients’ FATHER or BROTHER before age 55, or MOTHER or SISTER before age 65
What to ask about family history?
- Are parents living? If dead, ask at what age and cause
- Ask if parents had any known heart disease or stroke. If they did, ask what age they knew of heart problem or stroke (to determine if it was premature)
- Ask if siblings had heart attack or stroke
- For all 1st degree relatives, ask what that person’s risk factors were e.g. smokers, high BO
What must be done during a Physical Examination to Identify Cardiovascular Risk
Measure:
- weight
- height
- BMI (kg/m^2)
- waist circumference
- narrowest point between the lower ribs (costal margin) and the top of the hip (iliac crest) - BP (sitting)
- if elevated at sitting, measure again supine after 5 mins of lying down - Pulse
- listen for carotid bruits or blockage in carotid arteries by placing stethoscope over carotid pulse
- feel ankle (posterior tibial) and foot (dorsalis pdis) pulses for presence and strength - Physical signs of inherited dyslipidemia
What is considered an elevated waist circumference
In Caucasians > 102 cm in men or > 88 cm in women; In Asians or South-Asians > 90 cm in men or > 80 cm in women
What does an elevated waist circumference suggest
indicates abdominal obesity and is one criterion of the metabolic syndrome and a major predictor of insulin resistance
What are the physical signs of inherited dyslipidemia?
- corneal arcus (white ring overlying outer edge of iris in the eye)
- xanthelasma (flat or raised yellow patches on eyelids or just below eyes)
- planar xanthomas of the palms (orange-brown palm creases)
- tendon xanthomas (thickening or nodules in the Achilles tendons and possibly the extensor tendons of the hands and patellar tendons)
- in the case of very high triglycerides, eruptive xanthomas (single or bunches or reddish-yellow bumps over the back, buttocks, hands, elbows or feet)
What is the Framingham Risk Score (FRS)
The # of points achieved is converted into an estimate of their risk for having a heart attack or coronary death over the next 10 yrs, also based on outcomes of the Framingham Heart Study
What characteristics is the Framingham Risk Score (FRS) based on?
- Age
- Total cholesterol leve
- Smoking status
- HDL cholesterol
- Systolic BP depending on whether they are treated or untreated for high BP
When are upward adjustments of the FRS made?
- premature vascular disease in first degree relatives
- presence of other risk factors including elevated lipoprotein (a) [Lp(a)] or high sensitivity C-reactive protein (hs-CRP)
Can the The Framingham Risk Score provide an estimate of the lifetime risk of coronary disease?
No
Criticism of the FRS?
- based on a study done mainly in white men, underestimating risk in women
- underestimating long term risk associated with genetic dyslipidemias or other family history
- not accurately estimating risk in ethnic groups other than Caucasians
What are unmodifiable risk factors for Atherosclerosis
age, gender, and heredity
In the INTERHEART study, what are some confirmed strong risk factors for MI?
hypercholesterolemia, low HDL, smoking, high blood pressure, and diabetes, psychosocial stress and abdominal obesity.
According to the INTERHEART, what is protective against myocardial infarction
daily consumption of fruits and vegetables, regular physical activity, and regular alcohol intake
INTERHEART concluded that known modifiable risk factors account for ____% of the population attributable risk in men, and ____% in women, for myocardial infarction
- Men: 90%
- Women: 94%
What category contributes the largest # of points when scoring an individual’s risk of coronary disease by the FRS
Age
How does aging contribute to atherosclerotic plaque?
Over a lifetime an individual’s blood vessels are exposed to a variety of factors that damage the single cell-thick layer of endothelium lining the vessels, setting up a repair and inflammatory process that initiates the formation of atherosclerotic plaques
What are some of the damaging factors that damage the single cell-thick layer of endothelium lining the vessels, setting up a repair and inflammatory process that initiates the formation of atherosclerotic plaques?
- molecules in food e.g. trans or saturated fats and high dietary cholesterol, elevated levels of harmful lipoproteins [low density lipoproteins (LDL) or remnant lipoproteins)
- harmful chemicals in cigarette smoke
- elevated blood glucose
- elevated BP
- cytokines released into the blood stream from sites of inflammation
Which gender has an earlier onset of CHD generally in the population?
Men
Why do men have an earlier onset of coronary heart disease generally in the population than do women?
protective effects of estrogen on the blood vessel wall and endothelium in wome
How does menopause affect the risk of CHD in women?
After menopause, the risk of CHD rises sharply in women and to the same level as seen in men in older age group
Why does the risk of CHD rises sharply in women after menopause?
protective effects of estrogen on the blood vessel wall and endothelium in women is lost when estrogen production in women by the ovaries stops at menopause
How can the protective effect of estrogen be lost in premenopausal women
if they are diabetic
Does estrogen still confer protection in women who smoke or have genetic dyslipidemia?
estrogen still seems to confer some protection in women who smoke or have genetic dyslipidemia until they go through menopause.
What is dyslipidemia?
elevated LDL cholesterol and reduced HDL cholesterol
What indicates high LDL-C?
elevated levels of LDL particles OR elevated level of the main protein of LDL, apolipoprotein B (apoB)
Why is high LDL-C bad?
accumulate in the artery wall and be taken up either as aggregated LDL or oxidized LDL by macrophages or smooth muscle cells in the artery, leading to foam cell formation and atherosclerotic lesions
How do risk factors that damage the blood vessel endothelium aggravate the negative effects of LDL-C?
even lower levels of LDL can pass through the endothelium more easily to accumulate and cause harm
in the presence of known vascular disease or several major CV risk factors, the recommended level of LDL cholesterol is set lower. Why?
Several major CV risk factors of can damage the blood vessel endothelium, thus even low levels of LDL can pass thru the endothelium more easily and accumulate and cause harm
Does LDL or triglycerides correlate more strongly with CHD risk
LDL
How does triglycerides aggravate the harmful effects of LDL?
- inc TGs make LDL more likely to be digested and smaller and denser, making the LDL more harmful. Thus, high TGs can be atherogenic if LDL or apoB lvls are also elevated.
level of HDL cholesterol in blood correlates _____ with risk for CHD
inversely
What are the protective actions of HDL?
- ability to remove excess cholesterol delivered to arterial cells by LDL
- induce relaxation of the artery wall
What did the INTERHEART Study say was the strongest modifiable predictor of risk for myocardial infarction
ratio of apoB/apoA-I (importance of the balance between delivery of cholesterol into arteries by LDL and its removal by HDL)
How to tell whether all a patient’s high cholesterol is due to environmental factors like diet or exercise level or due to genetic (inherited) factors
If total cholesterol lvls higher than 6.5 mmol/l, LDL cholesterol higher than 4.5 mmol/l, TGs higher than 3 mmol/l, or HDL cholesterol lower than 0.7 mmol/l likely genetic factors, not the patients fault, and frequently will not be corrected with lifestyle measures alone
Since lifestyle measures alone won’t correct inherited dyslipidemia, what should be done?
presence of inherited dyslipidemia indicates the need for EARLIER USE OF MEDS to modify lipid lvls when other risk factors are present or there is a family history of premature vascular disease
How does smoking cause inc risk of CHD?
Cigarette smoke contains a large # of harmful chemicals that become dissolved in blood upon inhalation and damage the lining of arteries. These chemicals and the damage to the endothelium itself lead to constriction of blood vessels and reduction of BF to tissues inc the heart
the long term risk to blood vessels of having been a smoker is mainly gone after how long?
2 years
Quitting smoking results in a large reduction in the Framingham Risk Score in ____ individuals especially
younger
How might stress inc risk of CVD?
stress results in inc blood CORTISOL and ADRENALINE lvls, and DAMAGE to the blood vessel ENDOTHELIUM and ATHEROGENESIS
How does hypertension inc risk of CVD/CHD?
Chronic high BP can lead to DAMAGE to ENDOTHELIUM and a THICKENING of artery WALLS, impaired relaxation of arteries, which puts additional stress on the heart to pump against the higher resistance
What is the risk of myocardial infarction in diabetics vs. non diabetics?
Individuals with diabetes show a 2-4 fold increase in risk of MI compared to non-diabetics
What are the abnormalities seen in diabetes?
- increased small, dense LDL, elevated TGs, and low HDL
- glycosylation of proteins due to chronic high glucose has been thought to play a role in this risk
How does abdominal obesity inc risk of CVD/CHD?
secrete more inflammatory factors that either themselves, or through secondary mechanisms, lead to damage to the blood vessel endothelium and increase risk for atherosclerosis
How to identifying a family history of vascular disease, particularly if it is premature?
- elevated LDL cholesterol or low HDL cholesterol levels
- strong genetic determinants of high blood pressure and diabetes that increase an individual’s risk of these when they are present in other family members
- if early heart disease in the family difficult to identify, look at elevated Lp(a), which can then be measured in the patient
What does lipoprotein a aka Lp(a) consist of?
composed of one molecule of LDL with an additional protein, apo (a), unrelated to apoA-I on HDL, attached to the apoB portion of LDL via a disulfide linkage
Where is Lp(a) produced
liver
An individual’s Lp(a) level is determined by
inherited factors
Do drugs like the statins that lower LDL, lower Lp(a)?
No
How can the risk of high Lp(a) be markedly reduced
if plasma LDL levels are lowered
What are the reasons for increased risk with high Lp(a)?
High Lp(a) inc the leakiness of blood vessel endothelium or inc a tendency to form blood clots
What is CRP?
C-reactive protein is a marker of inflammation in the body
Where and when is CRP produced?
Produced mainly by LIVER in response to inc levels of inflammatory molecules including tumor necrosis factor alpha and interleukin 6 released from sites of inflammation.
Sites of inflammation that release TNFa and IL-6 include what?
- developing atherosclerotic lesions in artery walls
- visceral fat in people with abdominal obesity
- inflamed tissues in people with rheumatologic diseases such as rheumatoid arthritis or lupus
- the lungs of people with chronic lung disease
Does elevated CRP level tell you the source or site of the inflammation?
No
How does elevated CRP inc risk of CHD?
CRP contributes to atherosclerosis or blood clotting by itself
What does hs-CRP stand for
high sensitivity C-reactive protein
When is high sensitivity CRP (hs-CRP) an appropriate test to request in individuals?
in individuals at intermediate risk of coronary disease based on FRS in whom finding a high CRP would lead to a change in their management, including the use of cholesterol-lowering treatment
Is routine measurement of CRP a currently recommended assessment of cardiovascular risk?
No
Name some potential biomarkers for atherosclerosis?
- oxidized LDL
- subfractions of LDL (small dense LDL)
- myeloperoxidase (a mediator of lipoprotein oxidation)
- markers of inflammation including IL-6
- lipoprotein-associated phospholipase A2
- Specific gene polymorphisms
- patterns of protein expression (proteomics) and metabolite production (metabolomics)
