Cardiovascular Disease Prevention Part 2 Flashcards

1
Q

The goal of primordial prevention is ___ prevention. The goal of primary prevention is __ ___ disease event prevention. The goal of seondary prevention is ___ ___ prevention.

A

The goal of primordial prevention is disease prevention. The goal of primary prevention is atherosclerotic cardiovascular disease event prevention. The goal of secondary prevention is recurrent event prevention.

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2
Q

cardiac rehabilitation is an example of ___ prevention

A

In secondary prevention, some or, not infrequently, several of these events have already happened in an individual and the goal is to prevent or minimize the number of recurrent atherosclerotic cardiovascular disease related events. As can be seen from this info graphic, optimal chronic atherosclerotic cardiovascular disease care, i.e., cardiac rehabilitation, can be very effective in reducing the morbidity and mortality associated with atherosclerotic cardiovascular disease.

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3
Q

These are the ABCDEs of atherosclerotic cardiovascular disease event prevention

A
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4
Q

For most populations and most individuals, ___ is the most important driver of vascular inflammation based on duration of exposure.

However, it is also important because the process usually results in the diminished ability of the ___ ___ to resist those inflammatory drivers with advancing age.

A

For most populations and most individuals, AGE is the most important driver of vascular inflammation based on duration of exposure. However, age is also important because the aging process usually results in the diminished ability of the vascular endothelium to resist those inflammatory drivers with advancing age.

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5
Q

Yin and Yang of atherosclerotic cardiovascular disease

A

the Ying and Yang of atherosclerotic cardiovascular disease is the interplay between Exposure to the drivers of atherosclerosis and Susceptibility to those drivers. More specifically, it’s about exposure to vascular inflammation and one’s ability, or inability, to buffer or resist that vascular inflammation.

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6
Q

according to the SCORE evaluation, the lowest risk of CVD are those at the __ age with the least number of drivers of __ __.

A

according to the SCORE evaluation, the lowest risk of CVD are those at the youngest age with the least number of drivers of vascular inflammation. Conversely, the highest risk individuals, men in the oldest age bracket with the greatest exposure to the principal drivers of vascular inflammation, is expressed in dark red in the upper right

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7
Q

7 things that drive vascular inflammation

A
  1. blood sugar levels
  2. cholesterol levels
  3. BP levels
  4. obesity
  5. physical inactivity/sedentary behaviours
  6. tobacco abuse
  7. mental health issues like depression and anxiety.

Vascular inflammation is ameliorated by things such as weight maintenance, Mediterranean diet, stress reduction, smoking cessation or abstinence, and regular physical activity and exercise.

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8
Q

T?F the SCORE risk model tool is good at prediciting events in individuals based on theira ge and comorbidities.

A

false. Unfortunately, these tools are not very good at predicting events in individuals. In general, virtually every atherosclerotic cardiovascular disease event risk prediction model over predicts events in high-risk populations and under predicts events in low risk populations. This has confounded practitioners and clinical epidemiologists for decades. Libraries exist dedicated to explaining these discrepancies

Not everyone in a high-risk population has atherosclerosis. Similarly, not everyone in a low-risk population is free of atherosclerosis. Arguably, it is the presence of atherosclerosis which is the principal arbitrator of event rates and not simply the presence or absence of an inflammatory vascular milieu. When viewed within this disease expression environment, and from this perspective, it becomes obvious that high-risk individuals may not experience events while seemingly low-risk individuals may well experience events.

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9
Q
A

As can be seen from this figure, the higher the LDL-cholesterol concentration, the greater the expression of atherosclerosis and the more vascular beds in which it is evident. Importantly, most of the LDL-cholesterol levels expressed in this figure are within the so-called normal range for North America. But, once again, this “Normal” is not normal. It is simply typical for first-world populations.

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10
Q

Outline the clinical even threshold

A

It assumes an average LDL-C level of 125 mg/dL, which you can now rapidly calculate as being approximately 3.1 mmol/L. This means that the clinical event horizon or temporal threshold for adverse atherosclerotic cardiovascular disease events is somewhere in the range of 124 LDL years. Although this is approximately half the value observed in persons with homozygous and heterozygous familial hypercholesterolemia, it is important to understand that this is likely a threshold value as opposed to a value at which the median number of affected individuals will have already experienced asymptomatic atherosclerotic cardiovascular disease event, when LDL-C/years of exposure is extremely high.

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11
Q

Outline the blood pressure relationship with CVD event risk

A

even high-normal blood pressures creadily increase the cumulative incidence of CV events. Therefor, you dont need actual hypertension to increase your CVD risk

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12
Q

As we have seen, the Exposure side of the atherosclerosis equation is relatively easy to understand. High levels of vascular toxins present over long periods of time, usually one’s entire lifespan, epitomize Exposure and the subsequent development of atherosclerosis, as a consequence of severe vascular inflammation.

that is only one side of the equation to developing CVD. What is vascular susceptibility to atherosclerosis?

A

, it means that one’s vascular age or arterial age is significantly greater than one’s chronological age. Stated another way, it means if one is 40 years old, one’s arteries actually look or behave like they are 60-70 years old

In most of these circumstances, the origin or origins of vascular susceptibility are likely genotypically and phenotypically determined. Fundamentally, they relate to the inability of the vascular endothelium to generate sufficient antioxidant buffering capabilities to suppress or prevent vascular inflammation leading to atherosclerosis.

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13
Q

explain what genetics might cause someone to be suscpetible to CVD risk

A

In most of these circumstances, the origin or origins of vascular susceptibility are likely genotypically and phenotypically determined.

Fundamentally, they relate to the inability of the vascular endothelium to generate sufficient antioxidant buffering capabilities to suppress or prevent vascular inflammation leading to atherosclerosis.

- Nitric oxide is the endogenous vasodilating substance produced mostly within the vascular endothelium. Higher levels of nitric oxide, secondary to enhanced production, diminished destruction, or both are associated with lower levels of atherosclerosis. Nitric oxide suppresses vascular inflammation.

  • The same can be said for the presence or relative absence of oxidized LDL-C receptors on vascular endothelial cells. Fewer so-called LOX receptors lead to less atherosclerosis. And individuals whose platelets have less affinity for their vascular endothelium tend to generate lesser amounts of vascular inflammation and lesser amounts of atherosclerosis.
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14
Q
  • Nitric oxide is the endogenous vasodilating substance produced mostly within the vascular endothelium. ___ levels of nitric oxide, secondary to ___ production, ____ destruction, or both are associated with lower levels of atherosclerosis. Nitric oxide suppresses vascular inflammation.
A
  • Nitric oxide is the endogenous vasodilating substance produced mostly within the vascular endothelium. Higher levels of nitric oxide, secondary to enhanced production, diminished destruction, or both are associated with lower levels of atherosclerosis. Nitric oxide suppresses vascular inflammation.
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15
Q

we measure Susceptibility to atherosclerosis by :

A

we measure Susceptibility to atherosclerosis by determining whether individuals have arterial imaging evidence or functional evidence of atherosclerosis. If we only look at the Exposure side of the atherosclerosis equation, we must wait until individuals develop actual symptoms of CVD

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16
Q

How does coronary artery calcium scoring measure susceptivility to atherosclerosis

A

As arteries age, they calcify, and as they calcify, they become harder and stiffer (and remember stiffer means higher blood pressures).

  • the more calcification an individual had in their coronary arteries, the more susceptible they seem to be to adverse atherosclerotic coronary artery disease events

This technique utilizes a low energy, low radiation CT scan of the chest to identify the presence or absence of coronary artery calcification. As demonstrated in the previous lecture on Risk Stratification, the amount of coronary artery calcification is directly and proportionally related to the probability that an individual will subsequently experience symptomatic atherosclerotic cardiovascular disease or death. The only normal CACS is zero.

17
Q

T/F a person must be symptomatic to undergo coronary artery calcium score for susceptibility testing

A

false. the true power of any other imaging or functional technique which identifies the presence of presymptomatic atherosclerosis, lies in a finding of zero or true normal. Individuals with a zero coronary artery calcium score have an excellent prognosis with a very low rate of subsequent symptomatic atherosclerotic cardiovascular disease events, even into very old age.

18
Q

most sensitive method of visualizing early atherosclerosis

A

CT coronary artery angiography is currently the most sensitive way to identify early atherosclerosis within the coronary arterial circulation. Unlike invasive coronary angiography which identifies only the vessel lumen, CT coronary angiography images the entire coronary arterial wall. This means that plaque that does not intrude into the vessel lumen and does not cause any apparent stenosis that would be appreciated by invasive coronary angiography, can be identified within the arterial wall as a very early marker of atherosclerosis

19
Q

cons of CT angiography

A
  • allergies to dye
  • renal dysfunction or diabetics cannot use this method of imaging
  • more invasive that calcium imaging.

, CACS (calcium screening) is the preferred screening procedure with less radiation and no intravenous or contrast dye complications. CTCA is more sensitive than CACS, or any other current imaging technique, in the identification of coronary atherosclerosis, but it is not always required.

20
Q

Carotid Intima Media Thickness (CIMT).

The advantage of this technique is that it is noninvasive and transmits no radiation.

what is the principle disadvantage?

A

principal disadvantage is that its prognostic value becomes less robust as we age. Finding a significantly elevated CIMT in someone in their second or third decade is highly predictive of symptomatic adverse atherosclerotic disease events in subsequent decades.

In other words, as we get older, CIMT simply becomes a marker of age as opposed to a robust predictor of risk. And, in the absence of obvious carotid artery stenosis or obstruction, its clinical utility diminishes.

21
Q

__ ___ ___. This is a functional imaging test which assesses the ability of arteries to dilate under stress.The basic idea is that arteries that are normal, i.e., free of atherosclerosis, will dilate in response to flow stress. The flow stress is generated by transiently obstructing blood flow in the brachial artery with the blood pressure cuff, and then suddenly releasing the cuff after 2 to 3 minutes. The sudden, massive increase in forearm blood flow should result in dilation of the brachial artery if it is normal. If the artery fails to dilate, or actually constricts, then this suggests early evidence of atherosclerosis.

A

Flow Mediated Vasodilation (FMD).

22
Q

Multi-Ethnic Study of Atherosclerosis (MESA). The model uses both risk factor ____ and imaging evidence of ____ to atherosclerosis to predict events.

A

Multi-Ethnic Study of Atherosclerosis (MESA). The model uses both risk factor Exposure and imaging evidence of Susceptibility to atherosclerosis to predict events.

The panel on the right demonstrates severe coronary atherosclerosis very likely as a combination of severe Exposure to the drivers of atherosclerosis in vascular inflammation, in conjunction with significant Susceptibility to those drivers and their attendant vascular inflammation.

23
Q

statin use to treat atherosclerosis for event prevention

A

for those persons who have a calcium score of zero, i.e., normal, statins are of no benefit.

for those individuals who have a coronary artery calcium score of less than 100, there is benefit but over more than a decade, the benefit is relatively modest.

when calcium scores are more than 100, and the benefit of LDL-C lowering therapy becomes immediately obvious benefit.

Treating people with documented atherosclerosis in an effort to reduce events is makes sense. The greater the risk, the greater the logic in treatment. Treating people without documented atherosclerosis in an effort to reduce atherosclerotic CVD events makes little or sense.

24
Q

The atherosclerosis Susceptibility Substudy Multi-Ethnic Study of Atherosclerosis (MESA) uses ___ __ ___ scoring to detect subclinical atherosclerosis as a measure of the Susceptibility as well as utilizing the traditional cardiovascular disease risk factor levels as a measure of __ to the drivers of atherosclerosis.

A

The atherosclerosis Susceptibility Substudy Multi-Ethnic Study of Atherosclerosis (MESA) uses coronary artery calcium scoring to detect subclinical atherosclerosis as a measure of the Susceptibility as well as utilizing the traditional cardiovascular disease risk factor levels as a measure of Exposure to the drivers of atherosclerosis.

25
Q

T/F: In clinical practice, patients whose vascular age far exceeds their chronological age should, in most circumstances, have their atherosclerotic cardiovascular disease risk factors treated to the physiologic and biochemical values proven to improve clinical outcomes.

A

True