|
be established. Their SCD is both
their first and last cardiac event. 21
PATHOPHYSIOLOGY
MOST cardiovascular events are the
result of atherosclerosis in the major arteries( eg, the coronary arteries, the carotid arteries or intracerebral arteries). Atherosclerosis is an indo-
|
Nephron / CC BY-SA 3.0 / bit. ly / 41Letpc |
|||
lent process characterised by the | ||||
accumulation of lipid deposits( also | ||||
known as fatty plaques) in the subendothelial | ||||
space of medium- and | ||||
large-sized arteries( see figure 1). | ||||
Over time, these plaques expand and | ||||
are remodelled by inflammation, | ||||
fibrosis and local cellular proliferation | ||||
into advanced atherosclerotic | ||||
plaques, the latter characterised by a | ||||
fibrous cap over a necrotic lipid core. | ||||
Atherosclerotic plaques can press | ||||
into the lumen of arteries to limit | ||||
blood flow( known as stenosis) and | ||||
increase local shear pressure on the | ||||
endothelial surface. Cardiovascular | ||||
events are usually caused by plaque | ||||
rupture, where the endothelial surface | ||||
layer( cap) becomes denuded, | ||||
triggering the clotting cascade. This | ||||
can lead to blockage of the artery | ||||
( thrombosis) or distal embolisation | ||||
of the clot. | ||||
Box 1 lists the pathological | ||||
factors thought to influence the | ||||
increased rate of CVD in diabetes. 22 | ||||
In communicating this complex | ||||
pathobiology to our patients with |
T2DM, a simple metaphor like this can be used( see figure 2):“ Blood vessels function in our bodies just like the roads in our cities, allowing for a steady flow of traffic along |
Figure 1. Complex fibrofatty atherosclerotic plaque associated with stenosis in a coronary artery. |
|||
freeways and major arterial roads, and then venturing off into smaller and shorter streets until we reach our destination. Like any transport system, the health of the roads |
Box 1. Pathological factors influencing the increased rate of CVD in T2DM |
ASSESSING THE RISK OF CV EVENTS
ASSESS all people with T2DM for
their risk of having a cardiovascular
|
on this score, it is possible to categorise a patient’ s risk as low( less than 5 %), moderate( 5-10 %) or high risk( greater than 10 %). |
patients with high cardiovascular risk.
In some patients with a low or moderate risk score, a coronary artery
|
is critically important for maintaining healthy flow of traffic on them. If the surface of the road stays smooth, traffic can flow easily and get to where it needs to go. But over time, changes inevitably occur to the surface of any road due to fatigue and abrasion. A road will typically thicken in some places and become thinner in others, creating an uneven, bumpy surface. Underneath the surface, the packing of the soil beneath the pavement begins to weaken, while at the same time it is put under even more pressure by the stiffening upper crust. Importantly, these changes do not occur equally in all parts of the road. The sections |
• Greater plaque burden.
• Greater complexity of lesions.
• Greater coronary calcification.
• Greater extent of coronary ischaemia.
• More diffuse disease.
• More multivessel disease.
• More significantly affected vessels.
• Fewer normal vessels.
• Reduced coronary collateral recruitment.
• Reduced coronary vasodilatory reserve.
Source: Shaw JE et al 2017 22
flexible, just like our roads. This is
|
event, to direct the type and intensity of future management, including education, lifestyle change, pharmacotherapy and monitoring( see later). This should occur at the time of their diabetes diagnosis, although most patients will have had some consideration of their CVD risk previously because of shared antecedent risk factors( eg, obesity, prediabetes, metabolic syndrome). CVD risk is not usu-
This risk score incorporates patient data including age, sex, blood pressure, fasting lipid levels, smoking status, use of CVD medicines, postcode and history of AF. Specifically in people with diabetes, the Australian CVD Risk Calculator also incorporates additional risk factors including duration of diabetes, current level of glucose control( HbA1c), BMI, uACR and eGFR data to more accurately esti-
Many patients with T2DM will already have signs or symptoms of CVD or will have had a prior cardiovascular event.
|
calcium( CAC) score can be used to support consideration of a more intensive management strategy. 25 In particular, a CAC score of zero has a strong negative predictive value and generally excludes significant cardiovascular risk. In selected cases, an elevated CAC score can also be used to enhance treatment adherence. Assessment of carotid arteries using ultrasound can also be used to assess plaque burden. 26 However, these tests are not currently subsidised by Medicare for this purpose.
Screening for subclinical CVD( eg, exercise stress testing, stress echocardiogram) is not generally recommended in people with T2DM without
|
|
that easily become damaged and |
simply known as hardening of the |
any cardiac symptoms. Patients |
||
form potholes the fastest usually |
arteries. Our blood vessels may thin |
with sufficient CVD risk to warrant |
||
have the extra pressure of heavy |
in some places but thicken in oth- |
ally difficult to assess. Many patients |
mate cardiovascular risk. |
screening for this should already |
vehicles or have the added force of |
ers and may even start to bulge a lit- |
with T2DM will already have signs or |
It is understood that this CVD |
be intensively medically managed. |
braking and turning the corner. |
tle bit. This is known as plaque. Just |
symptoms of CVD or will have had |
risk calculator cannot incorporate all |
Nonetheless, all patients with T2DM |
“ Almost the same process of pro- |
as the softening of the road base |
a prior cardiovascular event. Others |
the risks identified in any individual |
and increased risk of CVD proba- |
gressive deterioration that happens |
ultimately leads to potholes, accu- |
will have heart failure or high-risk |
patient. Practitioners are therefore |
bly require an ECG, which will pro- |
to our roads also occurs in the arter- |
mulating cholesterol-rich plaques |
chronic kidney disease( denoted by |
encouraged to reclassify CVD risk, |
vide a valuable baseline for future |
ies and blood vessels of our body, where fatigue, abrasion and general wear and tear lead to changes known as atherosclerosis. As with the city roads, these changes do not occur equally in all parts of our |
in the walls of large arteries softens their resolve, and reduces their resistance to the stresses of regular use. If no pre-emptive maintenance is undertaken, the plaque becomes progressively unstable. |
a sustained eGFR less than 45mL / min / 1.73m 2, men with persistent urinary albumin-to-creatinine ratio [ uACR ] greater than 25mg / mmol, or women with persistent uACR greater than 35mg / mmol), which identifies |
particularly if the calculated risk is close to tipping into another category, based on other risk factors that may be present, including patient ethnicity, family history or serious mental illness( see box 2). Using this calcula- |
assessments.
FIRST CLINICAL PRESENTATION OF CVD
CVD is usually silent. Until suddenly,
|
blood vessels. Our largest blood |
And on one fateful day, a big load |
them as having a high risk of CVD. |
tor, most people with T2DM who are |
it is not anymore. Consequently, |
vessels, like our largest roads, are |
stresses an unstable arterial sur- |
In the remainder, it is recom- |
seen in Australian general practice |
ensure all patients at high risk of CVD |
under the greatest pressure and so |
face past its breaking point, eroding |
mended to undertake a formal |
are at high risk of CVD( see figure 4). |
( and their families) are familiar with |
are most vulnerable to atherosclerosis. Equally, in those sections of blood vessels where blood flow |
the surface and exposing the soft section underneath just like a pothole. This triggers a clot to form as a |
assessment of CVD risk using a risk calculator. 6 Endorsed by the RACGP, the Heart Foundation has developed |
Only a minority of patients with T2DM( less than one in eight) are likely to be estimated to have a low or |
the warning signs of a heart attack, stroke or limb-threatening peripheral vascular disease, and that they have a |
divides and needs to quickly turn a |
short-term repair job. But just like a |
the Australian CVD Risk Calculator |
moderate risk of CVD. Most of these |
proactive response plan that includes |
corner, the extra shear on the road |
single accident at peak hour on the |
( see figure 3), which generates a CVD |
patients will be under 40, where a |
an early and appropriate ambulance |
surface increases the wear and tear |
freeway, the flow of blood through |
risk score, representing the person’ s |
potentially long future of diabetes |
call. Delays in recognition and pres- |
and the risk of forming potholes. |
a damaged artery can quickly turn |
probability of dying or being hospi- |
ahead supports a more aggressive |
entation after an acute event can be |
As the years go by, the surface of our arteries also gets stiffer and less |
into a parking lot and nobody’ s going home.” 23 |
talised from a cardiovascular event within the next five years. 24, 25 Based |
approach to risk factor management identical to that recommended in |
the difference between life and death. A clear action plan of what to do in a |