Cardiovascular Disease Prevention Part 2 Flashcards
The goal of primordial prevention is ___ prevention. The goal of primary prevention is __ ___ disease event prevention. The goal of seondary prevention is ___ ___ prevention.
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.
cardiac rehabilitation is an example of ___ prevention
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.
These are the ABCDEs of atherosclerotic cardiovascular disease event prevention
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.
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.
Yin and Yang of atherosclerotic cardiovascular disease
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.
according to the SCORE evaluation, the lowest risk of CVD are those at the __ age with the least number of drivers of __ __.
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
7 things that drive vascular inflammation
- blood sugar levels
- cholesterol levels
- BP levels
- obesity
- physical inactivity/sedentary behaviours
- tobacco abuse
- 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.
T?F the SCORE risk model tool is good at prediciting events in individuals based on theira ge and comorbidities.
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.
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.
Outline the clinical even threshold
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.
Outline the blood pressure relationship with CVD event risk
even high-normal blood pressures creadily increase the cumulative incidence of CV events. Therefor, you dont need actual hypertension to increase your CVD risk
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?
, 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.
explain what genetics might cause someone to be suscpetible to CVD risk
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.
- 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.
- 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.
we measure Susceptibility to atherosclerosis by :
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